Ruby Bansal

Chemical degradation identified Human p38-MAPK as a host target to combat parasitic infections

This study shows that degrading host p38-MAPK with NR-7h reduces parasite load in Leishmania and Plasmodium infections and enhances antiparasitic therapy when combined with Amphotericin B.

Pleiotropic antimalarial activities and immunomodulation exhibited by Himalayan Buransh (Rhododendron arboreum) in human and rodent malaria models

This study demonstrates the antimalarial and immunomodulatory effects of Himalayan Buransh in vitro, in vivo, and in silico, showing potential as an adjunct therapy for drug-resistant malaria.

Targeting Leishmania donovani Sphingosine Kinase 1 using PF-543 enhances immune response and limits parasite load

This paper evaluates PF-543, a SphK1 inhibitor, against Leishmania donovani, showing reduced parasite load and enhanced immune response both in vitro and in vivo.

Gut microbiota-derived indole-3 acetic acid mitigates key hallmarks of metabolic dysfunction-associated steatotic liver disease (MASLD) in an NLRP3-dependent manner in in vitro and diet-induced mouse models

This study identifies indole-3 acetic acid (I3A) as an NLRP3 inflammasome inhibitor that mitigates MASLD hallmarks in vitro and in diet-induced mouse models.

Selective targeting of Plasmodium falciparum hexose transporter by phytochemical Ginsenoside Rg1 disrupts glucose metabolism and block development of parasite

This study identifies Ginsenoside Rg1 as a PfHT1 inhibitor that disrupts glucose metabolism and inhibits growth of both ART-sensitive and resistant Plasmodium falciparum parasites.

Evaluation of Immunopharmacological Efficacy of Live Leishmania donovani Overexpressing Ld_ζ1domain for Protection Against Experimental Human Visceral Leishmaniasis

This study evaluates the immunopharmacological efficacy of Leishmania donovani overexpressing Ld_ζ1domain as a vaccine candidate against visceral leishmaniasis, showing reduced parasite burden and enhanced immune response.

Schizophrenia-associated NRXN1 deletions induce developmental-timing- and cell-typespecific vulnerabilities in human brain organoids

This study shows NRXN1 deletions affect brain development differently in specific cell types and genetic backgrounds, leading to synaptic dysfunction in organoids.