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Channel: Blogs of Professor(Dr.) Pranab Kumar Bhattacharyya MD(calcutta.Univ) Pathology;

মাত্র এক বছরের মধ্যে সাতটি লাইফটাইম অ্যাচিভমেন্ট পুরস্কারে পুরস্কৃত অধ্যাপক ডঃ প্রবীন কুমার ভট্টাচার্য ।

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মাত্র এক বছরের মধ্যে সাতটি লাইফটাইম অ্যাচিভমেন্ট পুরস্কারে পুরস্কৃত অধ্যাপক ডঃ প্রবীন কুমার ভট্টাচার্য ।: নিজস্ব প্রতিবেদন : ২০২০ এর জানুয়ারি মাস থেকে ২০২১ সালের মার্চ মাসের মধে‍‍‍্য পুনরায় সাত...

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Indian icons education awards award 2021 life time achievements awards

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Life Time Achievements Awards of SCIENCE FATHER of ministry of corporate affairs Government of india

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 https://youtu.be/h2GXAfSBz48




Search Result of Publications of Bhattacharya PK in Pub Med ,NLM USA Bethesda http://www.ncbi.nlm.nih.gov/pubmed?cmd=search&term=Bhattacharya%20PK%5Bau%5D&dispmax=50

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1.
Barman B, Bhattacharya PK, Lynrah KG, Ete T, Issar NK.
J Clin Diagn Res. 2016 Jan;10(1):OD18-20. doi: 10.7860/JCDR/2016/17099.7151.
 Epub 2016 Jan 1.
2.
Zand B, Previs RA, Zacharias NM, Rupaimoole R, Mitamura T, Nagaraja AS,
 Guindani M, Dalton HJ, Yang L, Baddour J, Achreja A, Hu W, Pecot CV, Ivan C
, Wu SY, McCullough CR, Gharpure KM, Shoshan E, Pradeep S, Mangala LS, 
Rodriguez-Aguayo C, Wang Y, Nick AM, Davies MA, Armaiz-Pena G, Liu J,
 Lutgendorf SK, Baggerly KA, Eli MB, Lopez-Berestein G, Nagrath D,
 Bhattacharya PK, Sood AK.
J Natl Cancer Inst. 2016 Jan 26;108(6):djv426. doi: 10.1093/jnci/djv426.
PMID:
 
26819345
3.
Jamil MD, Hussain M, Lyngdoh M, Sharma S, Barman B, Bhattacharya PK.
J Neurosci Rural Pract. 2015 Oct-Dec;6(4):488-93. doi: 10.4103/0976-3147.169769.
4.
Rupaimoole R, Lee J, Haemmerle M, Ling H, Previs RA, Pradeep S,
 Wu SY, Ivan C, Ferracin M, Dennison JB, Millward NM, Nagaraja AS, 
Gharpure KM, McGuire M, Sam N, Armaiz-Pena GN, Sadaoui NC, 
Rodriguez-Aguayo C, Calin GA, Drapkin RI, Kovacs J, Mills GB,
 Zhang W, Lopez-Berestein G, Bhattacharya PK, Sood AK.
Cell Rep. 2015 Dec 22;13(11):2395-402. doi: 10.1016/j.celrep.2015.11.047. Epub 2015 Dec 10.
5.
Benito J, Ramirez MS, Millward NZ, Velez J, Harutyunyan KG, Lu H, Shi YX,
 Matre P, Jacamo R, Ma H, Konoplev S, McQueen T, Volgin A, Protopopova M,
 Mu H, Lee J, Bhattacharya PK, Marszalek JR, Davis RE, Bankson JA, Cortes
 JE, Hart CP, Andreeff M, Konopleva M.
Clin Cancer Res. 2016 Apr 1;22(7):1687-98. doi: 10.1158/1078-0432.CCR-14-3378. Epub 2015 Nov 24.
PMID:
 
26603259
6.
Kashyap R, Palai T, Bhattacharya PK.
Bioprocess Biosyst Eng. 2015 Dec;38(12):2417-26. doi: 10.1007/s00449-015-1478-4.
 Epub 2015 Oct 5.
PMID:
 
26437965
7.
Whiting N, Hu J, Shah JV, Cassidy MC, Cressman E, Millward NZ, Menter 
DG, Marcus CM,Bhattacharya PK.
Sci Rep. 2015 Aug 4;5:12842. doi: 10.1038/srep12842.
8.
Lai SY, Fuller CD, Bhattacharya PK, Frank SJ.
Clin Cancer Res. 2015 Nov 15;21(22):4996-8. doi: 10.1158/1078-0432.CCR-15-1214. Epub 2015 Jul 31.
PMID:
 
26232369
9.
Bhattacharya PK, Barman B, Roy A, Jamil M, Lyngdoh M, Mishra J.
Springerplus. 2015 Jun 30;4:302. doi: 10.1186/s40064-015-1081-9. eCollection 2015.
10.
Palai T, Kumar A, Bhattacharya PK.
Enzyme Microb Technol. 2015 Mar;70:42-9. doi: 10.1016/j.enzmictec.2014.12.010. Epub 2014 Dec 27.
PMID:
 
25659631
11.
12.
Lee Y, Zacharias NM, Piwnica-Worms D, Bhattacharya PK.
Chem Commun (Camb). 2014 Nov 7;50(86):13030-3. doi: 10.1039/c4cc06199c.
13.
Padmanabhan P, Young SM, Henstridge M, Bhowmick S, Bhattacharya PK, Merlin R.
Phys Rev Lett. 2014 Jul 11;113(2):027402. Epub 2014 Jul 8.
PMID:
 
25062229
14.
Khandekar DC, Palai T, Agarwal A, Bhattacharya PK.
Bioprocess Biosyst Eng. 2014 Dec;37(12):2529-37. doi: 10.1007/s00449-014-1230-5.
 Epub 2014 Jun 19.
PMID:
 
24938994
15.
Mehta Y, Gupta A, Todi S, Myatra S, Samaddar DP, Patil V, Bhattacharya PK,
 Ramasubban S.
Indian J Crit Care Med. 2014 Mar;18(3):149-63. doi: 10.4103/0972-5229.128705.
16.
Palai T, Kumar A, Bhattacharya PK.
Enzyme Microb Technol. 2014 Feb 5;55:40-9. doi: 10.1016/j.enzmictec.2013.12.003.
 Epub 2013 Dec 13.
PMID:
 
24411444
17.
Bhattacharya PK, Bhattacharya U, Bhattacharya R, Bhattacharya R,
 Bhattacharya S, Bhattacharya R, Mukherjee D, Mukherjee O, Mukherjee D, 
Barman DR, Das S, Dey A, Biswas RR, Sarkar S.
Indian J Hematol Blood Transfus. 2012 Sep;28(3):189-90. doi: 10.1007/s12288-011-0139-2.
 Epub 2012 Apr 8. No abstract available.
18.
19.
Cassidy MC, Chan HR, Ross BD, Bhattacharya PK, Marcus CM.
Nat Nanotechnol. 2013 May;8(5):363-8. doi: 10.1038/nnano.2013.65. Epub 2013 May 5.
PMID:
 
23644571
20.
Palai T, Bhattacharya PK.
J Biosci Bioeng. 2013 Jun;115(6):668-73. doi: 10.1016/j.jbiosc.2012.12.014. Epub 2013 Jan 18.
PMID:
 
23333643
21.
Palai T, Mitra S, Bhattacharya PK.
J Biosci Bioeng. 2012 Oct;114(4):418-23. doi: 10.1016/j.jbiosc.2012.05.012. Epub 2012 Jun 12.
PMID:
 
22695078
22.
Chakrabarti S, Bera M, Bhattacharya PK, Chakrabarty D, Manna AK, Pathak S, Maiti K.
J Indian Med Assoc. 2010 Dec;108(12):833-6.
PMID:
 
21661459
23.
Sarma JB, Bhattacharya PK, Kalita D, Rajbangshi M.
Indian J Med Microbiol. 2011 Jan-Mar;29(1):22-7. doi: 10.4103/0255-0857.76519.
PMID:
 
21304190
 
Free Article
24.
Mandowara A, Bhattacharya PK.
J Environ Manage. 2011 Jan;92(1):121-30. doi: 10.1016/j.jenvman.2010.08.015.
 Epub 2010 Sep 16.
PMID:
 
20843596
25.
Bhattacharya PK.
Natl Med J India. 2006 Sep-Oct;19(5):265-6. No abstract available.
PMID:
 
17203682
26.
27.
Sharma A, Thampi SP, Suggala SV, Bhattacharya PK.
Langmuir. 2004 May 25;20(11):4708-14.
PMID:
 
15969186
28.
29.
Water exclusion reaction in aqueous media: nitrone formation and 
Chatterjee A, Maiti DK, Bhattacharya PK.
Org Lett. 2003 Oct 16;5(21):3967-9.
PMID:
 
14535755
30.
Bhattacharya PK, Cha J, Barton JK.
Nucleic Acids Res. 2002 Nov 1;30(21):4740-50.
31.
Lenihan AS, Gurudev Dutt MV, Steel DG, Ghosh S, Bhattacharya PK.
Phys Rev Lett. 2002 Jun 3;88(22):223601. Epub 2002 May 16.
PMID:
 
12059418
32.
Delaney S, Pascaly M, Bhattacharya PK, Han K, Barton JK.
Inorg Chem. 2002 Apr 8;41(7):1966-74.
PMID:
 
11925195
33.
Bhattacharya PK, Barton JK.
J Am Chem Soc. 2001 Sep 12;123(36):8649-56.
PMID:
 
11535068
34.
35.
Bhattacharya PK, Pappelis AJ, Lee SC, BeMiller JN, Karagiannis CS.
Mech Ageing Dev. 1996 Dec 20;92(2-3):83-99.
PMID:
 
9080390
36.
Bhattacharya PK, Pappelis AJ, Karagiannis CS.
Mech Ageing Dev. 1996 Jul 5;88(1-2):83-94.
PMID:
 
8803925
37.
Mitra N, Mukherjee L, Bhattacharya PK, Moulik SP.
Indian J Biochem Biophys. 1996 Jun;33(3):206-12.
PMID:
 
8828291
38.
Iosseliani DG, Koval AN, Bhattacharya PK.
Int J Card Imaging. 1994 Jun;10(2):155-9.
PMID:
 
7963755
39.
Mitra N, Mukhopadhyay L, Bhattacharya PK, Moulik SP.
Indian J Biochem Biophys. 1994 Apr;31(2):115-20.
PMID:
 
7523281
40.
Bhattacharya PK, Karagiannis CS, Pappelis AJ.
Mech Ageing Dev. 1994 Jan;73(1):1-7.
PMID:
 
8028393
41.
Kar S, Kar K, Bhattacharya PK, Ghosh DK.
Antimicrob Agents Chemother. 1993 Nov;37(11):2459-65.
42.
Mukherjee J, Bhattacharya PK, Lahiri TK, Samaddar JC, Mehta R.
J Indian Med Assoc. 1993 Aug;91(8):202-3.
PMID:
 
8245491
43.
Iosseliani DG, Inoyatova II, Bhattacharya PK, Yarlikova EI.
Int J Cardiol. 1993 Aug;41(1):49-57.
PMID:
 
8225672
44.
Turley PJ, Wallis CR, Teitsworth SW, Li W, Bhattacharya PK.
Phys Rev B Condens Matter. 1993 May 15;47(19):12640-12648. No abstract available.
PMID:
 
10005459
45.
Borroff R, Merlin R, Pamulapati J, Bhattacharya PK, Tejedor C.
Phys Rev B Condens Matter. 1991 Jan 15;43(3):2081-2087. No abstract available.
PMID:
 
9997477
46.
Biswas D, Bhattacharya PK, Singh J.
Appl Opt. 1990 Sep 20;29(27):3900-4. doi: 10.1364/AO.29.003900.
PMID:
 
20577311
47.
Misra S, Sanyal T, Sarkar D, Bhattacharya PK, Ghosh DK.
Biochem Med Metab Biol. 1989 Dec;42(3):171-8.
PMID:
 
2597432
48.
Remillard JT, Wang H, Webb MD, Steel DG, Oh J, Pamulapati J, 
Bhattacharya PK.
Opt Lett. 1989 Oct 15;14(20):1131-3.
PMID:
 
19753078
49.
50.
Remillard JT, Wang H, Steel DG, Oh J, Pamulapati J, Bhattacharya PK.
Phys Rev Lett. 1989 Jun 12;62(24):2861-2864. No abstract available.
PMID:
 
10040110

Refrences of Pranab Kumar Bhattacharya of his Published article in Near Death Experiences in the Book

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Reference and Citation of Pranab kumar Bhattacharya on his publication Is there Science Behind the  Near Death Experence : Does Human Conciousness survives after death? Published  in Journal Annals of Tropical Medicine and Public Health of AHRO  2013; 6 (2) 15   in the book Understanding Dying, Death, and Bereavement by authors  By Michael R. Leming, George E. Dickinson  page no 146 and in page no 152

Understanding Dying, Death, and Bereavement by authors 

By Michael R. Leming, George E. Dickinson

2] Other References of the same article  by Payton Yerke Professor ChristensenEnglish 2010 
21 October 2014   at page no 3 and 12  on his article The Science of Ghosts and the Essence of the Human Soul


