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Manisha Dixit

Researcher at Council of Scientific and Industrial Research

Publications -  8
Citations -  205

Manisha Dixit is an academic researcher from Council of Scientific and Industrial Research. The author has contributed to research in topics: Internal medicine & Medicine. The author has an hindex of 2, co-authored 3 publications receiving 175 citations. Previous affiliations of Manisha Dixit include Academy of Scientific and Innovative Research.

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Journal ArticleDOI

miR-542-3p suppresses osteoblast cell proliferation and differentiation, targets BMP-7 signaling and inhibits bone formation

TL;DR: It is shown that miR-542-3p, a well-characterized tumor suppressor whose downregulation is tightly associated with tumor progression via C-src-related oncogenic pathways, inhibits osteoblast proliferation and differentiation and inhibits BMP-7-mediated osteogenesis.
Journal ArticleDOI

Enhanced immunoprotective effects by anti-IL-17 antibody translates to improved skeletal parameters under estrogen deficiency compared with anti-RANKL and anti-TNF-α antibodies.

TL;DR: Although anti‐RANKL and anti‐TNF‐α therapies had no effect on Ovx‐induced CD4+ T‐cell proliferation and B lymphopoesis, anti‐IL‐17 effectively suppressed both events with concomitant reversal of CD28 loss, and it is proposed that clinical trials using a humanized antibody against IL‐17 for treatment of postmenopausal osteoporosis is proposed.
Book ChapterDOI

Mutagenesis, Genetic Disorders and Diseases

TL;DR: This chapter would be highlighting the various mutagens, the changes that they introduce to the DNA base pairing, their repairing machinery pathway, and diseases that are caused by faulty repair machinery.
Journal ArticleDOI

IOF REGIONAL 2021 8th Asia Pacific Osteoporosis Conference: Oral Communication Abstracts

TL;DR: The present study suggested the regulation of eldecalcitol on apoptosis and ferroptosis of MLO-Y4 cells could be improved by ELD treatment as demonstrated by the enhancement in the protein expression of Nrf2 and GPX4, both of which are central regulators of ferroPTosis.
Journal ArticleDOI

Excess growth hormone triggers inflammation-associated arthropathy, subchondral bone loss, and arthralgia.

TL;DR: In this article , the effects of long-term excess growth hormone (GH) on the knee joint tissues were investigated, and the results indicated that treatment of acromegalic arthropathy should involve inhibition of ectopic chondrogenesis and chondrocyte hypertrophy.