ObjectiveThis study aims to systematically review the marketed traditional Chinese patent medicines for treating chronic gastritis （CG） in China. By analyzing their variety characteristics and prescription patterns， it seeks to provide references for clinical syndrome differentiation-based drug selection， treatment method optimization， and the design of high-quality clinical research. MethodsInformation on marketed traditional Chinese patent medicines for treating CG was collected. Microsoft Excel software was used to collate and statistically analyze representative drugs for each pathological stage， market status， syndrome types， and other contents. The Ancient and Modern Medical Case Cloud Platform （V2.3.9） was employed to analyze the formula composition patterns of standardized prescriptions. ResultsA total of 141 marketed traditional Chinese patent medicines for treating CG in China were included. Based on the disease's pathological progression， they can be classified into drugs for non-atrophic gastritis， atrophic gastritis， and precancerous lesions. Post-marketing research reveals that relevant evaluation is only conducted on 17 drugs， of which 2 involve pharmacoeconomic studies and 14 possess standardized evidence-based evidence. The primary dosage forms were capsules， granules， and tablets. From the 100 prescriptions screened according to inclusion/exclusion criteria， the varieties indicated for the stomach collateral stasis syndrome in atrophic gastritis accounted for the highest proportion. The main efficacy distributions were clearing heat， detoxifying， and relieving pain by promoting Qi circulation. Core drugs included Glycyrrhizae Radix et Rhizome， Paeoniae Radix Alba， and Aucklandiae Radix. Medicinal properties were predominantly warm and neutral. Flavors were mainly bitter， pungent， and sweet. The drugs primarily entered the spleen and stomach meridians. Analysis of the package inserts reveals that 67 products list "contraindications"， 110 include "precautions"， and 23 explicitly state "adverse reactions". ConclusionTraditional Chinese patent medicines for treating CG hold unique value in clinical practice. However， currently there are challenges such as insufficient clarity in syndrome type descriptions within package inserts and a relative lack of high-level evidence-based medical evidence， as well as pharmacoeconomic evaluations. Future efforts should focus on addressing these shortcomings by advancing research on syndrome characteristics and medication patterns based on syndrome differentiation， systematically conducting pharmacoeconomic evaluations， strengthening the accumulation of high-level evidence-based evidence， and， on this basis， improving patient medication adherence. This will comprehensively enhance the clinical application value and scientific connotation of this category of drugs.

ObjectiveTo decipher the mechanism by which Zuoguiwan （ZGW） treat hyperthyroidism in rats with kidney-Yin deficiency based on the dopamine receptor D4 （DRD4）/nicotinamide adenine dinucleotide phosphate （NADPH） oxidase 4 （NOX4） signaling pathway. MethodsThe rat model of kidney-Yin deficiency was induced by unilateral intramuscular injection of dexamethasone （0.35 mg·kg^-1）. After successful modeling， the rats were randomized into model， methimazole （positive control， 5 mg·kg^-1）， low-， medium-， and high-dose （1.85， 3.70， 7.40 g·kg^-1， respectively） ZGW， and normal control groups. After 21 days of continuous gavage， the behavioral indexes and body weight changes of rats were evaluated. The pathological changes of the renal tissue were observed by hematoxylin-eosin staining. The serum levels of thyroid hormones ［triiodothyronine （T₃）， thyroxine （T₄）， thyroid-stimulating hormone （TSH）］， renal function indexes ［serum creatine （Scr） and blood urea nitrogen （BUN）］， energy metabolism markers ［cyclic adenosine monophosphate （cAMP） and cyclic guanosine monophosphate （cGMP）］， and oxidative stress-related factors ［superoxide dismutase （SOD）， malondialdehyde （MDA）， and NADPH）］ were measured by enzyme-linked immunosorbent assay （ELISA）. Western blot was employed to analyze the expression of DRD4， NOX4， mitochondrial respiratory chain complex proteins ［NADH：ubiquinone oxidoreductase subunit S4 （NDUFS4） and cytochrome C oxidase subunit 4 （COX4）］， and inflammation-related protein ［tumor necrosis factor-alpha （TNF-α）， interleukin-6 （IL-6）， p38 mitogen-activated protein kinase （MAPK）］ pathway in the renal tissue. ResultsCompared with the normal group， the model group showed mental malaise， body weight decreases （P<0.01）， inflammatory cell infiltration in the renal tissue， a few residual parotid glands in the thyroid， elevations in serum levels of T₃， T₄， Scr， BUN， cAMP， cAMP/cGMP， MDA， and NADPH （P<0.01）， down-regulation in protein levels of TSH， SOD， and DRD4 （P<0.05， P<0.01）， and up-regulation in expression of NOX4， p-p38 MAPK/p38 MAPK， and inflammatory factors （P<0.01）. Compared with the model group， ZGW increased the body weight （P<0.05， P<0.01）， reduced the infiltration of renal interstitial inflammatory cells， restored the thyroid structure and follicle size， lowered the serum levels of T₃， T₄， Scr， BUN， cAMP， cAMP/cGMP， MDA and NADPH （P<0.05， P<0.01）， up-regulated the expression of TSH， SOD and DRD4 （P<0.05， P<0.01）， and down-regulated the expression of NOX4， p-p38 MAPK/p38 MAPK， and inflammatory factors （P<0.05， P<0.01）. Moreover， high-dose ZGW outperformed methimazole （P<0.05）. ConclusionBy activating DRD4， ZGW can inhibit the expression of NOX4 mediated by the p38 MAPK pathway， reduce oxidative stress and inflammatory response， thereby ameliorating the pathological state of hyperthyroidism due to kidney-Yin deficiency. This study provides new molecular mechanism support for the clinical application of ZGW.