3] Near-death experiences and science Written by Cornelia Fitsch
The pathologist PK Bhattacharya portrays that up to 48 percent of adults and up to 85 percent of children have at least once been in their lives a near-death experience .5 as many sufferers the NDE experience as a dream, and the influence of the temporal lobe can forget the experience (a region of the brain), the actual number of people who were so already exposed to an experience could be higher, and perhaps even at 100 percent figure.6 Today report especially those who suffered a cardiac arrest and was resuscitated by NDEs.7 However have more than 50 percent of patients who report NDEs, suffered at this time no cardiac arrest and not in acute danger to life befunden.8 near-death experiences are angesehen.9 by some scientists as proof of the immortality of the soul and as a proof of a 'life' after death


Scientific explanations


Despite many studies on near-death experiences, there is still no single theory, thereby causing this phenomenon. Scientists were able to show in 2002 that the electrical stimulation of a convolution in the side and back of the brain, the angular gyrus, OBEs trigger kann.11 The same could for the right temporal lobe (a brain region approximately above the right ear) proved werden.12 Bhattacharya presents However, this theory towards that werden.13 triggered when electrical stimulation is not the positive feelings, usually accompany NDEs, but fear, sadness and loneliness another explanation for OBEs could the so-called sleep paralysis, a part of REMPhase, sein.14 also for the NDE phenomenon of tunneling experience, there are scientific hypotheses. It could be a malfunction in the eye; as it would be possible that a lack of supply of the eye leads to oxygen and blood to those typical light phenomena. brain disease

Please Click on URL

1] https://books.google.co.in/books?id=gKCaBAAAQBAJ&pg=PA145&dq=pranab++bhattacharya&hl=en&sa=X&ved=0ahUKEwirmeCnzpXOAhUFT48KHbkCDFAQ6AEIJzAC#v=onepage&q=pranab%20%20bhattacharya&f=false

 2] https://www.suu.edu/hss/english/scriblerian/fall14/pdf/2010-argumentative-2nd-payton-yerke.pdf
 3] http://www.univie.ac.at/unique/uniquecms/?p=4444

Will You please like To Predict who are persons may be to win 2016 Nobel Prizes The date and time for the announcements of the Nobel Prizes -2016 are now set

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Will You please like To Predict who are persons may be to win 2016 Nobel Prizes The date and time for the announcements of the Nobel Prizes are now set.
 for Announcements of the 2016 Nobel Prizes . Please click onhttp://www.nobelprize.org/…/…/prize_announcements/index.html
PHYSIOLOGY OR MEDICINE - Monday 3 October, 11:30 a.m. at the earliest
PHYSICS - Tuesday 4 October, 11:45 a.m. at the earliest
CHEMISTRY - Wednesday 5 October, 11:45 a.m. at the earliest
PEACE - Friday 7 October, 11:00 a.m.
ECONOMIC SCIENCES - Monday 10 October, 11:45 a.m. at the earliest
LITERATURE - The date will be set later.
Times listed are local time in Sweden (CET).
http://www.nobelprize.org/mediaplayer/index.php?id=1459
Please note it also care fully that it is almost impossible to predict correct actually who will win the Nobel Prizes , because the nomination process is shrouded in darks for at least next 50 years . How ever one may just guess and comment on my predictions for 2016 Nobel prizes are like these . one may surely comment on this with proper justifications why he/she suggesting or defying my predictions


Who Deserves a Nobel Prize?

NOBEL PRIZE FOR PHYSIOLOGY OR MEDICINE
I find at present three possibilities in the following domains as possible candidates -:
A]" For TKI, Immantinib -: Prof Dennis J salmon 2] Prof NIcholus Lydon 3] Dr Bram J Duker 4]Charris L SAwers for Imantinib use is my first choice for several years together but not yet came truth
The Imatinib, drug is a staple of cancer treatment around the world, and continues to impress with it’s high success rate in treating CML patients. According to my study, the five year survival rate for CML patients before Imatinib was 30%. The survival rate for patients on imatinib is today 89%.[ please click on article at URLhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3422381/ [ titled as "Next Generation Therapy in Chronic Myeloid Leukemia" aauthors arePranab Kumar Bhattacharya,corresponding author1,2 Upasana Bhattacharya,1 Rupak Bhattacharya,3 Ritwik Bhattacharya,3 Soumyak Bhattacharya,3 Rupsa Bhattacharya,3 Dalia Mukherjee,3 Oindrila Mukherjee,4 Debasis Mukherjee,4 Debasis Roy Barman,1 Soma Das,1 Anuradha Dey,1 Ranu Roy Biswas,1 and Surajit Sarkar5
[1Department of Pathology & Hematology, Calcutta School of Tropical Medicine, C.R. Avenue, Kolkata, 73 WB India]
Additional article information for this  Article information
Next Generation Therapy in Chronic Myeloid Leukemia
Pranab Kumar Bhattacharya, Upasana Bhattacharya, [...], and Surajit Sarkar
Additional article information
TKIs Imatinib is an established first-line therapy CP of CML. Before Imatinib therapy, IFN-alpha was a treatment option for CML because it induced durable remissions in a subset of CP patients. However, because of IFN toxicity, and its limited and unpredictable efficacy, IFN-alpha was displaced by Imatinib, with its limited toxicity and marked efficacy in the treatment of most CML patients. Imatinib has limitations, but the 5-year survival rate with Imatinib is approx. 89% compared with Interferon and Cytarabin (70%). About 15–20% CML become resistant to Imatinib, and the resistance is found in association with a BCR/ABL mutation T315I or with G250E mutations. Treatment of Imatinib-resistance CML is thus a challenge in clinical hematology. In addition, clinical evaluation of Imatinib has shown adverse effects, such as fatigue, severe nausea, vomiting, oedema, fluid retention, muscle cramps, muscular skeletal pain, and cutaneous disorders. With the prolonged survival time in CML, which with Imatinib is a median 40 months, BCC, SCC, melanoma (30% cases), breast cancer (the authors have found 1 case), prostate cancer (1 case), GI cancer, GU bladder cancer including RCC, a few pancreatic and cholangiocarcinomas, and metastatic carcinoma of unknown origin have also been reported in various literature [1]. These investigators concluded that increased rates of cancers were found at a large range of sites and there was immune deficiency, regardless of the mechanism of deficiency. There have also been scattered reports of co-existence of CML with other lymphoid malignancies such as CLL and multiple myeloma [1, 2]. It has also been shown that heart failure occurs in 1 in 1,000 patients receiving Imatinib, and that it also alters bone metabolism. Imatinib costs more than the Interferon + Cytarabin combination. The effects of Imatinib (as well as other kinase inhibitors) on leukemic stem or initiating cells are limited, and so it has been advisable to take a low dose of Imatinib over a long period.
Now, the second generation TKIs, such as Dasatinib and Nilotinib, have appeared. A unique spectrum of adverse events has occurred and been reported for both these TKIs [3, 4]. For Dasatinib-treated patients, the occurrence of pleural effusion has been a clinical challenge, especially when pleural effusion becomes recurrent or is accompanied by pericardial effusion, pulmonary hypertension, or an infection. Also, potential risk factors such as a pre-existing cardiac disease, arterial hypertension, or auto-immune disorders have been described for these TKIs. Several non-hematologic adverse events have been described for Dasatinib, including diarrhea, skin rash, bleeding, viral re-activation, and sometimes also many opportunistic infections, which have been reported in patients receiving Dasatinib at a dose of 270 mg daily. Nilotinib-treated patients have developed increases in pancreatic enzymes, bilirubin, and fasting glucose levels. Other non-hematologic adverse events of Nilotinib include diarrhea, folliculitis-like skin rash, and bleeding. There are a few reports of severe peripheral arterial occlusive disease (PAOD) and other vascular occlusive events (infarction) in patients receiving Nilotinib [3, 4]. Several of these patients developed a rapidly progressive and highly resistant form of PAOD after switching from Imatinib to Nilotinib [3, 4]. The question is whether patients, who had a complete molecular response (CMR or MCyR) to Imatinib or Imatinib in combination with Interferon, could safely stop drug treatment? What should be done with relapses? Do TKIs act then? SCT is still the treatment for CML that is considered to be curative in patients with AP or blast-crisis CML. Other choices which are still in clinical trial include a vaccine called CMLVAX100 which is given along with Imatinib to see if there is an increase in its effectiveness. Research into this and other cancer vaccines is continuing. The oral agent AP24534 also appears to have some activity independent of Bcr-Abl mutation. Cortes and colleagues [5] conducted a trial of AP24534 in patients with refractory CML and other hematologic malignancies. This agent inhibits survival of cell lines expressing Bcr-Abl variants at an inhibitory concentration of less than 40 nM. It also inhibits Flt-3 and c-Src. And this agent has the advantage of being orally administered
Indian J Hematol Blood Transfus. 2012 Sep; 28(3): 189–190.
Published online 2012 Apr 8. doi: 10.1007/s12288-011-0139-2
PMCID: PMC3422381 This drug has also been found useful in certain gastrointestinal cancers like GIST Lung cancer and is currently being studied as a treatment for stroke and diabetes.
B ]  My second choice May be For CRISPR -: Emmanuelle Charpentier and Jennifer A. Doudna according myself they may be  potential candidates for Medicine /or chemistry winners for developing a method to edit genes known as CRISPR/. The technique holds potential to cure deadly genetic diseases including cancers by increase apoptosis.

