Barasat Government College

The structure, electronic, magnetic and optical properties of pyrite CrO2 at 46 GPa are extensively investigated for the first time using first-principles electronic structure calculations. Structural distortion is observed in the present material due to distortion in the CrO6 octahedra. The system is found to be half-metallic and ferromagnetic. The two available electrons are found to be distributed among all five Cr-3d orbitals. The three Cr-t2g (Cr-dxy, dyz, dxz) as well as the two Cr-eg (Cr-3d3z2- r2, Cr-3dx2- y2) orbitals are observed to be degenerate. The partial filling and delocalization of electrons in all five Cr-3d orbitals for the majority spin channel are responsible for the half-metallic behaviour of pyrite CrO2. The simultaneous effect of p-d hybridization and Cr–O antiferromagnetic coupling is responsible for ferromagnetism in the present material. The system remains half-metallic upon the application of U = 3 eV. The strength of ferromagnetism is enhanced at U = 3 eV. The Curie temperature Tc of pyrite CrO2 is significantly reduced to 146 K ( 156 K for U = 3 eV) at 46 GPa. The metallicity and anisotropy in the structure are observed in the investigation of the real [ _1() ] and imaginary [ _2() ] parts of the dielectric function. In the study of the energy loss function [ L() ], a significant electron energy loss is observed at a high pressure of 46 GPa. The system exhibits low dissipation or transparency up to 30 eV. The plasmon frequencies observed for L_xx() , L_yy() and L_zz() (x-, y- and z-components of [ L() ]) are 26.72, 26.65 and 26.34 eV, respectively, below which the system remains metallic. It is observed that the optical properties do not change substantially upon applying U=3 eV.

Psoriasis is a chronic, immune-mediated inflammatory disorder with systemic implications beyond its cutaneous manifestations. Its pathogenesis involves a complex interplay between genetic predisposition, environmental triggers, and immune dysregulation. The sustained crosstalk between dendritic cells (DCs) and T cells, which orchestrates the initiation and perpetuation of psoriatic inflammation. Plasmacytoid DCs, activated by nucleic acid-LL37 complexes, produce interferon-α that promotes myeloid DC maturation. These DCs secrete IL-12, IL-23, and TNF-α, driving differentiation of naïve T cells into Th1, Th17, and Th22 subsets. Effector T cells subsequently release cytokines such as IFN-γ, IL-17, and IL-22, which promote keratinocyte hyperproliferation, impaired differentiation, neutrophil recruitment, and angiogenesis. This DC-T cell axis forms a self-amplifying inflammatory loop that underpins disease chronicity. Conventional systemic agents, including methotrexate, cyclosporine, and retinoids, have demonstrated efficacy but are limited by nonspecific immunosuppression and significant toxicities. Advances in immunology have identified the IL-23/Th17 pathway as a pivotal therapeutic target, enabling the development of biologics and small-molecule inhibitors. Monoclonal antibodies targeting TNF-α, IL-12/23, IL-17, and IL-23 have revolutionized management, achieving high rates of sustained clearance with improved safety profiles. Additional strategies, such as PDE4 and JAK/STAT inhibitors, offer oral alternatives with targeted immunomodulation. Novel approaches, including tolerogenic DC therapy and neuroimmune modulation, hold promise for refining treatment and addressing disease heterogeneity. Effective immunotherapeutic strategies must therefore balance skin clearance with reduction of systemic inflammation and long-term comorbidity risk. Integrating mechanistic insights into DC-T cell interactions with emerging therapies provides a framework for personalized, safer, and more durable disease control.

Background Comparative evidence for glucagon-like peptide-1 receptor agonists (GLP-1 RAs) and sodium-glucose cotransporter-2 inhibitors (SGLT2Is) in chronic pancreatitis is limited. We compared outcomes between these therapies. Methods This retrospective TriNetX database study included adults with diabetes and chronic pancreatitis receiving a GLP-1 RA or SGLT2I. Propensity score matching yielded 3373 patients per cohort. Outcomes were assessed from day 1 through day 1825. Risk ratios (RRs) and hazard ratios (HRs) with 95% confidence intervals (CIs) were estimated. Results Recurrent acute pancreatitis occurred in 4.7% of GLP-1 RA recipients and 7.2% of SGLT2I recipients (RR, 0.649; 95% CI, 0.488–0.863; HR, 0.586; 95% CI, 0.437–0.786). GLP-1 RA use was also associated with lower recorded risks of exocrine pancreatic insufficiency (2.4% vs 4.7%; RR, 0.495; 95% CI, 0.374–0.657; HR, 0.473; 95% CI, 0.355–0.630), malnutrition (4.7% vs 7.6%; RR, 0.616; 95% CI, 0.499–0.760; HR, 0.601; 95% CI, 0.484–0.746), and all-cause mortality (8.7% vs 12.5%; RR, 0.697; 95% CI, 0.605–0.803; HR, 0.680; 95% CI, 0.586–0.790). No significant differences were observed for pancreatic pseudocyst, abnormal weight loss, pancreatic cancer, or subsequent opioid use. Conclusions GLP-1 RA use was associated with lower recorded risks of recurrent acute pancreatitis, exocrine pancreatic insufficiency, malnutrition, and mortality than SGLT2I use.

The present study explores the symbiotic relationships between the common freshwater mussel Lamellidens marginalis and two associated symbionts: water mites (Unionicola spp.) and ciliates (Conchophthirus spp.). Host mussels were collected from Banipur, Habra, West Bengal, India between August 2024 and March 2025, focusing on the prevalence, anatomical localization, and morphological diversity of the symbionts. Water mites exhibited a high prevalence of 71.8

Active XY models and active surfaces are two paradigmatic nonequilibrium systems with distinct microscopic origins. We show that the hydrodynamic theories for a quenched-disordered nonreciprocal random bond two-dimensional XY model and an inversion-symmetric active surface tangentially advected by quenched velocities are identical. This theory predicts sub-logarithmic phase order in the XY model and sub- or super-logarithmic positional order in the surface for short-range disorder with nonuniversal exponents, which vary continuously with the degree of transversality of the disorder variance. We argue that the nonreciprocal random bond XY model can disorder through vortex proliferation.