Comparative data on sequential transarterial chemoembolization (TACE) after stereotactic body radiation therapy (SBRT) in recurrent hepatocellular carcinoma (HCC) remain limited. This study aimed to evaluate the efficacy of this combination.

We retrospectively reviewed 152 patients with recurrent HCC who met predefined eligibility criteria; 109 received SBRT alone and 43 received SBRT plus TACE. To minimize selection bias, a 2:1 propensity score matching was performed, resulting in 68 patients in the SBRT-alone group and 36 in the SBRT plus TACE group for the final comparative analysis. Overall survival, progression-free survival, and local control were assessed using the Kaplan-Meier method.

The SBRT plus TACE group was associated with numerically higher survival rates, although this difference did not reach statistical significance. The cumulative one-, three-, and five-year overall survival rates were 91.2%, 76.3%, and 61.8% for SBRT alone, compared to 100.0%, 86.1%, and 77.5% for the combination therapy ( p = 0.069). The corresponding progression-free survival rates were 73.1%, 51.1%, and 32.3% versus 88.9%, 58.1%, and 52.3% ( p = 0.091). No acute grade ≥3 toxicities were observed in either group.

In this exploratory analysis of recurrent HCC, the combination of SBRT and TACE demonstrated a favorable trend toward improved survival compared with SBRT alone, without an increase in severe toxicity. While these findings did not reach statistical significance, they establish the safety profile of the combined approach and provide preliminary evidence supporting its potential therapeutic role. This hypothesis-generating study justifies and informs the design of larger, prospective trials to definitively evaluate the efficacy of this regimen.

Insulin resistance is a common extrahepatic manifestation of hepatitis C virus (HCV) infection (HCVi), but its mechanism is poorly understood. While systemic insulin resistance is documented, portal insulin dynamics, a key regulator of hepatic metabolism, remain unexplored. This study aimed to investigate the relationship between insulin, the gut-liver axis, and immunometabolic changes in patients with HCV.

HCV patients were evaluated before (HCVi; n = 29) and after sustained virologic response (SVR) achieved with sofosbuvir/velpatasvir treatment (SVR, n = 23) (NCT02400216). Liver biopsies, portal blood, and peripheral blood were collected at both phases. Statistical analyses were conducted using Wilcoxon rank-sum tests, Mann-Whitney tests, and Pearson’s correlation coefficients to assess differences and associations across insulin, glucose, cytokines, metabolites, immune cells, and hepatic liver transcriptomics to elucidate impaired insulin homeostasis in HCVi.

HCV patients had significantly reduced portal insulin compared to SVR (p = 0.02), while peripheral insulin, portal glucose, and peripheral glucose remained unchanged. Portal insulin correlated positively with proinflammatory cytokines and vascular injury markers and negatively with CD8/CD62L/CD45RA/CD3 cells (naive cytotoxic T-cells) and non-standard nucleotides. Hepatic transcriptomic analysis revealed portal insulin correlated positively with immune and negatively with amino acid pathways, reflecting insulin’s role in the perturbations of immunometabolism during HCVi.

Lower portal insulin during HCVi is associated with changes consistent with altered pancreatic insulin secretion and decreased hepatic insulin extraction. The observed correlations support a potential relationship between the immune response and insulin dynamics, indicating an interplay between the immune system, metabolism, and insulin in HCVi, with clinical implications for the management of dysglycemia.

Cervical cancer, driven mainly by persistent high-risk human papillomavirus infection, remains a major public health problem in Bangladesh, with 9,640 new cases and 5,826 deaths in 2022. Early detection of pre-cancerous cervical lesions (PCL) is essential, yet limited evidence exists on factors associated with PCL among Bangladeshi women. This study aimed to identify factors associated with PCL among women attending cervical cancer screening centers at selected tertiary hospitals.

