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Pathophysiology of alcoholic pancreatitis:An overview

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World Journal of Gastroenterology 2006年第46期12卷 7421-7427页

作者： parimal chowdhury Priya Gupta Department of Physiology and Biophysics University of Arkansas for Medical sciences Little Rock Arkansas United States

Use of alcohol is a worldwide habit regardless of socio- economic background. Heavy alcohol consumption is a potential risk factor for induction of pancreatitis. The current review cites the updated literature on the alcohol metabolism, its effects on gastrointestinal and pancreatic function and in causing pancreatic injury, genetic predisposition of alcohol induced pancreatitis. Reports describing prospective mechanisms of action of alcohol activating the signal transduction pathways, induction of oxidative stress parameters through the development of animal models are being presented.

关键词：酒精代谢胰腺功能胰腺炎病理生理综述

Nicotine as a mitogenic stimulus for pancreatic acinar cell proliferation

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World Journal of Gastroenterology 2006年第46期12卷 7428-7432页

作者： parimal chowdhury Kodetthoor B Udupa Departments of Physiology and Biophysics University of Arkansas for Medical Sciences 4301 W Markham Street Little Rock Arkansas 72205 United States Departments of Physiology and Biophysics and Geriatrics University of Arkansas for Medical Sciences 4301 W Markham Street Little Rock Arkansas 72205 United StatesMedical Service Central Arkansas Veterans Healthcare System Little Rick Arkansas 72205 United States

Cell proliferation is an important process in life for growth of normal and cancer cells. The signal transduction pathways activated during this process are strictly regulated. This editorial focuses on the role of nicotine, a mitogen, in the induction of signaling pathways resulting in proliferation of pancreatic tumor cells and compares these events with those in normal acinar cells isolated from the rat pancreas. The data shows striking similarities between these two cellular systems. In addition, the editorial reviews very recent literature of the contribution of MAPK signaling in cell lines associated with human diseases. A prospective cellular model of nicotine induced activation of MAPK cascade is presented.

关键词：胰腺腺细胞病理胰腺癌细胞增殖烟碱 ERK 有丝分裂 MAPK

Distribution of ^3H—nicotine in Rat Tissues Under the Influence of Simulated Microgravity

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Biomedical and Environmental Sciences 1999年第2期12卷 103-109页

作者： parimal chowdhury MICHAEL E. SOULSBY AND JAMES N. PASLEY (Department of Physiology and Biophysics, University of Arkansas for Medical Scienses, Little Rock, Arkansas 72205, USA) Univeristy of Arkansas for Medical Sciences 美国

Rat tail suspension offers a useful model to reproduce physiologic responses to *** present study was conducted in the head-down-tilt(HDT) rat model to assess changes in metabolism of body tissues employing 3H-nicotine. Twelve male rats were used in the study. Half of the rats were tail suspended at 30°for two weeks on a 12/12 light/dark cycle. During this period,body weight, food and fluid intakes were measured. At term, animals were anesthetized and injected IV withe a solution contaming 4 microuries of micotine. After 90 min the animals were sacrificed, exsanguinated and tissues (brain,blood,trachea,salivary gland,lung,heart,esophagus,spleen, kidneys and testes) were harvested. The distribution of 3H-nicotine per gram of each tissue was determinded and ealeulated as percent of total injected radioactivity. Final body weights of suspended ammals were significantly (P < 0.0 5) lower than those of eontrols(309±21 vs 350±11g). 3HNicotine waw retained in greatest amounts by the kindneys, followed inorder by salivary glands, spleen, and gastrointestinal tissues. compared to non-suspended control, the tissue retention of nicotine in suspended animals was decreased in the following tissues:esphyagus (25 %), aorta (25%). fundus (25%), trachea (22%), adrenals (18%), spleen (17 %), and pancreas (12 %). The decreased retention of mcotine in tissues from suspended animals may be indicative of the fluid shifts and changes in blood flow to those tissue beds. The lack of differnces in nicotine retention in liver and kidney between control and suspended groups may implicate a normal metabolic function of these organs even under simulated weightlessness.

