Chaihu Guizhi Ganjiangtang was first recorded in the Treatise on Cold Damage （Shang Han Lun）. This prescription is composed of Bupleuri Radix， Scutellariae Radix， Cinnamomi Ramulus， Zingiberis Rhizoma， Trichosanthis Radix， Ostreae Concha， and Glycyrrhizae Radix et Rhizoma. It has the effects of soothing Lesser Yang， warming the spleen， and stimulating the generation of body fluid. It is mainly used to treat digestive tract diseases such as chronic cholecystitis （CC）， irritable bowel syndrome， and non-alcoholic fatty liver disease. Dyspepsia caused by CC presents a variety of gastrointestinal symptoms such as abdominal pain， poor appetite， postprandial fullness， aversion to greasy food， soft stool， and bitter mouth， being a type of biliary dyspepsia. In modern medicine， dyspepsia caused by CC is mainly managed by medical treatment and surgical treatment. Internal medicine mainly focuses on reducing inflammation， promoting the function of gallbladder， resolving stones， alleviating spasms， and relieving the pain for CC， demonstrating definite short-term efficacy but suffering from single effects， high recurrence rate， and poor compliance. Although surgical treatment can cure cholecystitis， it is accompanied by the increased incidence of adverse events such as abdominal pain， diarrhea， and dyspepsia. Modern clinical studies have confirmed that Chaihu Guizhi Ganjiangtang can significantly alleviate the symptoms such as abdominal pain and dyspepsia of CC patients. Pharmacological studies have found that Chaihu Guizhi Ganjiangtang mainly contains active ingredients such as Bupleuri Radix saponins， baicalin， cinnamaldehyde， gingerol， Trichosanthis Radix polysaccharide， Ostreae Concha polysaccharide， and Glycyrrhizae Radix et Rhizoma total flavonoids. Chaihu Guizhi Ganjiangtang can ameliorate the symptoms of dyspepsia caused by CC by inhibiting inflammatory responses， improving gallbladder contraction and gastrointestinal motility， regulating the bile acid-intestinal flora axis and the brain-gut axis， and modulating blood lipids through multiple targets. By reviewing the previous literature， this article summarizes the research progress in the treatment of dyspepsia caused by CC with Chaihu Guizhi Ganjiangtang and its main active ingredients as well as the pathogenesis of this disease and puts forward the shortcomings and improvement strategies for the current research. The review aims to provide a reference for the further research on Chaihu Guizhi Ganjiangtang in the treatment of dyspepsia caused by CC.

OBJECTIVE To develope a predictive model for medication deviation risks during the hospital-to-home transition period in coronary heart disease （CHD） patients with initial treatment， aiming to assist medical staff in rapidly identifying high-risk groups for medication deviation. METHODS A total of 462 CHD patients with initial treatment from the Affiliated Hospital of North China University of Science and Technology （hereinafter referred to as “our hospital”） between January and July 2024 were enrolled. The patients were randomly divided into a modeling group and an internal validation group. The modeling group was further categorized into a medication deviation group and a non-medication deviation group based on whether medication deviations occurred. Similarly， 57 CHD patients with initial treatment from the cardiology department of our hospital between June and September 2025 were collected as an external validation group. Univariate analysis was used to screen predictive factors， followed by multivariate Logistic regression to construct the predictive model. Internal validation methods were employed to evaluate model performance， while external validation methods were used to test the model’s generalizability. RESULTS The 462 patients were divided into a modeling group （319 cases） and an internal validation group （143 cases）. In the modeling group， the medication deviation group （192 cases， 60.19%） and the non-medication deviation group （127 cases， 39.81%） were identified. Multivariate Logistic regression analysis revealed that age， medication type， medication adherence， and self-efficacy in rational medication use were predictive factors for medication deviations in CHD patients with initial treatment （ P ＜0.05）. The predictive model equation was logit P ＝ln[ P /（1－ P ） ] ＝1.321+1.732×age+4.091×medication type －4.360×medication adherence －3.081×self-efficacy in rational medication use. The model demonstrated good discrimination， with a Hosmer-Lemeshow goodness-of-fit test P -value of 0.439， an area under the receiver operating characteristic curve （AUC） of 0.870， sensitivity of 0.970， and specificity of 0.607. A risk nomogram with a total score of 350 points and a cutoff value of 110 points was plotted. The internal validation group showed an AUC o f 0.787 and a prediction accuracy of 77.6%， while the external validation group exhibited an AUC of 0.802 and a prediction accuracy of 73.7%. CONCLUSIONS This study successfully developed a predictive model for medication deviation risks during the hospital-to-home transition period in CHD patients with initial treatment. The model demonstrates excellent discrimination and predictive accuracy， effectively identifying high-risk populations for medication deviations. Age （＞70 years）， number of drug types≥5， poor medication adherence， and poor self-efficacy in rational medication use are independent risk factors for medication deviations.