An age-matched (±5 years) case-control study was conducted in two tertiary hospitals. Cases were women who tested colposcopy-positive for PCL, and controls were visual inspection with acetic acid-negative women attending the same screening centers. A total of 38 cases and 76 controls were included. Data were collected through face-to-face interviews using a structured questionnaire. Multivariable logistic regression identified factors associated with PCL, with significance set at p < 0.05.

A history of sexually transmitted infections (adjusted odds ratio (AOR) = 36.73; 95% confidence interval (CI): 3.25–414.83), pelvic infections (AOR = 6.48; 95% CI: 1.24–33.85), not living with a husband (AOR = 4.48; 95% CI: 1.06–18.90), and overweight/obesity (AOR = 3.58; 95% CI: 1.14–11.22) were significantly associated with higher odds of PCL. Menstrual irregularity, genital ulcer history, and number of lifetime sexual partners showed no significant association.

Sexually transmitted infections, pelvic infections, overweight/obesity, and not living with husband were identified as factors associated with PCL. Strengthened infection prevention, lifestyle counseling, and targeted health education may support ongoing cervical cancer prevention efforts in Bangladesh.

Human papillomavirus (HPV) is a double-stranded circular DNA virus with a genome of approximately 7–8 kb. This study aimed to establish an overlapping extension polymerase chain reaction method for the amplification of the entire genome of HPV16.

The HPV16 genome was divided into two larger fragments (with lengths of 3.9 kilobases and 5.3 kilobases, respectively), each of which had overlapping regions of more than 500 base pairs. A nested primer (outer primer: Fout/Rout; inner primer: Fin/Rin) was used to amplify each fragment. The key reaction parameters were optimized, including the selection of two highly accurate DNA polymerases; and a series of diluted samples (initial concentration of 2,000 copies/microliter, diluted to 2, 20, 200, and 2,000 copies/microliter) were used for amplification tests to evaluate the sensitivity of this method.

This study demonstrated high sensitivity for HPV16 detection, with effective amplification of samples as low as 2 copies/µL. For low-concentration samples (<200 copies/µL), the Thermo Fisher enzyme showed 50% and 75% effective amplification success rates at 2 copies/µL and 20 copies/µL, respectively, while the Vazyme enzyme achieved 0% success at both concentrations. Both enzymes enabled stable amplification of high-concentration samples (≥200 copies/µL). The amplified products matched the theoretical size, and Illumina sequencing confirmed Q30 ≥ 96% and >98% identity with the HPV16 reference sequence (K02718.1).

This study provides a highly sensitive and specific method for the full-genome sequence analysis of HPV16, which is applicable to HPV16 full-genome sequencing, variation analysis, and other research.

The optimal management strategy for adults with immune-tolerant (IT) chronic hepatitis B infection remains undefined. This study aimed to investigate the efficacy and predictive factors of a pegylated interferon (Peg-IFN)-based treatment strategy in IT patients with chronic HBV infection.

In this pilot, open-label, prospective study, 286 patients aged 18 to 60 years with IT characteristics were enrolled and allocated to one of three groups. The combination group received Peg-IFN for 48–96 weeks, with tenofovir disoproxil fumarate (TDF) initiated at week 12 and continued through week 96 (n = 103). The monotherapy group received TDF monotherapy alone (n = 125), and the control group was monitored without therapeutic intervention (n = 58).

No patients in the control group met any predefined efficacy endpoints. Intention-to-treat analysis showed that patients in the combination group achieved significantly higher virological response rates (71.8% vs. 53.6%, p = 0.005), hepatitis B e antigen seroconversion rates (15.5% vs. 1.6%, p < 0.001), and hepatitis B surface antigen (HBsAg) loss rates (10.7% vs. 0%, p < 0.001) compared with those in the monotherapy group at week 96. In the combination group, the cumulative rate of HBsAg loss was 5.4% at week 48 and increased to 11.8% by week 96. Independent predictors of achieving either hepatitis B e antigen seroconversion or HBsAg loss were baseline age under 30 years (odds ratio = 0.217, 95% confidence interval: 0.048–0.976, p = 0.046) and a decline in HBsAg level greater than 1 log10 IU/mL by week 24 (odds ratio = 13.976, 95% confidence interval: 2.506–77.932, p = 0.003).

