Acquired vaginal stenosis following caesarean delivery: a case report

Postpartum genital tract adhesions are infrequent and their reason has not been appraised. Though, severe dystocia and frequent pelvic examinations have been projected as possible causes. Here, we report a case of vaginal adhesions following caesarean section for obstructed labour that presented as irregular menstruation with desire to remove the PPIUCD. The patient was successfully treated with surgical resection

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Demographic profile of Cervical Cancer development: a hospital based study

Introduction: The present study is an attempt to detect Human papilloma virus infection along with its genotype in cancer cervix and its relation with demographic profile. Methods: Cervical cancer cases were enrolled in between Jan’ 2010 to Dec’ 2012. One sample was collected from non cancerous area of cervix for DNA extraction and two samples were collected from cancerous area of cervix from same patient, one for DNA extraction and other one for histopathological examination to confirm our clinical diagnosis. Extracted DNA was then checked for presence of HPV DNA by PCR amplification method using MY09/11 primer. HPV genotyping was done by using specific primer for HPV16 & HPV18. The cases were compared with their corresponding socio demographic profile. Results: The study showed 88.88% cases found to be HPV positive in cancerous area compared to 7.4% number in non cancerous area. Out of which 95.83% cases to be HPV 16 and only 4.16% were to be HPV 18 in cervical cancer cases. There were other significant risk factor association of cervical cancer with early marriage in 70.36% and high parity 87% of cases. Conclusion: The human papilloma virus type 16 & 18 are the major contributing factor along with other risk factors like early marriage, illiteracy and high parity for cervical cancer in our region

Epidemiology of cervical cancer development- a hospital based study

Introduction: The present study is an attempt to detect Human papilloma virus infection and immunomodulation status in the development of carcinoma cervix. Methods: Cervical cancer cases were enrolled in between Jan’ 2010 to Dec’ 2012. Cervical tissue biopsies from the both the cancerous region as well as the non cancerous control area of the cervix, and whole blood (3ml) were collected from all the study subjects. The tissue samples were collected either in PBS or RNA later solution in vials and stored in -80°C or liquid nitrogen till further use. Whole blood (2ml) was also collected from age matched voluntary female community controls (n=50), the plasma was separated, and stored at -20°C for cytokine analysis. Extracted DNA was then checked for presence of HPV DNA by PCR amplification method using MY09/11 primer. Th1 (IL-12) and Th2 (IL-10) were analysed both at protein as well as cervical tissue level. Results: The study showed 83.33% cases found to be HPV positive in cancerous area as well as in non cancerous area. There were other significant risk factor association of cervical cancer with early marriage in 70.36% and high parity 87% of cases. There is alteration of Th1 and Th2 ratio indicating immunomodulation plays an important role in the development of cervical cancer. Conclusion: The human papilloma virus infections are the major contributing factor as well as immunomodulation plays a major role in the development of cervical cancer in our region

Exploring the p53 connection of cervical cancer pathogenesis involving north-east Indian patients.

BackgroundAs per WHO, Cervical cancer (CaCx) is a global issue, being the fourth common cancer in women with incidence rate of 13.1 per 1 lakh women globally and accounting for 311000 deaths in the year 2018 itself globally. The molecular pathogenesis in Human papillomavirus (HPV) infected cases is inconclusive. The detection of molecular factors leading to progression of CaCx can be important in the diagnosis and management of the disease. p53 a known tumor suppressor gene having a regulative role in cell cycle has been highlighted as key factor in the prevention of cancer but its significance in CaCx cases has been variably documented. The present study therefore targeted to evaluate the significance of p53 profile in CaCx cases in ethnically distinct northeast Indian population.MethodsBlood and Tissue samples (N = 85) of cervical cancer patients were collected and screening for HPV was performed using PCR. Thereafter the differential mRNA expression(qPCR), Immunohistochemistry, Mutation (PCR direct sequencing method) of p53 was studied. Further p53 epigenetic profiling was done by Methylation specific PCR (MS-PCR) and western blotting by using p53 acetylation specific antibodies.ResultsOur findings revealed that the downregulation of p53 was associated with the progression of disease and the variation in downregulation based on p53 polymorphism was observed. Further hypermethylation and deacetylation of p53 was also found to be associated with the pathogenesis of CaCx. The downregulated expression and hypermethylation of p53 in lower grade of CaCx, together established its association with the progression of CaCx from lower to severe grade.ConclusionTherefore, in CaCx patients of northeast Indian population, malfunctioning of p53 is found to have significant role in cervical cancer progression

Abstracts of National Conference on Research and Developments in Material Processing, Modelling and Characterization 2020

This book presents the abstracts of the papers presented to the Online National Conference on Research and Developments in Material Processing, Modelling and Characterization 2020 (RDMPMC-2020) held on 26th and 27th August 2020 organized by the Department of Metallurgical and Materials Science in Association with the Department of Production and Industrial Engineering, National Institute of Technology Jamshedpur, Jharkhand, India. Conference Title: National Conference on Research and Developments in Material Processing, Modelling and Characterization 2020Conference Acronym: RDMPMC-2020Conference Date: 26–27 August 2020Conference Location: Online (Virtual Mode)Conference Organizer: Department of Metallurgical and Materials Engineering, National Institute of Technology JamshedpurCo-organizer: Department of Production and Industrial Engineering, National Institute of Technology Jamshedpur, Jharkhand, IndiaConference Sponsor: TEQIP-

Stratified analyses refine association between TLR7 rare variants and severe COVID-19

Summary: Despite extensive global research into genetic predisposition for severe COVID-19, knowledge on the role of rare host genetic variants and their relation to other risk factors remains limited. Here, 52 genes with prior etiological evidence were sequenced in 1,772 severe COVID-19 cases and 5,347 population-based controls from Spain/Italy. Rare deleterious TLR7 variants were present in 2.4% of young (<60 years) cases with no reported clinical risk factors (n = 378), compared to 0.24% of controls (odds ratio [OR] = 12.3, p = 1.27 × 10−10). Incorporation of the results of either functional assays or protein modeling led to a pronounced increase in effect size (ORmax = 46.5, p = 1.74 × 10−15). Association signals for the X-chromosomal gene TLR7 were also detected in the female-only subgroup, suggesting the existence of additional mechanisms beyond X-linked recessive inheritance in males. Additionally, supporting evidence was generated for a contribution to severe COVID-19 of the previously implicated genes IFNAR2, IFIH1, and TBK1. Our results refine the genetic contribution of rare TLR7 variants to severe COVID-19 and strengthen evidence for the etiological relevance of genes in the interferon signaling pathway