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Objective: Long‐term and high exposure to UV radiation can lead to the development of skin photoaging diseases. Therefore, there is an ongoing need for more natural and safe drugs to prevent or treat skin photoaging diseases. Methods: The Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform database were used to collect the active compounds and corresponding targets of Cnidii Fructus, Arnebiae Radix, Angelicae Sinensis Radix, Poria, and Borneolum. The GeneCards database and the NCBI Gene database were used to collect the targets of skin photoaging diseases. The STRING database was used to construct a protein–protein interaction network formed by the intersecting targets of drugs and diseases. The Metascape database was applied for Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis of the targets. Molecular docking between active compounds and targets was verified by Autodock. After that, the skin photoaging model of mice was established and treated with MP gel. The skin characterization on the back of mice was observed, and the ameliorative effect of MP gel on skin photoaging was evaluated by histological and epidermal thickness assays. The MDA content and SOD activity were measured. Caspase‐3 expression in mouse skin tissues was detected by immunohistochemistry, quantitative real‐time polymerase chain reaction assay, and Western blot. Results: The results of network pharmacology experiments showed that the natural drugs have multi‐component, multi‐target therapeutic disease characteristics. The results of animal studies showed that MP gel improved the health of photoaged skin, promoted skin structural integrity, had antioxidant properties and significantly inhibited caspase‐3 expression. Conclusion: The experimental validation of the results of the preliminary network pharmacology analysis was carried out in animal experiments, which confirmed part of the mechanism of action of MP gel in the prevention and treatment of skin photoaging. [ABSTRACT FROM AUTHOR]

Brucellosis is a worldwide zoonotic disease caused by Brucella spp. Human infection often results from direct contact with tissues from infected animals or by consumption of undercooked meat and unpasteurised dairy products, causing serious economic losses and public health problems. The male genitourinary system is a common involved system in patients with brucellosis. Among them, unilateral orchitis and epididymitis are the most common. Although the clinical and imaging aspect of orchi-epididymitis caused by brucellosis have been widely described, the cellular and molecular mechanisms involved in the damage and the immune response in testis and epididymis have not been fully elucidated. In this review, we first summarised the clinical characteristics of Brucella epididymo-orchitis and the composition of testicular and epididymal immune system. Secondly, with regard to the mechanism of Brucella epididymoorchitis, we mainly discussed the process of Brucella invading testis and epididymis in temporal and spatial order, including i) Brucella evades innate immune recognition of testicular PRRs；ii) Brucella overcomes the immune storm triggered by the invasion of testis through bacterial lipoproteins and virulence factors, and changes the secretion mode of cytokines; iii) Brucella breaks through the blood-testis barrier with the help of macrophages, and inflammatory cytokines promote the oxidative stress of Sertoli cells, damaging the integrity of BTB; iv) Brucella inhibits apoptosis of testicular phagocytes. Finally, we revealed the structure and sequence of testis invaded by Brucella at the tissue level. This review will enable us to better understand the pathogenesis of orchi-epididymitis caused by brucellosis and shed light on the development of new treatment strategies for the treatment of brucellosis and the prevention of transition to chronic form. Facing the testicle with immunity privilege, Brucella is like Bruce Lee in the movie Game of Death, winning is survival while losing is death. We summarized the clinical features and pathological changes of Brucellaepididymoorchitis. Our research reveals the pathogenesis of Brucella epididymoorchitis, which mainly includes the subversion of testicular immune privilege by Brucella and a series of destructive reactions derived from it. As a basic framework and valuable resource, this study can promote the exploration of the pathogenesis of Brucella and provide reference for determining new therapeutic targets for brucellosis in the future. [ABSTRACT FROM AUTHOR]

Objective: The aim of this investigation was to study the effects of Runt‐related transcription factor 2 (Runx2) on the junctional epithelium and alveolar bone. Methods: The attachment level of the junctional epithelium and the resorption of alveolar bone were analyzed by histology and scanning electron microscopy. The expression of amelotin was determined by immunohistochemistry, Western blot, and real‐time PCR. The ultrastructure of the dentogingival interface was observed by transmission electron microscopy. Results: The cKO mice demonstrated remarkable attachment loss, epithelial hyperplasia, and alveolar bone loss. The relative protein and mRNA expression of amelotin was increased in the junctional epithelium of the cKO mice. The attachment apparatus of the cKO mice showed ultrastructural deficiency. Conclusions: Loss of Runx2 led to the junctional epithelium and alveolar bone defects in mice. Runx2 may play a crucial role in maintaining the integrity of the dentogingival junction and the normal structure of alveolar bone. [ABSTRACT FROM AUTHOR]

