ObjectiveTo investigate the therapeutic effect of Astragali Radix-mediated changes in gut microbiota on treating type 2 diabetes （T2DM）. MethodsA 12-week randomized， placebo-controlled clinical trial enrolled eighty patients with newly diagnosed type 2 diabetes and poor glycemic control in the Qi deficiency type. All patients received insulin therapy. The observation group （40 cases） was administered with Astragali Radix Granules， while the control group （40 cases） received a placebo. Both treamtents were taken orally twice daily. Changes in gut microbiota were assessed by 16s rDNA sequencing. Serum glucagon-like peptide-1 （GLP-1） levels were measured using enzyme-linked immunosorbent assay （ELISA）. Glucose metabolism indicators including fasting blood glucose （FPG）， 2-hour postprandial blood glucose （2 h PG），glycated albumin（GA）， and glycated hemoglobin （HbA1c） were evaluated. Pancreatic function was evaluated using fasting C-peptide （FCP）， 2-hour postprandial C-peptide （2 h CP）， and C-peptide area under the curve （AUC_cp）. Traditional Chinese medicine （TCM） syndrome scores， clinical efficacy， and safety indicators were also observed. ResultsIn terms of glucose metabolism indicators， compared with the baseline， both groups exhibited significantly lower FPG， 2 h PG， GA and HbA1C （P<0.01），while FCP， 2 h CP and AUC_cp were significantly higher （P<0.01）. Compared with the control group after the treatment， the observation group showed significantly lower FPG， 2 h PG， GA and HbA1C（P<0.05， P<0.01），and significantly higher FCP， 2 h CP and AUC_cp （P<0.05， P<0.01）， indicating that Astragali Radix can improve glucose metabolism. In terms of the diversity of gut microbiota， no significant differences were detected in the Chao1， Shannon and Simpson indexes of the two groups compared with their respective baselines. However， compared with the post-treatment control group， the observation group demonstrated significant increases in the Chao1， Shannon and Simpson indexes （P<0.05， P<0.01）. The β-diversity analysis showed significant separation in gut microbiota composition before and after treatment in both groups， indicating that Astragali Radix can significantly alter the structure and improve the diversity of gut microbiota. At the phylum level， compared with the baseline， both groups showed a significant increase in the relative abundance of Bacteroidota（P<0.01）. The relative abundance of the potentially harmful phylum Proteobacteria was significantly lower in the observation Group after treatment （P<0.01）. Compared with the post-treatment control group， the observation group had a significantly higher relative abundance of Bacteroidota（P<0.01）. No significant difference was found in Firmicutes/Bacteroidota （F/B） ratio between the two groups after treatment， and other phyla showed no significant differences. At the genus level， compared with the baseline， the observation group exhibited a significant increase in Bacteroides （P<0.01） and a significant decrease in Escherichia-Shigella （P<0.01）， whereas no significant difference was seen in the control group . Compared with the control group after treatment， the observation group after treatment had a significantly higher relative abundance of Bacteroides （P<0.01）. No significant differences were seen in other genera. Linear discriminant analysis （LDA） identified potential characteristics taxa： in the observation group， Bacteroidota at the phylum level and Bacteroides and Dubosiella at the genus level， in the control group， Proteobacteria at the phylum level as well as Barnesiella and Staphylococcus at the genus level. Correlation analysis based on a heatmap revealed that GLP-1 levels were positively correlated with Firmicutes， F/B ratio and Fusobacterium， and negatively correlated with Bacteroidota， Proteobacteria， Bacteroides and Escherichia-Shigella. In terms of clinical efficacy， compared with the control group， the total effective rate of the observation group was significantly higher （P<0.05）. Compared with the baseline， the scores for shortness of breath， fatigue， weakness， spontaneous sweating and reluctance to speak significantly decreased in both groups （P<0.01）. Compared with the control group after treatment， the score for weakness was significantly lower in the observation group （P<0.01），indicating that Astragali Radix could improve clinical symptoms and alleviate weakness symptoms. In terms of safety， compared with the baseline， alanine aminotransferase （ALT） levels significantly decreased in both groups （P<0.05，P<0.01），indicating that Astragali Radix did not induce any significant abnormalities in liver and kidney functions. ConclusionAstragali Radix demonstrates the potential to significantly improve the gut microbiota environment in patients of newly diagnosed type 2 diabetes with Qi deficiency. The therapeutic effect may contribute to glycemic control， possibly mediated by an elevation in GLP-1 level. These findings may support its further clinical investigations and potential applications.

