Vidyasagar College (Bengali: বিদ্যাসাগর কলেজ) is a state government-aided public college, affiliated to the University of Calcutta, located in North Kolkata, West Bengal, India. The college offers both post-graduate and under-graduate courses in a number of subjects of arts and science. Founded in 1872, it was the first private college (now governmental) in India which was purely run, maintained and financed by Indians. Formerly known as Metropolitan Institution, it was named after its founder Pandit Ishwar Chandra Vidyasagar in 1917.The college is affiliated to Calcutta University, under UGC and accredited by NAAC. It follows semester based CBCS system. The college does not participate in NIRF ranking in college category. The college was a part of DBT STAR College Scheme. The college receives funding from State Government, UGC (via CU) and other GOI-affiliated institutes or schemes i.e RUSA, ICSSR, AICTE and NIEIT.
Cupric oxide (CuO) is a key p-type semiconductor in advancing third-generation solar cells. This study analyzes four heterojunction solar cells: CuO/Si, CuO/ZnO, CuO/SnO2, and CuO/CdS, using SCAPS simulations. Platinum (Pt) serves as the metal contact and indium tin oxide (ITO) is the substrate layer, offering higher efficiency than traditional Si substrates. The power conversion efficiency (PCE) of the Pt/CuO/CdS/ITO cell reaches an impressive 26.59
We study the fate of a forager who searches for food performing a random walk on lattices. The forager consumes the available food on the site it visits and leaves it depleted but can survive up to S steps without food. We introduce the concept of intermittent rest in the dynamics which allows the forager to rest with probability p upon consumption of food. The parameter p significantly affects the lifetime of the forager, showing that the intermittent rest can be beneficial for the forager for chosen parameter values. The study of various other quantities reveals interesting scaling behavior with p and also departure from usual diffusive behavior for 0.5 < p < 1. In addition to numerical simulations, the problem has been studied with analytical approach in one dimension and the results up to p < 0.5 agree with the numerical ones to a large extent.
The low-temperature metallic phase of 1T-TaS2 may originate from the current-and voltage-driven destabilization of the commensurate charge density wave in a strongly correlated Mott-insulator, alongside the robust yet rarely realized influence of intrinsic electronic distortions. Electrical pulse-driven transport, combined with the second harmonic response, reveals abrupt switching, negative differential resistance, and multiscale domain-wall reorganization. The free-energy analysis identifies a critical order parameter threshold for the Mott-metal transition, with scaling exponents (beta 1.3) consistent with two-dimensional percolation. The sparse limit fractal dimension Df 0.3 at 10 K, rising to 0.9 at 300 K, reflects the hierarchical evolution of the conductive pathways throughout the temperature. These findings establish a direct connection between fractal percolation, pulse-induced instabilities, and correlated electron transport, offering a framework for controlled access to nonequilibrium phase transitions in low-dimensional quantum materials.
The present in silico study provided the adaptive binding of seven physiologically active molecules, including four non-peptide hormones (cortisol, estradiol, triiodothyronine, melatonin) and three vitamins (methyltetrahydrofolate, pyridoxal phosphate, thiamine), alongside argireline as a benchmark, at hotspot-enriched interfaces of full C2AB-domain of Synaptotagmin 1 (Syt1), using molecular docking study and molecular dynamics (MD) simulations. Linear correlations of MD-features and nonlinear KPCA-IG–based ranking of features and ligands yielded deeper mechanistic insights. All ligands exhibited spontaneous binding with strong negative ΔGbinding values. Fifteen hotspots, clustered across the C2A, C2B, and C2AB–interlink regions, were dominated by hydrophobic and van der Waals interactions. Several hotspots and non-hotspots corresponded to Syt1 residues that are reported to link with Ca2+-dependent phenomena and membrane vesicular fusion. Solvent-excluded volume (VSE) analyses showed that local hotspot burial and global desolvation together influenced protein adaptability, distinguishing ligands with similar hotspots but divergent thermodynamics. Linear correlations established ΔGbinding as an indicator of hydrophobic hotspot burial. KPCA-IG identified ΔVSE and RMSD as dominant mechanistic features capturing cooperative induced-fit responses. Pyridoxal phosphate, melatonin and triiodothyronine emerged as mechanistically top adaptive binders, involving adjustable desolvation, hotspot expansion, optimal flexibility and pose retention. Methyltetrahydrofolate and cortisol showed intermediate burial-dominated cooperativity. Argireline, thiamine and estradiol exhibited ligand-specific burial-dominated, pose-locked and adaptability-limited bindings. Overall, our study demonstrates that desolvation control, induced-fit adaptability and structural flexibility, not ΔGbinding alone, govern Syt1-ligand binding, revealing Syt1 as a versatile presynaptic target for modulation by these bioactive molecules. ### Competing Interest Statement The authors have declared no competing interest. Department of Biotechnology (DBT), BINC (Bioinformatics National Certification), Ministry of Science and Technology, Government of India, BT/BI/10/078/2014
Riboflavin metabolism governs a myriad of redox-driven biochemical processes fundamental to energy production, cellular signaling, and biosynthesis. Flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN) act as obligatory prosthetic groups for a plethora of regulatory enzymes of key metabolic pathways, correlating riboflavin status directly to cellular energy flux and redox balance. Oxidative stress may disturb physiological activities of riboflavin metabolizing machineries. Chronic stress induces surge in levels of circulatory catecholamines including adrenaline which subsequently undergo auto-oxidation generating free radicals. Cardio-protective efficacy of melatonin is well-documented against cardiovascular diseases. In this study, subcutaneous administration of adrenaline in rats for 10 consecutive days induces an oxidative stress milieu in heart, mimicking a chronic stress model. Adrenaline precipitates antioxidant imbalance, tissue-morphological alterations and disruption of mitochondrial membrane potential accompanied by alterations in tissue riboflavin, FMN and FAD levels and prominent reductions in the activities of riboflavin metabolizing enzymes. Altered levels of these co-factors also disrupt cardiac energy metabolism. However, melatonin protects against these deleterious repercussions of adrenaline. Melatonin safeguards cardiac tissue from inflammation by restraining the surge in interleukin-1 beta, tumor necrosis factor-alpha and interleukin-10 and also from apoptosis by suppression of Caspase-8 and Caspase-3 levels. Intriguingly, isothermal titration calorimetric study revealed spontaneous binding of adrenaline with FAD and FMN. Melatonin also exhibits strong binding affinity for adrenaline. 1H-NMR spectroscopic studies unveiled fascinating findings concerning the site of interactions of adrenaline with FAD, FMN, and melatonin. Findings suggest that melatonin may impede binding of adrenaline with flavin co-enzymes plausibly by potential encounter and sequestration of adrenaline, FMN or FAD by melatonin. (c) 2026 Elsevier Inc. All rights are reserved, including those for text and data mining, AI training, and similar technologies.