Background: With the advancement of society, the cultivation of medical professionals equipped with solid theoretical knowledge, a strong sense of innovation, and critical thinking has become a crucial goal in the reform of medical higher education. Over recent years, the hybrid Problem-Based Learning (hPBL) model, a blend of Problem-Based Learning (PBL) and Lecture-Based Learning (LBL), has emerged as a novel approach in the medical education reform landscape of China. The application and efficacy of the hPBL model in medical experimental courses have piqued the interest of medical educators. The aim of this study was to appraise the application and effectiveness of the hPBL model in the experimental course of Medical Molecular Biology at Beihua University., Methods: Utilizing the "Rain Classroom" platform, students from the Preventive Medicine and Medical Imaging programs were allocated to either the hPBL or LBL method for their Medical Molecular Biology experimental courses. The hPBL model's impact on students' performance was evaluated across four domains: experimental theory, experimental operation, experimental report, and practical application. Questionnaires were employed to gauge students' experiences and perceptions., Results: The results indicated that the final assessment scores of the hPBL group were significantly superior to those of the LBL group. Moreover, the hPBL model effectively amplified students' self-learning capability, practical application skills, and communication competencies. Students expressed a high degree of satisfaction with this blended learning model., Conclusion: The hPBL model, which amalgamates PBL and LBL, has demonstrated its effectiveness in medical education. Its implementation in the experimental course of Medical Molecular Biology at Beihua University yielded positive outcomes, enhancing students' performance and satisfaction levels. Consequently, it is recommended that the hPBL model be further promulgated in other medical experimental courses., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Qu, Hou, Yu, Li, Xia and Dong.)

Hepatic fibrosis (HF) is a process that occurs during the progression of several chronic liver diseases, for which there is a lack of effective treatment options. Carthamus tinctorius L. (CTL) is often used in Chinese or Mongolian medicine to treat liver diseases. However, its mechanism of action remains unclear. In the present study, CTL was used to treat rats with CCl4‑induced HF. The histopathological, biochemical and HF markers of the livers of the rats were analyzed, and CTL‑infused serum was used to treat hepatic stellate cells (HSCs) in order to detect the relevant markers of HSC activation. Protein expression pathways were detected both in vitro and in vivo . Histopathological results showed that CTL significantly improved CCl4‑induced liver injury, reduced aspartate aminotransferase and alanine aminotransferase levels, promoted E‑cadherin expression, and decreased α‑smooth muscle actin (SMA), SOX9, collagen I and hydroxyproline expression. Moreover, CTL‑infused serum was found to decrease α‑SMA and collagen I expression in HSCs. Further studies showed that CTL inhibited the activity of the PI3K/Akt/mTOR pathway in the rat livers. Following the administration of the PI3K agonist 740Y‑P to HSCs, the inhibitory effect of CTL on the PI3K/Akt//mTOR pathway was blocked. These results suggested that CTL can inhibit HF and HSC activation by inhibiting the PI3K/Akt/mTOR pathway.

Hepatic fibrosis is chronic liver damage with many causes that has a relatively high death rate. The current study showed that long noncoding RNA (lncRNA) growth arrest-specific transcript 5 (GAS5), microRNA-23a (miR-23a), and phosphatase and tensin homolog (PTEN) play important roles in the pathological process of hepatic fibrosis but have a relatively unclear regulatory mechanism. This study aimed to investigate the roles of lncRNA GAS5, miR-23a, and PTEN in the pathological process of hepatic fibrosis and hepatic stellate cell (HSC) activation. We used carbon tetrachloride (CCl 4 ) intraperitoneal injections to establish a rat hepatic fibrosis model and exogenous transforming growth factor-β1 to establish an HSC activation model. Quantitative RT-PCR, Western blot, dual-luciferase reporter system, and RNA pull-down assays were used to investigate which microRNAs and lncRNAs participate in the process of hepatic fibrosis and HSC activation. miR-23a expression increased significantly in hepatic fibrosis tissues and activated HSCs. miR-23a interaction with and degradation of PTEN further influenced the downstream signaling pathway phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin/Snail (PI3K/Akt/mTOR/Snail), causing E-cadherin expression levels to decrease and α-smooth muscle actin and collagen I expression levels to increase. lncRNA GAS5 can be used as a sponge platform for miR-23a to decrease miR-23a expression levels competitively. We revealed the role of the lncRNA GAS5/miR-23a/PTEN/PI3K/Akt/mTOR/Snail signaling pathway in hepatic fibrosis, providing molecular targets for the treatment of hepatic fibrosis. NEW & NOTEWORTHY This is the first study revealing that microRNA-23a (miR-23a) promotes hepatic fibrosis through the phosphatase and tensin homolog/phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin/Snail signaling pathway, and long noncoding RNA (lncRNA) growth arrest-specific transcript 5 (GAS5) can act as a sponge platform for miR-23a. Therefore, lncRNA GAS5/miR-23a may bring molecular targets for hepatic fibrosis therapy.

Objective: To establish a convenient and accurate method of DNA molecular marker for the identification of corium stomachium galli., Method: Cytb mtDNA sequences of Gallus gallus domestica and three other species of poultry were downloaded from Genbank. Species-specific PCR primers were designed according to the differential DNA fragments of the cytb genes. PCR tests were performed with the DNAs extracted from G. gallus domestica, three other poultry species and domestic mammal animals., Result: The specific primers of G. gallus domestica could only amplify the cytb mtDNA of G. gallus domestica., Conclusion: The primers are specific to G. gallus domestica mtDNA and can used to discern Corium stomachium from the false medicine.