The theory of constitution in traditional Chinese medicine （TCM） has emerged as a new discipline in recent years. Constitution plays a vital role in the onset，progression，transformation，and prognosis of diseases. At present，some clinical scholars have adopted a novel diagnostic and treatment model of "constitution differentiation-disease identification-syndrome differentiation"，in which constitution is regarded as a core element throughout the diagnostic and therapeutic process. Constitution is closely associated with etiology，onset，pathogenesis，syndrome differentiation，and treatment. Against this background，the construction of animal models based on constitution holds far-reaching significance for advancing clinical research. This paper focuses on the construction and evaluation of rodent models with Qi-deficiency constitution，aiming to explore how to further induce Qi-deficiency syndromes and related disease states on the basis of Qi-deficiency constitution models，thereby developing an integrated animal model that embodies the trinity of "constitution-disease-syndrome". The establishment of this model not only provides a solid experimental foundation for the development of new therapies and drugs in TCM targeting specific constitutions，diseases，and syndromes，but also greatly promotes the modernization and scientific advancement of TCM theory. By comprehensively applying multidisciplinary technologies and methods，the study evaluates the model's validity，reliability，and practicality，with the aim of opening new avenues for future research in TCM and promoting the development of the field.

The theory of constitution in traditional Chinese medicine （TCM） has emerged as a new discipline in recent years. Constitution plays a vital role in the onset，progression，transformation，and prognosis of diseases. At present，some clinical scholars have adopted a novel diagnostic and treatment model of "constitution differentiation-disease identification-syndrome differentiation"，in which constitution is regarded as a core element throughout the diagnostic and therapeutic process. Constitution is closely associated with etiology，onset，pathogenesis，syndrome differentiation，and treatment. Against this background，the construction of animal models based on constitution holds far-reaching significance for advancing clinical research. This paper focuses on the construction and evaluation of rodent models with Qi-deficiency constitution，aiming to explore how to further induce Qi-deficiency syndromes and related disease states on the basis of Qi-deficiency constitution models，thereby developing an integrated animal model that embodies the trinity of "constitution-disease-syndrome". The establishment of this model not only provides a solid experimental foundation for the development of new therapies and drugs in TCM targeting specific constitutions，diseases，and syndromes，but also greatly promotes the modernization and scientific advancement of TCM theory. By comprehensively applying multidisciplinary technologies and methods，the study evaluates the model's validity，reliability，and practicality，with the aim of opening new avenues for future research in TCM and promoting the development of the field.

