Sepsis-induced acute lung injury (ALI) remains a leading cause of death in intensive care, yet targeted therapies are lacking. Kisspeptin-54 is a neuropeptide primarily known for reproductive regulation, though its role in sepsis is unexplored. This study investigated whether exogenous kisspeptin-54 protects against septic lung injury and examined the underlying mechanism. In a cecal ligation and puncture (CLP) mouse model, we observed reduced circulating kisspeptin-54 and downregulated pulmonary GPR54 expression during sepsis. Exogenous kisspeptin-54 improved 7-day survival, lowered clinical severity scores, and attenuated lung injury, as shown by reduced peritoneal inflammatory cell infiltration, decreased pulmonary vascular leakage and edema, and lower IL-1β and IL-18 levels. Mechanistically, kisspeptin-54 suppressed NLRP3 inflammasome components (NLRP3, ASC, cleaved caspase-1) in lung tissue while enhancing AMPK phosphorylation. These protective effects were reversed by the AMPK inhibitor compound C. To define individual responding leukocyte populations, convergent biochemical and morphological evaluations demonstrated that Kisspeptin-54 preferentially curbs pulmonary neutrophil accumulation over macrophages. In addition, cell-autonomous validation using the validated murine alveolar macrophage cell line MH-S confirmed that Kisspeptin-54 directly enhances AMPK phosphorylation, reduces NLRP3 expression by 48%, and suppresses cleaved caspase-1 maturation by 52%, thereby curbing supernatant IL-1β release. Baseline toxicity screening confirmed that therapeutic doses of Kisspeptin-54 alone are entirely non-toxic in healthy animals, while Compound C alone does not exacerbate background septic mortality. These findings indicate that kisspeptin-54 alleviates sepsis-induced ALI, and its protective effects are strongly aligned with AMPK-mediated suppression of NLRP3 inflammasome activation.

Endocrine-disrupting chemicals (EDCs) are attracting growing interest due to their effects on humans and on ecosystems. Among suspected EDCs, fluoride is a widespread pollutant in aquatic ecosystems, particularly as a result of fluoridation of drinking water. It has also been described to affect fish development. The aim of this study was to determine if chronic fluoride exposure could affect early life stages of rainbow trout (Oncorhynchus mykiss) especially their growth and thyroid hormone system. Trout embryos were exposed from 6 to 40 days post-fertilization, to 0, 1.5, 5, 17, 27.5, or 51.5 mg/L. Growth was significantly inhibited by the exposure with shorter larvae and delayed resorption of the yolk sac. Fluoride exposure increased axial skeleton malformations, but had no effect on the occurrence of edema or hemorrhage. Genes tshβ, dio1, dio2, dio3, and thrα, coding for proteins involved in the thyroid hormone system, were overexpressed in a dose-dependent manner. While histopathological changes of thyroid follicles were observed in larvae exposed to fluoride, no difference in the levels of thyroid hormones was highlighted. In conclusion, results indicate that fluoride exposure during early life stages of rainbow trout might affect their growth and development and exhibit multisite effects on the thyroid hormone system.

Hydrogen peroxide (H2O2) digestion is widely applied to remove natural organic matter (NOM) in microplastics (MPs) analysis. However, for sensitive polymers such as polyvinyl chloride (PVC), aggressive oxidation conditions may result in physical or chemical degradation. This study aims to evaluate nine H2O2 digestion protocols (25-70 °C, 6-48 h) to quantify the balance between the removal efficiency of NOM adsorbed on MP surfaces and PVC degradation. Using humic acid (HA) as a NOM proxy, we achieved 88.5% removal at 70 °C/48 h but observed significant PVC swelling (53.8% area increase). Fourier-transform infrared spectroscopy (FTIR) confirmed minimal chemical alteration (carbonyl index (CI), ≤ 0.081), though optical microscopy revealed temperature-dependent physical fragmentation. Crucially, we identify room temperature, 24 h as the optimal compromise, achieving approximately 61% NOM removal with ≤ 15% physical deformation. These findings help identify suitable conditions for PVC MP extraction in NOM-rich environments. This addresses a critical gap in MPs research.

Tuberculous tenosynovitis is a rare form of extrapulmonary tuberculosis characterized by an indolent course and nonspecific clinical findings, frequently leading to delayed diagnosis. Paradoxical inflammatory reactions during or after anti-tuberculosis therapy may further complicate clinical management and mimic disease relapse. This is a case study regarding a 54-year-old female veterinarian presented with a four-year history of progressive swelling and induration of the right index finger extending to the palm, accompanied by gradually worsening limitation of finger flexion and hand grasp. Magnetic resonance imaging demonstrated extensive flexor tenosynovitis with synovial proliferation. Tenosynovectomy revealed multiple rice bodies surrounding the flexor tendon. Histopathology showed well-formed granulomas without central necrosis, accompanied by focal stromal coagulative necrosis, while microbiological tests were negative. Tuberculous tenosynovitis was diagnosed based on clinical, radiological, and histopathological findings, and anti-tuberculosis therapy was initiated. The patient showed gradual clinical improvement over the nine-month course of treatment. However, one month after therapy completion, recurrent finger swelling with axillary and new epitrochlear lymphadenopathy developed. In the absence of evidence of relapse, a post-treatment paradoxical inflammatory reaction was suspected. Corticosteroid therapy resulted in rapid clinical improvement. This case highlights the diagnostic challenges of tuberculous tenosynovitis, particularly in patients with delayed presentation and negative microbiological findings, and underscores that paradoxical inflammatory reactions may occur even after completion of anti-tuberculosis therapy, potentially mimicking disease relapse.