ObjectiveTo investigate the mechanism by which Luoshi Neiyi prescription treats endometriosis （EMs） through the Toll-like receptor 4 （TLR4）/nuclear factor-κB （NF-κB） signaling pathway. MethodsAnimal experiments were conducted with 50 female SD rats， which were randomized into a sham operation group （10 rats） and a modeling group （40 rats）. An autologous endometrial transplantation method was used for the modeling of EMs. The 36 successfully modeled rats were randomly allocated into four groups （n=9 each）： The model group， the low-dose （7.87 g·kg^-1） Luoshi Neiyi prescription group， the high-dose （15.74 g·kg^-1） Luoshi Neiyi prescription group， and the dienogest （0.20 mg·kg^-1） group. The physiological status and ectopic lesion volumes of rats in each group were observed. Hematoxylin-eosin （HE） staining was used to observe the morphology of the eutopic endometrial tissue. Enzyme-linked immunosorbent assay （ELISA） was employed to measure the levels of inflammatory factors including interleukin-1β （IL-1β） and prostaglandin E₂ （PGE₂） in the serum of EMs rats. Immunohistochemistry was used to detect the expression of matrix metalloproteinase-9 （MMP-9） and vascular endothelial growth factor A （VEGFA） in the eutopic endometrial tissue. Western blot was adopted to determine the protein levels of TLR4， myeloid differentiation factor 88 （MyD88）， phosphorylated nuclear factor-κB （p-NF-κB）/NF-κB， MMP-9， and VEGFA in the eutopic endometrial tissue. In the cell experiments， the cell-counting kit-8 （CCK-8） assay was employed to screen the optimal concentration of Luoshi Neiyi prescription-containing serum， and a scratch assay was performed to assess the migration ability of iheESCs cells. Interventions with Luoshi Neiyi prescription-containing serum， resatorvid （TAK-242， a TLR4 inhibitor）， and lipopolysaccharides （LPS， a TLR4 agonist） were conducted， and Western blot was used to detect the expression of proteins related to the TLR4/NF-κB signaling pathway. ResultsThis experiment successfully replicated 36 EMs rat models. Compared with the sham operation group， the model group exhibited visible ectopic lesions on the abdominal wall and an increase in the writhing response score （P<0.01）. Furthermore， HE staining revealed the model group exhibited a thickened eutopic epithelium， stromal cell disarrangement， and evident infiltration of inflammatory cells. In addition， the model group showed elevated serum levels of IL-1β and PGE₂ （P<0.05， P<0.01）， increased positive expression of MMP-9 and VEGFA in the ectopic endometrial tissue （P<0.01）， and up-regulated protein levels of TLR4， MyD88， p-NF-κB/NF-κB， MMP-9， and VEGFA in the ectopic endometrial tissue （P<0.05， P<0.01）. Compared with the model group， all treatment groups exhibited a reduction in the ectopic lesion volume （P<0.01）. Furthermore， the writhing response scores were decreased in the high-dose Luoshi Neiyi prescription group and the dienogest group （P<0.05， P<0.01）. The pathological state of the ectopic endometrial tissue was alleviated to varying degrees in the treatment groups. Low-dose Luoshi Neiyi prescription reduced serum PGE₂ levels， and high-dose Luoshi Neiyi prescription and dienogest decreased serum IL-1β and PGE₂ levels in EMs rats （P<0.05， P<0.01）. The treatment groups showed decreased positive expression of MMP-9 and VEGFA in the ectopic endometrial tissue （P<0.05， P<0.01） and down-regulated protein levels of TLR4， MyD88， p-NF-κB/NF-κB， MMP-9， and VEGFA in the ectopic endometrial tissue （P<0.05， P<0.01）. The cell experiments showed that 5%， 10%， and 20% Luoshi Neiyi prescription-containing sera significantly reduced the viability and inhibited the migration of iheESCs. Compared with the control group， 5%， 10%， and 20% Luoshi Neiyi prescription-containing serum groups and the TAK-242 group showed reduced protein levels of TLR4， MyD88， p-NF-κB/NF-κB， MMP-9， and VEGFA （P<0.01）. Compared with the