Early and accurate prognostic assessment is crucial to avoid serious disease progression in patients with liver failure. Thyroid hormone is an important metabolic regulator involved in hepatic function. This review examines the pathophysiological regulation in detail of the hypothalamic-pituitary-thyroid axis in patients with liver failure and emphasizes the importance of thyroid profiling (thyroid-stimulating hormone, T3, and T4) in prognostic assessment and risk stratification. T3 can enhance liver regeneration. The clinical application of thyroid hormone replacement therapy in patients with acute-on-chronic liver failure complicated by non-thyroidal illness syndrome is controversial. This review aims to inform clinical practice regarding the relevance of thyroid hormone level assessment in liver failure and to provide novel insights into the prognostic evaluation and comprehensive care of liver failure complicated by thyroid dysfunction.

Acromegaly requires multimodal management. While surgery is first-line, many patients have persistent/recurrent disease. Gamma knife radiosurgery (GKRS) offers precise radiation, but data on its use as initial therapy remain limited. This study aimed to review the outcomes and report on our experience in treating patients with acromegaly using initial GKRS.

We retrospectively identified 33 patients with acromegaly who underwent GKRS from 1993 until 2016 at the Department of Radiotherapy, the Second Affiliated Hospital of Guangzhou Medical University. These patients had complete endocrine, radiological, and imaging data before and after GKRS. Furthermore, univariate and multivariate analysis was utilized to analyze the potential prognostic factors of endocrine remission and new-onset hypopituitarism.

Thirty-three patients were enrolled in the study. Fifteen patients (45.5%) were males and 18 (54.5%) were females. The median age was 44.0 years (range, 24.9–66.2 years). During a median follow-up of 65.6 months (range, 12.9–297.6), the median margin dose for GKRS was 15.0 Gy (range, 10.8–20.3 Gy). Endocrine remission was achieved in nine of the 33 patients (27.3%) over a mean follow-up of 85.1 months (range, 12.9–161.3). No prognostic factors demonstrated a significant association with endocrine remission. New-onset hypopituitarism occurred in eight patients (24.2%) after GKRS. The tumor control rate was 100%. Only one patient developed worsening visual dysfunction. No new cranial neuropathy was noted.

Initial GKRS for acromegaly provided effective tumor control and partial endocrine remission with a favorable safety profile, notably a low rate of new-onset hypopituitarism, representing a viable treatment option.

Helicobacter pylori infection represents a significant modifiable risk factor in the pathogenesis of gastric cancer. Nevertheless, conventional antibiotic treatments have increasingly proven inadequate due to challenges such as antibiotic resistance, microbial dysbiosis, and mucosal damage. In response to these issues, this review introduces an innovative intervention strategy based on the “nanotechnology-based 3R” approach (Remove H. pylori, Remodel the microenvironment, Repair the gastrointestinal tract), which aims to offer a comprehensive solution for managing H. pylori infection. This strategy comprises three principal components. Firstly, the utilization of pH/light/magnetic multi-responsive nanomaterials facilitates the precise eradication of the pathogen and its biofilm. Secondly, to address bacterial immune evasion, these nanomaterials are engineered to target and neutralize virulence factors such as VacA, thereby contributing to the reversal of the local immunosuppressive environment. Thirdly, the utilization of nanomaterials presents a promising approach for the concurrent repair of the mucosal barrier and the maintenance of intestinal microbiome homeostasis. Finally, this paper provides a comprehensive analysis of the specific mechanisms employed by typical nanomaterials, including metal-organic frameworks, charge-reversal nanoparticles, nanozymes, and antimicrobial peptide crystals. These mechanisms involve targeted microbial eradication, activation of autophagy, and the upregulation of tight junction proteins. Furthermore, the study delves into the critical roles played by multimodal external field stimulation and material–host interaction network analysis, which are essential for future clinical translation. Ultimately, this review suggests a potential roadmap for system-precision intervention that transcends the conventional “sterilization first” paradigm. Nonetheless, the current evidence regarding the efficacy and safety of this approach is predominantly derived from cell and mouse models. Therefore, its clinical applicability requires validation through studies involving large animal models and prospective clinical trials.

