Exploring the multilayered response of TB bacterium Mycobacterial tuberculosis to lysosomal injury.

Mtb subverts host immune surveillance by damaging phagolysosomal membranes, exploiting them as replication niches. In response, host cells initiate a coordinated LDR, integrating membrane repair, selective autophagy, and de novo biogenesis. This review delineates a systems-level model of lysosomal quality control governed by three critical regulatory axes: LGALS3/8/9, TRIM E3 ubiquitin ligases, and the AMPK-TFEB signaling pathway.

Artificial Intelligence in Gestational Diabetes Care: A Systematic Review.

Background: Artificial intelligence (AI) has emerged as a transformative tool for advancing gestational diabetes mellitus (GDM) care, offering dynamic, data-driven methods for early detection, management, and personalized intervention.

Objective: This systematic review aims to comprehensively explore and synthesize the use of AI models in GDM care, including screening, diagnosis, management, and prediction of maternal and neonatal outcomes. Specifically, we examine (1) study designs and population characteristics; (2) the use of AI across different aspects of GDM care; (3) types of input data used for AI modeling; and (4) AI model types, validation strategies, and performance metrics.

Resynchronization Therapy in a Coronary Venous Sinus Anomaly.

Anatomy: Coronary venous sinus is the major portal for cardiac venous drainage and plays a crucial role in electrophysiological procedures like left ventricular pacing.

Pathology: Although congenital anomalies of the coronary sinus are rare, we present a unique case of interrupted coronary sinus. The proximal segment drained normally into the right atrium, while the distal segment drained into a common channel that connected to the left subclavian vein via a persistent left superior vena cava.

Phagosomal escape and sabotage: The role of ESX-1 and PDIMs in pathogenesis.

() employs diverse virulence factors to evade immune defenses and persist intracellularly. The ESAT-6 secretion system-1 (ESX-1) type VII secretion system (T7SS) releases EsxA, EspA, and EspB, inducing phagosomal rupture and cytosolic access while triggering host defenses, including galectin recruitment and stress granule formation. To counteract host responses, utilizes phthiocerol dimycocerosates (PDIMs) to inhibit autophagy and LC3-associated phagocytosis (LAP) by suppressing NADPH oxidase (NOX2) recruitment and reactive oxygen species (ROS) production.