ObjectiveTo establish the self-reported core outcome set （COS） for patients with an example of a community study on heat-sensitive moxibustion for primary hypertension （PH）， to provide a reference for the selection of effectiveness evaluation indicators in community study on heat-sensitive moxibustion. MethodsA systematic literature search was conducted to collect outcomes used in randomized controlled trials and systematic review of heat-sensitive moxibustion for PH （Jan 2021）， and additional outcomes were added through patient and expert questionnaires （Feb 2021） to create a pool of outcome entries. A multidisciplinary expert Delphi survey was conducted to screen outcomes applicable to patient self-reporting （Apr 2021）， and the importance of outcome indicators was rated on a 5-Point Likert Scale. Finally， patient self-reported COS was determined through a consensus conference （June 2021）. ResultsA pool of patient self-reported indicators in the community study of heat-sensitive moxibustion treatment for PH was generated by standardizing and combining the outcome indicators based on the results of the literature search and the questionnaire survey， which consisted of totally 100 measurement tools or contents， excluding 51 indicators or measurement tools required measurement by specialized physicians or hospital equipment， and 49 items were retained to enter the initial list of indicator entries. For the first round of Delphi survey， the mean score for expert familiarity was 0.819， the mean score for basis of judgment was 0.710， and the expert authority coefficient was 0.765， with a total of 21 indicator measurement tools or contents deleted （significance score ≤ 75 or coefficient of variation ＞ 0.25）， 28 retained， and 3 new expert-added indicator entries added. In the second round of Delphi survey， the average score for expert familiarity was 0.859， the average score for basis for judgment was 0.763， and the expert authority coefficient was 0.811， with a total of 11 indicator measurement tools or contents deleted and 20 retained involving 5 domains. Following an expert consensus meeting， 8 outcome indicators were finalized for inclusion in the patient self-reported COS， including 6 indicators of effectiveness evaluation such as quality-of-life scores， blood pressure， traditional Chinese medicine symptom scores， cost-benefit， cardiovascular and cerebrovascular events， and adverse reactions/events， and 2 indicators of factors influencing effectiveness such as sensation of heat-sensitive moxibustion， and adherence. ConclusionIn this study， we initially established a criteria for evaluating the effectiveness in the community study on heat-sensitive moxibustion by constructing patient self-reported COS in the community study on heat-sensitive moxibustion for PH， which can provide a scientific research paradigm for the subsequent development of the community study on heat-sensitive moxibustion.

Background: and Purpose Ruptured intracranial aneurysms (RIA) are associated with a mortality rate of up to 40% in the Chinese population, highlighting the critical need for targeted treatment interventions for at-risk individuals. Although the impact of aldehyde dehydrogenase 2 (ALDH2) gene mutations on susceptibility to intracranial aneurysms (IA) is well documented, the potential connection between ALDH2 rs671 single-nucleotide polymorphism (SNP) and RIA remains unexplored. Given the increased prevalence of ALDH2 gene mutations among Chinese Han individuals, it is clinically relevant to investigate the link between ALDH2 rs671 SNP and IA rupture. Methods: A prospective study was conducted on 546 patients diagnosed with IA to investigate the association between ALDH2 rs671 SNP and the risk of IA rupture. Results: The ALDH2 rs671 SNP (ALDH2*2) was significantly more prevalent in patients with unruptured IA (UIA) than in those with RIA (32.56% vs. 18.58%, P=0.004). Multivariate logistic regression analysis revealed that people with the ALDH2 mutation (ALDH2*1/*2 and ALDH2*2/*2 gene type) had a significantly reduced odds ratio (OR=0.49; 95% confidence level [CI] 0.27–0.88; P=0.018) for RIAs. Age-specific subgroup analysis indicated that the ALDH2 mutation provided a stronger protective effect in individuals aged 60 years and above with IA compared to those under 60 years old (OR=0.38 vs. OR=0.52, both P<0.05). Conclusion The incidence of RIA was significantly higher in individuals with a normal ALDH2 gene (ALDH2*1/*1) than in those with an ALDH2 rs671 SNP (ALDH2*1/*2 or ALDH2*2/*2). ALDH2 rs671 SNP may serve as a protective factor against RIA in the Chinese Han population.