control group， the LPS group showed increased expression of the above proteins （P<0.01）. Compared with the LPS group， the LPS+5%， 10%， and 20% Luoshi Neiyi prescription-containing serum groups showed reduced expression of the above proteins （P<0.05， P<0.01）. ConclusionLuoshi Neiyi prescription may modulate the TLR4/NF-κB signaling pathway to reduce the inflammatory response and histopathological damage in the eutopic endometrium and suppress the adhesive， invasive， and angiogenic biological processes in the ectopic endometrial tissue， thereby exerting its therapeutic effect on EMs.

Abstract To clarify the service targets, service contents, and safeguard mechanisms of the basic public service program for student vision health management, the study grounded in the current status of child and adolescent myopia prevention and control in China and integrated with the practical experience and innovative practices of Wuhan National Demonstration Area for Student Vision Health Management, takes education as the main thread and schools as the base, consolidating resources from multiple stakeholders including education administrative departments, schools, families, and professional technical service institutions. Centering on four core components—vision health education, monitoring and record keeping, risk prevention and control, and dynamic management, the study constructs a multi tiered basic public service system for vision health management of primary and secondary school students. It further proposes the use of an intelligent management platform and a "three tier color coded early warning" mechanism (red, yellow, blue) to prevent and control student myopia at the source, providing schools with replicable and operable implementation pathways to enhance the level of student vision health management.

Objective To investigate the protective effect of epigallocatechin gallate(EGCG)on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP)-induced Parkinson's disease model mice.Methods Twenty-eight male C57BL/6J mice aged 6～8 weeks were randomly divided into four groups:the control group,the model group,the low-dose EGCG group[25 mg/(kg·d)],and the high-dose EGCG group[50 mg/(kg·d)].A Parkin-son's disease(PD)mouse model was established by intraperitoneal injection of MPTP at a dose of 30 mg/(kg·d)for 7 consecutive days.The protective effect of EGCG on MPTP-induced Parkinson's model mice was analyzed through behavioral index detection and Western blot method.Results(1)In the behavioral tests,compared with the model group,the movement distance and speed of mice treated with low-and high-dose EGCG were significantly improved(both P values<0.001).The mice in the high-dose EGCG treatment group also showed a significant advantage in the percentage of the central path distance(P<0.001).(2)Compared with the control group,the deposition of α-synuclein in the model group increased significantly(P<0.001).Compared with the model group,both the low-and high-dose EGCG groups reduced the deposition of α-synuclein(both P<0.001).(3)Compared with the control group,the expression levels of Beclin 1 and LC3 proteins in the substantia nigra region of mice in the model group decreased significantly(both P<0.001),while the expression level of p62 protein increased significantly(P<0.001).After treatment with EGCG,compared with the model group,the expression levels of Beclin 1 and LC3 proteins in mice of the low-dose EGCG group increased to varying degrees(P<0.01;P<0.001),and the expression level of p62 protein decreased significantly(P<0.001).In the high-dose EGCG group,the expression levels of Beclin 1 and LC3 proteins increased significantly(both P<0.001),and the expression level of p62 protein decreased significantly(P<0.001).Conclusion EGCG reduces alpha-synuclein deposition via the autophagy-lysosomal pathway and protects against MPTP-induced Parkinson's disease model mice.

