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| 1 | Dextran sodium sulfate colitis murine model: An indispensable tool for advancing our understanding of inflammatory bowel diseases pathogenesis显示文摘Inflammatory bowel diseases(IBD),including Crohn's disease and ulcerative colitis,are complex diseases that result from the chronic dysregulated immune response in the gastrointestinal tract. The exact etiology is not fully understood,but it is accepted that it occurs when an inappropriate aggressive inflammatory respon-se in a genetically susceptible host due to inciting environmental factors occurs. To investigate the path-ogenesis and etiology of human IBD,various animal models of IBD have been developed that provided indispensable insights into the histopathological and morphological changes as well as factors associated with the pathogenesis of IBD and evaluation of therapeutic options in the last few decades. The most widely used experimental model employs dextran sodium sulfate(DSS) to induce epithelial damage. The DSS colitis model in IBD research has advantages over other various chemically induced experimental models due to its rapidity,simplicity,reproducibility and controllability. In this manuscript,we review the newer publicized advances of research in murine colitis models that focus upon the disruption of the barrier function of the intestine,effects of mucin on the development of colitis,alterations found in microbial balance and resultant changes in the metabolome specifically in the DSS colitis murine model and its relation to the pathogenesis of IBD. | Derrick D Eichele Kusum K Kharbanda | 2017 | World Journal of Gastroenterology2017，23，33： | 50 |
| 2 | Treatment options for alcoholic and non-alcoholic fatty liver disease: A review显示文摘Alcoholic liver disease(ALD)and non-alcoholic fatty liver disease(NAFLD)are serious health problems worldwide.These two diseases have similar pathological spectra,ranging from simple steatosis to hepatitis to cirrhosis and hepatocellular carcinoma.Although most people with excessive alcohol or calorie intake display abnormal fat accumulation in the liver(simple steatosis),a small percentage develops progressive liver disease.Despite extensive research on understanding the pathophysiology of both these diseases there are still no targeted therapies available.The treatment for ALD remains as it was 50 years ago:abstinence,nutritional support and corticosteroids(or pentoxifylline as an alternative if steroids are contraindicated).As for NAFLD,the treatment modality is mainly directed toward weight loss and co-morbidity management.Therefore,new pathophysiology directed therapies are urgently needed.However,the involvement of several inter-related pathways in the pathogenesis of these diseases suggests that a single therapeutic agent is unlikely to be an effective treatment strategy.Hence,a combination therapy towards multiple targets would eventually be required.In this review,we delineate the treatment options in ALD and NAFLD,including various new targeted therapies that are currently under investigation.We hope that soon we will be having an effective multi-therapeutic regimen for each disease. | Sukhpreet Singh Natalia A Osna Kusum K Kharbanda | 2017 | World Journal of Gastroenterology2017，23，36： | 45 |
| 3 | Human immunodeficiency virus and hepatotropic viruses comorbidities as the inducers of liver injury progression显示文摘Hepatotropic viruses induced hepatitis progresses much faster and causes more liver-related health problems in people co-infected with human immunodeficiency virus(HIV). Although treatment with antiretroviral therapy has extended the life expectancy of people with HIV, liver disease induced by hepatitis B virus(HBV) and hepatitis C virus(HCV) causes significant numbers of non-acquired immune deficiency syndrome(AIDS)-related deaths in coinfected patients. In recent years, new insights into the mechanisms of accelerated fibrosis and liver disease progression in HIV/HCV and HIV/HBV co-infections have been reported. In this paper, we review recent studies examining the natural history and pathogenesis of liver disease in HIV-HCV/HBV co-infection in the era of direct acting antivirals(DAA) and antiretroviral therapy(ART). We also review the novel therapeutics for management of HIV/HCV and HIV/HBV coinfected individuals. | Murali Ganesan Larisa Y Poluektova Kusum K Kharbanda Natalia A Osna | 2019 | World Journal of Gastroenterology2019，25，4： | 12 |