Background: and Purpose Ruptured intracranial aneurysms (RIA) are associated with a mortality rate of up to 40% in the Chinese population, highlighting the critical need for targeted treatment interventions for at-risk individuals. Although the impact of aldehyde dehydrogenase 2 (ALDH2) gene mutations on susceptibility to intracranial aneurysms (IA) is well documented, the potential connection between ALDH2 rs671 single-nucleotide polymorphism (SNP) and RIA remains unexplored. Given the increased prevalence of ALDH2 gene mutations among Chinese Han individuals, it is clinically relevant to investigate the link between ALDH2 rs671 SNP and IA rupture. Methods: A prospective study was conducted on 546 patients diagnosed with IA to investigate the association between ALDH2 rs671 SNP and the risk of IA rupture. Results: The ALDH2 rs671 SNP (ALDH2*2) was significantly more prevalent in patients with unruptured IA (UIA) than in those with RIA (32.56% vs. 18.58%, P=0.004). Multivariate logistic regression analysis revealed that people with the ALDH2 mutation (ALDH2*1/*2 and ALDH2*2/*2 gene type) had a significantly reduced odds ratio (OR=0.49; 95% confidence level [CI] 0.27–0.88; P=0.018) for RIAs. Age-specific subgroup analysis indicated that the ALDH2 mutation provided a stronger protective effect in individuals aged 60 years and above with IA compared to those under 60 years old (OR=0.38 vs. OR=0.52, both P<0.05). Conclusion The incidence of RIA was significantly higher in individuals with a normal ALDH2 gene (ALDH2*1/*1) than in those with an ALDH2 rs671 SNP (ALDH2*1/*2 or ALDH2*2/*2). ALDH2 rs671 SNP may serve as a protective factor against RIA in the Chinese Han population.

Background: and Purpose Ruptured intracranial aneurysms (RIA) are associated with a mortality rate of up to 40% in the Chinese population, highlighting the critical need for targeted treatment interventions for at-risk individuals. Although the impact of aldehyde dehydrogenase 2 (ALDH2) gene mutations on susceptibility to intracranial aneurysms (IA) is well documented, the potential connection between ALDH2 rs671 single-nucleotide polymorphism (SNP) and RIA remains unexplored. Given the increased prevalence of ALDH2 gene mutations among Chinese Han individuals, it is clinically relevant to investigate the link between ALDH2 rs671 SNP and IA rupture. Methods: A prospective study was conducted on 546 patients diagnosed with IA to investigate the association between ALDH2 rs671 SNP and the risk of IA rupture. Results: The ALDH2 rs671 SNP (ALDH2*2) was significantly more prevalent in patients with unruptured IA (UIA) than in those with RIA (32.56% vs. 18.58%, P=0.004). Multivariate logistic regression analysis revealed that people with the ALDH2 mutation (ALDH2*1/*2 and ALDH2*2/*2 gene type) had a significantly reduced odds ratio (OR=0.49; 95% confidence level [CI] 0.27–0.88; P=0.018) for RIAs. Age-specific subgroup analysis indicated that the ALDH2 mutation provided a stronger protective effect in individuals aged 60 years and above with IA compared to those under 60 years old (OR=0.38 vs. OR=0.52, both P<0.05). Conclusion The incidence of RIA was significantly higher in individuals with a normal ALDH2 gene (ALDH2*1/*1) than in those with an ALDH2 rs671 SNP (ALDH2*1/*2 or ALDH2*2/*2). ALDH2 rs671 SNP may serve as a protective factor against RIA in the Chinese Han population.