Objective To investigate the protective effect of epigallocatechin gallate(EGCG)on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP)-induced Parkinson's disease model mice.Methods Twenty-eight male C57BL/6J mice aged 6～8 weeks were randomly divided into four groups:the control group,the model group,the low-dose EGCG group[25 mg/(kg·d)],and the high-dose EGCG group[50 mg/(kg·d)].A Parkin-son's disease(PD)mouse model was established by intraperitoneal injection of MPTP at a dose of 30 mg/(kg·d)for 7 consecutive days.The protective effect of EGCG on MPTP-induced Parkinson's model mice was analyzed through behavioral index detection and Western blot method.Results(1)In the behavioral tests,compared with the model group,the movement distance and speed of mice treated with low-and high-dose EGCG were significantly improved(both P values<0.001).The mice in the high-dose EGCG treatment group also showed a significant advantage in the percentage of the central path distance(P<0.001).(2)Compared with the control group,the deposition of α-synuclein in the model group increased significantly(P<0.001).Compared with the model group,both the low-and high-dose EGCG groups reduced the deposition of α-synuclein(both P<0.001).(3)Compared with the control group,the expression levels of Beclin 1 and LC3 proteins in the substantia nigra region of mice in the model group decreased significantly(both P<0.001),while the expression level of p62 protein increased significantly(P<0.001).After treatment with EGCG,compared with the model group,the expression levels of Beclin 1 and LC3 proteins in mice of the low-dose EGCG group increased to varying degrees(P<0.01;P<0.001),and the expression level of p62 protein decreased significantly(P<0.001).In the high-dose EGCG group,the expression levels of Beclin 1 and LC3 proteins increased significantly(both P<0.001),and the expression level of p62 protein decreased significantly(P<0.001).Conclusion EGCG reduces alpha-synuclein deposition via the autophagy-lysosomal pathway and protects against MPTP-induced Parkinson's disease model mice.

Objective To investigate the effect of miR-488-3p on renal tubular epithelial cell injury by regulating the cyclic guanosine monophosphate-adenosine monophosphate synthase(cGAS)-stimulator of interferon gene(STING)signaling pathway.Methods Human renal tubular epithelial HK-2 cells were divided into control,hypoxia-reoxygenation(HR),inhibition control,miR-488-3p inhibition,cGAS-STING pathway activator(RocA),and miR-488-3p inhibition+RocA groups.Quantitative real-time polymerase chain reaction was used to detect miR-488-3p expression in HK-2 cells.Cell viability was assessed using the CCK-8 assay.Enzyme-linked immunosorbent assay was used to measure the levels of interleukin(IL)-10,IL-1β,and tumor necrosis factor-α(TNF-α)in the culture supernatant of HK-2 cells.The DCFH-DA method was applied to detect the average fluorescence intensity of reactive oxygen species(ROS)in cells.Results Compared with the control group,the HR group showed increased miR-488-3p expression,IL-1β and TNF-α levels,average fluorescence intensity of ROS,malondialdehyde(MDA)levels,apoptosis rate,and protein expression of cleaved caspase-3,Bax,cGAS,and STING,whereas cell viability,IL-10 levels,and superoxide dismutase(SOD)activity were reduced in the HR group(P＜0.05).Com-pared with the HR and inhibition control groups,the miR-488-3p inhibition group exhibited decreased expression of miR-488-3p,IL-1β and TNF-α levels,average fluorescence intensity of ROS,MDA levels,apoptosis rate,and protein levels of cleaved caspase-3,Bax,cGAS,and STING,whereas cell viability,IL-10 levels,and SOD activity were increased(P＜0.05).Conclusion Downregulation of miR-488-3p expression mitigates HR-induced inflammation,oxidative stress,and apoptosis in HK-2 cells,thereby reducing cell damage.The under-lying mechanisms may be associated with an inhibition of the cGAS-STING signaling pathway.