| 4 | Primary duodenal neoplasms:A retrospective clinico-pathological analysis显示文摘AIM: To analyze the clinico-pathological spectrum of primary duodenal neoplasms. METHODS: A total of 55 primary duodenal neoplasms reported in the last 10 years after excluding ampullary and periampullary tumors were included in the study. Clinical details were noted and routine hematoxylin and eosin stained paraffin sections were studied for histological subtyping of the tumors. RESULTS: On histopathological examination primary duodenal neoplasms were categorized as: epithelial tumor in 27 cases (49.0%) including 10 cases of adenoma, 15 cases of adenocarcinoma, and 2 cases of Brunner gland adenoma; mesenchymal tumor in 9 cases (16.3%) consisting of 4 cases of gastrointestinal stromal tumor, 4 cases of smooth muscle tumor and I case of neurofibroma; lymphoproliferative tumor in 12 cases (21.8%), and neuroendocrine tumor in 7 cases (12.7%). CONCLUSION: Although non-ampullary/periampullary duodenal adenocarcinomas are rare, they constitute the largest group. Histopathological examination of primary duodenal tumors is important for correct histological subtyping. | Amanjit Bal Kusum Joshi Kim Vaiphei JD Wig | 2007 | World Journal of Gastroenterology2007，13，7： | 10 |
| 5 | Liver as a target of human immunodeficiency virus infection显示文摘Liver injury is a characteristic feature of human immunodeficiency virus(HIV) infection, which is the second most common cause of mortality in HIV-infected patients. Now it is recognized that liver plays a key role in HIV infection pathogenesis. Antiretroviral therapy(ART), which suppresses HIV infection in permissive immune cells, is less effective in hepatocytes, thereby making these cells a silent reservoir of HIV infection. In addition to direct hepatotoxic effects of HIV, certain ART treatment modalities provide hepatotoxic effects. The exact mechanisms of HIV-triggered chronic hepatitis progression are not elucidated, but the liver is adversely affected by HIV-infection and liver cells are prominently involved in HIV-elicited injury. These effects are potentiated by second hits like alcohol. Here, we will focus on the incidence of HIV, clinical evidence of HIVrelated liver damage, interactions between HIV and liver cells and the role of alcohol and co-infection with hepatotropic viruses in liver inflammation and fibrosis progression. | Murali Ganesan Larisa Y Poluektova Kusum K Kharbanda Natalia A Osna | 2018 | World Journal of Gastroenterology2018，24，42： | 5 |
| 6 | Role of alcohol in pathogenesis of hepatitis B virus infection显示文摘Hepatitis B virus(HBV)and alcohol abuse often contribute to the development of end-stage liver disease.Alcohol abuse not only causes rapid progression of liver disease in HBV infected patients but also allows HBV to persist chronically.Importantly,the mechanism by which alcohol promotes the progression of HBVassociated liver disease are not completely understood.Potential mechanisms include a suppressed immune response,oxidative stress,endoplasmic reticulum and Golgi apparatus stresses,and increased HBV replication.Certainly,more research is necessary to gain a better understanding of these mechanisms such that treatment(s)to prevent rapid liver disease progression in alcohol-abusing HBV patients could be developed.In this review,we discuss the aforementioned factors for the higher risk of liver diseases in alcohol-induced HBV pathogenies and suggest the areas for future studies in this field. | Murali Ganesan Allison Eikenberry Larisa Y Poluektova Kusum K Kharbanda Natalia A Osna | 2020 | World Journal of Gastroenterology2020，26，9： | 5 |