关键词： Gravitation Animals Male Nicotine Rats Rats, Sprague-Dawley Research Support, Non-U.S. Gov't Tissue Distribution Tritium Weightlessness Simulation

The genetics of nicotine dependence:Relationship to Pancreatic cancer

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World Journal of Gastroenterology 2006年第46期12卷 7433-7439页

作者： Stewart L MacLeod parimal chowdhury Department of Pediatrics University of Arkansas for Medical Sciences and Arkansas Children's Hospital Research Institute Arkansas Center for Birth Defects Research and Prevention Little Rock AR United States Department of Physiology University of Arkansas for Medical Sciences Little Rock AR United States

SmoKing or tobacco products continues to De a major cause of worldwide health problems. Epidemiological studies have shown that tobacco smoking is the greatest risk factor for the development of pancreatic cancer. Smokers who are able to quit smoking can reduce their risk of pancreatic cancer by nearly 50% within two years, however, their risk of developing pancreatic cancer remains higher than that of non-smokers for 10 years. Nicotine is the major psychoactive substance in tobacco, and is responsible for tobacco dependence and addiction. Recent evidence suggests that individuals have genetically based differences in their ability to metabolize nicotine, as well as genetic differences in the psychological reward pathways that may influence individual response to smoking initiation, dependence, addiction and cessation. Numerous associations have been reported between smoking behavior and genetic polymorphisms in genes that are responsible for nicotine metabolism. In addition, polymorphisms in genes that encode neurotransmitters and transporters that function in psychological reward pathways have been implicated in differences in smoking behavior. However, there is a large degree of between-study variability that demonstrates the need for larger, well-controlled case-control studies to identify target genes and deduce mechanisms that account for the genetic basis of inter-individual differences in smoking behavior. Understanding the genetic factors that increase susceptibility to tobacco addiction may result in more effective tobacco cessation programs which will, in turn, reduce the incidence of tobacco related disease, including pancreatic cancer.

关键词：烟碱依赖胰腺癌遗传因素抽烟遗传多态性尼古丁代谢

Tissue Distribution of [^3H]—Nicotine in Rats

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Biomedical and Environmental Sciences 1993年第1期6卷 59-64页

作者： parimalchowdhury RYUICHIRODOIPHILLIPL.RAYFORD LOUISW.CHANG Departments DepartmentsDepartments of Physiology BiopgysicsToxicologyUniversity of Arkansas for Medical Sciences4301W.Markham StLittle RockA R 72205USAof Physiology and BiophysicsUniversity of Arkansan for Medical Sciences4301W.Markham StLittle RockA R 72205USAof Physiology and ToxicologyUniversity of Arkansas for Medical Sciences4301W.Markham StLittle RockA R 72205USA

This study was conducted in adult male Sprague -- Dawley rats to determine the distribution of [3H]-nicotine in blood and tissues following a bolus injection and a constant infusion of pure nicotine. The animals were anesthetized and injected with either 0.5 ml of nicotine solution or given a constant infusion of the same nicotine solution with identical amounts of radioactive nicotine. After sacrifice, blood, brain, trachea, salivery gland, esophagus, lung, heart, liver, fundus, antrum, spleen, pancreas, duodenum, jejunum, ileum, cecum, colon, kidneys, adrenal gland, and testes were collected and measured for radioactivity by scintillation counting. The distribution of nicotine was found highest in kidneys by both routes of administration. Higher accumulations were also found in salivary and adrenal glands, fundus, antrum, duodenum, jejunum, ileum and colon. Retention of nicotine via constant infusion was significantly higher in esophagus, fundus antrum, spleen, cecum, pancreas, testes, heart and muscle when compared with bolus injection. Six-fold increase in retention of blood levels of nicotine were found with constant infusion. (P<0.05). The results indicate that longer retention of nicotine occurs in blood and other specific tissues such as esophagus, fundus, antrum, spleen, cecum, pancreas, testes, heart and muscle via constant exposure. These data may implicate the predisposition of these tissues to pathologic manifestations.