C] Alexander Y. Rudensky, Shimon Sakaguchi, and Ethan M. Shevach my third choice for in medicine for discovering how immune cells called regulatory T cells(Treg ) and a protein called Foxp3 works together
For physics Prize -:
,. My long years Predictions [after i was correct on  professor peter higgs for Higg's particle and quantum teleportation] were and still it is prof. Alan Guth (b. 1947). In 1979 or a little back, Prof Alan Guth developed the theory that finally became known as “cosmic inflation theory of Big Bang  and he first published his work in 1981 in journal Physics review and next in journal Nature. Cosmic inflation is the idea that at a very early time (approximately 10-36 s. after the Big Bang) the universe passed through a phase of exponentially rapid expansion. Alun Guth hypothesized that this expansion was driven by a positive vacuum energy density (negative vacuum pressure). In 2006, an orbiting telescope—the Wilkinson Microwave Anisotropy Probe (WMAP)—provided observational evidence corroborating the cosmic inflation hypothesis though the Nature of WIMP not clear before physicist.
Alain Aspect (b. 1947) for his hypothesis on correctness of Bell’s Theorem, stating that either the realism condition or the locality condition on elementary particles must fail. His Hypothesis that a light source can be split into two beams, which are then if passed through polarisers with randomized settings. When the polarities of the two beams were subsequently measured, they were found to be statistically correlated. This finding has been interpreted to mean that the locality condition is indeed violated (quantum non-locality is real). Today, Aspect is a Research Director at the prestigious National Center for Scientific Research (CNRS), in Paris.
My fourth choice is that I may probably like to see that the prize may go to the entire LIGO collaboration, considering that there were thousands of scientist involved in demonstrating Einstein’s predictions. or for the Graviton particle as gravity as a particle instead a force. But I do also understand that the Nobel committee (Royal Swedish academy of Science) will prefer to award it to maximum three individuals, and there are 3 who are kind obvious. However 2016 might be rather too early for this Nobel award, considering the nominations were due by Feb 1,2016 but probably someone knew the gravitational waves discovery was imminent and nominated them much later .yet or  to   P. A. R. Ade, K.W. Yoon,C. L. Wong, and /or as a team  for  BICEP2 or Detection of B-Mode Polarization at Degree Angular Scales by BICEP2 experiment  for  first gravitational wave published in PHYSICAL REVIEW LETTERS  PRL 112, 241101 (2014)20 JUNE 2014 
Nobel prize in Literature-:
Since 1901, the Nobel Prize in Literature has been awarded annually to an author only from any country written in any languages who has, in the words from the will of Alfred Nobel, produced "in the field of literature the most outstanding work in an ideal direction". Though individual works are sometimes cited as being particularly noteworthy, here "Work" refers to an author's work as a whole. The Swedish Academy decides who, if anyone will receive the prize in any given year. The academy announces the name of the chosen laureate in early October. It is one of the five Nobel Prizes established by the will of Alfred Nobel in 1895; the others are the Nobel Peace Prize, Nobel Prize in Chemistry, Nobel Prize in Physics, and Nobel Prize in Physiology or Medicine.http://nobelprize.org/nobel_prizes/literature/nomination/. Selection of Nobel Laureates
The Swedish Academy http://www.svenskaakademien.se/en is responsible for the selection of the Nobel Laureates in Literature, and has 18 members. The Swedish Academy was founded in 1786 by Swedish King Gustav III. The Academy is composed of 18 members whose tenure is for life long. Known as "De Aderton" (The Eighteen), current members of the Academy include distinguished Swedish writers, linguists, literary scholars, historians and a prominent jurist. The Nobel Committee for Literature is the working body that evaluates the nominations and presents its recommendations to the Swedish Academy, and comprises four to five members.
Who is eligible for the Nobel Prize in Literature?
The candidates eligible for the Literature Prize are those nominated by qualified persons (see below) who have received an invitation from the Nobel Committee to submit names for consideration. Other persons who are qualified to nominate but have not received invitations may also submit nominations. No one can nominate himself or herself . In months September – Academy members confer. Having read the work of the final candidates, members of the Academy discuss the merits of the different candidates' contributionsThe Nobel Committee for Literature 2016 Members are Per Wästberg (Chairman) FD, Writer Kjell Espmark FD, Emeritus Professor, Writer Anders Olsson Professor, Writer Kristina Lugn Writer Horace Engdahl
Professor, Writer Associate Members Sara Danius Professor, Writer Katarina Frostenson
Writer https://www.nobelprize.org/…/l…/prize_awarder/committee.html
the Nobel Prize for Literature could conceivably go to anyone and the Nobel Committee often gives the award to writers who are rather relative unknowns in the national or international community based on what is known as odds ratio? Several odds are there. one such Prominent are Ladbrokes’s odds which are probably based on betting actions for winning the prize, but not the reality one The more people in a given place bets on a particular writer for winning the Nobel Prize , the shorter becomes the odds. The shorter the odds, just because a writer is a favorite of the weirdos who spend their hard-earned money betting on cultural prizes and of course obvious that odds doesn’t mean that that same writer is a favorite for the Nobel Swedish Academy always. According me based on odds
one of such is Japanese novelist and spaghetti-enthusiastHaruki Murakami ( his odds in japan 5/1 to 6/1 to highest odd in US 500/1), He's /was for last few years together probably one of the most decorated possible candidates having won nearly every major literary prize in Japan, the Jerusalem Prize, the Franz Kafka Prize, the International Catalunya Prize, the Welt-Literaturpreis, World Fantasy Award, and the Hans Christian Andersen Literature Award but not the Pulitzer award yet . So what ? He has honorary Doctorates of Letters from Yale, Princeton, Tufts, Hawaii. He's politically outspoken in both his works and in person and as of late has taken to criticizing Japan's nuclear programs and their ongoing disputes with China over the Senkaku islands.
Another such candidate may be American writersJoyce Carol Oates (highest odd from 8/1 in ER to 1600/1 US and or Mr Philip Roth currently all have 8/1 to 10/1 odds to maximum 1/800 may be favourite to committee . Bt my favorite isMilan Kunderasince 2019 and he has highest odd 50/1in ER US lowest odd. Kundera was born in Brno, in what was then Czechoslovakia and is now the Czech Republic. He studied BA in literature at the Charles University in Prague, but switched to film studies. After graduation, he taught at the Institute for Advanced Cinematographic Studies. Kundera joined the Communist Party in 1948, but was expelled in 1950 for “anti-party activities”—an incident which formed the basis for his first novel, The Joke, published in Paris in 1967 (I read it .) He was readmitted to the Communist party in 1956, and expelled again in 1970. In 1975, he went into exile in France. In 2008, he was accused by French govt of having worked for the Communist secret police—a charge he vehemently denies. Three remarkable early novels—The Joke, The Farewell Waltz (1972), and Life Is Elsewhere(1973), together with a book of short stories (Laughable Loves[1969])—established Kundera as a distinctive, tragicomic voice at the intersection of the existentialist novel and the theater of the absurd. However, it was The Immortality(the book impressed me) , Book of Laughter and Forgetting (1978) and The Unbearable Lightness of Being (1984) that catapulted him onto the international stage. In these books, the author inserts his characters—with their typical human obsessions concerning aldurism extramarital love pleasure vigorous sex, death, politics all mixed and the philosophy meaning of life—into the high drama of recent Czech history. In addition to his nine novels (the last four of which were composed directly in French), Kundera has written verse, plays, and several volumes of literary sexual and philosophical reflection. Illuminating both his fiction and his essays is a vision of the novel as the best means of revealing the many-sided truth about the human predicament.
For Peace Prize -:
Thousands of people are eligible to submit nominations for the Peace Prize. The Norwegian Nobel committee typically receives as more than 200 nominations, according to the Associated Press.
 If one goes through excerpt from the will of Alfred Nobel for peace prize[ urlhttp://www.nobelprize.org/alfred_nobel/will/ ] it is said"---- one part to the person who shall have done the most or the best work for fraternity between Nations of standing armies or for holding and promotion of peace Congress The prizes for physics and chemistry shall be awarded by the Swedish Academy of Sciences; that for physiology or medical works by the Karolinska Institute in Stockholm; that for literature by the Academy in Stockholm, and that for champions of peace by a committee of five persons to be elected by the Norwegian Sorting. ". So far to my knowledge 96 peace Nobel prize awarded since 1901-2015 and amongst 103 individuals awarded Nobel peace prize , of which 65 awarded to single one Laureate ;02 prize shared among three person; 26 organization were given It was not awarded on 19 occasions: as in 1914-1916, 1918, 1923, 1924, 1928, 1932, 1939-1943, 1948, 1955-1956, 1966-1967 and 1972. Three persons were nominated several occasions but evaluation came as no.They were 1) Joseph Stalin in 1945;1947; 1948 2) Mahatma Gandhi for 1937;1938;1939;1948.he is however called missing NL 3) Adlof Hitler was nominated in 1939 [http://www.nobelprize.org/nobel.../facts/peace/index.html ] .Leo Tolstoy; EMRemorque!; Pablo Casals and Nicholas Roerich were also nominated several occasions but not awarded who really deserved peace prize. From India many personal were nominated ( from 1901- 1964 total valid nominated for which expert committee evaluated their candidature)of which Jawharlal Nehru was nominated on several occasions (1950; 1957; 1953;1954;1955;1960;1961)but denied. Other Indians nominated were from Bengal Hari mohon banerjee ( 1934;1936;1937;1939 1941) ; sri Arobindo (1950 ); Sanjib chaudhury Bengal Rau;Raja manikan .Sarbapalli Radhakrisnan was nominated in following years (1951;1953;1956; 1957; 1958;1959;1960;1961;1963;1964) besides them vinoba Bhave was also nominated sevetal occasions.Maria Montessori who fought for children education and her educational methods still followed by many English median schools of india was nominated several occasions but denied https://www.facebook.com/nobelprize/photos/a.164901829102.119895.81239734102/10153912234954103/?type=3&theater] 

  This year my choice For Peace Nobel  Prize

 References  1] : "Who Deserves a Nobel Prize? Post your message". Nobelprize.org. Nobel Media AB 2014. Web. 1 Oct 2016. <http://www.nobelprize.org/nobel_prizes/who-deserves.html?pageNum_GetGreetings=2&totalRows_GetGreetings=399





For the relativistic formula for the kinetic energy, ordinary subatomic particles are confined in an infinite well of velocity of Light [c]. So it may be however considered that Faster than Light Particle (FTL) speed phenomenon may exist in this Universe. On the other hand to day even physicists and...
OPENSCIENCEONLINE.COM







What is the 2nd Quantum Revolution? Reference of 22. (1) in the article Blogs of Professor(Dr.) Pranab Kumar Bhattacharyya MD(cal.Univ) Pathology;

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Boston Commons High Tech Networkwhat-is-the-2nd-quantum

 




The cosmic Web,the seed of galaxies WHIMDarkenergy

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comment 

 comments no 3 published  

Is the universe a sponge?

Authors are

Rupak Bhattacharya Professor( Dr.) Pranab kumar Bhattacharya Upasana Bhattacharya Ritwik Bhattacharya Rupsa Bhattacharya Dalia Mukherjee Ayeshi Mukherjee Debasis Mukherjee Hindole Banerjee Runa Mitra


Universe consisted of mysterious Dark energy (70%), Dark matter(25%) and that make up now 95% of matter in the universe which revel it self as gravity. Enormous filaments and blobs of dark matter in early universe condensed as universe condensed. Within the cosmic webs, all galaxies, stars, planets were next created. Galaxies are not dotted randomly throughout universe but are generally either concentrated in groups or in clusters, which are connected again by multitude of filaments and voids. These filamentary distributions of galaxies explained by vast quantities of dark matter enveloping galaxies and filamentary cold gas flowing within them ,responsible for star formation within them and the dark matter ISM is the dominant mass in the universe. Galaxies over passing time , clumped itself in a filamentary networks . In the cosmic web hypothesis, all spherical structures appeared probably first within filaments, growing in between them, followed by the great walls [planar structures] connecting the filaments of cosmic Web Massive filamentary structures observed at relatively small distances from us. These filaments located about 6.7 billion light-years away from us and extends over at least 60 million light-years even. 'superclusters' are also filamentary cluster–cluster bridges. Computerized numerical simulations shows balance between dark matter and dark energy , determines both how universe expands and how regions of unusually high or low matter density evolved with time. Most of baryons in the local universe are also missing in that they are not in galaxies or in the previously detected gaseous phases. Rupak Bhattacharya and Pranab Bhattacharya here are authors suggest that these missing baryons are so predicted may be in a moderately hot phase, 1E5 to 1E7 K, largely in form of giant cosmic filaments that connect the denser virialized clusters and groups of galaxies. These filaments can be detected through absorption lines they produce in the spectra of background Active Galactic Nucleus . Models show that the highest covering fraction of such filaments occurs in super clusters and the archive has two AGNs projected behind super clusters, both of which show absorption systems (in Lyalpha LybetaOVI) at the super cluster red shift The universe is so permeated by a network of filaments, sheets, and knots collectively forming a “cosmic web.” The discovery of the cosmic web, especially through its signature of absorption of light from distant sources by neutral hydrogen in the intervening intergalactic medium, exemplifies the interplay between theory and experiment that drives science and is one of the great examples in which numerical simulations have played a key and decisive role. We authors in this article recount the milestones in our understanding of cosmic structures; summarizing its impact on astronomy, cosmology, and physics; and look ahead by outlining the challenges faced as we prepare to probe the cosmic web at new wavelengths.


 This  abstract  article The cosmic Web,the seed of galaxies WHIM  aqnd Darkxenergy   " in abstract  form  published in this Blog  is Strictly Copy Righted material to Prof.(Dr.) Pranab Kumar Bhattacharya under his Intellectual Property Right(IPR)  Copy Right Acts  under sections-/301 / 306/3D/107/1012( a,) (b ) / RDF and Protect Intellectual Property Right ACT of USA-2012. Please do not ever try to infringe to avoid huge  amount  damage suit charge  in several cores INR / or civil suit / or  even criminal proceedings in IPR Courts of India or in any other courts of India Professor Bhattacharya  will deem fit it so . Please do not try or take any sort of  attempts to infringe any thing [ besides reading  or liking or commenting or E mailing  if any if you have ]   or engaging yourself in  kinds  of plagiarism for yours own safety purpose from Plagiarism suit or infringement of Copy Right act suit .  You are not  ever permitted to reproduce any things  from his/ their postings/ published articles/comments/blogs/posts or sharing in his Face book etc or even use for your's fair uses also or dissemination for others knowledge or teaching or public or published  reproduce  as per IPR acts and laws for ever.These terms are however will not  be applicable for Professor Dr Pranab Kumar Bhattacharya's  only daughter miss Upasana Bhattacharya , other authors and to  all his family members who can use these articles and postings in this Blog  or his face book  for their beneficiary acts in future or ever in manner they desire to use.

This Paper was sent to following journals  and Comments of Editors are enclosed
 1] Journal of Theoretical Physics 

























This Paper was sent to following journals  and Comments of Editors are enclosed
 1] Journal of Theoretical Physics 




























Natural history of liver fibrosis progression in patients confected with hepatitis c virus and human immunodeficiency virus type 1

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Revista da Sociedade Brasileira de Medicina Tropical

Print version ISSN 0037-8682
On-line version ISSN 1678-9849

Rev. Soc. Bras. Med. Trop. vol.49 no.6 Uberaba Nov./Dec. 2016

http://dx.doi.org/10.1590/0037-8682-0402-2015  LETTER

1Department of Pathology, Murshidabad District Medical College,
Beharampore, Murshidabad, West Bengal, India.
2Department of Pathology, Calcutta School of Tropical Medicine
 Kolkata, West Bengal, India.

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SPARC authors amendedCopy Right rules-2006  of US  when & if accepted for any other blogs, 
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Article 13

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RESEARCH & REVIEWS : JOURNAL OF SPACE SCIENCE & TECHNOLOGY

 Vol 5, No 3 (2016) > Bhattacharya

Table of Contents

Articles





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WHERE FROM MASS CAME IN THE UNIVERSE?- DID THE MASS ORIGINATED FROM A ZERO REST MASS LESS PARTICLE IN HIGGS FIELD Published in  RRJOST Journal  Vol 5, No 3 (2016) > Bhattacharya et al   belongs still  only to Professor (Dr.) Pranab kumar Bhattacharya,MD (Calcutta Univ.), FIC Path (India),WBMES and the other authors here in chronology, as per copy right rules of IPR- 1996 applicable in India-2006 under IPR law under sections 306/301/3D/107/1201 (a), (b)and PIP copy Right Acts of US 2012, SPARC authors amended Copy Right rules-2006 of US even when and  though  accepted and published RRJoST of STM  Group journals  for any other blogs, or  as a reference, or for publication in  other research indexed journals or in books or for next Research on it or as reference material or published as paper/article/communication/comments in any Indexed journal/journals or as an article in any open access journals or as a commissioned article, the copy right clearance must be sought from authors and then also this article will be under RDF Copy Right rules of IPR of Professor (Dr.) Pranab Kumar Bhattacharya. No persons or any  journal editorial board members(RRJOST of STM Journal group /reviewers/book authors from any states/places of any country or from any places within country India or any citizen of India or of Indian origin forever are not authorized by Professor Dr. Pranab kumar Bhattacharya  WBMES to use the article’s any contents , ideas, concepts, hypothesis, any scientificallymeaningful syllables/words/sentences from this published article in the published article  of Prof. Pranab kumar Bhattacharya without his/future copy right owner’s written permission and Copy Right clearance, even for any one’s personal knowledge gain or for his/her fair use even/dissemination of any information or knowledge/or application in any field of physics, astronomy, applied mathematics/Particle physics (Will be considered then as Plagiarism by Prof. (Dr.) P.K Bhattacharya), [except such all permission is always remain granted to other authors ,their first degree blood relatives in whatever manner they want to use this article for ever. This isThe copy right of this article Schrödinger cat's experiment's interpretation and parallel Universe or Multiple Universe?” belongs only

to Professor (Dr.) Pranab kumar Bhattacharya, MD (Calcutta Univ.), FIC Path (India), WBMES and the other authors here in chronology, as per copy right rules of IPR- 1996 applicable in India-2006 under IPR law under sections 306/301/3D/107/1201 (a), (b) and PIP copy Right Acts of US 2012, SPARC authors amended Copy Right rules-2006 of US even when and though  accepted and published for RRJOST  or any other blogs, as a reference, or for
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under RDF Copy Right rules of IPR of Professor (Dr.) Pranab Kumar Bhattacharya.
No persons or journal editorial board members/reviewers/book authors from any states/places of any country or from any places within country India or any citizen of India or of Indian origin forever are not authorized by Professor Dr. Pranab kumar Bhattacharya to use the article’s any contents , ideas, concepts,
hypothesis, any scientifically meaningful syllables/words/sentences from this published article in the Blogs of Prof. Pranab kumar Bhattacharya without his/future copy right owner’s written permission and Copy Right clearance, even for any one’s personal knowledge gain or for his/her fair use even/dissemination of any information or knowledge/or application in any field of physics, astronomy, applied mathematics/Particle physics (Will be
considered then as Plagiarism by Prof. (Dr.) P.K Bhattacharya), [except such all permission is always remain granted to other authors ,their first degree blood relatives in whatever manner they want to use this article for ever. This is official declaration as class 1 Group-A, Gazated officer in WBMES cadare of
Department of Health and family welfare Government of West Bengal, India.

