Metabolic syndrome (MetS) is associated with a plethora of different comorbidities. Exploring its key molecular mechanisms, such as advanced glycation end product and its receptor (AGE/RAGE) pathway, holds great potential. Numerous sources agree that targeting the AGE/RAGE pathway is a potential therapeutic strategy for MetS. However, the regulation of AGE/RAGE by microRNAs (miRNAs) in the context of MetS is still poorly understood. This review aimed to provide a systematic picture of the influence of miRNAs on AGE/RAGE in the context of MetS, with a particular focus on its ligands and receptors. This review achieves this in two ways: through an inductive “bottom-up” approach realized by a classical descriptive literature search, and through a deductive/synthetic “top-down” approach based on carefully selected miRNA profiling studies in MetS and its comorbidities. Although the initial inductive approach allowed the identification of some miRNAs of interest, almost all articles on this topic focus on the regulation of processes exclusively involved in atherogenesis. The new deductive approach has broadened the research horizon: It has enabled the discovery of new promising miRNAs and allowed for ranking different comorbid pathologies in MetS according to the degree of miRNA dysregulation of AGE/RAGE. Thus, in addition to atherosclerosis, significant miRNA dysregulation of AGE/RAGE was also described in MetS, particularly in immune cells, as well as in subcutaneous adipose tissue in obesity. This review, along with the novel approaches to systematizing the data contained therein may contribute to the understanding of MetS pathogenesis and the search for targets for the treatment of MetS.

Familial hypobetalipoproteinemia (FHBL), caused by apolipoprotein B (APOB) variants, disrupts APOB-containing lipoprotein synthesis, leading to reduced serum total cholesterol, low-density lipoprotein cholesterol, and APOB. Heterozygous carriers are often asymptomatic, while homozygotes exhibit severe manifestations like malabsorption, vitamin deficiencies, and hepatic steatosis. In recent years, FHBL has attracted increasing attention due to its association with liver disease and its role as a unique monogenic model of steatotic liver disease independent of cardiometabolic risk factors. Mechanistically, lipid overload, endoplasmic reticulum stress, oxidative damage, and impaired autophagy may drive hepatocellular injury and fibrosis. Challenges include insufficient diagnosis, sparse epidemiological data, and unclear disease progression. Enhanced genetic testing, mechanistic research, and longitudinal studies are critical to improving diagnosis, risk assessment, and therapies for FHBL-associated liver disease.

The incidence of early-onset pancreatic cancer (EOPC) is rising, yet optimal treatment strategies remain unclear. While adjuvant chemotherapy (ACT) has shown survival benefits in pancreatic ductal adenocarcinoma, its specific role in EOPC patients following neoadjuvant chemotherapy (NACT) and surgery remains underexplored. This study aimed to assess the clinical benefit of ACT in EOPC patients after NACT.

This retrospective cohort study analyzed pancreatic ductal adenocarcinoma patients from the SEER database (2006–2019) who received NACT followed by curative resection. Propensity score matching (1:1) was used to balance covariates such as tumor, lymph node, metastasis stage, chemotherapy, and radiotherapy. Overall survival (OS) and cancer-specific survival (CSS) were compared between patients with EOPC (<50 years) and average-onset pancreatic cancer (AOPC, ≥50 years). Multivariate Cox regression analysis was performed to identify prognostic factors.

After propensity score matching (124 EOPC vs. 124 AOPC), EOPC patients had significantly longer median OS (41.0 vs. 29.0 months, P = 0.042) and CSS (48.0 vs. 30.0 months, P = 0.016). ACT was an independent prognostic factor for EOPC (OS: hazard ratio = 0.495, 95% confidence interval 0.271–0.903, P = 0.022; CSS: hazard ratio = 0.419, 95% confidence interval 0.219–0.803, P = 0.009), but not for AOPC (P > 0.05). Subgroup analysis revealed that EOPC patients with tumor, lymph node, metastasis stage II disease or those receiving ACT derived the greatest survival benefit.

