Ovarian cancer (OC) is a major global health problem. The main treatments are surgery and chemoradiotherapy. A drawback of the latter is that repeated treatments are likely to lead to cancer cells developing resistance to the drug, resulting in recurrence, development of metastases, and poor prognosis for patients. Consequently, there is interest in combining chemoradiotherapy with treatment using active components extracted from natural products. One such component is resveratrol (RVT), which is a natural anti-tumor ingredient extracted from plants. Although there are many reviews on the biological activity of RVT, only a few studies have been performed to investigate the diversity of protein binding of RVT with OC and the application of various novel drug formulations containing RVT to treat OC. The review presented here may provide some ideas for the prevention and treatment of OC.

Combined traumatic brain injury (CTBI) remains a leading cause of disability/mortality among workers, yet which routine biochemical tests that predict infectious complications remain controversial. We aimed to identify the most informative serum markers for early diagnosis and prognosis of such complications.

In this retrospective observational study, 80 acute CTBI patients (40 without vs. 40 with mainly bacterial infectious complications) and 40 healthy controls were analyzed. Serum collected at 24, 72, and 168 h was assayed for protein fractions, metabolic markers, lipid peroxidation indices, antioxidant activity, endogenous intoxication markers, acids/minerals, and relevant enzymes.

The study found that the most important prognostic indicator for infectious complications was a simultaneous increase in α1-globulins, β-globulins, diene conjugates, superoxide dismutase, medium- and low-molecular-weight substances in erythrocytes, erythrocyte oligopeptides, and lactate at 24 h after injury (p < 0.001). A significant increase in sialic acids, uronic acids, total Ca and P, and low-density lipoproteins was observed at 72 h after injury (p < 0.001). Notably, individual components from the 24-h panel demonstrated high standalone predictive value, with areas under the curve of diene conjugates (0.91), erythrocyte oligopeptides (0.87), β-globulin (0.86), α1-globulin (0.82), and superoxide dismutase (0.82), respectively. The elevation of these biomarker profiles was significantly correlated with worse clinical outcomes, including longer intensive care unit stay and ventilation duration.

This study identified a set of biochemical markers associated with infectious complications in patients with CTBI. These biochemical parameters may serve as additional diagnostic and prognostic criteria for the management of infectious complications in patients with СTBI.

Congenital portosystemic shunts (CPSS) are rare vascular anomalies characterized by abnormal communication between the portal and systemic venous systems, resulting in partial or complete diversion of portal blood away from the liver. These shunts can give rise to a broad spectrum of clinical manifestations, including hyperammonemia (with or without encephalopathy), hepatopulmonary syndrome, and portopulmonary hypertension. Notably, these complications often occur in the absence of portal hypertension. Advances in diagnostic imaging, particularly Doppler ultrasound, computed tomographic angiography, and magnetic resonance imaging, have enhanced the early detection and classification of CPSS. Treatment approaches vary depending on shunt type and clinical severity and may include interventional closure via embolization or surgical ligation. Most persistent or symptomatic shunts require immediate intervention. Recent studies have also identified potential genetic and embryological mechanisms contributing to CPSS development, offering new insights into their pathogenesis. This review aims to summarize current knowledge on the epidemiology, pathophysiology, clinical presentation, diagnostic evaluation, and management of CPSS, and to highlight their consideration in patients with hepatic encephalopathy or unexplained liver disease.

Gliomas remain a major challenge in brain cancer treatment. Although genetic mutations have been widely studied, recent research indicates that epigenetic changes, which alter gene activity without changing the DNA sequence, also contribute significantly to tumor growth and treatment resistance. This review seeks to elucidate the principal drivers and modulators of brain tumor development, emphasizing the complex interaction between tumor metabolism and epigenetic regulation. It highlights how metabolic intermediates influence chromatin structure and transcriptional events driving glioma progression. Metabolic intermediates, such as acetyl-CoA and S-adenosylmethionine, serve as essential epigenetic cofactors, directly impacting chromatin structure and gene expression. Additionally, metabolic disorders like diabetes not only frequently coexist with gliomas but also exacerbate tumor progression through mechanisms such as inflammation, oxidative stress, and epigenetic reprogramming. Tumors located near brain regions controlling heart function may also increase the risk of sudden death, particularly in diabetic patients. The review proposes a comprehensive framework to understand glioma development by linking metabolism, epigenetics, and overall health. This integrated perspective leads to novel personalized treatment approaches, targeting both the tumor and the patient’s broader metabolic health, with the potential to improve survival rates and quality of life for glioma patients.