| 7 | Revisiting the morphology of pelvicalyceal system in human cadaveric kidneys with a systematic review of literature显示文摘Objective:Renal collecting system macroscopically consists of minor calyx,major calyx,renal pelvis and ureter.Stone in renal collecting system is a common presentation in everyday urological practice.The prevalence of renal calculi ranges from 4%to 20%in different geographical distribution.Anatomical variation in renal collecting system plays a significant role in formation of calculi in its parts.The large extra renal pelvis leads to stagnation of urine for longer durations and formation of stones.The stone free rate after percutaneous nephrolithotomy and extra corporeal shock wave lithotomy is significantly related to anatomical factors,particularly the type of renal pelvis and dimensions(length and width)of lower infundibulum.Previous authors described the morphology of pelvicalyceal system in a highly variable manner and the available anatomical description of pelvicalyceal system is contradictory and incomplete.Hence an attempt has been made to provide the precise anatomy of pelvicalyceal system in adult human kidneys.Methods:We studied 196 formalin embalmed kidneys to note the number of infundibulum,major and minor calyces.The location and shape of pelvis were also studied.Results:The intra-renal pelvis was narrow and had funnel shaped appearance in 95 of total 196(48.5%)specimens,and the extra-renal pelvis was dilated as balloon shaped in 43 of 196(21.9%)specimens.In 41(20.9%)specimens,the renal pelvis was having partially intra-and extra-renal in location.Bilateral symmetry was found in only 27.1%of 196 renal collecting systems.The length of lower infundibulum was more than 22 mm in 19(9.7%)of 196 cases which directly affects the stone clearance rate during open and endoscopic surgeries on pelvicalyceal system.Conclusion:This study provides the accurate morphological details of the shape and dimensions of renal pelvicalyceal system to help the urologists and nephrologists. | Kusum Rajendra Gandhi Sushama Chavan | 2019 | Asian Journal of Urology2019，6，3： | 5 |
| 8 | Relationship between oxidative stress and hepatic glutathione levels in ethanol-mediated apoptosis of polarized hepatic cells显示文摘AIM:To investigate the role of reactive oxygen species(ROS) in ethanol-mediated cell death of polarized hepatic(WIF-B) cells.METHODS:In this work,WIF-B cultures were treated with pyrazole(inducer of cytochrome P4502E1,CYP2E1) and/or L-buthionine sulfoximine(BSO),a known inhibitor of hepatic glutathione(GSH),followed by evaluation of ROS production,antioxidant levels,and measures of cell injury(apoptosis and necrosis).RESULTS:The results revealed that ethanol treatment alone caused a significant two-fold increase in the activation of caspase-3 as well as a similar doubling in ROS.When the activity of the CYP2E1 was increased by pyrazole pretreatment,an additional two-fold elevation in ROS was detected.However,the CYP2E1-related ROS elevation was not accompanied with a correlative increase in apoptotic cell injury,but rather was found to be associated with an increase in necrotic cell death.Interestingly,when the thiol status of the cells was manipulated using BSO,the ethanol-induced activation of caspase-3 was abrogated.Additionally,ethanol-treated cells displayed enhanced susceptibility to Fas-mediated apoptosis that was blocked by GSH depletion as a result of diminished caspase-8 activity.CONCLUSION:Apoptotic cell death induced as a consequence of ethanol metabolism is not completely dependent upon ROS status but is dependent on sustained GSH levels. | Benita L McVicker Pamela L Tuma Kusum K Kharbanda Serene ML Lee Dean J Tuma | 2009 | World Journal of Gastroenterology2009，15，21： | 5 |
| 9 | Role of transmethylation reactions in alcoholic liver disease显示文摘Alcoholic liver disease is a major health care problem worldwide. Findings from many laboratories, including ours, have demonstrated that ethanol feeding impairs several of the many steps involved in methionine metabolism. Ethanol consumption predominantly results in a decrease in the hepatocyte level of S-adenosylmethionine and the increases in two toxic metabolites, homocysteine and S-adenosylhomocysteine. These changes, in turn, result in serious functional consequences which include decreases in essential methylation reactions via inhibition of various