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Kundu, I.

Publications and source records attributed to Kundu, I..

2 recordsLinked to original sources

Gender-specific MetS prediction using pathophysiological determinants: Beyond diagnostic constraints

Metabolic syndrome (MetS), constituted by obesity, hyperglycemia, hypertension, and dyslipidemia, is a growing public health concern due to its associated risk with cardiovascular and other metabolic disorders. Early-stage detection and prevention of MetS are key factors in an effective management strategy. Thus, the current study aimed to develop a risk score for MetS progression based on features pertaining to its pathophysiology, that can facilitate early detection and treatment strategies. A multivariate logistic regression model was developed using a representative feature from MetS pathophysiological pathways of inflammation, endothelial dysfunction, and hepatic dysregulation. The model was built on NHANES dataset and validated in Chinese and Indian datasets. The model performance evaluated using ROC resulted in an AUC of 0.81 in training and 0.87 and 0.79 for Chinese and Indian validation datasets, respectively. In conclusion, a MetS predictive model built on three MetS pathophysiological determinants was developed and validated in distinct datasets. HighlightsO_LIA MetS prediction model, trained on NHANES data, is validated with two datasets of varied ethnicity. C_LIO_LIThe three parameter model, independent of MetS diagnostic criteria, is reflective of inflammation, endothelial dysfunction, and hepatic dysregulation. C_LIO_LIThe model achieved an AUC of 0.81 in NHANES data; 0.87 and 0.79 for Chinese and Indian validation datasets respectively. C_LI

bioinformatics↗

A recombinant fragment of Human surfactant protein D binds Spike protein and inhibits infectivity and replication of SARS-CoV-2 in clinical samples

RationaleCOVID-19 is an acute infectious disease caused by the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). Human surfactant protein D (SP-D) is known to interact with spike protein of SARS-CoV, but its immune-surveillance against SARS-CoV-2 is not known. ObjectiveThis study aimed to examine the potential of a recombinant fragment of human SP-D (rfhSP-D) as an inhibitor of replication and infection of SARS-CoV-2. MethodsrfhSP-D interaction with spike protein of SARS-CoV-2 and hACE-2 receptor was predicted via docking analysis. The inhibition of interaction between spike protein and ACE-2 by rfhSP-D was confirmed using direct and indirect ELISA. The effect of rfhSP-D on replication and infectivity of SARS-CoV-2 from clinical samples was studied by measuring the expression of RdRp gene of the virus using qPCR. Measurements and Main ResultsIn-silico interaction studies indicated that three amino acid residues in the RBD of spike of SARS-CoV-2 were commonly involved in interacting with rfhSP-D and ACE-2. Studies using clinical samples of SARS-CoV-2 positive cases (asymptomatic, n=7 and symptomatic, n=8 and negative controls n=15) demonstrated that treatment with 5M rfhSP-D inhibited viral replication by ~5.5 fold and was more efficient than Remdesivir (100 M). Approximately, a 2-fold reduction in viral infectivity was also observed after treatment with 5M rfhSP-D. ConclusionsThese results conclusively demonstrate that the calcium independent rfhSP-D mediated inhibition of binding between the receptor binding domain of the S1 subunit of the SARS-CoV-2 spike protein and human ACE-2, its host cell receptor, and a significant reduction in SARS-CoV-2 infection and replication in-vitro.

immunology↗