Problem: Recurrent pregnancy loss (RPL) is the spontaneous loss of two or more consecutive pregnancies prior to 20 weeks of gestation, occurring in 1% of the reproductive-age population. It is a major cause of infertility in India with a staggering 7.46% prevalence rate.
View Article and Find Full Text PDFRegulated oxidative stress (OS) is important during pregnancy. Sporadic studies suggest the significance of deregulated OS in hepatitis E virus (HEV) infected pregnancy, but with limited reactive oxygen species (ROS) or antioxidant markers. The present novel study, therefore, aimed to evaluate the significance of ROS-antioxidant imbalance and resulting altered OS in HEV infected pregnancy complications like preterm delivery (PTD) and outcome.
View Article and Find Full Text PDFBackground: Lacunae exist in understanding the underlying etiology in majority of recurrent pregnancy loss (RPL) cases. Given the significance of regulated immune-modulation in pregnancy, and the central role of pro-inflammatory TNF-α plays in it; this study targeted to appraise the significance of TNF-α profile in RPL pathogenesis in an ethnically distinct population from Assam, India.
Methods: Term delivery, medically terminated pregnancy (MTP) and RPL cases (based on ASRM criteria) were enrolled with no anatomical and chromosomal abnormalities or pathological infections; and blood and/or placenta/product of conceptus (POC) tissue samples were collected with informed consent.
With the background of association of oxidative stress and Hepatitis E virus (HEV) infection in pregnancy complications the present novel study aimed to evaluate the significance of changes in maternal homocysteine levels and the related mechanism(s) in the pathophysiology of HEV related pregnancy complications and negative outcomes. Term delivery (TD, N = 194) and HEV-IgM positive pregnancy cases [N = 109] were enrolled. Serum and placental homocysteine levels were evaluated by ELISA and immunofluorescence and in turn correlated with serum Vitamin B12 levels.
View Article and Find Full Text PDFBackground: As 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.
View Article and Find Full Text PDFPap smear is often employed as a screening test for diagnosing cervical pre-cancerous and cancerous lesions. Accurate identification of dysplastic changes amongst the cervical cells in a Pap smear image is thus essential for rapid diagnosis and prognosis. Manual pathological observations used in clinical practice require exhaustive analysis of thousands of cell nuclei in a whole slide image to visualize the dysplastic nuclear changes which make the process tedious and time-consuming.
View Article and Find Full Text PDFThe diagnosis of cervical dysplasia, carcinoma in situ and confirmed carcinoma cases is more easily perceived by commercially available and current research-based decision support systems when the scenario of pathologists to patient ratio is small. The treatment modalities for such diagnosis rely exclusively on precise identification of dysplasia stages as followed by The Bethesda System. The classification based on The Bethesda System is a multiclass problem, which is highly relevant and vital.
View Article and Find Full Text PDFWhile a publicly available benchmark dataset provides a base for the development of new algorithms and comparison of results, hospital-based data collected from the real-world clinical setup is also very important in AI-based medical research for automated disease diagnosis, prediction or classifications as per standard protocol. Primary data must be constantly updated so that the developed algorithms achieve as much accuracy as possible in the regional context. This dataset would support research work related to image segmentation and final classification for a complete decision support system (https://doi.
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