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| 1 | All ileo-cecal ulcers are not Crohn's:Changing perspectives of symptomatic ileocecal ulcers显示文摘AIM To investigated clinical,endoscopic and histopathological parameters of the patients presenting with ileocecal ulcers on colonoscopy.METHODS Consecutive symptomatic patients undergoing colonoscopy,and diagnosed to have ulcerations in the ileocecal(I/C) region,were enrolled.Biopsy was obtained and theirclinical presentation and outcome were recorded.RESULTS Out of 1632 colonoscopies,104 patients had ulcerations in the I/C region and were included in the study.Their median age was 44.5 years and 59% were males.The predominant presentation was lower GI bleed(55,53%),pain abdomen ± diarrhea(36,35%),fever(32,31%),and diarrhea alone(9,9%).On colonoscopy,terminal ileum was entered in 96(92%) cases.The distribution of ulcers was as follows:Ileum alone 40%(38/96),cecum alone 33%(32/96),and both ileum plus cecum 27%(26/96).The ulcers were multiple in 98% and in 34% there were additional ulcers elsewhere in colon.Based on clinical presentation and investigations,the etiology of ulcers was classified into infective causes(43%) and noninfective causes(57%).Fourteen patients(13%) were diagnosed to have Crohn's disease(CD).CONCLUSION Non-specific ileocecal ulcers are most common ulcers seen in ileo-cecal region.And if all infections are clubbed together then infection is the most common(> 40%) cause of ulcerations of the I/C region.Cecal involvement and fever are important clues to infective cause.On the contrary CD account for only 13% cases as a cause of ileo-cecalulcers.So all symptomatic patients with I/C ulcers on colonoscopy are not Crohn's. | Jay Toshniwal Romesh Chawlani Amit Thawrani Rajesh Sharma Anil Arora Hardik L Kotecha Mohan Goyal Vijendra Kirnake Pankaj Jain Pankaj Tyagi Naresh Bansal Munish Sachdeva Piyush Ranjan Mandhir Kumar Praveen Sharma Vikas Singla Rinkesh Bansal Vineet Shah Sunita Bhalla Ashish Kumar | 2017 | World Journal of Gastrointestinal Endoscopy2017，9，7： | 5 |
| 2 | Pantoprazole Improves Glycemic Control in Type 2 Diabetes: A Randomized, Double-Blind, Placebo-Controlled Trial显示文摘 | Pawan Kumar Singh Debasish Hota Pinaki Dutta Naresh Sachdeva Amitava Chakrabarti Anand Srinivasan Inderjeet Singh Anil Bhansali | 2012 | The Journal of Clinical Endocrinology & Metabolism2012，，11： | 1 |
| 3 | Utility of Glycated Hemoglobin in Diagnosing Type 2 Diabetes Mellitus: A Community-Based Study显示文摘 | Padala Ravi Kumar Anil Bhansali Muthuswamy Ravikiran Shobhit Bhansali Pinaki Dutta J. S. Thakur Naresh Sachdeva Sanjay Kumar Bhadada Rama Walia | 2010 | The Journal of Clinical Endocrinology & Metabolism2010，，6： | 1 |
| 4 | Stem cell-like memory T cells:Role in viral infections and autoimmunity显示文摘Stem cell-like memory T(TSCM)cells possess stem cell properties including multipotency and self-renewal and are being recognized as emerging players in various human diseases.Advanced technologies such as multiparametric flowcytometry and single cell sequencing have enabled their identification and molecular characterization.In case of chronic viral diseases such as human immunodeficiency virus-1,CD4+T_(SCM) cells,serve as major reservoirs of the latent virus.However,during immune activation and functional exhaustion of effector T cells,these cells also possess the potential to replenish the pool of functional effector cells to curtail the infection.More recently,these cells are speculated to play important role in protective immunity following acute viral infections such as coronavirus disease 2019 and might be amenable for therapeutics by ex vivo expansion.Similarly,studies are also investigating their pathological role in driving autoimmune responses.However,there are several gaps in the understanding of the role of T_(SCM) cells in viral and autoimmune diseases to make them potential therapeutic targets.In this minireview,we have attempted an updated compilation of the dyadic role of these complex T_(SCM) cells during such human diseases along with their biology and transcriptional programs. | Meenakshi Sachdeva Shivangi Taneja Naresh Sachdeva | 2023 | World Journal of Immunology2023，13，2： | 0 |
