Fullerene (C & C)-Meso-Tris-4-Carboxyphenyl Porphyrin Dyads Inhibit Entry of Wild-Type and Drug-Resistant HIV-1 Clades B and C.

The biological applications of noncationic porphyrin-fullerene (P-F) dyads as anti-HIV agents have been limited despite the established use of several cationic P-F dyads as anti-cancer photodynamic therapy (PDT) agents. This article explores the potential of amphiphilic non-cationic porphyrin-fullerene dyads as HIV-1 inhibitors under both PDT (light-treated) and non-PDT (dark) conditions. The amphiphilic P-F dyads, PBC and PBC, demonstrated enhanced efficacy in inhibiting the entry and production of HIV-1 (subtypes B and C).

Cutaneous Manifestations of Systemic Lupus Erythematosus and Their Correlation With Cardiac Involvement.

Systemic lupus erythematosus (SLE) is a chronic autoimmune disorder characterized by widespread immune dysregulation that affects multiple organ systems, including the skin and cardiovascular system. The crosstalk between different cell death pathways-such as apoptosis, necroptosis, and neutrophil extracellular trap (NETosis), plays a pivotal role in the pathogenesis of SLE, influencing both cutaneous and cardiac manifestations. Cutaneous lupus erythematosus (CLE) is one of the most common early signs of SLE, affecting up to 80% of patients.

Purine but Not Pyrimidine De Novo Nucleotide Biosynthesis Inhibitors Strongly Enhance the Antiviral Effect of Corresponding Nucleobases Against Dengue Virus.

Every year, dengue virus affects hundreds of millions of individuals worldwide. To date, there is no specific medication to treat dengue virus infections. Nucleobases, the base of a nucleoside without ribose, are understudied as potential treatments for viral infections.

Sepsis-Associated Acute Kidney Injury: Pathophysiology and Treatment Modalities.

Sepsis-associated acute kidney injury (S-AKI) is a critical complication that significantly contributes to the morbidity and mortality of sepsis patients. This narrative review explores the complex and multifactorial pathophysiology of S-AKI, which involves hemodynamic alterations, microcirculatory dysfunction, endothelial damage, inflammatory responses, oxidative stress, and direct tubular injury. Conventional perspectives linking S-AKI primarily to reduced renal blood flow are now being reconsidered, with growing insights highlighting the significance of microcirculatory dysfunction and endothelial activation as key contributors.