OBJECTIVE: To investigate the detection patterns, clinical phenotypic characteristics, and differences in diagnostic timeliness of Klinefelter syndrome (KS) across prenatal and postnatal stages, with an aim to provide a basis for optimizing strategies for early screening, diagnosis, and intervention. METHODS: A retrospective study was conducted to analyze data from two phases. The prenatal diagnosis group included 33,302 pregnant women who underwent amniocytic karyotyping due to advanced maternal age, abnormal ultrasound findings, or high-risk non-invasive prenatal testing (NIPT). The postnatal diagnosis group included 52,101 patients who underwent peripheral blood karyotyping due to primary infertility, abnormal external genitalia, or growth and developmental abnormalities. Additionally, medical histories of adult diagnosed patients were reviewed retrospectively to identify early occult symptoms. This study was approved by the Medical Ethics Committee of Chengdu Women's and Children's Central Hospital (Ethics No.: LCYJ-2025-030). RESULTS: In the prenatal group, 96 cases of KS were detected (detection rate 0.29%). The primary indications for referral were NIPT indicating sex chromosome abnormalities (45.83%), advanced maternal age (16.66%), and ultrasound abnormalities (17.70%). In the postnatal group, 128 cases of KS were detected (detection rate 0.25%). Clinical presentations were primarily primary infertility/azoospermia (77.34%), and the patients were predominantly adults (84.40%). Retrospective analysis revealed that adult patients presented with specific physical signs that had been overlooked during childhood. CONCLUSION As KS lacks typical early clinical manifestations, diagnosis is often delayed until adulthood when reproductive needs arise, showing a pattern of "passive detection" and resulting in missed opportunities for optimal intervention. By conducting a comparative analysis of prenatal diagnostic data and postnatal retrospective data, a risk association model linking prenatal screening indications with childhood-specific signs was developed. This study has provided empirical evidence for establishing a multidisciplinary, full life-cycle management system of "screening ~ diagnosis ~ monitoring ~ intervention" helping to shift from "passive detection in adulthood" to "proactive management across the entire life course," and laid a foundation for improving early diagnosis rate and long-term quality of life for patients.
Humans ; Klinefelter Syndrome/genetics* ; Female ; Adult ; Pregnancy ; Retrospective Studies ; Prenatal Diagnosis/methods* ; Male ; Phenotype ; Karyotyping ; Young Adult ; Adolescent ; Middle Aged