methyltransferases. Of particular interest to our laboratory is the inhibition of three important enzymes, phosphatidylethanolamine methyltransferase, isoprenylcysteine carboxyl methyltransferase and protein L-isoaspartate methyltransferase. Decreased activity of these enzymes results in increased fat deposition, increased apoptosis and increased accumulation of damaged proteins- all of which are hallmark features of alcoholic liver injury. Of all the therapeutic modalities available, betaine has been shown to be the safest, least expensive and most effective in attenuating ethanol-induced liver injury. Betaine, by virtue of aiding in the remethylation of homocysteine, removes both toxic metabolites (homocysteine and S-adenosylhomocysteine), restores S-adenosylmethionine level, and reverses steatosis, apoptosis and damaged proteins accumulation. In conclusion, betaine appears to be a promising therapeutic agent in relieving the methylation and other defects associated with alcoholic abuse. | Kusum K Kharbanda | 2007 | World Journal of Gastroenterology2007，13，37： | 3 |
| 10 | Lack of hepcidin expression attenuates steatosis and causesfibrosis in the liver显示文摘AIM: To investigate the role of key iron-regulatory protein, hepcidin in non-alcoholic fatty liver disease(NAFLD). METHODS: Hepcidin(Hamp1) knockout and floxed control mice were administered a high fat and high sucrose(HFS) or a regular control diet for 3 or 7 mo. Steatosis, triglycerides, fibrosis, protein and gene expression in mice livers were determined by histological and biochemical techniques, western blotting and realtime polymerase chain reaction. RESULTS: Knockout mice exhibited hepatic iron accumulation. Despite similar weight gains, HFS feeding induced hepatomegaly in floxed, but not knockout, mice. The livers of floxed mice exhibited higher levels of steatosis, triglycerides and c-Jun N-terminal kinase(JNK) phosphorylation than knockout mice. In contrast, a significant increase in fibrosis was observed in knockout mice livers within 3 mo of HFS administration. The hepatic gene expression levels of sterol regulatoryelement-binding protein-1c and fat-specific protein-27, but not peroxisome proliferator-activated receptoralpha or microsomal triglyceride transfer protein, were attenuated in HFS-fed knockout mice. Knockout mice fed with regular diet displayed increased carnitine palmitoyltransferase-1a and phosphoenolpyruvate carboxykinase-1 but decreased glucose-6-phosphatase expression in the liver. In summary, attenuated steatosis correlated with decreased expression of lipogenic and lipid storage genes, and JNK phosphorylation. Deletion of Hamp1 alleles per se modulated hepatic expression of beta-oxidation and gluconeogenic genes. CONCLUSION: Lack of hepcidin expression inhibits hepatic lipid accumulation and induces early development of fibrosis following high fat intake. Hepcidin and iron may play a role in the regulation of metabolic pathways in the liver, which has implications for NAFLD pathogenesis. | Sizhao Lu Robert G Bennett Kusum K Kharbanda Duygu Dee Harrison-Findik | 2016 | World Journal of Hepatology2016，8，4： | 3 |
| 11 | Methionine metabolic pathway in alcoholic liver injury显示文摘 | Kusum K. Kharbanda | 2013 | Current Opinion in Clinical Nutrition and Metabolic Care2013，，1： | 3 |
| 12 | Citric acid:An efficient and green catalyst for rapid one pot synthesis of quinoxaline derivatives at room temperature显示文摘有 1,2-dicarbonyl 混合物的 o-phenylenediamines 的冷凝作用在乙醇在房间温度在更高的收益面对柠檬性的酸负担得起相应 quinoxaline 衍生物,并且大多数反应在不到 1 min 被完成。 | Radhakrishnan Mahesh Arghya Kusum Dhar Tara Sasank T.V.N.V. Sappanimuthu Thirunavukkarasu Thangaraj Devadoss | 2011 | Chinese Chemical Letters2011，22，4： | 3 |