SD/Professor (Dr.) Pranab kumar
Bhattacharya MD (Calcutta Univ) FIC path,
WBMES
Professor (detailment) 
Department of Pathology
School of Tropical Medicine, Kolkata
108 CR Avenue Kolkata-700073
Department of Health and Family Welfare
(Medical Education Wings); Govt. of West
Bengal; India
Member and Member Secretary of Board of
Studies (BOS) UG/PG/DCP.

Title- “West Bengal clinical establishment ( Registration, Regulation, and transparency ) bill-2017- Rest of India can take lesions from West Bengal for such a regulatory body in every state as a part of health care reform

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 Professor Dr Pranab kumarBhattacharya MD( Calcutta Univ) FIC path Professor of Pathology Murshidabad Medical college Behrampore Murshidabad  West Bengal;  Runa Mitra MA ( university of Calcutta) social worker   Barrackpore ; Sagorika Dutta choudhury Correspondent Ajka; news Paper


 In India health care system is mixed type i.e. both the public & private medicare health system runs parallel and side by side. In public health care system governed by the state or central government is almost at free of costs in majority of provinces in India with some kinds of national program on vaccination and eradication of some infectious diseases like malaria, Chickengunia ,dengue, leprosy, kala-azar, tuberculosis, NRHM but these tropical diseases even in this 21 century claims a good numbers of life . Preventive health care in chronic diseases like, diabetes, COPD, cardiovascular , Stroke hypertension ,cancer psychiatric illness etc that costs too much financial burden for any family is over looked usually till date. Health is a state government affair mostly. Private health care system consist of private practitioners , private nursing homes and private health care institutions, private diagnostic centres and these private hospitals , nursing homes and diagnostics are big profitable health industries in health economics mainly targeting for business without any regulatory bodies or commissions from end of government and vigilance laws and acts to regulate their functions so long through licenses for doing such trades or business from the government level with trade licenses issued & permission to them to carry on business with ailments . The lands are usually provided by the government for establishment i.e. for hotel like buildings or Air conditioned rooms and for many infrastructures human resources ( Doctors and nurses) are also recruited by them either from government medical colleges having post graduate/post doctoral degrees or retired faculties and specialists from public hospitals with huge percentage of incentives or with persons having foreign diplomas like MRCP FRCS MRCS most of which are not recognized by the highest councils ( So far it was regulatory bodies in India) like Medical councils of India with its state branch offices like in West Bengal state West Bengal Medical councils So in India out of pocket expenditure in health was/is huge in relation to any other welfare countries, unprotected by nationalized health insurances and about roughly 60 millions of 129 millions populations are pushed towards poverty almost every years because of mushrooming private Medicare health industries and house holds are unable to afford such treatment for illness typically for cardiovascular causes diabetes mellitus with or without complications septicemia End stage renal disease liver diseases cancer septicemia , organ failure and transplants of either stem cells or biologic molecules and people had to sell house lands valuables every things for hospital treatment at least in West Bengal state . However this authors never say that all private hospitals doctors and nurses are corrupted or bad but many private care industries misuses the health system and causes harassment to people for so long years together. So there needed some sort of reform in health system which are pro-poor and has universal access to health care in this country

 The present Indian government (2017) health department in march 2017 for the first time since independence in 1947 declared its political intention to set up its intention in health care system spending to provide free supply of medicine free diagnosis and free emergency essential services to reduce house hold out of pocket expenditure that present government health department of west Bengal provinces did in 2014 July for the public hospitals run by government But it needs policies, strategy and priority selections and increase of expenditure of GDP for health (which is in 2017-18 budget is 1.3%) to at least 3.5 to 5% and must be in time bound manner and to support universal accesses to health services be it in public and private care like Obama health care in USA or NHS care in UK The policy according to me * offering Free medicines of quality and good bio availability ** offering free diagnostic including radiology digital x ray CT scan , Serological pathological bacteriological tests*** New comprehensive primary health care packages for cardiovascular diseases , Diabetes, dialysis, cancer if it is in private health care industries done under a fixed government rate and capping of fees , billing system by making new laws and acts( besides 1985 clinical establishment acts) through some regulatory bodies with power of judiciary system In India there are almost 30,000 primary health centres and 500 community health centres where facilities infrastructure and human resources are rudimentary particularly in relation to free supply of medicine, diagnostic, palliative care, and mental health care. In addition to existing national level health care allocation of funds should be directed so towards 1) Free screening for Diabetes mellitus through FBS HBA1C and free supply of medicine /insulin /drugs 2) Screening of hypertension at free of cost with treatment to reduce stroke Acute Myocardial infarction and death 3) Screening for breast cancer at free of cost with proper treatment if and when detected 4) Screening for pre cancerous lesions for oral cancer (OSMF) and oral cancer 5) Screening for Lung cancer at free of cost and treatment 6) Target for elimination of Leprosy Kalaazar and tuberculosis by 2025 Target for elimination of malaria and dengue by 2025 by vaccine 8) To reduce pre mature death from diabetes mellitus type 2, cancer COPD by 25% at least by 2025 Problem is political will in our country India to increase GDP in health care system at public hospitals and with human resources- as most post graduates post doctoral specialists being trained in public medical colleges and hospitals joining in private health care institutions for lucrative salaries incentives lavish life styles The problems in health care system in west Bengal I author do identify • Huge load of patients – almost 70% - 73% patients rushes to medical colleges from districts rural sub divisional hospitals • Overcrowding – due to faulty referral system or not working • High bed occupancy rate and non availability of beds – one bed is often shared by 2-3 patients due to non referral system in public hospitals by order of supreme court when admissions is through emergency • Waiting time for any investigations it is variable in different public hospitals. But in medical colleges often one to three months due to lack of human resources non availability of sufficient technicians and reagents to tests. However waiting time is much less in west Bengal then waiting time in UK USA with high GDP expenditures in health and that resulted health tourism • Non availability of free bed side care by nurses and Group D staffs – they are in adequate in numbers. Nurses are microscopic and GDA Sweepers and other Group D staffs are not available and as such most patient party have little choices to hire private attendants or ayah at cost of approx 150/= INR per shift(12 hours) and thus costs RS 300/= INR per day in most medical colleges- though system of paid attendants in west Bengal state discontinued by previous left front government a decade ago • Most importance is cleanliness


 The health care system of west Bengal provinces as well rest of India has been struggling for decades( since 1990s) There had been numerous complaints against private health care institutes for long years together . They used to charge exorbitant rates without providing proper treatment and in many cases quarries regarding ailments and estimated costs of treatment are not properly addressed with clarity and consent There had been accesories when the body of the diseased had not released by private hospitals on account of non clearance of dues , The violence  that were witnessed recently in West Bengal in private hospitals of metro cities in kolkata is the result of accumulated anger we do consider . The state government of West Bengal has shown the courage to stop the unethical practice indulged in by the hospital authorities by a new bill In west Bengal Provinces in march 2017 a new bill has been signed by the Governor of West Bengal named as “West Bengal clinical establishment ( Registration, Regulation, and transparency bill-2017) and through this bill a commission has been formed which will tabs on approximately 2000 private hospitals and nursing homes in the state of West Bengal

 • The commission will hear complains of negligence against private health care institutions managerial staffs health technicians nurses doctors working there and this panel may order cancellation of licenses closer of that particular establishment Seizer of the property of managerial staffs doctors nurses who are at fault or found guilty of causing grievous injury or death . This panel can file FIR if it finds a clinical establishment is guilty in violating registration or license norms and if charges are proved the persons including / hospital CEOs/ Managerial staffs/ doctors/nurses/ technicians can be jailed up to 3 years . This commission will also cap charges for indoor & outdoor services doctors fees structure and investigation charges and needs 
• This kind of steps I consider is a very good step for access of all in health care system and also for the rest of India can take a lesion from government of West Bengal for such a regulatory body in every state


• West Bengal new Regulatory laws on private hospitals however set off central versus state battle amongst leadership of Indian medical Association(IMA) – the country’s largest Private association of doctors when the IMA of West Bengal chapter uniamously decided to support the new bill and laws IMA national president objected to certain clauses in “West Bengal clinical establishment ( Registration, Regulation, and transparency bill-2017”relating to prosecution for 3 years and compensation in grievous injury or death (up to 50 Lakhs INR ) without any valid reasons as this bill will not affect an honest doctor and when private health care intuitions mostly are den of malpractices and were without accountability for so long years together

• The National president of IMA  Dr KK Aggarwal told there were alternative forums like consumer forum. He told there should be consumer court or a regulatory commission. There should be single windows accountability.  But how much CPA laws were effective for so many long years? Status of CPA was not enough clear whether one aggrieved person on same ground can file two separate cases on one incidence with both the court of laws and consumer forum? And more over regarding power of consumer forum/ court verdicts can be challenged to high court and supreme court and private hospitals are more powerful players for money He also  told for omission of  criminal charges  against doctors  unless there is intention to harm the patients. But the new act  suggest that any one causing death  or injury of any types to a  patient  through negligence  should be  liable to  punishment  in under Indian penal code(IPC)  and any person violating  the conditions of registration
  or license  under act should be  liable to imprisonments up to three years


So my personal view that the bill is not against the honest doctors private practioners whose numbers are more and maximum


 • However before the bill come to as acts or rules I shall request the commission to consider following points if I am not wrong 
1) Post mortem examination should be must if and when charge of negligence on death
 2) when and if negligence cannot be proved the doctor/nurses/ technician should be paid by the order of the commission for the legal expenditure , spoiling reputation , and mental pressure he/she bears 
3) Mal handling of doctors on duty must be arrested immediately
 4) Banning of all quacks in west Bengal 
5) Case compensation and jail should be also for the managerial staff CEO who is policy makers for private hospitals and not doctors 
6) Fixing guide lines for Ethical medical practices in private health care institutions 
7) Fixing Guide line to improve bonding in individual doctors encouraging more communications and inform consent with patient’s party 
8) Encouraging audit system in practice of private health care clinical establishments in regard to investigations prescriptions of drugs in generic and doctor patients relationship after the bill is implemented 
9) Monthly if possible weekly death review committee report should be sent to health department 
10) Educating doctors on sociological issues 
11) Protection of Doctors be it private and public against civic legislative and social mal-handling & Exploitation by private hospital managements 
12) Empowering doctors to take steps legally against frivolous complains malicious defamatory press statements and unlawful harassment


 This article Title-  “West Bengal clinical  establishment ( Registration, Regulation,  and Transparency ) bill-2017-  Rest of India can  take lesions  from West Bengal for such a regulatory body  in every state  as a part of health care reform  " published in this Blog  is Strictly Copy Righted material to Prof.(Dr.) Pranab Kumar Bhattacharya under his Intellectual Property Right(IPR)  Copy Right Acts  under sections-/301 / 306/3D/107/1012( a,) (b ) / RDF and Protect Intellectual Property Right ACT of USA-2012. Please do not ever try to infringe to avoid huge  amount  damage suit charge  in several cores INR / or civil suit / or  even criminal proceedings in IPR Courts of India or in any other courts of India Professor Bhattacharya  will deem fit it so . Please do not try or take any sort of  attempts to infringe any thing [ besides reading  or liking or commenting or E mailing  if any if you have ]   or engaging yourself in  kinds  of plagiarism for yours own safety purpose from Plagiarism suit or infringement of Copy Right act suit .  You are not  ever permitted to reproduce any things  from his/ their postings/ published articles/comments/blogs/posts or sharing in his Face book etc or even use for your's fair uses also or dissemination for others knowledge or teaching or public or published  reproduce  as per IPR acts and laws for ever.These terms are however will not  be applicable for Professor Dr Pranab Kumar Bhattacharya's  only daughter miss Upasana Bhattacharya , other authors and to  all his family members who can use these articles and postings in this Blog  or his face book  for their beneficiary acts in future or ever in manner they desire to use.