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.

Liver fibrosis is characterized by the excessive deposition of extracellular matrix, a process primarily driven by activated hepatic stellate cells (HSCs), and currently lacks effective therapy. Cathepsin K (CTSK) exhibits context-dependent roles across organ systems in fibrosis, but its function in liver fibrosis is unclear. This study aimed to investigate the role and underlying mechanisms of CTSK during liver fibrosis.

CTSK expression was analyzed in human fibrotic liver samples via transcriptomic analysis and confirmed in murine fibrosis models. The function of CTSK was investigated in both primary HSCs and LX-2 cells by assessing its effects on cell activation, proliferation, apoptosis, and the underlying signaling pathways following CTSK overexpression. The therapeutic potential was evaluated using an adeno-associated virus serotype 8 to overexpress CTSK in two etiologically distinct murine fibrosis models.

CTSK was upregulated in activated HSCs and fibrotic livers. Furthermore, we discovered that it mediates a negative feedback loop to inhibit the TGF-β/Smad pathway via Smad7/Smurf2-dependent TGF-β receptor-I degradation, thereby suppressing HSC activation and proliferation. CTSK also induced mitochondrial apoptosis through Bax/Bcl-2 imbalance and caspase-3 activation. Together, these actions contribute to the anti-fibrotic effect of CTSK. Notably, adeno-associated virus serotype 8-mediated CTSK overexpression attenuated liver fibrosis across multiple murine models.

Our study demonstrates that elevated CTSK functions as an endogenous protective factor that attenuates liver fibrosis. CTSK mediates negative feedback inhibition of the TGF-β pathway while concurrently promoting the mitochondrial apoptosis pathway. The dual anti-fibrotic mechanisms identify CTSK as a promising therapeutic target for liver fibrosis.

To observe the clinical efficacy of Jiawei Lizhong Tang combined with dorsal Yu acupoint embedding in patients with non-alcoholic steatohepatitis (NASH).

A total of 118 patients with NASH who attended the Department of Gastroenterology at Liuzhou Hospital of Traditional Chinese Medicine from January 2020 to December 2022 were selected as study subjects. The participants were randomly assigned to either the control group or the observation group using a random number table, with 59 cases in each group. The control group received treatment with Western medicine (compound glycyrrhizin capsule), whereas the observation group received treatment with traditional Chinese medicine combined with thread embedding (Jiawei Lizhong Tang combined with dorsal Yu acupoints embedding). Both groups received a treatment course of 12 weeks. The following anthropometric indicators were measured: weight, waist circumference, and body mass index. Liver function was assessed by measuring alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyltransferase (GGT), and total bilirubin (TBIL). Lipid profile indicators included triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C). Blood glucose indicators included fasting blood glucose, fasting insulin (FINS), and insulin resistance index (HOMA-IR). Additionally, liver stiffness measurement (LSM), controlled attenuation parameter (CAP), and liver/spleen CT ratio were assessed. Clinical efficacy was evaluated at the end of the treatment period.

After 12 weeks of treatment, significant improvements were observed in weight, waist circumference, BMI, serum ALT, AST, GGT, TBil, TG, TC, LDL-C, HDL-C, fasting glucose, FINS, HOMA-IR, LSM, CAP, and liver/spleen CT ratio in both groups compared to baseline (P＜0.05). The improvements in these indicators were significantly better in the observation group than in the control group after treatment (P＜0.05).