ObjectiveTo analyze the epidemiological and etiological characteristics of a cluster of human metapneumovirus (HMPV) infection in a kindergarten in Gongshu District of Hangzhou City in May 2024, and to provide reference for the prevention and control of similar outbreaks. MethodsAn on-site investigation was conducted using an epidemiological case investigation form. Throat swab specimens collected from cases were screened for 13 respiratory pathogens using real-time fluorescent polymerase chain reaction (PCR). For HMPV nucleic acid positive specimens, the F gene of HMPV was used as the target gene for amplification and sequencing. The sequencing results were then compared with sequences in GenBank database to determine the virus subtypes and perform phylogenetic analyses. ResultsThe outbreak occurred in a kindergarter junior class with a total of 28 preschoolers and 3 teachers and childcare workers. A total of 11 cases (10 preschoolers and 1 teacher) were identified, including 8 male cases and 3 female cases. Clinical manifestations included fever in all 11 cases (100.00%), cough in 8 cases (72.72%), catarrhal symptoms in 4 cases (36.36%), and headache in 3 cases (27.27%). All symptoms were mild, and no severe cases were observed. A total of 11 throat swab samples were collected. Real-time fluorescent PCR test results showed that 3 samples were positive for HMPV nucleic acid, 2 samples were positive for both HMPV and Streptococcus pneumoniae, and 1 sample was positive for both HMPV and rhinovirus. The sequences of the 6 HMPV nucleic acid positive specimens were amplified and analyzed using specific primers, and all were determined to be HMPV subtype A2b. The F gene fragment sequence showed the highest similarity to PV081665.1/Brazil/2024 (99.65%), and also exhibited high similarity to PP683455.1/Indonesia/2021 (99.48%), PV016275.1/Beijing/2024 (99.31%), and PV052230.1/USA/2024 (99.13%). ConclusionThis cluster of acute respiratory tract infection was caused by HMPV subtype A2b, with co-infection of rhinovirus and Streptococcus pneumoniae. The F gene fragment sequences of the HMPV in this outbreak were highly homologous to those of the A2b strains isolated from Brazil, Beijing, Indonesia, and the the United States.

ObjectiveTo investigate the association between single and combined exposure to arsenic （As）， mercury （Hg）， and cadmium （Cd） in urine and hearing loss in adults. MethodsA total of 400 adult patients were recruited for the study， comprising 200 participants in the normal hearing group and 200 in the hearing loss group. General demographic information of the study subjects was collected by a self-administered questionnaire， morning urine samples were tested for As， Hg， and Cd concentrations， and hearing status was assessed by Pure Tone Audiometry. A binary Logistic regression model was used to explore the association between the concentrations of the three metals in urine and hearing loss， and a Bayesian kernel-machine regression （BKMR） model was used to further explore the association between the concentrations of the three metal mixtures and hearing loss. ResultsAfter correction for urinary creatinine， As， Hg， and Cd concentrations were higher in the hearing loss group than those in the normal hearing group （P<0.05）. Binary Logistic regression indicated that concentrations of As， Hg， and Cd were positively associated with hearing loss， and the risk of hearing loss was significantly higher in the second quartile of Cd concentration compared to the first quartile （OR=2.000， 95%CI： 1.009-3.964）. BKMR modeling analysis showed that the combined exposure levels of As， Hg， and Cd significantly increased the risk of hearing loss， with Cd being the most important contributor （posterior inclusion probability=0.412）， and that there were potential interactions between As and Cd， and Cd and Hg. ConclusionCombined exposure to As， Hg， and Cd in urine is significantly associated with adult hearing loss， with Cd being the primary contributor in the exposure combination. The interactions between As and Cd， as well as Cd and Hg， may have adverse effects on hearing loss.

