Endometrium is the innermost layer of the uterus that respond to and synthesize estrogens in connection with its synchronized thickening and shedding during menstrual cycle. Since its thickening is essential for implantation of the embryo, its hyperplasia at chronicity could lead to uterus-associated infertility. if untreated. Qualitative and quantitative analysis of phytochemical constituents, antioxidant efficacy, and GC–MS analysis of M. pudica leaf extract were done. The antiproliferative efficacy of the extract was assessed by MTT assay, fluorescent staining, and mRNA studies of apoptotic-related genes in endometrial cancer cells (Ishikawa and AN3CA). About 25 female rats were assigned to five groups, control (Group 1) and DES-induced endometrial hyperplasia (Groups 2–5). in this, Groups 3–5 were treated with M. pudica leaf extract at increasing doses to assess its restorative efficacy in terms of estrous cycle, structure of ovary, and uterine weight adopting quantification of hormones, ROS, and mRNA expression of genes associated with inflammation (IL-6, NCOR1, and DLK1), angiogenesis (VEGF), and progression of endometrial hyperplasia (ARID1A, SMARCA4, PIK3CA and KRAS). Administration of M. pudica leaf extract restored the estrous cycle, bringing to normalcy the structure and function of the ovary and uterus, balancing hormones, and reducing inflammation. The expression of ARID1A and SMARCA4, were enhanced while those of genes associated with proliferation, angiogenesis, and inflammation were mitigated. M. pudica leaf extract is potentially effective as a therapeutic agent against endometrial hyperplasia and its cancer cell proliferation by restoring nearly all the dysregulations up to mRNA expression level.
The spread of multidrug-resistant bacteria in water bodies poses a significant public health concern. Efflux pumps represent critical mechanisms of antimicrobial resistance, regulated by genetic repressors that aid bacterial adaptation to environmental stress. This study profiles the diversity of efflux pump genes and genetic repressors in the surface waters of the Cereja (Bragança) and Uraim (Paragominas) rivers in the Amazon region of Brazil. Surface water samples were collected along a gradient of anthropogenic impact, and environmental DNA was sequenced on the Illumina platform. The resulting sequencing data were subsequently subjected to metagenomic analysis, which identified a higher abundance of efflux pump genes in the Cereja River compared to the Uraim River, dominated by the RND and SMR families. Additionally, two-component system (TCS) repressor genes, particularly cbrB, were successfully recovered and modeled using Swiss-Model homology modeling. The higher coverage of the cbrB repressor gene in anthropogenically impacted sites underscores its regulatory role in bacterial stress responses, suggesting its potential application as a novel biomarker of environmental pollution and antibiotic resistance spread in aquatic ecosystems.
Endothelial Glycocalyx (eGCX) degradation is a major pathophysiological event in sepsis, contributing to endothelial dysfunction, vascular permeability, inflammation, microvascular thrombosis, and organ failure. Despite its importance, eGCX-targeted therapies are not currently incorporated into standard sepsis management. This systematic review summarized clinical and preclinical evidence on therapeutic and experimental strategies aimed at preserving or restoring eGCX integrity in sepsis. PubMed, Scopus, Web of Science, the Cochrane Library, and Google Scholar were searched through August 2026. Eligible human and animal studies evaluated eGCX-directed interventions in sepsis or experimental sepsis models. Outcomes included circulating biomarkers such as syndecan-1, heparan sulfate, and hyaluronan, microcirculatory measures including perfused boundary region, and structural assessment by microscopy. Risk of bias was assessed using RoB 2, SYRCLE, and ROBINS-I. Twenty-one studies were included, comprising 17 animal and 4 human studies. Interventions included ascorbic acid, sulodexide, doxycycline, activated protein C, heparin-based therapies, antithrombin, recombinant thrombomodulin, therapeutic plasma exchange, colivelin, liposomal nanocarriers of preassembled eGCX, and rhamnan sulfate. Several interventions reduced eGCX shedding, improved endothelial barrier or microvascular function, and, in some experimental models, preserved or restored eGCX ultrastructure. Overall, the eGCX represents a promising therapeutic target in sepsis; however, most evidence remains preclinical, and well-designed clinical studies using standardized eGCX outcomes are needed. eGCX preservation can be a target of interest in sepsis using several promising interventions. These interventions include ascorbic acid, sulodexide, doxycycline, activated protein C, heparin-based therapies, plasma-derived and recombinant antithrombin, recombinant thrombomodulin, therapeutic plasma exchange, colivelin, liposomal nanocarriers of preassembled eGCX, and rhamnan sulfate.