Objective To analyze the influencing factors of postoperative hypoxemia after whole lung lavage (WLL) in patients with pneumoconiosis and to evaluate the predictive value of lung ultrasound scores. Methods A total of 757 patients with pneumoconiosis who underwent unilateral large-volume WLL were selected as the research subjects by continuous sampling method. The patients with hypoxemia after large-volume WLL were assigned to the observation group (82 cases), and those without hypoxemia were assigned to the control group (675 cases). Patients′ basic information and clinical data of the two groups were collected using a retrospective investigation method. The binary logistic regression analysis was used to analyze the influencing factors of hypoxemia after large-volume WLL in patients with pneumoconiosis, and receiver operating characteristic (ROC) curve analysis was conducted to assess the predictive value of ultrasound indicators. Results The combined rate of postoperative hypoxemia in the patients was 10.8% (82/757). The multivariate logistic regression analysis showed that the risk of hypoxemia in patients aged ≥65 years was higher than that in patients aged <65 years (P<0.05). The risk of hypoxemia was higher in patients with increased pre-extubation lung ultrasound score than those with lower pre-extubation lung ultrasound score (P<0.01). Patients with a higher partial pressure of carbon dioxide in arterial blood (PaCO₂) had a higher risk of concurrent hypoxemia than those with a lower pressure (P<0.01), while patients with lower arterial partial pressure of oxygen (PaO₂) had a higher risk of concurrent hypoxemia than those with higher PaO₂ (P<0.01). Pearson correlation analysis showed that lung ultrasound scores were negatively correlated with PaO₂ and positively correlated with PaCO₂ (both P<0.01). The ROC curve analysis showed that the area under the curve was 0.855, the 95% confidence interval was 0.828 to 0.879, the diagnostic sensitivity was 84.2%, and the specificity was 75.1%. Conclusion Age, pre-extubation lung ultrasound score, and PaCO₂ are risk factors for hypoxemia after WLL in patients with pneumoconiosis, while PaO₂ is a protective factor. Pre-extubation lung ultrasound scoring demonstrates good accuracy in predicting postoperative hypoxemia among pneumoconiosis patients after WLL.

OBJECTIVE: To investigate the clinical characteristics and genetic etiology of a child with Cortical dysplasia, complex, with other brain malformations 4 (CDCBM4) and epilepsy due to a TUBG1 gene variant. METHODS: A child diagnosed with CDCBM4 and epilepsy at the Children's Medical Center of the Affiliated Hospital of Guangdong Medical University in May 2024 was selected as the study subject. Clinical data were retrospectively analyzed. Peripheral venous blood samples were collected from the child and her parents for genomic DNA extraction. Trio-based whole-exome sequencing (WES) was performed, and candidate variants were validated by Sanger sequencing. According to the Standards and Guidelines for the Interpretation of Sequence Variants established by the American College of Medical Genetics and Genomics (ACMG), candidate variants were classified for pathogenicity. This study was approved by the Medical Ethics Committee of the Affiliated Hospital of Guangdong Medical University (Ethics No.: PJ2021-097). RESULTS: The child, a 4-month-old female infant, had no special facial features, normal limb muscle strength, and increased muscle tone of infantile onset, with generalized tonic-clonic seizures as the main manifestation. During seizures, she exhibited head retroflexion, tightly closed eyes, and tonic convulsions of the limbs, occurring approximately 2-3 times per day. Electroencephalogram suggested bilateral anterior predominant medium-to-high amplitude 7-8 Hz mixed rhythm discharges. Head MRI revealed ventricular system dilatation and pachygyria. Trio-WES results indicated that the child has harbored a TUBG1 gene variant of c.776C>T (p.Ser259Leu). Sanger sequencing verification showed that neither of her parents had carried the same variant, confirming it as de novo in origin. According to the ACMG guidelines, the variant was rated as pathogenic (PS2+PS3+PM2_Supporting+PP3). Combining the child's clinical phenotype, the child was diagnosed as CDCBM4 with epilepsy. CONCLUSION Children with CDCBM4 and epilepsy due to TUBG1 gene variants may show pachygyria or agyria and commonly present with intellectual and motor developmental delays and seizure disorders of variable severity. The heterozygous TUBG1 c.776C>T (p.Ser259Leu) variant is likely the genetic etiology underlying this disorder. The results of this study has expanded the mutational spectrum of the TUBG1 gene associated with CDCBM4 and epilepsy.
Humans ; Female ; Epilepsy/genetics* ; Malformations of Cortical Development/genetics* ; Infant ; Phenotype ; Exome Sequencing ; Microtubule-Associated Proteins/genetics*