Background Cadmium (Cd) is a highly toxic heavy metal. Chronic low-dose cadmium exposure can lead to renal tubular dysfunction. However, the precise mechanisms by which cadmium induces renal tubular injury through disruption of intracellular metabolic networks remain incompletely understood. Objective To investigate the toxic effects of cadmium exposure on human renal tubular epithelial cells (HK-2) and to elucidate the associated metabolic regulatory network from the perspective of metabolic reprogramming. Methods An in vitro HK-2 cell injury model was established using 5 μmol·L⁻¹ cadmium chloride (CdCl₂). The expression of the renal injury marker kidney injury molecule-1 (KIM-1) was determined by Western blot (WB). Glycolytic capacity was evaluated by metabolic flux analysis. Mitochondrial reactive oxygen species (ROS) production was assessed with a fluorescent probe. Mitochondrial membrane potential (MMP) was evaluated after JC-1 staining. Intracellular adenosine triphosphate (ATP) levels were measured using an ATP assay kit. In addition, untargeted metabolomics analysis was conducted to characterize alterations in the intracellular metabolic fingerprint profile and to explore the metabolic pathway changes underlying cadmium-induced renal tubular epithelial cell injury. Results Cadmium exposure induced injury in HK-2 cells, as indicated by mitochondrial membrane depolarization, increased mitochondrial ROS levels, and decreased intracellular ATP levels. Metabolic flux analysis further revealed significant metabolic reprogramming, characterized by compensatory increases in basal glycolytic rate and maximal glycolytic capacity. Untargeted metabolomics showed depletion of the long-chain acylcarnitine pool and deficiency of key metabolic cofactors, suggesting impaired fatty acid oxidation and mitochondrial energy metabolism. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis indicated that the differential metabolites were mainly enriched in oxidative phosphorylation and glycerophospholipid metabolism. Correlation analysis showed that acylcarnitines were negatively correlated with nucleic acid metabolism-related metabolites, whereas ATP was positively correlated with lysophosphatidylcholine, suggesting that cadmium exposure-induced mitochondrial dysfunction may be accompanied by abnormal DNA metabolism and lipid peroxidation. Conclusion Cadmium exposure could induce impaired mitochondrial function, and promote glycolytic metabolic reprogramming in renal tubular epithelial cells. These findings provide new insights into the metabolic mechanisms underlying cadmium-induced nephrotoxicity and may help identify potential metabolic targets for intervention.

OBJECTIVES: To investigate the molecular mechanism underlying Leber hereditary optic neuropathy (LHON) caused by the m.3472T>C (p.Phe56Leu) mutation. METHODS: From a cohort of 1397 LHON patients, three large pedigrees (WZL122, WZ676, WZ706) carrying the m.3472T>C mutation were identified and selected for this study. Immortalized lymphoblastoid cell lines were established from peripheral blood samples obtained from two affected individuals carrying the homoplasmic m.3472T>C mutation (derived from one Han Chinese LHON pedigree) and two genetically unrelated, matched healthy controls. The MitoTool software was used to analyze the complete mitochondrial DNA sequence to determine the haplogroup background, and the conservation of the mtDNA mutation site was evaluated using the MitoMap database. The secondary structure of the ND1 protein was predicted and analyzed using online prediction software. The three-dimensional structure and molecular interaction changes of wild-type and mutant ND1 proteins were visualized and analyzed using PyMOL. Western blotting was performed to determine the expression levels of key proteins. Cellular ATP levels were measured using a chemiluminescence assay. Mitochondrial membrane potential and intracellular reactive oxygen species (ROS) levels were assessed by flow cytometry. RESULTS: mtDNA haplotype analysis showed that the subjects all belonged to the East Asian mitochondrial haplogroup D4. The m.3472T>C mutation results in the substitution of a highly conserved phenylalanine with leucine (p.Phe56Leu) in the ND1 subunit of mitochondrial complex Ⅰ, which may alter the structure and function of ND1. In lymphoblastoid cell lines carrying the m.3472T>C mutation, manifestations of mutant ND1 instability were observed, including reduced ND1 protein levels, diminished mitochondrial ATP production, decreased mitochondrial membrane potential, and increased mitochondrial ROS production. Concurrently, the expression levels of the antioxidant enzymes catalase and SOD2 were elevated (all P<0.01). These findings collectively suggest impaired complex Ⅰ function. CONCLUSIONS The m.3472T>C mutation contributes to the pathogenesis of LHON by disrupting the structural stability of the ND1 subunit in complex Ⅰ, leading to mitochondrial dysfunction.