A Peg-IFN-based treatment strategy significantly increases response rates compared with TDF monotherapy or observation in patients with IT characteristics.

Cardiorenal syndrome is associated with high morbidity and mortality and is characterized by bidirectional interactions between cardiac and renal dysfunction. The advent of sodium-glucose cotransporter 2 inhibitors (SGLT2i) and the nonsteroidal mineralocorticoid receptor antagonist finerenone has substantially changed the therapeutic landscape. Combination therapy with SGLT2i and finerenone may provide additional benefits through complementary mechanisms, representing a potential paradigm shift in the management of cardiorenal syndrome. In this review, we examine the pathophysiological pathways that characterize cardiorenal syndrome, clinical data from major randomized controlled trials, and the rationale for the concomitant use of these two drug classes. SGLT2 inhibitors significantly reduce hospitalization for heart failure, slow renal function decline, and provide benefits in both heart failure with reduced ejection fraction and heart failure with preserved ejection fraction, irrespective of diabetes status. Finerenone has been shown to reduce the risk of cardiovascular events and chronic kidney disease progression in patients with type 2 diabetes and chronic kidney disease, with a more favorable safety profile than steroidal mineralocorticoid receptor antagonists. Emerging evidence suggests that combination therapy may reduce hospitalizations for heart failure and slow renal disease progression beyond the effects of either monotherapy. However, implementation of these therapeutic options requires careful patient selection, ongoing monitoring of renal function and electrolytes, and close collaboration between cardiologists and nephrologists.

Reporting quality in clinical research is critical for evidence-based medicine and reproducibility of clinical studies. Previous work has mostly focused on the reporting quality of clinical trials and observational longitudinal studies. However, few studies have examined the reporting quality of trend analyses. Moreover, the reporting of recommended statistical metrics in trend analyses remains largely unclear. Therefore, we assessed the reporting quality of trend analyses based on reporting of recommended statistical metrics. We systematically searched the PubMed for the trend-analysis articles published in 10 leading medicine and oncology journals over an 11-year period (2008–2018). Studies published after 2019 were excluded due to a sudden, significant increase in publication numbers during and immediately after the COVID-19 pandemic. Only original articles, research letters, and meta-analyses/systematic reviews were included. We scored the reporting quality of these articles based on whether they reported p-values, effect sizes, beta/coefficient/slope/annual-percentage-change (APC). 297 articles met the inclusion criteria. Among these, 193 (66.0%) reported p-values and 216 (72.7%) reported effect sizes. Only 13 (5.8%) analyses reported neither p-values/effect sizes nor beta/coefficient/slope/APC. In multivariable regression models, authors affiliated with epidemiology departments were less likely to report effect sizes, whereas those from statistics departments were more likely to do so. Interestingly, U.S.-based senior authors (versus non-U.S.) more likely reported p-values. No factors were independently associated with reporting APC. Overall, the reporting quality of trend analyses in leading medicine and oncology journals appears moderate and warrants improvement. We thus call for increased awareness and further research on reporting quality in trend analyses in oncology research and beyond.

Liver transplant rejection significantly affects patient prognosis. Myeloid-derived suppressor cells (MDSCs), known for their potent immunoregulatory functions, represent a promising target for managing liver transplant rejection. This study aimed to systematically characterize the diversity of MDSC subsets and their context-dependent functions, particularly within the context of transplant tolerance.

We analyzed clinical and murine liver transplants using single-cell RNA sequencing, bulk RNA sequencing, flow cytometry, multiplex immunohistochemistry, and co-culture assays to phenotype MDSC subsets.

