Autoimmune hepatitis (AIH) frequently coexists with extrahepatic autoimmune diseases (EADs), but their prevalence, characteristics, progression, and treatment effect in the Han Chinese population remain unclear. This study aimed to evaluate the prevalence and spectrum of EADs and to assess their clinical features, disease course, and treatment outcomes in Han Chinese patients with AIH.

Medical records of 371 Han Chinese patients with AIH (diagnosed from March 2016 to October 2023) were retrospectively analyzed.

Among the 371 AIH patients, 304 (81.94%) were female, with a median age of 52.5 years (interquartile range, 46.0–61.0). A total of 23.98% (89/371) had at least one EAD, including 27.06% (82/303) in type 1 AIH, 11.11% (7/63) in antibody-negative AIH, and none in type 2. A single EAD was the most common (20.21%, 75/371). The most frequent EADs were Sjogren’s syndrome (8.63%) and autoimmune thyroid disease (8.36%). Compared with patients without EADs, those with EADs had lower alanine aminotransferase, red blood cell, and hemoglobin levels, but higher aspartate aminotransferase/alanine aminotransferase ratio and antinuclear antibody (ANA) positivity (all P < 0.05). ANA positivity was independently associated with EADs (odds ratio = 2.209, 95% confidence interval = 1.242–3.927, P = 0.007). After three months of treatment, the complete biochemical response rate was lower in the EADs group than in the non-EADs group (40.0% vs. 55.3%, P = 0.024), whereas no significant differences were observed at 6, 12, 24, or 36 months (all P > 0.05).

In the Han Chinese population, 23.98% of AIH patients had EADs, with Sjogren’s syndrome and autoimmune thyroid disease being the most common. ANA positivity was a significant risk factor for EADs. EAD patients had a poorer initial treatment response at three months, but comparable long-term biochemical response from six months.

In the past decade, immune checkpoint inhibitors (ICIs) have dramatically changed cancer treatment, significantly improving outcomes for patients with various malignancies. Nonetheless, their widespread application has resulted in a rise in immune-related adverse events due to excessive immune activation, including immune-mediated hepatotoxicity (IMH). IMH can cause serious complications and even death, underscoring the need for early prediction and intervention. This review outlines the current understanding of risk factors and predictive biomarkers for IMH in cancer patients undergoing ICI therapy, with risk factors divided into patient-associated, tumor-associated, and agent-associated categories. Higher IMH risk is related to female sex, younger age, extreme BMI, Asian ethnicity, and chronic liver disease. Cancer type, prior ICI treatment, dual ICI combination therapy, and the concurrent use of chemotherapy, targeted agents, or other hepatotoxic drugs (e.g., acetaminophen, statins) also increase the risk of IMH. Potential predictive biomarkers encompass circulating blood cells, serum proteins, autoantibodies, cytokines, gene profiles, and the gut microbiome. Despite promising findings, the predictive value of these biomarkers remains inconsistent, and no definitive biomarker has been established for routine clinical use. Large-scale prospective studies are essential to verify the predictive value of these biomarkers and facilitate their integration into clinical practice, thereby providing deeper insights into the early identification and individualized management of IMH during ICI therapy.

The rate of functional cure (HBsAg loss) remains unsatisfactory following pegylated interferon (PEG-IFN) treatment in chronic hepatitis B. To optimize PEG-IFN administration, this study aimed to evaluate virological markers to predict functional cure and/or hepatitis B e antigen (HBeAg) loss.

Relevant studies assessing virologic markers for predicting functional cure and HBeAg loss after PEG-IFN therapy were systematically retrieved from PubMed, Embase, the Cochrane Library, and Web of Science up to November 2023. Predictive effectiveness was evaluated via the summary receiver operating characteristic curve.

We analyzed 38 studies (6,179 patients). HBsAg decline at week 24 had the greatest discriminative ability according to the area under the receiver operating characteristic curve (AUROC) (0.89) and sensitivity (0.88) for predicting functional cure, whereas baseline HBsAg had a comparable AUROC (0.86) and highest specificity (0.79), with both being significantly better than baseline hepatitis B core-related antigen and hepatitis B virus (HBV) RNA (all P < 0.001). For HBeAg loss or seroconversion, HBV RNA, HBV DNA, HBeAg, and HBeAg decline at week 12, as well as HBV DNA and HBeAg decline at week 24, all exhibited comparable predictive values (AUROC = 0.75–0.78). HBV RNA and HBeAg levels at week 24 showed optimal sensitivity (0.87), and HBeAg decline at week 12 had the highest specificity (0.83).

HBsAg decline at week 24 and baseline HBsAg levels are better predictors of functional cure than novel virologic markers, while on-treatment HBV RNA and HBeAg levels and dynamic changes are the most reliable indicators for HBeAg loss.

Breast cancer (BCA) is one of the most common cancers worldwide, with a high rate of incidence and mortality. This review provides global information on BCA therapy using curcumin. Chemotherapy, as an effective treatment for different stages of BCA, and curcumin, generally regarded as safe compound and an alternative to synthetic drugs, have been described for the treatment of BCA. A few parameters, including nano-curcumin versus bulk curcumin and its encapsulated form versus its corresponding free form, have been discussed. Curcumin, a safe and edible compound with antitumor properties, is a promising medicinal compound for the treatment of BCA. Encapsulation of curcumin enhances its stability and anticancer efficiency. Nano-curcumin exhibits superior properties when compared to its bulk counterparts, leading to notable interactions and effects.

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.

Cirrhotic ascites develops when portal hypertension and arterial under-filling chronically activate neuro-hormonal pathways that drive renal sodium-water retention. Augmented proximal tubular sodium reabsorption, predominantly mediated by the apical sodium/hydrogen exchanger 3 (NHE3), plays a fundamental role in this process. Given the spatial coupling of NHE3 and the sodium-glucose cotransporter 2 (SGLT2), selective SGLT2 inhibition reduces NHE3 activity via functional suppression within the apical microdomain. The increased sodium chloride delivery to the macula densa augments tubuloglomerular feedback and modulates the renin–angiotensin–aldosterone system. Early clinical investigations, ranging from case reports and retrospective analyses to pilot randomized trials, indicated potential benefits in controlling ascites and reducing decompensation events. However, their limited sample size, heterogeneous endpoints, and predominantly observational design constrain the generalizability of the findings. This review concentrates on the molecular mechanisms and emerging clinical evidence supporting the therapeutic potential of SGLT2 inhibitors in the management of cirrhotic ascites.

Hepatocellular carcinoma (HCC) is a malignant tumor with high incidence and mortality rates worldwide, in which immune evasion mechanisms play a crucial role in its progression and treatment. Natural killer group 2D ligands (NKG2DL), as key molecules activating immune cells, significantly influence the immune evasion of liver cancer through their regulatory mechanisms. This review summarizes the regulatory mechanisms of NKG2DL expression, including genetic, signaling pathway, non-coding RNA, and stress response modulation, and discusses their expression patterns and clinical relevance in HCC. Studies have shown that the expression status of NKG2DL not only impacts patient prognosis and therapeutic response but also provides potential targets for HCC immunotherapy. Future research should focus on the molecular networks regulating their expression and their synergy with immunotherapy to provide a theoretical basis for developing more precise diagnostic and personalized treatment strategies for HCC.