Objective To systematic evaluate the impact of applying the clinical nursing pathway(CNP)on epidural anesthetic analgesia natural delivery.Methods The randomized controlled trial(RCT)and quasi-experimental researches on the application of CNP in epidural anesthetic analgesia natural delivery were retrieved from PubMed,Cochrane Library,Embase,Web of Science,China Knowledge Network database,Wanfang database,VIP and the Chinese Biomedical Literature Database.The retrieval time limit was from January 1,2014,to July 31,2024 with no language limitation.The meta analysis on the included studies was performed by applying RevMan5.4.1.Results A total of 5 RCTs and 2 quasi-experimental studies were in-cluded,involving 979 parturients with deliveries.The meta analysis showed that compared with the conven-tional nursing,CNP could shorten the duration of the first stage of labor(MD=—1.06,95％CI:—1.95——0.17,P=0.02)and the duration of the second stage of labor(MD=—0.12,95％CI:—0.21——0.03,P=0.006);decreased the rate of perineal lateral incision(RR=0.73,95％CI:0.65-0.83,P＜0.001)and inci-dence rate of postpartum urinary retention(RR=0.35,95％CI:0.20-0.63,P＜0.001);and shortened the time to lactation initiation(SMD=—1.52,95％CI:—2.38——0.66,P＜0.001).There was no influence on reducing postpartum 24 h hemorrhage amount(SMD=—0.51,95％CI:—1.23-0.21,P=0.16).The study subjects were divided into the primipara women subgroup and unclassified parturients subgroup.Compared with the conventional nursing group,compared with the conventional nursing,CNP had no impact on the dura-tion of the first stage of labor(MD=—0.32,95％CI:—0.61-0.98,P=0.63)and the duration of the second stage of labor(MD=—0.11,95％CI:—0.25-0.04,P=0.15)in the primipara women subgroup.CNP could reduce the postpartum 24 h hemorrhage volume in the unclassified parturients subgroup(SMD=—1.47,95％CI:—1.72——1.21,P＜0.001).Conclusion Application of CNP in parturients labor analgesia could reduce the perineal lateral incision rate and incidence rate of postpartum urinary retention and shorten the time to lac-tation initiation.Due to the heterogeneity among studies,the impact of CNP on the labor duration and the bleeding amount within postpartum 24 h still requires more high-quality studies to be conducted in the future for verification.

Parkinson disease (PD) is a complex neurodegenerative disorder characterized by a variety of motor and non-motor symptoms. Many studies have shown that the transmembrane protein 175 (TMEM175) gene may be a potential target for the treatment of PD and other neurodegenerative disorders, but the specific pathogenic mechanism remains unclear. TMEM175 is a lysosomal protein-coding gene that encodes a lysosomal proton channel protein. This article reviews the research advances in the characterization of the TMEM175 gene and its encoded proteins, the clinical features of mutant PD, and related pathogenic mechanism. It is shown that the TMEM175 gene has an impact on the pathogenesis of PD, and patients with different mutation sites tend to have different ages of onset and clinical features. Compared with the patients without TMEM175 mutations, the patients with TMEM175 mutations tend to have an earlier age of onset, more severe motor symptoms, and more susceptibility to cognitive impairment and non-motor symptoms. This article systematically reviews the TMEM175 gene, in order to assist in the early diagnosis of PD and the discovery of new disease-modifying therapies and treatment strategies.