Single-cell RNA sequencing analysis of human and murine samples revealed MDSC involvement in transplant rejection. In mice, MDSC scores followed a normal distribution during the first week post-transplant and correlated with clinical flow cytometry data at one month. A distinct LDLR+ monocytic MDSC (M-MDSC) subset was identified and confirmed through spatial mapping by multiplex immunohistochemistry. Flow cytometry demonstrated dynamic changes in LDLR+ M-MDSCs across tissues (liver, spleen, peripheral blood, bone marrow, and lymph nodes), with a peak during acute rejection. Co-culture experiments showed that LDLR−/− M-MDSCs exhibited reduced Arg-1/iNOS expression and an impaired capacity to induce inhibitory receptors (TIGIT, PD1, CTLA-4) or suppress effector molecules (GZMB, IFN-γ, IL-2) in CD8+ T cells.

These findings highlight the critical role of MDSCs in liver transplant rejection. LDLR+ M-MDSCs exhibited enhanced immunosuppressive properties, underscoring their potential clinical relevance in mitigating rejection and promoting immune tolerance.

This narrative review provides a detailed and comprehensive examination of hemoadsorption therapy and its role in treating severe poisoning. First, the global problem of suicidal and nonsuicidal self-injury is described, with regional differences in the types of poisons used noted. Lower- and middle-income countries are disproportionately affected by pesticides compared to high-income countries. Organophosphates often constitute the majority of pesticide poisoning in many of these countries. Next, we review the history of hemoadsorption therapy from its early origins to its current evolution. The key physical and chemical principles underlying extracorporeal therapy and its effectiveness are described. A review of the literature examining the evidence for the efficacy of hemoadsorption therapy in poisoning is presented. Current evidence-based guidelines are summarized, including toxin types, clinical indications, and the extracorporeal therapies recommended. Emerging evidence regarding the use of hemoadsorption therapy for severe organophosphate and calcium channel blocker poisoning is also considered. A care pathway for considering hemoadsorption in poisonings where formal guidelines are lacking is proposed. Both the hemoadsorption strategies used and the potential adverse effects of this therapy are discussed. For this narrative review, the PubMed/Medline was searched from inception to April 30, 2025, using the terms (“hemoperfusion” OR “hemadsorption”) AND (“poisoning”). Clinical trials, randomized controlled trials, and meta-analyses were included, along with additional relevant studies identified through a manual review of references. The role of modern resin bead hemoadsorption therapy for severe poisoning is expanding to include removal of commonly encountered poisons that are protein-bound and have a large volume of distribution. Using a multicycle approach, hemoadsorption therapy has shown improved outcomes for both calcium channel blockers and organophosphate poisoning.

Acute liver failure (ALF) is a severe hepatic injury associated with high short-term mortality. Our previous study found that 1,5-anhydroglucitol (1,5AG) levels correlate with clinical outcomes in patients with liver failure. This study aimed to explore the potential effects and mechanisms of 1,5AG in ALF.

An experimental model of ALF was established using LPS and D-GalN. 1,5AG was administered to mice by gavage before modeling. Empagliflozin was then administered to reduce 1,5AG levels in mice. Peroxisome proliferator-activated receptor alpha (PPARα) agonists were also used to explore the role of 1,5AG in mice with liver failure.

1,5AG pretreatment significantly increased ALT and AST levels, aggravated histological damage and hepatocyte apoptosis, and increased mortality in ALF mice. Transcriptomic analysis and western blot validation revealed that 1,5AG significantly inhibited the PPARα signaling pathway and its downstream target, fibroblast growth factor 21. Empagliflozin treatment reduced 1,5AG levels, alleviated liver injury and hepatocyte apoptosis, and promoted the PPARα signaling pathway in ALF. PPARα agonists effectively reversed the effects of 1,5AG on ALF, thereby alleviating liver damage, pathological injury, and hepatocyte apoptosis.

1,5AG exacerbated liver injury in ALF mice by inhibiting the hepatic PPARα pathway, thereby promoting hepatocyte apoptosis.