| 5 | Thyroid dysfunction and developmental anomalies in first degree relatives of children with thyroid dysgenesis显示文摘Background: Familial clustering in patients withpermanent congenital hypothyroidism (CH) caused bythyroid dysgenesis (TD) has been reported in developedcountries. There is no information on familial TD fromdeveloping countries.Methods: A total of 312 first degree relativesbelonging to 80 families of children with TD (group 1)and 40 families of age-matched normal children (group2) were screened by thyroid ultrasonography, serum totalthyroxine (T4) and thyroid stimulating hormone (TSH).Results: Thyroid scintigraphy revealed agenesis in78.7% of the patients, ectopic gland in 15%, and hypoplasiain 6.2%. The mean thyroid volumes were similar in parentsand siblings of both groups. Eight (10.6%) mothers in group1 were identified to have thyroid hypoplasia as comparedwith none in group 2 (P=0.03). Serum TSH was signifi cantlyhigher in group 1 than in group 2 (P=0.004). Sixteen (7.8%)subjects (6 mothers, 5 fathers, and 5 siblings) in group 1were found to have subclinical hypothyroidism as comparedto none in group 2 (P<0.05). Four families were identifiedto have thyroid developmental anomalies and abnormalthyroid functions accounting for 5% of cases of familial TDin our cohort.Conclusions: Thyroid developmental anomalies andthyroid function abnormalities are more frequent in firstdegree relatives of children with TD as compared with acontrol population. These findings suggest that possiblythere is a genetic component of TD in Indian patients. | Lakshminarasimhan Sindhuja Devi Dayal Kushaljit Singh Sodhi Naresh Sachdeva Anish Bhattacharya | 2016 | World Journal of Pediatrics2016，12，2： | 0 |
| 6 | Role of nucleic acid sensing in the pathogenesis of type 1 diabetes显示文摘During infections,nucleic acids of pathogens are also engaged in recognition via several exogenous and cytosolic pattern recognition receptors,such as the toll-like receptors,retinoic acid inducible gene-I-like receptors,and nucleotide-binding and oligomerization domain-like receptors.The binding of the pathogen-derived nucleic acids to their corresponding sensors initiates certain downstream signaling cascades culminating in the release of type-I interferons(IFNs),especially IFN-αand other cytokines to induce proinflammatory responses towards invading pathogens leading to their clearance from the host.Although these sensors are hardwired to recognize pathogen associated molecular patterns,like viral and bacterial nucleic acids,under unusual physiological conditions,such as excessive cellular stress and increased apoptosis,endogenous self-nucleic acids like DNA,RNA,and mitochondrial DNA are also released.The presence of these self-nucleic acids in extranuclear compartments or extracellular spaces or their association with certain proteins sometimes leads to the failure of discriminating mechanisms of nucleic acid sensors leading to proinflammatory responses as seen in autoimmune disorders,like systemic lupus erythematosus,psoriasis and to some extent in type 1 diabetes(T1D).This review discusses the involvement of various nucleic acid sensors in autoimmunity and discusses how aberrant recognition of self-nucleic acids by their sensors activates the innate immune responses during the pathogenesis of T1D. | Darshan Badal Naresh Sachdeva Deep Maheshwari Preetam Basak | 2021 | World Journal of Diabetes2021，12，10： | 0 |
| 7 | Pancreatic fat in type 2 diabetes:Causal or coincidental?显示文摘Type 2 diabetes(T2D)is a multifactorial metabolic disorder affecting more than 450 million people across the globe.With the increasing prevalence of T2D and obesity,the role of fat accumulation at sites other than subcutaneous adipose tissue has received significant attention in the pathophysiology of T2D.Over the past decade and a half,a pressing concern has emerged on investigating the association of pancreatic fat accumulation or pancreatic steatosis with the development of disease.While a few reports have suggested a possible association between pancreatic fat and T2D and/or impaired glucose metabolism,a few reports suggest a lack of such association.Pancreatic fat has also been linked with genetic risk of developing T2D,prediabetes,reduced insulin secretion,and beta cell dysfunction albeit some confounding factors such as age and ethnicity may affect the outcome.With the technological advancements in clinical imaging and progress in assessment of pancreatic beta cell function,our understanding of the role of pancreatic fat in causing insulin resistance and development of various etiologies of T2D has significantly improved.This review summarizes various findings on the possible association of pancreatic fat accumulation with the pathophysiology of T2D. | Soham Mukherjee Deep Maheshwari Rimesh Pal Naresh Sachdeva | 2023 | World Journal of Meta-Analysis2023，11，3： | 0 |
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