| 13 | Effect of forest fire on soil microbial biomass and enzymatic activity in oak and pine forests of Uttarakhand Himalaya, India显示文摘Background:Forest fire incidences in the Himalayan region of Uttarakhand,India are very common in summers.Pine and oak are the principal and dominant species of Himalayan subtropical forest and Himalayan temperate forest,respectively.Forest vegetation influences the physicochemical and biological properties of soil and forest fire in pine and oak forests may have a different effect on the physicochemical and biological properties of soil.Therefore,the present study was carried out to assess the impact of forest fire on soil microbial properties,enzymatic activity,and their relationship with soil physicochemical properties in the advent of forest fire in the pine and oak forests of the Garhwal region of Uttarakhand Himalaya,India.Results:The soil microbial biomass carbon and nitrogen,soil basal respiration,and acid phosphatase activity decreased,whereas dehydrogenase activity increased at burnt sites of both forest types.The overall change in soil microbial biomass carbon was 63 and 40%at the burnt oak forest and burnt pine forest,respectively.Dehydrogenase activity and acid phosphatase activity showed a strong positive correlation with soil organic matter(r=0.8)and microbial indices,respectively.The ratio of soil microbial biomass carbon/nitrogen was reduced at burnt sites of both forest types.Factor analysis results showed that fire had a significant impact on soil characteristics.The soil basal respiration was linked with macro-and micronutrients at burnt sites,whereas at control sites,it was linked with physicochemical properties of soil along with nutrients.Conclusion:Forest fire had a significant impact on soil properties of both forest types.The impact of forest fire on soil microbial biomass carbon was stronger in the oak forest than in the pine forest.Forest type influenced soil enzymatic activity at burnt sites.The bacterial community was dominated over fungi in burnt sites of both forests.Soil microbial indices can be used as a selective measure to assess the impact of fire.Furthermore,forest type plays an important role in regulating the impact of forest fire on soil properties. | Devanshi Singh Priyanka Sharma Ujjwal Kumar Achlesh Daverey Kusum Arunachalam | 2021 | Ecological Processes2021，10，1： | 2 |
| 14 | Alcohol Consumption Decreases Rat Hepatic Creatine Biosynthesis Via Altered Guanidinoacetate Methyltransferase Activity显示文摘 | Kusum K. Kharbanda Sandra L. Todero Jordan C. Moats Ryan M. Harris Natalia A. Osna Paul G. Thomes Dean J. Tuma | 2014 | Alcohol Clin Exp Res2014，，3： | 2 |
| 15 | Prolonged feeding with guanidinoacetate, a methyl group consumer, exacerbates ethanol-induced liver injury显示文摘AIM To investigate the hypothesis that exposure to guanidinoacetate(GAA, a potent methyl-group consumer) either alone or combined with ethanol intake for a prolonged period of time would cause more advanced liver pathology thus identifying methylation defects as the initiator and stimulator for progressive liver damage.METHODS Adult male Wistar rats were fed the control or ethanolLieber De Carli diet in the absence or presence of GAA supplementation. At the end of 6 wk of the feeding regimen, various biochemical and histological analyses were conducted. RESULTS Contrary to our expectations, we observed that GAA treatment alone resulted in a histologically normal liver without evidence of hepatosteatosis despite persistence of some abnormal biochemical parameters. This protection could result from the generation of creatine from the ingested GAA. Ethanol treatment for 6 wk exhibited changes in liver methionine metabolism and persistence of histological and biochemical defects as reported before. Further, when the rats were fed the GAA-supplemented ethanol diet, similar histological and biochemical changes as observed after 2 wk of combined treatment, including inflammation, macroand micro-vesicular steatosis and a marked decrease in the methylation index were noted. In addition, rats on the combined treatment exhibited increased liver toxicity and even early fibrotic changes in a subset of animals in this group. The worsening liver pathology could be related to the profound reduction in the hepatic methylation index, an increased accumulation of GAA and the inability of creatine generated to exert its hepato-protective effects in the setting of ethanol.CONCLUSION To conclude, prolonged exposure to a methyl consumer superimposed on chronic ethanol consumption causes persistent and pronounced liver damage. | Natalia A Osna Dan Feng Murali Ganesan Priya F Maillacheruvu David J Orlicky Samuel W French Dean J Tuma Kusum K Kharbanda | 2016 | World Journal of Gastroenterology2016，22，38： | 2 |