Hermetia illucens (Diptera: Stratiomyidae) is an economically important insect widely used in organic waste bioconversion, sustainable animal feed production, and biomaterial generation. Accurate identification is essential because morphology alone may be challenging during immature stages. This study integrated morphological characterization with DNA-based identification to provide baseline morphological and molecular characterization of H. illucens from the Jeddah region of western Saudi Arabia. Adult H. illucens were collected from organic waste-rich agricultural environments in Jeddah, Saudi Arabia, and reared under controlled laboratory conditions. Adult and larval morphology was documented using stereomicroscopy based on established diagnostic characters. DNA was extracted from larvae, and partial mitochondrial COI and nuclear 28 S rRNA regions were amplified using universal primers. Sequences were aligned with GenBank sequences, and phylogenetic analyses were performed using MEGA X. The life cycle of H. illucens comprised egg, larva, prepupa, pupa, and adult stages. Adults showed characteristic morphological features, including a metallic black body, translucent abdominal windows, distinctive antennae, blue halteres, and sexual dimorphism of the terminalia. Larvae had an elongated, 11-segmented cylindrical body with a sclerotized head capsule and chewing mouthparts. Both COI and 28 S rRNA regions were successfully amplified and confirmed the specimens as H. illucens. COI sequences yielded 15 haplotypes and clustered with H. illucens sequences from Latin and South America, forming two clades. Integrating morphological examination with mitochondrial and nuclear DNA markers provides a reliable framework for H. illucens identification and establishes baseline morphological and molecular reference data for Saudi Arabian populations.
Asthma is a chronic inflammatory airway disease, and airway epithelial cell injury is closely associated with disease progression. TRIM27, as an E3 ubiquitin ligase, plays a significant role in immune-inflammatory responses. This study aims to investigate the role of TRIM27 in airway epithelial cell injury and inflammation. House dust mite extract (HDM)-induced mouse or 16HBE cell models were constructed to simulate asthma in vivo and in vitro. Lung histopathological injury was assessed via HE and PAS staining. Bronchoalveolar lavage fluid (BALF) inflammatory cell counts and ELISA were used to measure inflammation levels. Cell viability and apoptosis was detected by CCK-8, flow cytometry and TUNEL staining. RT-qPCR and Western blot were employed to detect related gene and protein expression. TRIM27 was upregulated in both in vivo and in vitro asthma models. TRIM27 knockdown alleviated HDM-induced lung histopathological damage in mice, reduced goblet cell hyperplasia and inflammatory cell infiltration, and decreased inflammatory cytokine levels. In vitro experiments showed that TRIM27 knockdown partially restored HDM-induced decline in cell viability, inhibited apoptosis, ROS generation, and inflammatory cytokine release. Mechanistic studies revealed that HDM stimulation activated the NF-κB/MAPK pathway, while TRIM27 knockdown suppressed its activation. Further research demonstrated that TRIM27 activates the NF-κB/MAPK pathway by promoting TRAF3 ubiquitination and degradation. TRAF3 knockdown can weaken the beneficial effects of TRIM27 knockdown. TRIM27 activates the NF-κB/MAPK signaling pathway by promoting TRAF3 ubiquitination and degradation, thereby exacerbating airway epithelial cell injury and inflammatory response, and promoting asthma progression.