Empirical and theoretical studies can be distinguished among the areas of investigation of the renin-angiotensin-aldosterone system (RAAS) and its relationship with the development of cardiovascular diseases. Theoretical work is based mainly on the bioinformatic analysis of key elements of RAAS (genes, proteins, metabolites), on calculations and predictions of protein interactions, and on mechanisms of RAAS gene expression regulation. An associative gene network based on big data analysis allows us to reveal relationships among the proteins, regulatory pathways, and biological processes acting in RAAS, as well as to identify new diagnostic markers, therapeutic targets, putative molecular mechanisms of the development of RAAS-associated diseases, drug interactions, and drug toxicity.

The reconstruction and analysis of associative gene networks were performed using ANDSystem. The regulation of RAAS-associated gene expression was analyzed by transcription factor (TF) binding sites (TFBSs) prediction in the proximal promoters of these genes and by studying interactions between TFs themselves using the Ensembl Biomart web service and AnimalTFDB 4.0. The recognition of potential TFBSs in RAAS gene promoters was performed using MoLoTool.

According to the centrality criteria of the RAAS associative gene network, the following proteins were identified as exerting a significant influence on information interplay between network components: IL6, EDN1, TNFA, MK01, LEP, and JUN. Analysis of the ten identified TFs and their TFBSs among the genes in the RAAS network under study revealed clusters of three to 26 genes regulated by them.

Components with the highest values of centrality and vertex degrees were identified in the reconstructed associative gene network of the RAAS, and ten TFs supposed to regulate 26 RAAS genes were determined.

Clove essential oil (CEO) derived from Syzygium aromaticum and miswak (Salvadora persica) contains bioactive compounds with antimicrobial properties. Due to the growing interest in alternatives to conventional antibiotics, this study aimed to evaluate the in vitro antimicrobial efficacy of CEO, miswak, and their combination against key peri-implantitis pathogens.

The antimicrobial activities of CEO, miswak, and their combinations were tested against Fusobacterium nucleatum, Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, and Prevotella intermedia. Disc diffusion and serial dilution methods were used to measure the inhibition zones and minimum inhibitory concentrations, respectively. Doxycycline served as a standard antibiotic for comparison, while ethanol was used as a negative control. Data were analyzed using one-way analysis of variance and Tukey’s honestly significant difference test, with significance set at α = 0.05.

CEO exhibited inhibition zones of 10–16 mm, comparable to that of doxycycline (13–16 mm), whereas miswak (6–13 mm vs. 1–14 mm) and the CEO–miswak combination (8–14 mm vs. 0–14 mm) showed lower activity. Mean minimum inhibitory concentration values were lowest for doxycycline (1.73 ± 0.46 µg/mL), followed by CEO (2.37 ± 0.24 µg/mL) and CEO–miswak combination (2.92 ± 0.12 µg/mL). Statistical analysis showed that the CEO–miswak combination was less effective than CEO (p = 0.0326) and doxycycline (p = 0.0001), but not different from miswak (p = 0.9836). CEO showed slightly greater activity than miswak (p = 0.0605).

Among the natural extracts tested, CEO exhibited superior antimicrobial efficacy, whereas miswak was less effective. The combination of CEO with miswak did not enhance antimicrobial efficacy, suggesting antagonistic interactions between their bioactive compounds.

Tenofovir alafenamide (TAF) has demonstrated comparable efficacy to tenofovir disoproxil fumarate (TDF), with improved renal and bone safety, in Chinese participants with chronic hepatitis B enrolled in two Phase 3 trials. This study aimed to evaluate the long-term virologic efficacy, serological and biochemical responses, resistance, and renal and bone safety of TAF over eight years in this population.