Parkinson Disease

Objective To investigate the effect of miR-488-3p on renal tubular epithelial cell injury by regulating the cyclic guanosine monophosphate-adenosine monophosphate synthase(cGAS)-stimulator of interferon gene(STING)signaling pathway.Methods Human renal tubular epithelial HK-2 cells were divided into control,hypoxia-reoxygenation(HR),inhibition control,miR-488-3p inhibition,cGAS-STING pathway activator(RocA),and miR-488-3p inhibition+RocA groups.Quantitative real-time polymerase chain reaction was used to detect miR-488-3p expression in HK-2 cells.Cell viability was assessed using the CCK-8 assay.Enzyme-linked immunosorbent assay was used to measure the levels of interleukin(IL)-10,IL-1β,and tumor necrosis factor-α(TNF-α)in the culture supernatant of HK-2 cells.The DCFH-DA method was applied to detect the average fluorescence intensity of reactive oxygen species(ROS)in cells.Results Compared with the control group,the HR group showed increased miR-488-3p expression,IL-1β and TNF-α levels,average fluorescence intensity of ROS,malondialdehyde(MDA)levels,apoptosis rate,and protein expression of cleaved caspase-3,Bax,cGAS,and STING,whereas cell viability,IL-10 levels,and superoxide dismutase(SOD)activity were reduced in the HR group(P＜0.05).Com-pared with the HR and inhibition control groups,the miR-488-3p inhibition group exhibited decreased expression of miR-488-3p,IL-1β and TNF-α levels,average fluorescence intensity of ROS,MDA levels,apoptosis rate,and protein levels of cleaved caspase-3,Bax,cGAS,and STING,whereas cell viability,IL-10 levels,and SOD activity were increased(P＜0.05).Conclusion Downregulation of miR-488-3p expression mitigates HR-induced inflammation,oxidative stress,and apoptosis in HK-2 cells,thereby reducing cell damage.The under-lying mechanisms may be associated with an inhibition of the cGAS-STING signaling pathway.

【Objective】 To explore the effectiveness of creating the obstructive sleep apnea hypopnea syndrome (OSAHS) animal model of glossocoma using the botulinum toxin type A in white rabbits, and to explore the effectiveness and safety of magnetic traction hyoid suspension operation in the OSAHS animal model of glossocoma. 【Methods】 A total of 12 adult male experimental white rabbits were randomly divided into two groups. The animals in the experimental group were injected with 0.4 mL (10 U) of botulinum toxin type A in the genioglossus muscle to construct the OSAHS animal model of glossocoma. The animals in the control group were injected with 0.4 mL of normal saline. We designed and 3D printed a polyacrylate shell that could be loaded with inner and outer neodymium iron boron (NdFeB) magnets. After the modeling, a polyacrylate shell with the inner magnet device was fixed on the hyoid bone of the animals in the experimental group. All animals in the experimental group wore the polyacrylate orthotic neck brace containing the outer magnet 10 days after the operation. The arterial blood oxygen detector was used to record the oxygen saturation (SaO2) of the femoral artery, and multi-slice CT plain scan was used to measure the diameter of the narrowest part of the upper airway. 【Results】 The animals in the experimental group gradually showed decreased activity, labored breathing, blue lips and ear margins and other manifestations of hypoxemia 5 days after intramuscular injection of botulinum toxin type A in the genioglossus, and their body weight dropped from (3.72±0.21)kg to (3.40±0.20)kg, the average SaO2 of the femoral artery decreased from (93.84±5.14)% to (84.00±3.35)%, and the diameter of the narrowest part of the upper airway decreased from (4.83±0.47)mm to (3.52±0.83)mm (P<0.05). In the control group, the animals’ weight, the average SaO2 of the femoral artery, and the diameter of the narrowest part of the upper airway did not significantly change before and after injection of normal saline into the genioglossus muscle (P>0.05). The animals in the experimental group completed the magnetic traction hyoid suspension surgery. After wearing the orthotic neck brace containing an external magnet for hyoid magnetic traction, the food intake and activity of the animals in the experimental group increased, the color of the lips changed from purple to pink, the SaO2 of the femoral artery increased significantly to (90.44±5.95)%, and the diameter of the narrowest part of the upper airway increased significantly to (4.42±0.15)mm (P<0.05). 【Conclusion】 The genioglossus muscle injection of botulinum toxin type A in white rabbits could successfully establish the OSAHS animal model of glossocoma. Magnetic traction hyoid suspension surgery in the treatment of OSAHS animal model could effectively correct the upper airway stenosis related symptoms and hypoxemia caused by glossocoma.