This article has been published 1]  as a comment at British Medical journal The BMJ opinion to the blog article   by  Avinash Supe: Violence against doctors cannot be tolerated March 29, 2017               

2]  This article has been published also as comments  at British Medical journal  The BMJ opinion  

Tessa Richards: Patients combat corruption in healthcare December 20, 2016


BMJ 2014348 doi: https://doi.org/10.1136/bmj.g3169 (Published 08 May 2014)Cite this as: BMJ 2014;348:g3169
Please note  it very carefully that, The Copy Right of this article belongs only 
to Professor Pranab kumarBhattacharya MD(cal) FIC path(Ind) and other authors
 in chronological order  , as per copy right rules of IPR 1996 applicable in India-2006
 under sections 307/ 306/ 3D/107/2012 and PIP Acts of US 2012SPARC authors amended 
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e: The role of the microbiome in human health and disease: an introduction for clinicians : Relative abundances of Gammaproteobacteria and relative paucity of anerobic bacteria precede Necrotising Enterocolitis in low birth weight baby

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BMJ 2017356 doi: https://doi.org/10.1136/bmj.j831 (Published 15 March 2017)


Necrotising enterocolitis is a catastrophic necro inflammatory injury to the intestine in low birth weight infants (5-10% of very low birth weight babies) through out the age of 2 months-9 months, and their mortality rate is about 25% and present treatment is bowel resections. Necrotising enterocolitis is associated positively with various antibiotics and found negatively with human milk and very costly probiotics. DNA analysis of stool culture in study of gut microbes shows commonly organisms such as Gram negative bacilli, Actinobacteria, and firmicutis, Propionibacteria, Bifidobacteria, and bacteriods are preventives of necrotising enterocolitis when overproduction of Gram negative facultative baccili and potentially pathogenic organisms such as E coli Enterobacter, Klebsiella and other obligate anaerobic bacteria particularly clostridia develops in the infant guts before necrotising enterocolitis and results in dysbiosis and ultimately necrotising enterocolitis.
The question is whether these Gram negative bacteria are associated with necrotising enterocolitis and result from dysbiosis. These Gram negative bacteria elicit mucosal injury to the bowel that resembles necrotising enterocolitis and we find that antibiotics can, however, diminish mucosal injury. TLR 4 which binds with bacterial lipopolysaccharides is implicated in cellular processes that actually underlie the cause of necrotising enterocolitis.
Anaerobic bacteria responding to microbiota-accessible carbohydrates produce short chain fatty acids, especially acetate, propionate and butyrate, which are anti-inflammatory too. Oral aminoglycosides which reduce populations of Gram negative gut bacteria but do not inhibit anaerobic bacteria may thus protect against necrotising enterocolitis though it is said that antibiotics use is a risk factor for necrotising enterocolitis and associated with lower proportion of protective anaerobes and lower proportion of Gamma proteobacteria.
Necrotising enterocolitis may be related to a lack of gut bacterial diversity.
So the question is, can probiotics with Bifidobacterium breve prevent necrotising enterocolitis?
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The Cosmic Web, the Seed of Galaxies- are also made of Warm Intergalactic Medium(WHIM) and Dark Energy

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Authors affiliation : BSc(Calcutta University ), MSc (Jadavpur Univ), of residence 7/51Purbapalli, Sodepur, Dist 24 Parganas(north), Kol 110,West Bengal, India. Free lancer Theoretical Physicist.Author σ: Professor, MD(Calcutta Univ) ; FIC Path(India), Professor of department of Pathology(detailment), Calcutta School of Tropical Medicine,108, C.R Avenue; Kolkata-73, West Bengal, India. Author ρ: Student, Mahamayatala, Garia, kol-84, only daughter of Prof.PK Bhattacharya.
 Author Ѡ: B.com(Calcutta Univ). Author ¥: MSc (PUSHA New. Delhi, India) of residence7 /51 Purbapalli, Sodepur, Dist 24 parganas(north), Kolkata-110, West Bengal, India, Author χ: Calcutta Univ, Swamiji Road, South Habra, 24 Parganas(north) West Bengal, India. Author ν: BHM( IGNOU).Author Ѳ: Student. Author ζ: Bsc(Calcutta Univ) of Residence Swamiji Road, South Habra, 24 Parganas(north), West Bengal, India. Author £: of residence7/51 Purbapalli, Sodepur, Dist 24parganas(north), Kolkata-110,West Bengal, India. Author €: MA (Calcutta University) BK Mitra Palliative care unit Barrackpore North 24 parganas West Bengal India.
Now published in
Global Journal of Science Frontier Research A Physics and Space Science Volume XVII Issue V ersion I Year 2017 page 57-68

of the PDF Please go at page 74 to 85 GJSFR-A 
Classification: FOR Code: 029999
This is a research/review paper, distributed under the terms of theCreative Commons Attribution-Noncommercial 3.0 Unported License http://creativecommons.org/licenses/by-nc/3.0/), permitting all non commercial use, distribution, and reproduction in any medium, provided the original work is properly cited]
Abstract- Universe consisted of mysterious Dark energy (70%), Dark matter(25%) and that makeup now 95% of matter in the universe which revel it self as gravity. Enormous filaments andblobs of dark matter in early universe condensed as universe condensed. Within the cosmicwebs, all galaxies, stars, planets were next created. Galaxies are not dotted randomlythroughout universe but are generally either concentrated in groups or in clusters, which areconnected again by multitude of filaments and voids. These filamentary distributions of galaxiesexplained by vast quantities of dark matter enveloping galaxies and filamentary cold gas flowingwithin them, responsible for star formation within them and the dark matter ISM is the dominantmass in the universe. Galaxies over passing time, clumped itself in a filamentary networks
click at URL https://globaljournals.org/GJSFR_Volume17/E-Journal_GJSFR_(A)_Vol_17_Issue_1.pdf
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Save Women from Cervical Cancer in Low Middle Income Countries and Middle Income Countries

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Professor of Pathology, Murshidabad Medical College, India
Received: April 29, 2015 | Published: May 01, 2017
*Corresponding author: Pranab Kumar Bhattacharya, Professor of Pathology, Murshidabad Medical college, (university of Calcutta) FIC path, Berhampore station road, Berhampore Court, District -Murshidabad, West Bengal, India, Tel: 9231510435; Email: 

Abbreviations

HICS:Incidences Rate Between High; LICS:Low Income Countries; LMICS:Low Middle Income Countries; VIA: Visual Inspections with Acetic Acid; ISH: In Situ Hybridization; IHC: Immunohistology; UN: the United Nations; NCD: Non Communicable Diseases

Editorial

No women should die of cervical cancer in this day and age and yet each year more than 2,60,000 women world wide in Low and middle income countries die of this cancer only. There is dramatic disparity in the incidences rate between high (HICS) and low income countries (LICS) and this disparity is likely to be due to differential access to screening of cervical pre cancerous lesions, treatment facilities available in primary level and taking preventive measures with new HPV-9 vaccines- as use of Human papilloma virus vaccinations continues to be lag in the low middle income countries (LMICS). Dramatic benefits were observed from vaccinations of HPV and early cervical pre- cancerous lesions [1]. The new HPV-9 vaccine which includes 9 or more HPV types there is good chance after several decades cervical cancer screening may no longer be warranted. But that is for the high income countries. What about for LMICS and MICS like India or in West Bengal Province of India? Hundreds and millions of women are already beyond the age of adolescence and age of vaccination and remains without screening and preventive treatment due to lack of human resources like trained pathologists & laboratory technicians as resource personals and this author apprehends that some 25 millions women will die of cervical cancer by next 25 years in MICS and LMICS.
We and government know that successful methods that could reduce the incidence of cervical cancer are Pap smear, colposcopy and biopsy and new 9 HPV vaccines. But women in LMICS has almost nil access to biopsy & Pap smear due to lack of adequate trained pathologists in rural, urban, suburban districts, sub divisional, and state general level public hospitals. The basic tools for cervical screening already exists and getting better and better(new Bethesda classification -2014 thin prep smear fluid based cytology and HPV detection) in high income countries but still out of reach for millions of women in LMC and MICS like India only due to lack of human resources and budgetary allotment by the government.
 One notable advances in screening methods is visual inspections with Acetic Acid (VIA) which allows trained health workers to spot cervical abnormalities with just a speculum examination available even at primary health center (primary care level) of West Bengal , India The high cost bearing but highly sensitive molecular tests by In situ Hybridization (ISH) or by Immunohistology (IHC) that detect HPV infections- is not accessible for remote villages urban semi urban hospitals except in some Medical colleges of West Bengal state as it needs sophisticated laboratory infrastructure like thin prep, monoclonal primary and secondary antibodies or PCR or FISH technology and trained pathologists. However both Visual inspections with Acetic Acid (VIA) and Molecular identifications of HPV are now acceptable screening methods by WHOM also. There has been much improvement in preventive treatment using technologies such as Cryo pen and thermal coagulation and conventional cryotherapy. Advances in the uses of mobile phones for tracking health information and reaching patients and the explosive growth of their availability in MICS and LMICS is another opportunity to improve cervical cancer prevention. So a state or a country must have political will to take advantages of knowledge and technologies to provide sufficient human resources (here pathologists, technicians, health workers) training. Providing budget for in situ hybridization or immunohistology or immunocytochemistry and extending even to primary care or community care. Fortunately in 2017 Government of India included it as national health program in 2017 declared. The United Nations (UN) summit on non communicable diseases (NCD) held in 2011 and listing WHO for screening and treatment of cervical pre-cancerous lesions to prevent cervical cancer is a feasible proposition for LICS and MICS.
Why the LICS are not much interested in the effective cervical, Lung cancer, breast cancer screening diabetes, hypertension, stroke, prostate cancer screening in the national health program? They are enable to in funding in many health issues like eradications of malaria ,dengue, polio, wide spread treatment of HIV –AIDS, 5% reduction of mortality of children, and tobacco control program, malaria dengue vaccine development program when signs of global commitments are emerging in 2015 as five years initiative “ taking cervical cancer Prevention: Protecting all women and girls”.
  1. According this author for the MICS like India has to build
  2.  Efficient screening services and in India and west Bengal provinces of India there is much shortage of Pathologists, laboratory technicians and health workers.
  3. In India the health system is week and both private and public mixed type and private care health system never participate in national health program as there is no profit in this system.
  4. In adequate health information system.
  5. Tracking individual patients is lacking.
  6. Monitor program performance is lacking.
  7. Vaccination campaign in adolescent girls to be done.
  8. Proper training of pathologists to identify pre cancerous lesions in low resource setting if possible by VIA.
 Of course molecular testing like HPV and its sub typing using cervical or vaginal smears form sophisticated laboratories in cities and Medical colleges( all medical colleges do not have this facility yet) after collecting it from rural sub divisional districts hospitals even by self collections from homes or communities by health workers possible and providing HPV 9 vaccinations [9VHPV – a new Vaccine 0,5 ml contains 30ug HPV-6, 40ug HPV 11, 60ug HPV 16, 20ug, HPV 18 virus like particles and 20ug HPV 31, 21ug HPV 33, 20ug HPV 45, 20ug HPV 58 virus like particles] for those who are positive for HPV types 11, 16,18,31 in India is the most effective ways in closing the burden but probably will not be enough effective one because
  1. pathologists/cytopathologists will not be opting for it to work as it becomes too much burden for a pathologists to screen every day hundred slides of Pap cervical smears [from self experiences].
  2. Technicians will not perform ISH and IHC as it takes DNA based technology and time consuming dedicated monoclonal antibody staining requires somewhat like 4-5 hours time unless there is automated immuostainers are provided.
  3. There will be cultural barrier for women to test PaP smear and biopsy.
  4. Enhancing accuracy, yields and efficient screening remain absent due to lack of adequate training amongst pathologists/cytopathologists (for liquid based cytology of cervical smears and vaginal smears as per Bethesda classification 2014[2].
  5. HPV vaccine may cause some harm to some few people but balance between benefits and harms suggests vaccinations.
 So this author considers that if MICS and LMICS can provide equalities access to rural women and poor or poorer women screening by PaP smear liquid based cytology with HPV testing more than once and screening of older women at least for once can expect greater disease burden reduction by effective treatment for those who are positive for Pap smear or HPV 11, 16 & 18 in west Bengal and in India.