The treatment of NASH with Jiawei Lizhong Tang combined with dorsal Yu acupoint embedding effectively improves patient condition, reduces liver function damage, regulates blood lipids, insulin resistance, and hepatic steatosis. The therapeutic effect is superior to that of Western medicine therapy.

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.

Infectious diarrhea is a gastrointestinal illness that results in around 1.7 billion cases and 525,000 deaths annually, particularly among children under five, according to the World Health Organization. While some Cameroonian medicinal plants show promise for treating diarrhea, many plants are used without established scientific evidence of their efficacy. These plants include Tithonia diversifolia (T. diversifolia) and Solanum torvum (S. torvum), which are traditionally used to treat diarrheal symptoms. This study sought to investigate the anti-Shigella activity of leaf extracts from T. diversifolia and S. torvum.

Extracts from T. diversifolia and S. torvum were obtained by successive maceration in solvents of increasing polarity, including hexane, dichloromethane, ethyl acetate, methanol, and water. The as-prepared extracts (10) were evaluated for antibacterial activity against selected Shigella species using an in vitro experiment. The mode of action of the bioactive extracts was determined in Shigella through growth kinetic analysis.

Hexane extract from S. torvum (St-HEX-F) and dichloromethane extract from T. diversifolia (Td-DCM-F) inhibited the growth of Shigella flexneri NR-518 and Shigella boydii NR-521 with minimum inhibitory concentration (MIC) values of 500 and 1,000 µg/mL, respectively. Shigella flexneri and Shigella boydii were the most sensitive strains, whereas Shigella sonnei was the most resistant strain. Bacterial growth kinetics revealed that St-HEX-F and Td-DCM-F are bacteriostatic at MIC and bactericidal at 2×MIC and 4×MIC.

Extracts from T. diversifolia and S. torvum possess anti-Shigella activity and could be used as a potential source of active ingredients for developing new treatments against diarrhea caused by multidrug-resistant Shigella.

Metabolic dysfunction-associated steatotic liver disease (MASLD) affects approximately 32% of the US adult population. The present study aimed to utilize the All of Us electronic health record-linked large cohort to assess seven metabolic risk factors (MRFs) simultaneously, the impact by ethnicity and age, and clinical presentations of MASLD.

This study included a MASLD group (n = 15,060) and a frequency-matched control group (n = 75,300). Multivariable analyses were performed to compare the frequencies of MRFs and clinical outcomes between the two groups. Type 1 diabetes was not included in the multivariable analysis. Subgroup analyses were conducted according to race and ethnicity, as well as age.

The overall frequency of MASLD was 6.0%. Compared with the control group, individuals with MASLD had significantly higher independent frequencies of obesity (66.1% vs. 41.3%), type 2 diabetes (39.5% vs. 16.9%), hypertension (64.3% vs. 38.6%), hyperlipidemia (59.8% vs. 37.3%), obstructive sleep apnea (28.9% vs. 13.4%), and hypothyroidism (21.2% vs. 13.4%). Obesity was identified as the strongest independent MRF among Asians, Whites, and Hispanics, particularly in individuals younger than 50 years, whereas hypertension was the strongest independent MRF in Blacks. MASLD was also associated with significantly higher frequencies of cardiac events, including coronary artery disease (17.1% vs. 9.4%) and myocardial infarction (7.1% vs. 4.2%); hepatic events, including cirrhosis (7.5% vs. 1.1%) and hepatocellular carcinoma (0.5% vs. 0.1%); and elevated liver enzymes, including alanine aminotransferase (27.7% vs. 10.1%), aspartate aminotransferase (18.0% vs. 6.4%), and alkaline phosphatase (19.8% vs. 13.1%), compared with the control group.

Our study demonstrated that obesity, hypertension, hyperlipidemia, type 2 diabetes, obstructive sleep apnea, and hypothyroidism were independent MRFs for MASLD overall, but the ranking of these MRFs by odds ratios could vary by ethnicity and age. MASLD presents with significantly higher rates of alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase elevation, as well as cardiac and hepatic events.