Debates persist regarding the efficacy and safety of azvudine, particularly its real-world outcomes. This study involved patients aged ≥60 years who were admitted to 25 hospitals in mainland China with confirmed SARS-CoV-2 infection between December 1, 2022, and February 28, 2023. Efficacy outcomes were all-cause mortality during hospitalization, the proportion of patients discharged with recovery, time to nucleic acid-negative conversion (T _NANC), time to symptom improvement (T _SI), and time of hospital stay (T _HS). Safety was also assessed. Among the 5884 participants identified, 1999 received azvudine, and 1999 matched controls were included after exclusion and propensity score matching. Azvudine recipients exhibited lower all-cause mortality compared with controls in the overall population (13.3% vs. 17.1%, RR, 0.78; 95% CI, 0.67-0.90; P = 0.001) and in the severe subgroup (25.7% vs. 33.7%; RR, 0.76; 95% CI, 0.66-0.88; P < 0.001). A higher proportion of patients discharged with recovery, and a shorter T _NANC were associated with azvudine recipients, especially in the severe subgroup. The incidence of adverse events in azvudine recipients was comparable to that in the control group (2.3% vs. 1.7%, P = 0.170). In conclusion, azvudine showed efficacy and safety in older patients hospitalized with COVID-19 during the SARS-CoV-2 omicron wave in China.

The 2024 American Society of Clinical Oncology(ASCO)Annual Meeting was held in Chicago,the United States,from May 31 to June 4 in 2024.In recent years,antibody-drug conjugates(ADCs)have become one of the most popular targeted therapies because of their high specificity,efficacy,and low toxicity,making them a focal point in this ASCO meeting.Currently,over 100 ADCs are under investigation,demonstrating the considerable development potential of ADCs in the field of targeted cancer therapy.The aforementioned conference reported several recent research advancements regarding ADCs for the treatment of breast cancer(BC).This review summarizes the latest progress of ADCs in BC treatment discussed at the confer-ence.

Objective:To explore the clinical features, histopathological morphology, and differential diagnosis of lymphoepithelioma-like carcinoma with abnormal expression of follicular dendritic cell markers.Methods:From 2020 to 2021, 4 cases of lymphoepithelioma-like carcinoma with abnormal expression of follicular dendritic cell markers diagnosed in Fujian Cancer Hospital (2 cases) and the Second Affiliated Hospital of Fujian Medical University (2 cases) were collected. Different ancillary procedures such as HE, special stains, immunohistochemistry, and in situ hybridization techniques were used to assess the histopathological features and immunophenotypes. The clinical data were collected and literature was reviewed.Results:All 4 cases of lymphoepithelioma-like carcinoma with abnormal expression of follicular dendritic cell markers were male. They were 32, 45, 67 and 39 years old, respectively. The main clinical manifestations were bloody phlegm, abdominal pain, fatigue and anorexia. The clinical stages at diagnosis were stage Ⅳ (3 cases) and stage Ⅱ (1 case). Cases 2 and 3 had two pathological examinations at different sites, with a total of six pathological examinations. The histomorphology showed singly scattered or nests of tumor cells in a background of abundant small lymphocytes. The tumor cells were enlarged and pleomorphic, some appeared polygonal with inconspicuous cell borders, and they were arranged in a syncytial pattern. There were megakaryocytes, multinucleated tumor cells, and a few spindle-shaped cells seen. Atypical mitosis was commonly noted. By immunohistochemistry, the tumor cells were positive for CKpan(5/6), CK8/18(4/4), CAM5.2(2/5), CK-H(0/4), CK-L(3/4), EMA(4/5), CK5/6(3/6), p63(1/6), p40(1/6), E-cadherin (4/6), SSTR2(6/6), PD-L1(5/5), LCA(0/6), vimentin(5/6), CD2 (6/6), CD23(6/6), CD35(5/6), CXCL-13(4/5) and D2-40(1/5). The Ki-67 proliferative index was 60%-95%. In situ hybridization for EBER were all positive (6/6). Special stain for reticulin showed positive staining surrounding nests of tumor cells.Conclusions:The expression of follicular dendritic cell markers in lymphoepithelioma-like carcinoma is very rare, which may be related to EBV infection. Occasionally, it can overlap with follicular dendritic cell sarcoma by morphology and immunophenotype, which can lead to misdiagnosis. Only by combining clinical information, morphological characteristics and immunophenotype can an appropriate diagnosis be made.