Objective:To evaluate the clinical value of peripheral blood monocyte subset analysis in the diagnosis and treatment of chronic myelomonocytic leukemia (CMML) .Method:We retrospectively enrolled 51 patients newly diagnosed with CMML at Guangdong Provincial People's Hospital between June 1, 2020, and December 31, 2024, according to the WHO 2022 diagnostic criteria. Twenty-three patients with other myeloid neoplasms (excluding CMML) and peripheral monocytosis (absolute count ≥0.5×10 9/L and percentage ≥10%) were included as the control group. All patients underwent bone marrow aspiration for examinations including bone marrow smears, biopsies, cytogenetics, and gene mutation analysis to establish a definitive diagnosis. Concurrently, flow cytometry was used to determine the proportions of peripheral blood monocyte subsets: classical (MO1, CD14 +CD16 -) , intermediate (MO2, CD14 +CD16 +) , and non-classical (MO3, CD14 lowCD16 +) . Differences between the groups were compared, and diagnostic efficacy was evaluated using receiver operating characteristic (ROC) curves. Result:Among the 51 CMML patients, the proportion of the peripheral blood MO1 subset was significantly higher than that in patients with other myeloid neoplasms ( P=0.027) , whereas there were no significant differences in the MO2 and MO3 subsets (all P>0.05) . Further analysis revealed that 43 (84.31%) of the CMML patients met the WHO diagnostic threshold for the MO1 subset (≥94%) , while the remaining 8 patients did not; 46 patients (90.20%) had MO3 subset proportions below the threshold proposed by Hudson (≤1.13%) , while the remaining 5 patients were above this threshold. In-depth analysis showed that among the 8 patients who did not meet the WHO criteria, 7 were experiencing inflammation. Similarly, all 5 patients who did not meet the Hudson criteria were in an inflammatory state. Subsequent ROC curve analysis of this cohort identified a cut-off value for the MO1 subset of 97.55% [Area Under the Curve (AUC) =0.661, P=0.027], which aligns with the WHO criteria. Conclusion:Peripheral blood monocyte subset analysis, particularly MO1 subset analysis, can effectively assist in CMML diagnosis, but exclusion of inflammatory conditions is required.

Objective:To investigate the clinical characteristics and genetic etiology of a child with Cortical dysplasia, complex, with other brain malformations 4 (CDCBM4) and epilepsy due to a TUBG1 gene variant. Methods:A child diagnosed with CDCBM4 and epilepsy at the Children′s Medical Center of the Affiliated Hospital of Guangdong Medical University in May 2024 was selected as the study subject. Clinical data were retrospectively analyzed. Peripheral venous blood samples were collected from the child and her parents for genomic DNA extraction. Trio-based whole-exome sequencing (WES) was performed, and candidate variants were validated by Sanger sequencing. According to the Standards and Guidelines for the Interpretation of Sequence Variants established by the American College of Medical Genetics and Genomics (ACMG), candidate variants were classified for pathogenicity. This study was approved by the Medical Ethics Committee of the Affiliated Hospital of Guangdong Medical University (Ethics No.: PJ2021-097).Results:The child, a 4-month-old female infant, had no special facial features, normal limb muscle strength, and increased muscle tone of infantile onset, with generalized tonic-clonic seizures as the main manifestation. During seizures, she exhibited head retroflexion, tightly closed eyes, and tonic convulsions of the limbs, occurring approximately 2-3 times per day. Electroencephalogram suggested bilateral anterior predominant medium-to-high amplitude 7-8 Hz mixed rhythm discharges. Head MRI revealed ventricular system dilatation and pachygyria. Trio-WES results indicated that the child has harbored a TUBG1 gene variant of c. 776C>T (p.Ser259Leu). Sanger sequencing verification showed that neither of her parents had carried the same variant, confirming it as de novo in origin. According to the ACMG guidelines, the variant was rated as pathogenic (PS2+ PS3+ PM2_Supporting+ PP3). Combining the child′s clinical phenotype, the child was diagnosed as CDCBM4 with epilepsy. Conclusion:Children with CDCBM4 and epilepsy due to TUBG1 gene variants may show pachygyria or agyria and commonly present with intellectual and motor developmental delays and seizure disorders of variable severity. The heterozygous TUBG1 c. 776C>T (p.Ser259Leu) variant is likely the genetic etiology underlying this disorder. The results of this study has expanded the mutational spectrum of the TUBG1 gene associated with CDCBM4 and epilepsy.