References

  1. Markowitz LE , Liu G , Hariri S, Steinau M , Dunne EF, et al. (2016) Prevelance of HPV after introduction of vaccination on program in the united states. Pediatrics 137(3): 1-9.
  2. Nayar R, Wilbur DC (2015) The Pap Test and Bethesda 2014 Cancer Cytopathol 123(5): 121-132
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  4. Professor Pranab kumar Bhattacharya
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Septicemia and Shock: Pathogenesis and Novel Therapeutic Strategies

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Septicemia and Shock: Pathogenesis and Novel Therapeutic Strategies

   Authored By

Beharampore, Murshidabad, West Bengal, India
2] 7/51 Purbapalli PO -Sodepur District 24 Parganas(north) West Bengal Kolkata-70001 India
[3] Swamiji Road , South habra District 24 Parganas(north) West Bengal Kolkata-70001 India
 [4]  B K Mitra Palliative care unit  Barrackpore District 24 Parganas(north) West Bengal Kolkata-70001 India 
Email-:  profpkb@yahoo.co.in     Mobile -9231510435


 Abstract and  research data/ result and analysis not given for this article here much intentionally to prevent plagiarism unless and untill  published in a high index journal


 [ NEJM] sent and in review process now t 


 The overall mortality in patients with sepsis is approximately 30%; this figure increases to 50% or greater in patients with septic shock, and sepsis continues to be seen as a major clinical challenges in ITU  or ICU or CCU .  Sepsis is usually associated with exacerbated production of both pro- and anti-inflammatory cytokines, which are detectable within blood .These “half-angel/half-devil” properties are fully illustrated in sepsis. While the cytokines are a prerequisite to fight infection, their overzealous production is also deleterious for patients. The highest levels of cytokines  are found in plasma of non-surviving patients from sepsis : can they be markers and causative agents of poor outcome in severe sepsis? . Only, the level of the chemokine “RANTES” is inversely considered as  associated with the APACHE II score and with poor outcomes. The link, interplay and network of cytokines taking place during sepsis are illustrated by the correlations between the levels of most pro- and anti-inflammatory cytokines. Excessive release of anti-inflammatory cytokines may be according to myself  associated  also with the immune dys-regulation observed in sepsis. However, despite the presence of huge amounts of anti-inflammatory cytokines and molecules targeting specifically interleukin-1 (IL-1) (i.e. IL-1 receptor antagonist) and tumor necrosis factor (TNF) (i.e. soluble TNF receptors), there is no indication that their levels are sufficient to fully counteract these pro-inflammatory cytokines. TNF was initially thought to be the “hub of the cytokine network”. Although TNF contributes to favor the production of many other cytokines within a complex cascade, there are numerous examples, which illustrate that its presence is not a prerequisite for these productions.     It is acknowledged that severe sepsis/ or septic shock is a major problem in clinical  bed side medicine,  and yet the extent of the problem and its basic immunology remains poorly defined to us. The problem of sepsis is further complicated by the remarkably diverse spectrum of illness encompassed under the term “sepsis”. Sepsis may  range in severity from mild systemic inflammation without significant clinical consequences to multi system failure(MODS)  as in septic shock with an exceedingly high mortality rate. Sepsis also connotes a clinical syndrome that may occur in any age group, in markedly different patient populations, and in response to a multitude of microbial pathogens from multiple different anatomic sites within the human body.

Although protocols could be tailored by each hospital, all the protocols a required to include a 3-hour bundle consisting of receipt of the following care within 3 hours: obtaining of a blood culture before the administration of antibiotics, measurement of the serum lactate level, and the administration of broad-spectrum antibiotics. Protocols are also required to include a 6-hour bundle, consisting of the administration of a bolus of 30 ml of intravenous fluids per kilogram of body weight in patients with hypo tension or a serum lactate level of 4.0 mmol or more per liter, the initiation of vasopressors for refractory hypotension, and the re measurement of the serum lactate level within 6 hours after the initiation of the protocol.  An association between time to treatment and outcome among patients with sepsis or septic shock treated in the emergency department during a state wide initiative mandating protocolized care.  It is found that a longer time to completion of a 3-hour bundle of care for patients with sepsis and the administration of broad-spectrum antibiotics were each associated with higher risk-adjusted in-hospital mortality. A recent meta-analysis of 11 observational studies, however, showed no significant mortality benefit of the administration of antibiotics within 3 hours, as compared with after 3 hours, after triage in the emergency department (odds ratio, 1.16; 95% CI, 0.92 to 1.46) or within 1 hour after the recognition of shock (odds ratio, 1.46; 95% CI, 0.89 to 2.40).[1]. There  may be several biologic explanations for the association between the time to completion of a 3-hour treatment bundle and outcome of sepsis. First, more rapid the administration of antibiotics it reduces pathogen burden, modifies the host response, and could reduce the incidence of subsequent organ dysfunctions. Second, clinicians who decide more quickly to measure the serum lactate level may identify heretofore unrecognized shock and are more prepared to deliver lactate-guided resuscitation than clinicians who are slower to measure the serum lactate level — a strategy that may improve outcome in randomized trials.[2]  Third, physicians have broad variation in how they identify sepsis, even when they are presented with similar cases.[3] Fast delivery of sepsis treatment, even within the structure of mandated protocols, requires a prompt clinical suspicion of both infection and worsening organ dysfunction.

 Broad spectrum Antibiotics are essential to the treatment of bacterial sepsis as they reduce the bacterial burden. The impact of bacterial resistance found to be very important in a range of conditions. Resistance to antibiotics can be defined genotypically, phenotypically and clinically through pharmacokinetic/pharmacodynamic studies and their correlations with clinical outcomes. Although the kinetics of antibiotics has been shown to be favorably altered in sepsis, a range of studies in sepsis has revealed that for most pathogens resistance contributes to significant increases in mortality. This has been clearly demonstrated in bacteraemia, including community- and hospital-acquired infections, and with bacteraemia caused by vancomycin-resistant enterococci, methicillin-resistant staphylococci, and extended-spectrum producing gram-negative bacterias. Significant mortality increases have also been seen with ventilator-associated pneumonia and serious infections requiring admission to intensive care. Gentotypic and phenotypic resistance in coagulase-negative staphylococci causing bacteraemia, and in invasive pneumococcal disease has not shown differences in mortality. In the latter case, dosage regimens have to date been adequate to overcome laboratory-defined resistance. Early indications are that de-escalating therapy from broad-spectrum initial coverage after results of cultures and susceptibility tests become available does not jeopardise outcomes, and further prospective studies are warranted. There is now convincing evidence that broad-spectrum initial therapy to cover the  likely pathogens and their resistances pending culture results is mandatory in sepsis to minimise adverse outcomes.


Monocytes/macrophages play  also a key role in host defense mechanism  by phagocytosing invaded pathogens, or in  presenting antigens to immune cells, and producing numerous inflammatory  cytokine mediators. Expression of many proteins and genes  is  up regulated  in activated human monocytes, a whole picture of pathophysiologic function of activated human monocytes has not yet been drawn. Serial analysis of gene expression (SAGE) procedure when  are used  to lipopolysaccharide (LPS)-stimulated human monocytes  more than 12,000 different transcripts can be sequenced. In addition, the Long SAGE can be used in LPS-stimulated monocytes to increase the accuracy of corresponding gene identification. Comparison of gene expression profile with that of resting monocytes revealed the whole LPS-inducible gene expression profile. The functional classifications of LPS-inducible genes( greater than 8 fold increase compared with resting monocytes) in monocytes showed that 25% of inducible genes were identified to encode cytokines and chemokines, followed by proteins related to metabolism (11%), cell surface antigens (9%), nuclear proteins (8%), proteases (6%), proteins related to extracellular transport (4%) and intracellular transducers (4%). Moreover, 14% of LPS-inducible genes still encode proteins with unknown function.

HMGB1 is a member of the high mobility group protein super family that had been widely studied as nuclear proteins that bind DNA, stabilize nucleosomes, and facilitate gene transcription. Surprisingly, a series of recent discoveries revealed a cytokine activity of HMGB1, that when secreted into the extracellular milieu, mediates downstream inflammatory responses in endotoxemia, arthritis, and sepsis. HMGB1 is properly defined as a "cytokine" because it stimulates pro inflammatory responses in monocytes/macrophages, is produced during inflammatory responses in vivo in standardized models of systemic and local inflammation, mediates delayed endotoxin lethality, and is required for the full expression of inflammation in animal models of endotoxemia, sepsis, and arthritis. HMGB1 is either actively secreted by monocytes/macrophages or passively released from necrotic cells from any tissue. These pathways are central for the biology of HMGB1 as a cytokine, since they provide key mechanisms that integrate the inflammatory response to infectious and non-infectious cell injuries. Receptor signal transduction of HMGB1 occurs in part through the receptor for advanced glycation end-products (RAGE) expressed on monocytes/ macrophages, endothelial cells, neurons, and smooth muscle cells. HMGB1 is a “late-acting” cytokine, because it first appears in the extracellular milieu 8-12 hours after the initial macrophage response to pro-inflammatory stimuli. Knowledge of the cytokine role of HMGB1 has implications for understanding "downstream" cytokine cascades, regulation of delayed innate immune responses, and targeting treatment towards these processes. Effectiveness of delayed treatment with HMGB1 blockade up to 24 hours after induction of experimental sepsis offers a unique window of opportunities to allow rescue from lethal sepsisHMGB1 is a member of the high mobility group protein super family that has been widely studied as nuclear proteins that bind DNA, stabilize nucleosomes, and facilitate gene transcription. Surprisingly, a series of recent discoveries revealed a cytokine activity of HMGB1, that when secreted into the extracellular milieu, mediates downstream inflammatory responses in endotoxemia, arthritis, and sepsis. HMGB1 is properly defined as a "cytokine" because it stimulates proinflammatory responses in monocytes/macrophages, is produced during inflammatory responses in vivoin standardized models of systemic and local inflammation, mediates delayed endotoxin lethality, and is required for the full expression of inflammation in animal models of endotoxemia, sepsis, and arthritis. HMGB1 is either actively secreted by monocytes/macrophages or passively released from necrotic cells from any tissue. These pathways are central for the biology of HMGB1 as a cytokine, since they provide key mechanisms that integrate the inflammatory response to infectious and non-infectious cell injuries. Receptor signal transduction of HMGB1 occurs in part through the receptor for advanced glycation end-products (RAGE) expressed on monocytes/ macrophages, endothelial cells, neurons, and smooth muscle cells. HMGB1 is a “late-acting” cytokine, because it first appears in the extracellular milieu 8-12 hours after the initial macrophage response to pro-inflammatory stimuli. Knowledge of the cytokine role of HMGB1 has implications for understanding "downstream" cytokine cascades, regulation of delayed innate immune responses, and targeting treatment towards these processes. Effectiveness of delayed treatment with HMGB1 blockade up to 24 hours after induction of experimental sepsis offers a unique window of opportunities to allow rescue from lethal sepsis

The recent success of several important trials has fuelled interest in further therapeutic developments. Here, I review the many different strategies that are being investigated, focusing in particular on those that are in late pre-clinical, or early clinical development. These can be broadly divided into three groups: strategies aimed at bacterial targets, strategies aimed at disorders of immune regulation in the host, and finally, other novel strategies based on modifying host response like super antigens . Which, if any, of these will prove successful in large clinical trials is unknown. Nevertheless, the fact that sepsis has finally proved tractable as a target for new drug development lends support to those who believe that at least some of the compounds identified in this paper will prove to have clinical benefit..........(continued  but not published in the blog for safety purpose)  

 Reference

1] Sterling SA, Miller WR, Pryor J, Puskarich MA, Jones AE. The impact of timing of antibiotics on outcomes in severe sepsis and septic shock: a systematic review and meta-analysis. Crit Care Med 2015;43:1907-191

2]Jansen TC, van Bommel J, Schoonderbeek FJ, et al. Early lactate-guided therapy in intensive care unit patients: a multicenter, open-label, randomized controlled trial. Am J Respir Crit Care Med 2010;182:752-761

3]Rhee C, Kadri SS, Danner RL, et al. Diagnosing sepsis is subjective and highly variable: a survey of intensivists using case vignettes. Crit Care 2016;20:89-89


Please note  it very carefully that, The Copy Right of this article belongs only 
to Professor Pranab kumarBhattacharya MD(cal) FIC path(Ind) and other authors
 in chronological order  , as per copy right rules of IPR 1996 applicable in India-2006
 under sections 307/ 306/ 3D/107/2012 and PIP Acts of US 2012SPARC authors amended 
Copy Right rules-2006  of US  when & if accepted for any other blogs, as a reference, or publication  or Research  or  reference material  or published as paper or article in open access journals as a commissioned article  and then  also this article will be under RDF Copy Right rules of 
IPR of Prof PK Bhattacharya.
 No persons/  nor any Private care Hospitals/ nor any Nursing homes/ and their health care
 provider doctors nurses paramedical staffs from any states of  country India or any citizen of India or of Indian origin are for ever authorized by Professor Pranab kumar Bhattacharya to use  any  scientifically meaningful  syllables/words  /sentences/ new drugs/protocolos/ from this
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 one’s personal or for his/her fair use even/ treatment of his or her patients/ dissemination of  
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Article 7

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  • nications, satellite reception, quantum computation and high-efficiency multi-junction solar cells for electricity generation are just some of the exciting fields that exemplify the rich consequences of his work,” Yang continued.(More…)
  • (More…)
  • (More…) ANKED SELECTED SOURCES

    There is a fair bit of math and physics along the way, some parts get pretty heavy into it, but mostly th Quantum was an excellent history of the quantum revolution that began in the early 20th century. [1] [2]
     [3]
     [4]    [5]
     [6] [7]  [8]
     [9] [9]  [9]
    Max Planck worked on the ‘Black Body’ problems started the quantum revolution in 1900. [10] POSSIBLY USEFUL

    In this work the author managed to give a superb account of the development of thought about quantum by bringing to life all the great physicists involved (Planck, Einstein, Born, Bohr, Schringer, de Broglie, Wien, Pauli, Heisenberg, Dirac, Boltzmann, Compton, Bohm, von Neumann, Bell) through vivid vignettes of their scientific accomplishments, interpersonal relations and the historical background. [1]   [1] [1]
     [2] [1]  [2] [1]  [1]  [1]  [1]  [2]  [2]  [2]  [2]
    [1] [1]  [1]  [3]
     [1]  [1]  [1]  [1]Quantum sets the science in the context of the great upheavals of the modern age.                  He also provides what I’ve found to be the best and most coherent account of the history of the development of quantum theory that I’ve read, managing, at the same time, to bring alive many of the key physicists and mathematicians involved, and not just Neils Bohr and Albert Einstein who are in the book’s titl There are a lot of popular science books on quantum theory but this one is different in that its aim is to question what’s meant by reality.      I’m not up on the latest developments relating to quantum blah blah, so I really don’t know if I should call it quantum mechanics, or theory, or physics.            [1] [1]  [1]  [1]
     [1]  [1]
     [1] [1]
     [2]  [1]  [1]  [1]  [1]  [1] [1]  [1]  [1]  [1]  [1]  [1]  [1] [1]  [1]  [1]  [1]  [1]
     [1]  [1]  [1]  [1]
     [1]  [1]
     [1]  [1]
     [1]  [1]   [1]  [1]  [1]  [1] [1]
     [1] [1] [3]  [2]  [2]
    [1]   [1]
    [1]
      [1]
     [1]  [11]  [1]
     [11]
    What is relevant, however, is that testing of D-Wave products has been a back-and-forth battle, with claims of superior performance relative to classical computers later giving way to claims of no real advantage for the “quantum” approach (I leave it to the reader as to whether the scare quotes are warranted). [4]  [4]    [4]
      [7]  [12]  [4]  [4] [13]  [4]  [4]
      [14]  [4]
    t well versed in both quantum mechanics and computer/algorithm theory) is that interpreting the technobabble–particularly when it?                  [4]  [12]  [4]
     [13]
     [6]“Mobile phone communications, satellite reception, quantum computation and high-efficiency multi-junction solar cells for electricity generation are just some of the exciting fields that exemplify the rich consequences of his work,” Yang continued.           