Participants completing the three-year double-blind phase were eligible to receive open-label TAF 25 mg/day for up to an additional five years (totaling eight years). Analyses of viral suppression (HBV DNA < 29 IU/mL), alanine aminotransferase normalization, serological responses, resistance surveillance, and safety outcomes were conducted.

Among 334 enrolled participants, 212 of 227 participants randomized to TAF continued open-label TAF (TAF-TAF), and 99 of 107 participants on TDF switched to open-label TAF (TDF-TAF). At Year 8, 79.3% (180/227) and 78.5% (84/107) of participants in the TAF-TAF and TDF-TAF groups, respectively, achieved viral suppression (missing = failure); rates increased to 95.2% (180/189) and 95.5% (84/88) when excluding missing data. Alanine aminotransferase normalization rates remained high and comparable between groups. Serologic response rates continued to increase over time, with higher rates observed in the TAF-TAF group. Estimated glomerular filtration rate (by Cockcroft-Gault) and hip/spine bone mineral density remained stable in the TAF-TAF group through eight years; the small declines in these renal and bone parameters observed during double-blind TDF treatment improved after switching to open-label TAF. No resistance to TAF was detected.

Long-term TAF treatment demonstrated durable virologic efficacy, sustained biochemical and serological responses, and favorable renal and bone safety over eight years in Chinese participants with chronic hepatitis B.

Metabolic dysfunction-associated steatotic liver disease (MASLD) and sarcopenia frequently coexist, yet their causal relationship and underlying mechanisms remain poorly defined. This study aimed to investigate whether a bidirectional causal link exists between MASLD and sarcopenia and to identify the molecular mediators involved in liver-muscle crosstalk.

We applied Mendelian randomization to test the causal effect of sarcopenia-related traits on MASLD risk. To capture distinct clinical features, we established complementary mouse models, including diet-induced and genetic (ob/ob) MASLD models, a stelic animal model, and a drug-induced muscle atrophy model. Multi-tissue transcriptomic profiling was performed on liver and muscle to uncover altered pathways.

Complementing prior genetic evidence establishing MASLD as a causal factor for sarcopenia, our Mendelian randomization analysis revealed that diminished muscle mass and muscle function contribute to an elevated risk of MASLD. In mice with MASLD, we observed loss of muscle mass, reduced strength, and ectopic lipid deposition in skeletal muscle. Conversely, muscle atrophy exacerbated hepatic steatosis, inflammation, and fibrosis in MASLD mice. Transcriptional profiling revealed that sarcopenia impairs hepatic metabolic homeostasis by enhancing fatty acid uptake and impairing oxidative phosphorylation, while MASLD, in turn, promotes muscle dysfunction by exacerbating inflammatory responses and metabolic dysfunction. We further identified C-C motif chemokine ligand 2 as a key myokine that drives MASLD, and adrenomedullin as a key hepatokine that triggers sarcopenia.

Our findings suggest a potential bidirectional causal relationship between MASLD and sarcopenia, which may be partially mediated by C-C motif chemokine ligand 2 and adrenomedullin.

Cardiac pacemaker implantation is a primary therapy for various arrhythmic disorders; however, safety concerns persist in India. This study aimed to evaluate two-year safety outcomes of cardiac pacemakers, implantable cardioverter-defibrillators, and cardiac resynchronization therapy devices in a tertiary care setting.

In this prospective cohort study, data collection was conducted over a one-year enrolment period (February 2023 to January 2024), encompassing patient demographics, pacemaker implantation details, indications, and comorbidities. Patients were prospectively followed for a total of two years from enrolment—during the data collection period and for an additional year, to record device-associated adverse events. Ethical approval was obtained (IECJNMC/1662), and data were analyzed using SPSS.