Objective:To evaluate the effect of an electronic balance aid in balance rehabilitation training for patients with acute peripheral vestibular injury by comparing the outcomes of medication-only treatment and medication combined with vestibular rehabilitation using an electronic balance aid.Methods:This was a randomized controlled trial. The study subjects included 98 patients (40 males and 58 females, aged 25-69 years) diagnosed with idiopathic sudden sensorineural hearing loss (ISSNHL) with vertigo or vestibular neuritis, who were treated in the Department of Otorhinolaryngology-Head and Neck Surgery of Tianjin First Central Hospital from November 2022 to November 2023. All patients were randomly divided into the experimental group and the control group at a 1∶1 ratio using the sealed envelope method. Control group (conventional drug treatment): Patients received medication treatment for 2 weeks, including betahistine mesilate tablets, vitamin B1 tablets, methylcobalamin tablets, ginkgo biloba tablets, diphenhydramine hydrochloride injection (within 3 days of onset), metoclopramide hydrochloride injection, and glucocorticoids. Experimental group (conventional drug treatment+device training): On the basis of the same medication treatment as the control group, patients received vestibular rehabilitation training using an electronic balance aid (20 minutes per session, once a day,≥5 days per week, for a total of 2 weeks). SPSS software was used to compare the total scores of the Dizziness Handicap Inventory (DHI), the total scores of the Sensory Organization Test (SOT), and sensory analysis indicators between the two groups before and after treatment.Results:After treatment, vertigo symptoms significantly improved in both groups. DHI: The total DHI score in the control group decreased from 77.9±1.8 before treatment to 20.2±2.3 after treatment ( P<0.001). In the experimental group, the total DHI score decreased from 73.5±2.1 before treatment to 8.6±0.9 after treatment ( P<0.001). The difference in total DHI scores between the two groups after treatment was statistically significant, with the experimental group showing a lower score ( t=-4.616, P<0.001). The improvement in DHI scores was also more pronounced in the experimental group compared to the control group ( t=2.004, P=0.048). SOT: The total SOT score in the control group increased from 52.90±0.95 before treatment to 73.3±1.1 after treatment ( P<0.001). In the experimental group, the total SOT score increased from 54.9±0.8 before treatment to 83.5±0.9 after treatment ( P<0.001). The difference in total SOT scores between the two groups after treatment was statistically significant, with the experimental group showing a higher score ( t=7.104, P<0.001). The improvement in SOT scores was also more pronounced in the experimental group compared to the control group ( t=6.532, P<0.001). Sensory Analysis Indicators Proprioception (SOM): In the experimental group, the proprioception score significantly increased after treatment compared with before treatment ( t=-2.338, P=0.029), while, there was no statistically significant difference in the proprioception score of the control group before and after treatment ( P=0.537). Before treatment, there were no statistically significant differences in visual, vestibular, or visual dependence scores between the two groups (all P>0.05). After treatment, the visual, vestibular, and visual dependence scores of both groups significantly increased compared with those before treatment (all P<0.05); moreover, the post-treatment visual, vestibular, and visual dependence scores of the experimental group were significantly higher than those of the control group (all P<0.05). Conclusion:Compared with medication-only treatment, the combination of an electronic balance aid and medication for the treatment and rehabilitation training of patients with acute peripheral vestibular injury can significantly improve the therapeutic effect in the short term.

Hepatic stellate cells (HSCs) are the primary fibrogenic cells in the liver, and their activation plays a crucial role in the development and progression of hepatic fibrosis. Here, we report that retinoid X receptor-alpha (RXRα), a unique member of the nuclear receptor superfamily, is a key modulator of HSC activation and liver fibrosis. RXRα exerts its effects by modulating calcium/calmodulin-dependent protein kinase kinase β (CaMKKβ)-mediated activation of AMP-activated protein kinase-alpha (AMPKα). In addition, we demonstrate that K-80003, which binds RXRα by a unique mechanism, effectively suppresses HSC activation, proliferation, and migration, thereby inhibiting liver fibrosis in the CCl₄ and amylin liver NASH (AMLN) diet animal models. The effect is mediated by AMPKα activation, promoting mitophagy in HSCs. Mechanistically, K-80003 activates AMPKα by inducing RXRα to form condensates with CaMKKβ and AMPKα via a two-phase process. The formation of RXRα condensates is driven by its N-terminal intrinsic disorder region and requires phosphorylation by CaMKKβ. Our results reveal a crucial role of RXRα in liver fibrosis regulation through modulating mitochondrial activities in HSCs. Furthermore, they suggest that K-80003 and related RXRα modulators hold promise as therapeutic agents for fibrosis-related diseases.