Regression of cirrhosis-my current understanding

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* Professor  Department of Pathology; Murshidabad Medical college ; Berhampore station road; Berhampore court ;  Murshidabad  District ;West Bengal; India and Professor of Pathology(on Deputation)  Calcutta school of Tropical Medicine ; 108 CR Avenue Kolkata-700073 West Bengal

** Associate Professor,  Dept of Pathology , Calcutta School of Tropical Medicine,   108, CR Avenue Kolkata -700073  West Bengal 

*** of all Residents 7/51 purbapalii sodepur 24 parganas north west Bengal India

 **** Swamiji Nagar South Habra North 24 parganas West Bengal India

*****  BK Mitra Palliative  care institute Barrackpore North 24 parganas West Bengal India


Corresponding authors

Pranab kumar Bhattacharya; MD ( University of Calcutta) FIC path  WBMES * Professor  Department of Pathology Murshidabad Medical college Berhampore Murshidabad West Bengal India and Professor of Pathology Calcutta school of Tropical Medicine ; 108 CR Avenue Kolkata-700073 West Bengal  

 Mobile- 9231510435 

Copyright- Belongs to Professor Dr. Pranab  Kumar Bhattacharya as per Copyright Laws of IPR

Abstract -:

 The anatomical and histo pathological   state of chronic liver diseases is a balance between the effects of liver injury and repair  . As cirrhosis develops and progress the fibrous bands tends to be thick and widened with evidence of histological  activity and Cirrhosis  is more of a macro nodular pattern . If the  cause of  ensuing liver injury  is removed or  if effective  treatment of underlying  liver injury diseases are ensured , regeneration of hepatocytes dominates over fibrosis  resulting   enlargement of regenerative nodules and expansion  against septae as well as  lyses of sepate. Nodules surrounded by thin sepate  then  coalesce  first giving rise to  macro nodular  pattern cirrhosis. Incomplete septal cirrhosis  is morphological  land mark  in this dynamic process of regeneration  and repair and thus  these authors  postulate  that  incomplete cirrhosis  is a feature of regressing  cirrhosis  rather than a separate entity  as it was told by Poper H etal in 1966                      
Keyword     Histopathological Sub classification of Cirrhosis; Regression of Cirrhosis, Histological criteria of Regression  of cirrhosis, incomplete Cirrhosis  
Introduction- Cirrhosis is defined as a diffuse process characterized by fibrosis and the conversion of normal liver architecture into structurally &functionally abnormal nodule. A new patho physiological relevant definition of cirrhosis state and cirrhosis is the collection of anatomic changes in the liver that results from presence of wide spread imbalance of hepatic blood flow where inflow exceeds the outflow capacity in cirrhosis fibrous septea develops when there is formation of parechymal extinction lesions with loss of contagious hepatocytes. Parenchymal  extinction lesions accumulates to form confluent regions of extinctions that results in morphological pattern recognizable of cirrhosis. Activation of hepatic fibroblasts is mediated mainly by inflammatory or congestive mechanism.
So Cirrhosis becomes the end stage of liver fibrosis and it results from a variety of chronic liver insults we know, which includes, congenital, metabolic, toxic, inflammatory and various infective causes and cirrhosis leads to complete  morphologic alteration of liver and switch from lobular to a nodular organization associated with vascular remodeling & biochemical changes

Clinical Staging of Cirrhosis

Clinical Staging of Cirrhosis is based on the factors that predict death. The utility of clinical sub classification is meant mainly for identification of patients who will require liver transplant. Broadly clinically Cirrhosis have been classified as I) compensated cirrhosis II) de-compensated cirrhosis. Now de-compensated cirrhosis is defined by the clinically defected ascities, varicial  hemorrhage, hepatic encephalopathy with jaundice and all these complications results from portal hypertension and or liver cells functional insufficiency. The hepatic venous pressure gradient (HVPG) is used for sub classification and predictor of poor outcome. Advantage of HVPG is that a trans jugular liver biopsy can be obtained during the same procedure, which can help histological & hemodynamic correlations.
Histological sub-classification of Cirrhosis- Though liver biopsy is an invasive procedure and mostly today replaced by fibroscan, however it is still the gold standard for diagnose of liver disorders, for staging of chronic liver diseases and for establishing the diagnosis. Liver biopsy provides more information regarding patho physiology of the diseases and has added advantages that it can be reviewed retrospectively. Several  histopathological features has been evaluated to correlate with severity of chronic liver disease including cirrhosis. The three features which are most important and significant are nodule size, septal fibrosis / and width to correlate with clinical outcome. With increasing severity of liver diseases, the amount of fibrosis increases and parenchymal mass of hepatocytes decreases. Along similar liver, a reported case of conversion from  micronodular to macronodular cirrhosis are associated with clinical improvement.
The Lannec group of expert liver pathologists  first proposed classification of cirrhosis in the following manner-based or nodule size and septal thickness
Stage-4a-: Definite or probable Cirrhosis, Thin Septa, 1(one) broad septum can be allowed.
Stage-4b-: At least two(2) broad Septa, but no very broad septum.
Stage-4c-: At least One( 1) very broad septum or many minute nodules.
Septa are defined as broad when the thickness is equivalent the size of the small module and as very broad septa when the thickness is greater than the size of nodule.
Laennec  system of fibrosis & staging of cirrhosis correlated with not only HVPG but also with severity of varies and ascities. In the Laennc system fibrosis septae  are described as broad when the thickness is equivalent to the size of the nodule and very thick when the thickness is greater than the size of the nodule.
However Nagula et al sub-classified cirrhosis, when they did study on chronic hepatitis C patients showed small nodules and thick septae  were more likely to have HVPG greater than 10mm Hg pressure. In their  study they compared the size of the nodule to width of liver biopsy and showed that small nodules were less than 1mm, large nodules were greater than 2mm, thin septae  were less than 0.2mm and thick septae  were greater than 0.4mm and they devised a scoring system to categorize cirrhosis into Category A and Category B, based on nodule size and septal thickness.

Most Recent Classification system

                The most recent classification was done Jain-Garciawhere the histologic criteria had been better defined in more objective ways. The Jain-Garcia system that their author followed  are based on different histological criteria to classify cirrhosis. For classification of cirrhosis the type of predominant (>2/3 septa)  or nodules in the biopsy is taken into account to classify, otherwise considered as mixed as it is given below
                Nodule                                                                 Septa                                                                    Score
Large Nodule (>2mm)=1                               Thin septae (<0.1mm)=3                                                      <4(Stage-4a)
Mixed Nodules =2                                           Intermediate septae (0.1-0.2mm)=2                4(Stage 4b)
Small Nodules (<1mm)=3                             Thick septae  (>0.2mm)=4                                    >4(Stage4c)
Collagen proportionate is important in sub classifying chronic liver disease for Hepatitis C  patients to be done with Elastic Vangesion Stain(EVG) Stain or Sirius stain . Fibrosis   is expressed  as the area occupied by collagen as a proportion  of total biopsy area referred as collagen proportionate area and collagen proportionate area correlate well with clinically significant portal hypertension. This procedure is done by these  authors  by Sirus Red Stained sections using computer assisted digital imaging technology. However crude assessment of collagen can also be done by a well trained histopathologist in good in good  bi ocular Microscope too.
Why this Sub Classification required?

There are evidences, both in animal models and in human that liver fibrosis and even cirrhosis can be regressed or  completely revert to normal  liver architecture and function, either on cessation of the cause of liver injury or treatment of the underlying cause. In 1979, there was a land mark  published paper in journal Pathology Annual  by Perez Tamzyao, who first described the  evidence for reversal of fibrosis and cirrhosis in both animal model and in human. They demonstrated first that arrest of fibrogenic  stimulus can cause reversion of liver fibrosis induced by CCl4 intoxications or bile duct ligation in rat models . We today know that following antiviral treatment of hepatitis B, a shift from fully developed hepatitis B induced cirrhosis  to incomplete septal cirrhosis . The best demonstration of such reversibility of cirrhosis is demonstrated in patients with hepatitis C virus (HCV) or hepatitis B virus (HBV) cirrhosis treated effectively with drug  sofusbuvir( for genotypes 1, 2, 3, 4, 5, and 6)  or with velpatasvir, or with γ-interferon(peginterferon) , . In additions there are also several reports  of histo pathological proof (Stage 4c cirrhosis) in auto Immune hepatitis , hereditary heamochromotosis, secondary briliary cirrhosis and occasional cases of wilson’s disease.
The morphological features of regressing cirrhosis in human have been defined above. Regression of cirrhosis involves two main processes, namely decrease in fibrosis and repopulation of fibrogenic region by regenerating hepatocytes. There is not decrease of amount fibrous tissue and collagen tissue which may be assessed by sinus red stain followed by computer assisted digital images or by vangision stain and reticulin stain followed by morphometric measurement of fibrous area. There will be thinning of fibrous septa with disappearance of shunting vessels where the septa and septa becomes incomplete gradually thinned out and finally disappear. Bile ductular proliferation will disappear quickly in a regressing liver where as sinusoidal capillaries proliferation and peri sinusoidal fibrosis become inconsistent regression of fibrosis is associated with partial or full restoration lobular organization. There are eight parameters which represent hepatic repair complex or regression of cirrhosis. 1)Perforated delicate septa, 2)isolated thick collagen fibers,3)delicate peri portal fibrous spikes,4) portal tract remnants,5)hepatic vein remnants with prolapsed hepatocytes ,6)hepatocytes within portal tracts or split septa.
 A New Concept of Incomplete Septal Cirrhosis

 Histo pathologically different pattern of Cirrhosis can be described which depends on interplay between hepatocyte injury, regeneration  and fibrosis . Morhphologically Cirrhosis is usally  termed Micronodular or macronodular or mixed type . There is another type of Cirrhosis which was  introduced  by Popper .H etal as incomplete septal cirrohosis(9) – a type of  macronodular  cirrhosis  in which slender  incomplete septae  demarcate  larger inconspicuous  nodules . On needle biopsy of liver  apart from  then  1) incomplete septa  render 2)  a vague nodule  formation  to the liver . Incomplete  Septal cirrohosis  is also associated with 3) Hypoplastic  Portal tract 4) Increase in venous chanels 5) Abnormal spacing between portal  tracts  and veins 6) Crowding of Reticulin fibers between  adjacent zones of Hyperplastic Parenchyma 7) hepatocyte cell plate thickening  8) dilated Sinusiods
 Regression of Cirrohosis is best demonstrated in Chronic Hepatitis B and Chronic Hepatitis C after effective treatment  with drug  sofusbuvir( for genotypes 1, 2, 3, 4, 5, and 6)  or with velpatasvir, with or without Ribavirin  or with γ-interferon(peginterferon) . Regression may be demonstrated  also in Alcoholic cirrohosis  in compensated state after abstinence  of alcohol and with antifibrogenic drugs

 Similarly Histopathological  improvement beween pared liver biopsies  is also observed  after weight loss, hypocaloric diet, Blood sugar control , control of hyperlipidimia   and exercise  in established  NASH  or NAFLD related cirrhosis . There are  many reports  of regression of cirrohosis  in autoimmune hepatitis  after treatment with Prednisilone and Azothiaprine

 In contrast  features of  regressions  have not been yet well established in primary billiary  cirrhosis , primary sclerosing cholangitis  and vascular obliterative  disease

Progression versus Regression  assessment  by pathologists

 As a pathologist  while we authors evaluate liver biopsy  from a case of  established cirrhosis  we must try to evaluate whether cirrhosis is progressive or regressive as per Wanless criteria(10). This should be assessed in paired liver biopsies taken after  significant  time interval of complete treatment. A biopsy Length of at least 2-3 cm or presence of 11 complete portal tract are considered adequate liver biopsy for this purpose