关键词： Tissue Distribution of Nicotine in Rats

Molecular signaling mechanisms of apoptosis in hereditary non-polyposis colorectal cancer

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World Journal of Gastrointestinal Pathophysiology 2012年第3期3卷 71-79页

作者： Samar Hassen Nawab Ali parimal chowdhury Department of Applied Science College of Science and Mathematics University of ArkansasLittle Rock AR 72204 United States Department of Physiology and Biophysics University of Arkansas for Medical SciencesLittle Rock AR 72205 United States

Colorectal cancer is the second most leading cause of cancer related deaths in the western countries. One of the forms of colorectal cancer is hereditary non-polyposis colorectal cancer (HNPCC), also known as "Lynch syndrome". It is the most common hereditary form of cancer accounting for 5%-10% of all colon cancers. HNPCC is a dominant autosomal genetic disorder caused by germ line mutations in mismatch repair genes. Human mismatch repair genes play a crucial role in genetic stability of DNA, the inactivation of which results in an increased rate of mutation and often a loss of mismatch repair function. Recent studies have shown that certain mismatch repair genes are involved in the regulation of key cellular processes including apoptosis. Thus, differential expression of mismatch repair genes particularly the contributions of MLH1 and MSH2 play important roles in therapeutic resistance to certain cytotoxic drugs such as cisplatin that is used normally as chemoprevention. An understanding of the role of mismatch repair genes in molecular signaling mechanism of apoptosis and its involvement in HNPCC needs attention for further work into this important area of cancer research, and this review article is intended to accomplish that goal of linkage of apoptosis with HNPCC. The current review was not intended to provide a comprehensive enumeration of the entire body of literature in the area of HNPCC or mismatch repair system or apoptosis; it is rather intended to focus primarily on the current state of knowledge of the role of mismatch repair proteins in molecular signaling mechanism of apoptosis as it relates to understanding of HNPCC.

关键词： Colorectal cancer Hereditary non-polyposis colorectal cancer Apoptosis Molecular signaling mechanisms DNA mismatch repair proteins

Retrieval and Amplification of DNA from Unstained Histopathological Sections

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Biomedical and Environmental Sciences 1993年第3期6卷 211-216页

作者： DONNAC.MONTAGUE BEVERLYD.LYN-COOK parimalchowdhury LOUISW.CHANG University NationalUniversityUniversity of Arkansas for Medical SciencesDeparments of Pharmacology/ToxicologyCenter for Toxicological ResearchJeffersonAR72079USAof Arkansas for Medical SciencesDepartments of Pharmacology/ToxicologyPhysiologyof Arkansas for Medical SciencesDepartments of Pharmacology/ToxicologyNational Center for ToxicologicalResearchJeffersonAR 72079USA

Testing of compounds for carcinogenic potential in vivo involves various experimental designs. A few of these techniques are directed to demonstrate the genotoxicity and mutagenicity of the compound by histopathology. These changes shown by histochemical means include monoclonal antibody directed cellular markers. Development of the polymerase chain reaction technique (PCR) for amplification of DNA has facilitated the investigation of molecular events related to the formation of malignant neoplasms. We describe here a method for screening tissues for mutations of the H-ras gene using monoclonal antibodies directed toward normal and mutant p21 proteins. Formalin-fixed, paraffin-embedded tissue sections are used to subsequently confirm the gene mutation by PCR amplification of the H-ras gene. The results indicated a successful application of this technique to demonstrate the presence of p21 oncoprotein in the tissues tested.

关键词： Retrieval and Amplification of DNA from Unstained Histopathological Sections DNA