| 16 | Lysosome and proteasome dysfunction in alcohol-induced liver injury显示文摘The review describes research findings on the influence of alcohol consumption on two crucial catabolic systems in hepatocytes:the lysosome and the ubiquitin-proteasome system(UPS).The lysosome is a membrane-bound organelle that degrades all aging and/or damaged organelles and hydrolyzes all forms of macromolecules.The UPS is mostly proteolytic.It carries out the majority of its functions in the soluble portion of the cytoplasm(cytosol)and degrades nearly all intracellular proteins,particularly those with short half-lives,so that their levels are tightly controlled.Our review will briefly discuss the epidemiology of alcohol abuse and the spectrum of alcohol-induced liver disease(AILD).We will explain why ethanol(EtOH)metabolism,but not EtOH alone,is hepatotoxic.Then,we will summarize how heavy drinking alters hepatic catabolic systems,resulting in liver enlargement that develops from hepatocyte swelling due,in part,to aberrant accumulation of undegraded lipid droplets(steatosis)and undegraded proteins(proteopathy).Our detailed description of each catabolic system will highlight its discoverer(s)and emphasize each system’s characteristics.Most important,we will review the evidence that chronic EtOH consumption disrupts hepatic lysosome biogenesis and inhibits the UPS by impeding hepatic proteasome activity.It will become evident that each of these EtOH-induced defects has far-reaching functional consequences.Finally,we will describe current and potential therapeutic interventions for alleviating EtOH-induced liver injury.The most effective intervention is the cessation of EtOH consumption.However,there are other potential approaches using natural or synthetic compounds that activate autophagy or the proteasome to enhance the degradation of accumulated lipid droplets or proteins,respectively,which could alleviate AILD.These approaches,now in their early stages of investigation,will also be discussed in this review. | Terrence M.Donohue.Jr Natalia A.Osna Kusum K.Kharbanda Paul G.Thomes | 2019 | Liver Research2019，3，3： | 2 |
| 17 | Roles of syndecan-1, bcl6 and p53 in diagnosis and prognostication of immunoproliferative small intestinal disease显示文摘瞄准:在 immunoproliferative 的诊断和预知评估 syndecan-1, bcl6 和 p53 的角色小肠的疾病(IPSID ) 并且学习 kappa (kappa ) 和人字缝尖(人字缝尖) 的侧面轻链和 IgA 重链。方法:学习由 IPSID 的 11 个盒子和包括了 11 正常肠粘膜和回肠的 11 高等级 B 房间淋巴瘤的控制的类似的数字组成了。分析的参数包括了临床的侧面,生物化学并且另外的实验室调查,放射线学并且组织检查所见包括免疫组织化学。结果:所有 IPSID 箱子有可论证的浆液 IgA 重链和重粘膜血浆房间渗入。根据 Galian 的组织学的阶段,有有舞台 A 的 4 个病人并且 7 与舞台 B。kappa 和人字缝尖轻链在 7 个病人是过去表示的;1 舞台 A H pylori 的耐心的有的 H pylori 积极的活跃胃炎和根除导致了疾病宽恕。舞台 A 活体检视为 syndecan-1 有更高的表示,当舞台 B 为 bcl6 和 p53 有更高的表示时。Syndecan-1, kappa 和人字缝尖轻链和 IgA 重链与 bcl6 和 p53 显示出反的关系。所有病人与 doxycycline 被对待。砍政体在得了坦率的淋巴瘤的 5 个病人被增加。三由于广泛的机关渗入死于疾病。结论:象 syndecan-1, kappa 和人字缝尖轻链和 IgA 重链一样的某些免疫标记能具有在识别早阶段 IPSID 的许多帮助。舞台 B IPSID 比上演 IPSID 为 bcl6 和 p53 显示出更高的表示。bcl6 和 p53 表情与一个更多的病沉重期舞台和好攻击的瘤行为相关。 | Kim Vaiphei Neeraj Kumari Saroj Kant Sinha Usha Dutta Birinder Nagi Kusum Joshi Kartar Singh | 2006 | World Journal of Gastroenterology2006，12，22： | 2 |
| 18 | Proteomics reveal a concerted upregulation of methionine metabolic pathway enzymes, and downregulation of carbonic anhydrase-III, in betaine supplemented ethanol-fed rats显示文摘 | Kusum K. Kharbanda Vasanthy Vigneswara Benita L. McVicker Anna U. Newlaczyl Kevin Bailey Dean Tuma David E. Ray Wayne G. Carter | 2009 | Biochemical and Biophysical Research Communications2009，，4： | 2 |
| 19 | Alcoholic Liver Disease and Methionine Metabolism显示文摘 | Kusum Kharbanda | 2009 | Semin Liver Dis2009，，02： | 2 |
| 20 | Accumulation of proteins bearing atypical isoaspartyl residues in livers of alcohol-fed rats is prevented by betaine administration: Effects on protein- l -isoaspartyl methyltransferase activity显示文摘 | Kusum K. Kharbanda Mark E. Mailliard Cheryl R. Baldwin Michael F. Sorrell Dean J. Tuma | 2007 | Journal of Hepatology2007，，6： | 2 |
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