This study aimed to analyze temporal trends and the clinical-epidemiological profile of visceral leishmaniasis (VL)-HIV coinfection in Brazil between 2009 and 2024. This ecological time-series and descriptive cross-sectional study used data from the Brazilian Information System for Notifiable Diseases (SINAN, acronym in Portuguese) covering eight states with the highest VL incidence: Bahia, Ceará, Maranhão, Minas Gerais, Mato Grosso do Sul, Pará, São Paulo, and Tocantins. Annual coinfection rates were calculated as the ratio between the number of reported VL-HIV coinfection cases and the resident population of the respective state in the same year, multiplied by 100,000. Temporal trends were evaluated using segmented regression to estimate the annual percentage change (APC). Correlation analyses (Spearman), categorical associations (Pearson's chi-squared test), differences in means (Student's t-test), and binary logistic regression (odds ratio - OR) for symptoms were also performed. An increasing trend in coinfection rates was observed in Bahia (APC = 4.2), Mato Grosso do Sul (APC = 19.7), Pará (APC = 10.4), and Tocantins (APC = 8.4). Ceará and Minas Gerais showed an initial increase followed by a decline. A moderate positive correlation was observed between VL cases and coinfection (ρ = 0.313; p < 0.001). Coinfected individuals had a higher mean age (37.9 versus 27.3 years; p < 0.001) and were predominantly male (72.4% versus 59.8%). Mixed-race individuals were the most prevalent, with a higher proportion of Black individuals among coinfected patients. Symptoms associated with coinfection included fever (OR = 2.44), jaundice (OR = 1.69), and edema (OR = 1.56), whereas weight loss, hepatomegaly, and associated infection were associated with lower odds. VL-HIV coinfection shows heterogeneous patterns, with increasing trends in endemic states and distinct temporal segments across Federative Units. These findings reinforce the need for integrated strategies for surveillance, diagnosis, and treatment.

Hydrogels combining the biochemical complexity of the native extracellular matrix (ECM) with the tunable properties of protein-based biomaterials are promising for neural tissue engineering. In this study, decellularized spinal cord meninges (dSCM) were combined with water-soluble hydrophilic silk fibroin (hSF) and enzymatically crosslinked using a horseradish peroxidase/H2O2 system to develop composite hydrogels. A detergent-free, sonication-assisted decellularization method effectively removed cellular components while preserving matrix integrity, reducing residual double-stranded DNA to below 50 ng mg-1 dry weight and retaining key ECM constituents, including collagen and glycosaminoglycans. Hydrogels prepared at different dSCM:hSF ratios showed composition-dependent structural and mechanical behavior, with the 1:0.5 and 1:1 formulations exhibiting the most favorable compressive stiffness and viscoelastic performance. Structural, thermal, and morphological analyses further indicated that hSF incorporation improved matrix stability and contributed to more controlled swelling and degradation behavior. Biological evaluation showed that the 1:0.5 formulation promoted neovascularization in the chorioallantoic membrane assay without evident adverse inflammatory response. In addition, SH-SY5Y cells maintained high viability and showed increased expression of the neuronal-associated markers β-III tubulin and MAP2 over time. Overall, these findings suggest that dSCM:hSF hydrogels provide a promising platform for neural tissue engineering.

Acute respiratory diseases (ARDs) are among the most common illnesses of the 21st century and serve a leading cause of temporary disability. They are also a frequent trigger for the development of acute kidney injury (AKI), which, when progressing to acute kidney failure (AKF), requires costly treatment, including hemodialysis. The risk of AKF increases with age, especially in the presence of comorbidities. The proportion of AKF patients in intensive care units reaches 10-15%. This article presents clinical observations of two female patients of middle and advanced age who developed AKF following ARI. In biochemical blood tests, both Patient A (58 years old) and Patient D (85 years old) exhibited significantly elevated levels of C-reactive protein (CRP: 384 mg/L and 285.4 mg/L, respectively), interleukin-6 (IL-6: 197.0 pg/mL and 143 pg/mL, respectively), and D-dimer (3.88 mg FEU/L and 8.11 mg FEU/L, respectively). These changes were accompanied by an increase in serum creatinine (Scr: 339 mol/L and 160 mol/L, respectively) and a marked decrease in glomerular filtration rate (GFR: 12 mL/min and 25 mL/min, respectively). With conservative therapy, the general condition of the patients improved, and there was a significant reduction in CRP levels (17.7 mg/L and 104 mg/L, respectively), IL-6 (48.2 pg/mL and 67.7 pg/mL, respectively), and Scr (64 mol/L and 84.7 mol/L, respectively), as well as an increase in GFR (92 mL/min and 57 mL/min, respectively). However, serum cystatin C and D-dimer levels remained above threshold values throughout dynamic monitoring. CONCLUSION: In patients with severe ARI, the development of AKF is associated with elevated CRP, IL-6, and D-dimer levels. Increased serum cystatin C levels may serve as a predictor of chronic kidney disease in the future.