Among 183 patients, 95% received cardiac pacemakers, 3% cardiac resynchronization therapy devices, and 2% implantable cardioverter-defibrillators. The data comprised 58% males (mean age, 63 years). The adverse event rate was 5.5% (10/183), distributed as 3.8% device infection, 1.09% lead dislodgement, and 0.54% generator dysfunction, with no statistical difference between males and females (P > 0.05). Different age groups, various indications, and several comorbidities showed no significant disparities (P > 0.05) between males and females. The Cox model showed no significant effect of several predictors on the occurrence of adverse events (P > 0.05). The Kaplan–Meier survival curve revealed a higher incidence of adverse events in the first six months, followed by stabilization. Adverse events were appropriately documented and reported to the Indian Pharmacopoeia Commission.

The observed adverse event rate of 5.5% supports previous Indian and international data; however, the smaller sample size and short follow-up duration warrant further investigation for more specific outcomes.

Irinotecan is a camptothecin derivative that exerts its antitumor effects after conversion into the active metabolite 7-ethyl-10-hydroxycamptothecin (SN-38), and it is widely used for the treatment of various advanced solid tumors. However, irinotecan-induced neutropenia (IIN) remains one of its most common and clinically significant hematological toxicities, increasing the risk of infection, treatment interruption, dose reduction, and poor therapeutic outcomes. This review aims to summarize the pathogenesis, risk factors, and management strategies of IIN to provide practical guidance for its clinical prevention and standardized management. Current evidence suggests that IIN is mainly associated with SN-38-mediated topoisomerase I inhibition and mitochondrial injury in hematopoietic stem cells, leading to impaired neutrophil production. The risk of IIN is influenced by irinotecan dosage, UGT1A and transporter gene polymorphisms, baseline patient characteristics, organ function, and concomitant chemotherapy. Preventive and therapeutic strategies include genotype-guided dose adjustment, careful dose optimization, oral alkalinizing agents, granulocyte colony-stimulating factor support, and modulation of intestinal microbiota. In conclusion, IIN is a multifactorial and potentially manageable adverse reaction. Integrating pharmacogenetic testing, individualized dosing, supportive care, and emerging approaches such as microbiota-based interventions may improve the safety and continuity of irinotecan-based chemotherapy.

The incidence and mortality of stroke are gradually increasing. In this context, post-stroke neuronal loss and the related long-term complications, along with costly treatment strategies, are significant concerns for healthcare professionals, and effective, convenient, and inexpensive therapeutic modalities are required. Natural and easily accessible herbal remedies may be the optimal option in post-stroke recovery. This narrative review aims to summarize the neuroprotective properties of Withania somnifera (Ashwagandha) and its therapeutic efficacy in neuronal plasticity and recovery after stroke. Original research articles, reviews, and case studies were sourced from databases such as PubMed, Web of Science, Scopus, Google Scholar, Medline, and Embase. Only full articles published in English up to July 2025 were considered. Keywords including W. somnifera, Ashwagandha, stroke, cerebral ischemia, neurodegeneration, neuronal loss, and post-stroke recovery were utilized for the literature search. It has been found that various plant parts of W. somnifera are abundant in bioactive compounds. The neuroprotective effects of W. somnifera are documented in numerous diseases. Nevertheless, W. somnifera is reported to be involved in modulating various biological pathways to mitigate neuroinflammation, apoptosis, and oxidative stress in stroke. W. somnifera promotes cell proliferation and enhances neurogenesis. Preclinical experiments on murine models show the effectiveness of W. somnifera in post-stroke recovery by enhancing neural plasticity and reducing neuronal loss in the infarct area. Furthermore, W. somnifera boosts neurotransmitter levels, improves motor functions, and enhances memory. It also decreases neutrophil infiltration in the infarct region and lessens neuronal loss. Therefore, the application of W. somnifera may prove advantageous in facilitating post-stroke recovery by enhancing neural function. However, well-designed clinical trials are needed to confirm the efficacy of W. somnifera in post-stroke recovery in humans.