Despite therapy with potent antiviral agents, chronic hepatitis B (CHB) patients remain at high risk of hepatocellular carcinoma (HCC). While metabolites have been rediscovered as active drivers of biological processes including carcinogenesis, the specific metabolites modulating HCC risk in CHB patients are largely unknown. Here, we demonstrate that baseline plasma from CHB patients who later developed HCC during follow-up exhibits growth-promoting properties in a case-control design nested within a large-scale, prospective cohort. Metabolomics analysis reveals a reduction in long-chain acylcarnitines (LCACs) in the baseline plasma of patients with HCC development. LCACs preferentially inhibit the proliferation of HCC cells in vitro at a physiological concentration and prevent the occurrence of HCC in vivo without hepatorenal toxicity. Uptake and metabolism of circulating LCACs increase the intracellular level of acetyl coenzyme A, which upregulates histone H3 Lys14 acetylation at the promoter region of KLF6 gene and thereby activates KLF6/p21 pathway. Indeed, blocking LCAC metabolism attenuates the difference in KLF6/p21 expression induced by baseline plasma of HCC/non-HCC patients. The deficiency of circulating LCACs represents a driver of HCC in CHB patients with viral control. These insights provide a promising direction for developing therapeutic strategies to reduce HCC risk further in the antiviral era.

Epilepsy is a chronic neurological disorder affecting ~65 million individuals worldwide. Abnormal synaptic plasticity is one of the most important pathological features of this condition. We investigated how ubiquitin-specific peptidase 47 (USP47) influences synaptic plasticity and its link to epilepsy. We found that USP47 enhanced excitatory postsynaptic transmission and increased the density of total dendritic spines and the proportion of mature dendritic spines. Furthermore, USP47 inhibited the degradation of the ubiquitinated α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) subunit glutamate receptor 1 (GluR1), which is associated with synaptic plasticity. In addition, elevated levels of USP47 were found in epileptic mice, and USP47 knockdown reduced the frequency and duration of seizure-like events and alleviated epileptic seizures. To summarize, we present a new mechanism whereby USP47 regulates excitatory postsynaptic plasticity through the inhibition of ubiquitinated GluR1 degradation. Modulating USP47 may offer a potential approach for controlling seizures and modifying disease progression in future therapeutic strategies.
Animals ; Receptors, AMPA/metabolism* ; Neuronal Plasticity/physiology* ; Seizures/physiopathology* ; Disease Models, Animal ; Mice, Inbred C57BL ; Mice ; Ubiquitin Thiolesterase/genetics* ; Male ; Excitatory Postsynaptic Potentials/physiology* ; Ubiquitination ; Dendritic Spines/metabolism* ; Hippocampus/metabolism*

On August 31， 2025， the Asian Pacific Association for the Study of the Liver （APASL） updated and released management of acute variceal bleeding： updated APASL guidelines （2025 edition）， which systematically elaborates on the definition， diagnosis， assessment， and treatment of acute variceal bleeding. This article gives an excerpt of the recommendations in this guideline.

This paper summarized Professor LI Yueqing's clinical experience in treating prostate cancer by stages from the perspective of deficiency and stasis. It is believed that the onset of prostate cancer is due to kidney deficiency， while blood stasis is the core pathogenesis， and dampness-heat， phlegm-turbid， and cancer toxins are the key pathological factors in the progression of the disease. The pathogenesis in the early stage of the disease is kidney qi depletion and dampness， heat and phlegm coagulation； in the middle stage， it is spleen and kidney depletion， phlegm coagulation and blood stasis； and in the late stage， the pathogenesis changes into yin deficiency and essence depletion， and stasis-turbid toxin obstruction. For treatment， the basic principle is to supplement and boost kidney qi， enrich and nourish the kidney yin. The main treatment methods are draining dampness， dissolving phlegm， dispelling stasis， clearing heat and resolving toxins， and the method of invigorating blood and dispelling stasis runs through the whole course of treatment. In the early stage， radical treatment is mainly used， and Longshe Yangquan Decoction （龙蛇羊泉汤） with modifications is supplemented to clear and drain dampness and heat. In the middle stage， androgen deprivation therapy is the basic treatment， and Bushen Tongqiao Decoction （补肾通窍汤） with modifications is used in combination to nourish the spleen and kidney， dissolve phlegm and dispel stasis. In the late stage， Dabuyin Pills and Liuwei Dihuang Pills （大补阴丸合六味地黄丸） with modifications is mainly used to enrich yin and supplement essence， resolve toxins and dissolve stasis， and prevent cancer recurrence.