Ruchi Jakhmola-Mani

Ms. Ruchi Jakhmola-Mani

orcid

Research Focus & Metrics

Academic Career Length

11Years (2016-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 January 2016 in Aquatic Toxicology
Verified
Journal Article
Closed access
AKAllan V. Kalueff
Allan V. Kalueff
DEDavid J. Echevarria
David J. Echevarria
SHSumit Homechaudhuri
Sumit Homechaudhuri
ASAdam Michael Stewart
Adam Michael Stewart
ACAdam D. Collier
Adam D. Collier
CSCai Song
Cai Song

2 March 2021 in Cellular and Molecular Neurobiology
Verified
Journal Article
Closed access
PDF file
NDNitu Dogra
Nitu Dogra
RJRuchi Jakhmola-Mani
Ruchi Jakhmola-Mani
Deepshikha Pande KatareDeepshikha Pande Katare
Deepshikha Pande Katare

6 May 2016 in Scientific Reports
Verified
Journal Article
Open access
KMKhyati Mittal
Khyati Mittal
RJRuchi Jakhmola-Mani
Ruchi Jakhmola-Mani
Deepshikha Pande KatareDeepshikha Pande Katare
Deepshikha Pande Katare
Type 3 Diabetes (T3D) is a neuroendocrine disorder that represents the progression of Type 2 Diabetes Mellitus (T2DM) to Alzheimer’s disease (AD). T3D contributes in the increase of the total load of Alzheimer’s patients worldwide. The protein network based strategies were used for the analysis of protein interactions and hypothesis was derived describing the possible routes of communications among proteins. The hypothesis provides the insight on the probable mechanism of the disease progression for T3D. The current study also suggests that insulin degrading enzyme (IDE) could be the major player which holds the capacity to shift T2DM to T3D by altering metabolic pathways like regulation of beta-cell development, negative regulation of PI3K/AKT pathways and amyloid beta degradation.

28 October 2020 in Journal of Biomolecular Structure and Dynamics
Verified
Journal Article
Closed access
RJRuchi Jakhmola-Mani
Ruchi Jakhmola-Mani
NSNikita Sehgal
Nikita Sehgal
NDNitu Dogra
Nitu Dogra
SSShikha Saxena
Shikha Saxena
Deepshikha Pande KatareDeepshikha Pande Katare
Deepshikha Pande Katare
COVID-19, emerged at the end of 2019 have dramatically threatened the health, economy, and social mobility of people around the world and till date no medication is available for its treatment. An amazing herb, Nigella sativa, having antiviral, antihypertensive, anti- diarrhoeal, analgesics, and anti-bacterial properties, needs to be explored for its efficacy against SARS-CoV-2, the causative agent of COVID-19. In-silico studies were carried out to understand the role of its bioactive constituents in COVID-19 treatment and prevention. Firstly, the disease network was prepared by using ACE2 (Angiotensin-II receptor), as it is the entry site for virus. It was used to decipher the mechanism of SARS-COV-2 infection in humans. Second, the target receptors for N. sativa were predicted and protein interaction studies were conducted. Further, docking studies were also performed to analyse it for treatment purpose as well. This study concludes that pathways undertaken by N. sativa bioactive constituents were similar to the pathways followed in SARS-COV-2 pathology, like renin-angiotensin system, kidney functions, regulation of blood circulation, blood vessel diameter, etc. Also, in docking studies, the constituents of N. sativa, α-hederin, Thymohydroquinone and Thymoquinone were observed to be efficiently binding to ACE2. Also, the bioactive phytoconstituents are involved in molecular pathways like HIF1, VEGF, IL-17, AGE-RAGE, chemokine and calcium signaling pathways which can be majorly helpful in combating hypoxia and inflammation caused due to compromised immune system and oxidative stress. Therefore, N. sativa standardized extract having the above phytoconstituents could be useful in COVID-19 and hence opens a new treatment line.

19 January 2023 in Metabolic Brain Disease
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Journal Article
Closed access
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NDNitu Dogra
Nitu Dogra
RJRuchi Jakhmola-Mani
Ruchi Jakhmola-Mani
APAngamba Meetei Potshangbam
Angamba Meetei Potshangbam
SBShilpa Buch
Shilpa Buch
Deepshikha Pande KatareDeepshikha Pande Katare
Deepshikha Pande Katare

1 November 2021 in CNS & Neurological Disorders - Drug Targets
Verified
Journal Article
Closed access
PDF file
RJRuchi Jakhmola-Mani
Ruchi Jakhmola-Mani
AIAnam Islam
Anam Islam
DKDeepshikha Pande Katare
Deepshikha Pande Katare
Aim: Poor nutritional effect of junk food induces injuries to the liver and the brain but still most of the developing nations survive on these diets to compensate for the fast-paced lifestyle. The aim of the study is to infer the protein-connections behind the liver-brain axis and identify the role of these proteins in causing neurodegenerative disorders. Background: Chronic consumption of fructose and fat-rich food works as a toxin in the body and has the ability to cause a negative metabolic shift. Recently a study was published in Annals of Internal Medicine (2019) citing the loss of vision and hearing in a 14-year-old boy whose diet was strictly restricted to fries and junk-food for almost a decade. This puts the entire body on insulin resistance and related co-morbidities and causes simultaneous damaging effects on the liver as well as the brain. This work provides insights into the liver-brain axis and explains how the liver is involved in brain related disorders. Objective: In this study, transcriptomic data related to chronic eating of junk-food was analyzed and simultaneous damage that happens in the liver and the brain was assessed at the molecular level. Method: Transcriptomic study was taken from the GEO database and analysed to find out the genes dysregulated in both the liver and the brain during this metabolic stress. Cytoscapev3.7 was used to decipher the signalling between the liver and the brain. This connection between both is called as the liver-brain axis. Results: The results obtained from our study indicate the role of TUBB5-HYOU1-SDF2L1-DECR1- CDH1-EGFR-SKP2-SOD1-IRAK1-FOXO1 gene signature in the decline of concurrent liver and brain health. Dysregulated levels of these genes are linked to molecular processes like cellular senescence, hypoxia, glutathione synthesis, amino acid modification, increased nitrogen content, synthesis of BCAAs, cholesterol biosynthesis, steroid hormone signalling and VEGF pathway. Conclusion: The results obtained from our study indicate the role of TUBB5-HYOU1-SDF2L1-DECR1- CDH1-EGFR-SKP2-SOD1-IRAK1-FOXO1 gene signature in the decline of concurrent liver and brain health. Dysregulated levels of these genes are linked to molecular processes like cellular senescence, hypoxia, glutathione synthesis, amino acid modification, increased nitrogen content, synthesis of BCAAs, cholesterol biosynthesis, steroid hormone signalling and VEGF pathway.