General

Progression

 Regression

 Area

 Enlarged with chronic inflammation & fibrosis

Normal or enlarged , but with fibrosis only

Bile ducts

 Preserved or absent

Usually preserved

 Hepatic Artery

 May be prominent due to formation of vascular shunts

 Prominence of hepatic arterioles persist

Portal veins

 Obscured due to obliterative venopathy

Obscuring portal veins

Interface Activity

 Frequently active interface hepatitis, cholestasis , ductular proliferation

 inactive

 Fibrous Septa

 With or without bridging: Pattern of septal fibrosis depends on Etiology _: broad inflamed septa in case of viral hepatitis 

More delicate sinusoidal fibrosis in Alcohol, Toxic  and Metabolic conditions

 Thinned delicate ( even bridging) may  exhibit . Discontinuty ,Perforation


Parenchymal Hepatocytes

 May or may not show characteristic histological feature of Etiology

 May be residual feature of underlying cause present

 Hepatic cellular complex

Absent

Present


References
①Kutami R, Girgrah N, Wanless IR etal. The Laennec grading system for assessment of hepatic fibrosis: validation by correlation with wedged hepatic vein pressure as clinical feature.  Heptalogy 32:407A:2000
②Wanless IR,Sweeney G,Dhilon A.P etal “Lack of progressive hepatic Fibrosis during long term therapy with deferiprone in subjects with transfusion dependent Beta Malassemia  Blood .” 100:1566-9:2002.
③Nagula S, Jain D, Groszmann R.J etal- Histological-hemodynamic correlation in cirrhosis- a histological classification of the severity of cirrhosis. J. Hepatol-44:177-7,2006
④Pierre Bedosa, Guadal Pepe-Garcia-Tsao, Dhanpat Jain “Cirrhosis regression and Sub classification.”                Surgical Pathology 6:295-309:2013
⑤Calvaruso V, Burroughs A.K, Standish R etal “computer assessed Image analysis of Liver collagen: relationship to Ishak scoring and hepatic venous pressure gradient” Heptalogy 49.1236-44:2009
⑥Friedman S.L, Bansal MB “reversal of hepatic fibrosis- fact or fantasy? “ Hepatogy 43:82-88:2006
⑦Perez-Tamzyo R ”Cirrhosis of the Liver: a reversible disease? “ Pathol.Annu 14(2):183-213 1979
⑧Czaja A.J, Carpenter HA. Decreased fibrosis during Cortico Steroid Therapy of auto immune hepatitis. J.Hepatol 40:646-52:2004
(9) Poper H  What is the major types of Hepatic Cirrhosis In Ingelflinger F, Relman A ; Finland  M Eds Controversy in Internal Medicine  Philadelphia ,Publishers Saunders  1966 : 233-243

(10)  Wanless I R , Nakashime E, Shirman M  Regression of  Human cirrhosis : Morphological Features and the genesis of incomplete  septal cirrhosis  Arch.Pathol. Lab. Med 12:1599-1607: 2000

Please note  it very carefully that, The Copy Right of this article Regression of cirrhosis-my current understanding " belongs only to Professor Pranab kumarBhattacharya MD(calcutta university ) FIC path(Ind)  , as per copy right rules of IPR 1996 applicable in India-2006 sections 307/ 306/ 3D/107/2012 and PIP Acts of US 2012SPARC authors amended Copy Right rules-2006  of US  when & if accepted for any other blogs, 
as a reference, or publication  or Research  or  reference material  or published as paper or article
 in open access journals as a commissioned article  and then  also this article will be under RDF 
 Copy Right rules of IPR of Prof PK Bhattacharya.
 No person from any states of  country India or any citizen of India or of Indian origin are for ever
 authorized by Professor Pranab kumar Bhattacharya to use  any  scientifically meaningful 
syllables/words  /sentences from this published blog article in the Blogs of Prof Pranab kumar Bhattacharya 
MD(cal) FIC path(ind.) in Blog spot.com  without his / future copy right  owner ‘s written permission  &
 copy Right clearance, even for any one’s personal or for his/her fair use even/ dissemination of  
any information( Will be considered  then as Plagiarism) , [except such all permission is always
 remain granted to other authors ,their first degree blood relatives in what ever manner they want 
to use this article  for ever from the date of publication in ProfPranab Kumars Bhattacharya 
MD(cal) FIC path(ind)  Blog at blog spot.com   or for digital preservation of  the article in National
 Level Science Library(NSDL) US or of other countries.- by declaration- 
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Mahatma Gandhi Excellance award of India International Friendship Society New Delhi To Prof Dr Pranab kumar Bhattacharya

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 Mahatma Gandhi Excellence award of India International Friendship Society 
New Delhi To be Awarded  in4th October 2017 at  new delhi 
 Patrons of the society are  http://www.globalfriendshipday.org/patronsandmembers.php
 any News Paper is allowed to print the news 

India International Friendship Society was founded as a non-Profit non-Governmental Organization (NGO)in the year …… on four very strong pillars – friendship, patriotism, commitment and ethical values.The guiding force of the Society is based on the noble philosophy of serving the cause of motherland - headed by one of the most distinguished personalities of India possessing some rare attributes like uprightness and discipline, loyalty and concern - the former CBI Director Sardar Joginder Singh.
Objective:-
The activities of the Society move round the nucleus of patriotism created by the founders. The organization has been relentlessly working towards creating a congenial and healthy environment for the Non-Resident Indians reveal the emotional feelings towards their motherland that they always nurture and actively participate in the developmental projects of the country.

Indians are bestowed with extraordinary talent and skill – which is manifested across the world where Indians stand out in distinction and excellence in their respective fields of activities. The Society has been working with patriotically spirited objective to promote and strengthen greater unity and friendship between resident and non-resident Indians and to create a congenial atmosphere of rapport and closeness as well as greater mutual understanding for the NRIs to invest in Indian projects on industries, services and social welfare.

As appreciation and recognition, the Society also confers prestigious awards to Indian and non-Indian nationals who has made significant contributions in country’s socio-economical developments and glorified the country by their exquisite work anywhere in the world.

Aim & Objects of the society :-

To develop social and cultural cooperation between our progressive people and of all countries.
To honestly share and exchange important evolution between any two countries in culture, education, sports and others.
To arrange conferences, seminars and exhibitions and producing and distributing relevant literature, including books and journals for universal benefit from them.
To celebrate festivals for each other and exchange greetings on such occasions to make friendship more deeper and practical.
To arrange visits of different delegations to friendly countries to meet people in all fields and vocations, including science and technology and education.
To arrange money and other infrastructure for new joint ventures established in close cooperation or help of the other society or its members.
To exchange scientific and technical education.
To arrange meeting with Government Ministries to promote Society's aim and objective.
To act in the best interests of the Government, the country and the members of the Society.
To enroll members throughout the world among people of Indian origin. Person who receive the award will be the member of society.
To establish and develop the international friendship and fraternity and foster the bondage of humanity and service by different schemes and programmes.
To honour its member with "Award and Certificate of Excellence" for outstanding leadership in the field, such as education, medical services, engineering, architecture and other exceptional performance of high order and services. This society, however, reserves the right to present or not to present the Award(s) even after the selection of the candidate without assigning any reasons whatsoever, without being answerable to anyone. No legal or any other action can be taken against the society. The applies to the jurisdiction of Delhi State.
To collect a most reasonable delegate fee from the Awardee, in order to raise the necessary funds. The delegate fee, however, is strictly voluntary and no delegate is under any obligation to pay.
In case any information is lost, the Awardees can collect his Award at a later date from New Delhi.

ACHIEVEMENT AND VERY SHORT BIOGRAPHY OF PROF.(Dr.) PRANAB KUMAR BHATTACHARYA FOR ANY NATIONAL/ INTERNATIONAL AWARDS NOMINATIONS

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Achievements and Shortest Biography of Prof. Dr.Pranab Kumar Bhattacharya, Retired WBMES

( DOB -1956)

                                                                               


Prof. Dr.Pranab Kumar Bhattacharya, WBMES  (Retired)                                 p.k.b=2016.jpg

Ex Professor,and Head Dept. of Pathology, 

Academic building,, 2nd floor, 

Calcutta School of Tropical Medicine, 

108,C.R.Avenue, Kolkata 700 073, West Bengal Department of Health and Family Welfare                                                   

Government of West Bengal

Email profpkb@yahoo.co.in

whatsapp & mobile -:9231510435.

            

                                


       TO WHOM IT MAY CONCERN 


MBBS from The Medical College, Kolkata”, University of Calcutta, W.B(year -: january 1981); M.D ( Pathology) fromInstitute of PostGraduate Medical Education & Researchof University of Calcutta (year-: December 1989), Fellows of Indian College of Pathology (FICPATH year-: december 1997), Presently Retiered as “Professor”& head(at Department of Pathology, Calcutta School of Tropical Medicine, Kolkata, West Bengal  & Ex Professor of Pathology at Murshidabad Medical College, Berhampore , West Bengal India. He was Ex-Professor and  Ex- Head of Pathology at Calcutta School of Tropical Medicine and Ex supervisor , convener ,member of Board of Studies for UG/PG/PD and D.C.P (at Calcutta School of Tropical Medicine) courses of  West Bengal University of Health Sciences (WBUHS); also Ex Professor & Head of Pathology at Regional Institute of Ophthalmology, The Medical College, Kolkata. He was Additional Professor in Pathology at IPGME&R ,Kolkata and was Professor of West Bengal University of Health Sciences(WBUHS) at University college of Medicine ,Kalyani,  Nadia, West Bengal ( in 2011 ) . He acquired vast teaching, administrative and also diplomatic experiences in Government services (Both in WBHS and in WBMES cadre ),under the Health and Family Welfare department of West Bengal government ,Swasthya Bhavan, Salt lake city, Kolkata -93  , spanning more than  three and half decades (37 years 08months of Services).He also have credited himself as very much popular and one of the most knowledgeable MCI /NMC Recognized Doctoral /Post Graduate teacher( Teacher NO- PAT-900415 ); university Examiner; MD /PhD Thesis Guide and Adjudicators in discipline Pathology in this country/as well in the state of West Bengal and worked as teacher in Pathology in all capacities in previous five tire promotional system of WBMES cadre in West Bengal state of India  he  retired now  . His date of superannuation was 31.03.2021 from WBMES cadre services as "Professor of Pathology" in equivalent officiating ranks of "special secretary" to the government of West Bengal.


Publications 

He has been regularly publishing most spectacular and excellent scientific articles, as Editorials / Review articles/ case reports / as comments / Rapid responses published/ Responses/ Letters to the Editor / Electronic letters/ correspondences/  and  his original research papersin Indian National level and of International level reputed, external double blinded peer reviewed, indexed journals of Biomedicine and of Science, like Physics/  Particle Physics/, Theoretical Physics/, Space Sciences, Astronomy / Astrophysics/ Astrobiology journals  with very high or topmost impact factors by Reuter Thomson /ISI/Copernicus/COPUS/Excerpta Medicus or Elsevier Science/ Researchgate/ Pub Facts/ Pub-lon/ Pubmed / Google scholar/ science Gate with his tween sibling brothers Mr.Rupak Bhattachrya, Mr. Ritwick Bhattacharya , his sister Mrs. Dalia Mukherjee and his only  daughter Miss Upasana Bhattacharyaunder hisown Intellectual Property Rights (all acts and laws) Copyright as a registered personal , RDF Copyright , PIP Copyright-2012 USA  and in Copyright works, USA . 

 

Published Research Papers-:


He published so far 327 Research Papers/Articlesin various journals of National and International repute ( including in Science of AAAS.org USA, PNAS USA, the BMJ , BMJ opinion, BMJ Blogs , JAMA, JCI, Nejm, The Lancet, RSBMT, JCP, ICPJ, ATMPH, Blood,  cell, and Nature journal)  in National and International conferences of academic bodies as Abstracts. 


He has more than 270 citations references of his published articles in International Journals ,books, MD/ MS Thesis of WBUHS / or University of Calcutta  and in books chapters by various international authors. He owns  a blog in his name at  Google blogs spot  with more than 355  posts  by himself and his Associate authors . Average viewers of his free blogs articles published are 90,000 every year.  from all over the world.

Awards Received and nominated for awards  -:

He was the recipient of several (09)  Medals , Prizes of University of Calcutta, 98 Certificates of merits , Excellences and Medals of college , and of various academic bodies ,Organizations and many Guest speakers, Chairpersons , Judges of  free and award papers presentation, conference & scientific webinar participation certificates including certificate of his excellences.He is recipient of Rashtriya Gaurav Award of India (conferred  2016 August) and” Glory of India Award”( conferred 2016 er),Bharat Ratna Dr. APJ Abdul Kalam Award for Excellence in Astronomy, On Theoretical physics  ( conferred 2017 January) ; Mother Teresa  Peace Prize (conferred  2017 May);Mahatma Gandhi Excellence award (conferred  October 2017), Mahatma Gandhi Life Time achievement award ( conferred 2019 May ) and Glory of India Gold Medal ( Conferred May 2019) from India International Friendship Society (IIFS) of New Delhi, India, and Bangkok  Thailand in 2016 , 2017and 2019.  He was selected for “Jewel of India Prize”” of IIFS, New Delhi  in 2019. He was awarded Best Citizen of India award ( 2017).  He was selected for  Rashtriya Pratibha ( for most  Talented Personality in India) Award of  Indo Socio Development Association( March 2018)  ; He was Selected forI-Proclaim Annual Research Awards - 2017  as Lifetime Achievement</