EOPC patients exhibit superior survival following NACT and surgical resection compared to AOPC, with ACT further enhancing outcomes in this subgroup. These findings support the use of tailored ACT for EOPC and underscore the need for prospective validation.

Prognostic scores are valuable tools for predicting survival in patients with chronic liver disease. Recently, the albumin-bilirubin (ALBI) score has emerged as a potential prognostic indicator in liver-related conditions. This study aimed to compare the prognostic efficacy of the ALBI score with the Model for End-stage Liver Disease (MELD), MELD-Na+, and Child-Turcotte-Pugh (CTP) scores in predicting survival among patients with alcohol-associated liver disease (ALD).

This study included consecutive ALD patients admitted to the Medicine and Gastroenterology wards of MKCG Medical College and Hospital, Berhampur, Odisha, India, between November 2019 and November 2022. Upon hospitalization, baseline characteristics, clinical and laboratory parameters, ALBI, MELD, MELD-Na+, and CTP scores were recorded. The accuracy of these scores in predicting survival up to three years was compared.

A total of 490 ALD patients were included. Higher ALBI scores were observed in patients who died during hospitalization (p < 0.001), at 28 days (p < 0.001), 90 days (p < 0.001), six months (p < 0.001), one year (p < 0.001), two years (p < 0.001), and three years (p < 0.001), compared to those who survived. However, the area under the receiver operating characteristic (AUROC) curves showed that the ALBI score was inferior to MELD, MELD-Na+, and CTP scores in predicting survival at admission [AUROC: ALBI (0.719), MELD-Na+ (0.823), MELD (0.817), CTP (0.770)] and at three years [AUROC: ALBI (0.755), MELD-Na+ (0.787), MELD (0.758), CTP (0.784)]. Furthermore, Cox regression analysis revealed that components used in the MELD, MELD-Na+, and CTP scores—such as serum creatinine, serum sodium, and hepatic encephalopathy—were independent predictors of mortality, whereas the components of the ALBI score (serum albumin and serum bilirubin) were not.

All hospitalized ALD patients had a grade 3 ALBI score, with significantly higher scores observed among non-survivors compared to survivors. However, MELD, MELD-Na+, and CTP scores were superior to the ALBI score in predicting survival both during hospitalization and over a three-year follow-up period.

Huo Xue Tong Luo Capsule (HXTL) has been clinically used to treat osteonecrosis of the femoral head, osteoporosis, and other bone and joint diseases with promising effects. Our previous study has shown that HXTL can promote osteogenesis in mesenchymal stem cells by inhibiting lncRNA-Miat expression through histone modifications. However, the mechanism by which HXTL treats postmenopausal osteoporosis (PMOP) remains unclear. In this study, we used network pharmacology-based mechanism prediction, molecular docking, and pharmacological validation to investigate the mechanism of HXTL in treating PMOP.

The key candidate targets and relevant signaling pathways of HXTL for PMOP treatment were predicted using network pharmacology and molecular docking analysis. RAW264.7 cells were used for Western blot to validate the predicted mechanistic pathways. The ovaries of mice were surgically removed to simulate PMOP. The effect of HXTL on PMOP was evaluated using tartrate-resistant acid phosphatase staining and immunohistochemical assays in vivo.

Network pharmacology analysis suggested that HXTL interacted with 215 key targets linked to PMOP, primarily affecting the PI3K-AKT signaling pathway. Molecular docking showed that the main components of HXTL exhibited strong binding affinity to NFATc1, p-PI3K, and p-AKT1. Furthermore, our in vitro results confirmed that HXTL suppressed the PI3K-AKT signaling pathway. In vivo, HE and tartrate-resistant acid phosphatase staining results showed that HXTL inhibited osteoclast formation and protected bone mass.

This research demonstrated that HXTL could inhibit osteoclast formation and prevent bone loss induced by ovariectomy in mice by inhibiting the PI3K-AKT signaling pathway. These findings provide important evidence for the clinical application of HXTL in treating PMOP.

