Temporal lobe epilepsy (TLE) is the most common focal epilepsy, with many patients developing drug-resistant epilepsy. Surgical interventions, including stereoelectroencephalography (SEEG)-guided temporal lobe resection (TLR) and SEEG-guided responsive neurostimulation (RNS), are key treatment options. This systematic review compares the efficacy and safety of these interventions in drug-resistant TLE.

A systematic review was conducted following the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) 2020 guidelines. A comprehensive search of multiple databases was performed (January 23–February 14, 2025). Eligible studies included adult patients with drug-resistant TLE undergoing SEEG-guided TLR or RNS (where SEEG was used pre-implant for localization). Primary outcomes assessed included seizure freedom, seizure reduction, adverse events, and quality of life (QoL) improvements. Quality assessments were performed using appropriate tools for randomized and observational studies.

Fifteen studies met the inclusion criteria, with sample sizes ranging from 10 to 440 participants. SEEG-guided TLR achieved an average seizure freedom rate of 58.5% (range: 32–85%) and a mean seizure reduction of 75% (range: 60–90%). SEEG-guided RNS resulted in an average seizure freedom rate of 12.85% and seizure reduction of 63.2%, with variability across studies. QoL improvements were reported in 80–82% of patients. Adverse events were infrequent but varied between interventions.

This review highlights the effectiveness of SEEG-guided TLR and RNS in managing drug-resistant TLE. While both interventions reduce seizure burden and improve QoL, seizure freedom rates are higher with resection. However, gaps remain in understanding long-term cognitive outcomes and demographic influences on treatment response. Future research should address these factors to refine patient selection and optimize epilepsy care.

Therapy-related B-lymphoblastic leukemia (B-ALL) following treatment for multiple myeloma is a rare occurrence. Despite its rarity and the lack of recognition by the World Health Organization as a distinct disease entity, previous publications indicate its possible emergence following myeloma treatment.

The patient is a 65-year-old gentleman with a history of IgG kappa multiple myeloma, status post multiple lines of therapy. The patient presented with a fever, and a complete blood count showed cytopenia. Bone marrow morphologic evaluation revealed numerous blasts. Immunophenotypic analysis demonstrated that these blasts were B lymphoblasts, despite MYC and unusual surface kappa light chain expression. A diagnosis of B-ALL with surface kappa light chain expression post-myeloma treatment was made. Ancillary studies indicated that the B-ALL and the previous myeloma were clonally unrelated. Next-generation gene sequencing revealed pathogenic mutations in KDM6A and KRAS.

This case highlights the potential for therapy-related B-ALL following myeloma treatment, a phenomenon deserving further investigation. The expression of surface light chain in blasts can present a diagnostic pitfall.

Mitochondrial respiratory complexes (Complexes I–V) and their assembly into respiratory supercomplexes (SCs) are fundamental to liver bioenergetics, redox homeostasis, and metabolic adaptability. Disruption of these systems contributes to major liver diseases, including non-alcoholic fatty liver disease, alcoholic liver disease, drug-induced liver injury, viral hepatitis, and hepatocellular carcinoma, by impairing adenosine triphosphate synthesis, increasing oxidative stress, and altering metabolic pathways. Recent advances have clarified the structural-functional interdependence of individual complexes within SCs, revealing their dynamic remodeling in response to physiological stress and pathological injury. These insights open opportunities for clinical translation, such as targeting SC stability with pharmacological agents, nutritional strategies, or gene therapy, and employing mitochondrial transplantation in cases of severe mitochondrial failure. Precision medicine approaches, incorporating multi-omics profiling and patient-derived models, may enable individualized interventions and early detection using SC integrity as a biomarker. By linking molecular mechanisms to therapeutic strategies, this review underscores the potential of mitochondrial-targeted interventions to improve outcomes in patients with liver disease.

Infection control is essential for the success of prosthodontic and oral implant procedures, as microbial contamination can lead to serious complications such as denture stomatitis and peri-implantitis. While synthetic disinfectants like chlorhexidine are commonly used, they may cause side effects including irritation, toxicity, and the development of microbial resistance over time. Natural products derived from plants, animals, and minerals are currently being explored as safer alternatives. Compounds such as epigallocatechin gallate from green tea; eugenol from clove oil; quercetin, thymol, cinnamaldehyde, and flavonoids from propolis; and terpinen-4-ol from tea tree oil have shown strong antimicrobial and anti-biofilm properties. These natural agents are not only effective against harmful oral bacteria but also promote healing, are more biocompatible, environmentally friendly, and are often preferred by patients. However, challenges remain regarding their routine clinical use. The strength and composition of natural agents can vary, and there is a lack of consistent product standards, clinical trials, and comprehensive safety data. Currently, these products are not approved by the U.S. Food and Drug Administration for dental use and are only available as over-the-counter remedies. Production costs and scalability must also be evaluated in comparison with synthetic alternatives. Emerging technologies, such as nanocarriers and targeted delivery systems, are being developed to enhance the effectiveness of natural agents in dental applications. Further clinical research and the establishment of clear regulatory guidelines are necessary to support their integration into clinical practice. Natural disinfectants hold significant potential to become valuable, safe, and sustainable tools for maintaining hygiene in prosthodontics and oral implantology.

Immunoinflammatory skin diseases are characterized by an imbalance in immune homeostasis, and their chronic inflammatory processes involve a complex regulatory network of CD4+ T cell differentiation. With the widespread use of biologics (e.g., interleukin-17/interleukin-23 inhibitors) in psoriasis, atopic dermatitis, and other diseases, the adverse effects triggered by the phenomenon of CD4+ T cell-mediated immune drift have attracted significant attention, with the skin being the primary target as an immune organ. In this paper, we provide a review of the clinical features of the skin and the mechanisms of immune drift caused by different types of biologics, as well as the therapeutic modalities.

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.

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.

Parenteral nutrition (PN)-associated cholestasis (PNAC) is frequently diagnosed in premature infants; however, not all PN-exposed infants develop PNAC. We propose that, in premature infants receiving PN and varying amounts of enteral feeds, differences in the gut microbiome and fecal bile acid content are associated with PNAC development. This study aimed to examine the fecal microbiome and bile acid content of premature infants on PN to determine if there is a relationship with the development of PNAC.

Twenty-two preterm infants had serial bilirubin measurements and fecal samples collected during their neonatal intensive care unit admission. Fecal samples underwent 16S rRNA gene sequencing and bile acid analysis. Binomial regression, adjusting for postmenstrual age with feed amount as a moderator, was used to assess the impact of the fecal microbiome and bile acids on PNAC development.

Cholestatic patients (n = 11) had greater PN and antibiotic exposure (p = 0.020; p = 0.010) and longer neonatal intensive care unit stays (p = 0.0038) than non-cholestatic patients. Microbiome richness was higher in non-cholestatic infants (p < 2E-16), with no difference in β diversity (p = 1.0). Cholestatic infants had a significantly higher abundance of Proteobacteria and Fusobacteriota and a lower abundance of Bacteroidota (p < 2E-16). Akkermansia was abundant in all infants on low feeds; as feed volume increased, Akkermansia abundance significantly increased in non-cholestatic infants (p < 2E-16). Bile acid analysis demonstrated significantly lower deoxycholic acid concentrations in cholestatic infants (p < 2E-16). Metagenomic analysis revealed an increase in Proteobacteria requiring augmented stress responses in non-cholestatic infants.

This is the first study to directly explore the relationship between PNAC susceptibility, the microbiome, and fecal bile acids in preterm infants. The microbiome and bile acid patterns identified here may inform the development of targeted therapeutics for this vulnerable population.

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.