Spinal cord injury (SCI) significantly impacts the central nervous system, with limited effective treatments available. Brain-derived neurotrophic factor (BDNF) plays a crucial role in neuronal growth, survival, and regeneration after SCI. MicroRNAs, particularly miR-124-3p, have been implicated in SCI pathophysiology. However, the relationship between miR-124-3p and BDNF in the context of SCI remains unclear. This study aimed to investigate the correlation between miR-124-3p expression and BDNF levels in a rat model of spinal cord injury and to assess how the timing of injury affects this relationship.

This study included 72 male Wistar rats divided into three groups: intact (n = 8), sham (n = 32), and SCI (n = 32). SCI diagnosis was confirmed through behavioral-motor function analysis using the Basso, Beattie & Brenham score and histological examination with crystal violet staining. The expression levels of miR-124-3p and BDNF were assessed using real-time polymerase chain reaction in all groups at four time points (one hour, one day, three days, and seven days post-injury).

In the SCI group, a marked reduction in miR-124-3p expression was observed relative to both the sham and intact groups. Conversely, there was a substantial elevation in BDNF expression within the SCI group in comparison to the sham and intact groups. The findings underscore a negative association between miR-124-3p expression and BDNF messenger RNA levels.

The downregulation of miR-124-3p and concurrent upregulation of BDNF suggest a potential regulatory role of miR-124-3p in modulating BDNF expression during SCI. These findings provide new insights into the molecular mechanisms underlying SCI and suggest that miR-124-3p and BDNF could serve as potential therapeutic targets. Further research is needed to explore the translational potential of these findings for developing novel diagnostic and therapeutic strategies for SCI.

Nanobiotechnology has driven transformative advancements in healthcare, particularly in the development of innovative solutions for wound treatment, a persistent and costly global health concern. Among these advancements, the combination of biopolymers and metallic nanoparticles has attracted considerable interest due to their excellent biocompatibility and potent antimicrobial activity. This scoping review explores recent technological progress in wound care, with a focus on alginate-based dressings functionalized with metallic nanoparticles. Alginate, a highly versatile biopolymer, was frequently employed in diverse formats, including hydrogels, sponges, beads, films/membranes, and fibers, across the analyzed studies. Silver nanoparticles were the most extensively investigated agents, owing to their well-established efficacy and the development of strategies to mitigate associated risks. Other metallic nanoparticles were also reported, contributing to a growing body of evidence supporting their therapeutic relevance. The synergistic integration of alginate and metallic nanoparticles has shown promising potential to enhance the performance of wound dressings, representing a significant step forward in the design of next-generation materials for effective and targeted wound management.

Breast cancer remains one of the most common cancers affecting women globally, with late detection frequently contributing to its high mortality rate. Multiple factors drive these delays, including a lack of awareness, financial constraints in low-income countries, and limited access to non-invasive and accurate biomarkers. This review aims to introduce biomarkers, particularly hematological and biochemical serum markers, as essential, non-invasive, and accurate tools for improving the diagnosis, prognosis, and therapeutic management of breast cancer. Hematological markers are measurable blood parameters that reflect physiological and pathological processes such as inflammation, infection, cardiovascular stress, autoimmune conditions, and cancer. Routinely measured hematological markers, such as the neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, and red blood cell indices, are typically obtained from standard tests like the complete blood count. Regular monitoring through complete blood count is essential during cancer treatment to evaluate changes in blood cell counts and detect potential adverse effects. Because of their affordability, minimal infrastructure requirements, and broad accessibility, hematological parameters have been increasingly studied for their association with high-risk factors in breast cancer, particularly in resource-limited settings. Their utility underscores their critical role in improving patient outcomes across diverse healthcare environments. This review summarizes the clinical value of various hematological and serum-based biochemical markers in the screening and diagnosis of breast cancer. Prediction methods that incorporate hematological and serum-based biochemical parameters can support screening, diagnosis, and staging. Overall, individual or combined blood indicators hold significant potential to enhance diagnostic accuracy and effectiveness.