Objective: To study the association between ankyloglossia and sagittal mandibular development impairment as well as lower anterior dental crowding, providing a reference for clinical practice. Methods: This study was approved by the hospital's Medical Ethics Committee. A total of 100 patients aged 7-13 years were enrolled from January 2024 to January 2025, comprising 50 patients with ankyloglossia (case group) and 50 individuals with a healthy lingual frenulum (normal group). Clinical examination was performed to assess lingual frenulum length, Kotlow classification, and the simplified Hazelbaker assessment tool for lingual frenulum function (HATLFF) score. Cephalometric radiographs were used to measure the A-point-nasion-B-point (ANB) angle, sella-nasion-B-point (SNB) angle, and mandibular total length (condylion-gnathion [Co-Gn]). Dental cast analysis was conducted to evaluate lower anterior teeth crowding. Data were compared between the two groups. Pearson correlation analysis was used to examine the relationships between the lingual frenulum length, simplified HATLFF score, and cephalometric/dental cast parameters (ANB, SNB, Co-Gn, lower anterior crowding). The diagnostic value of ankyloglossia for mandibular development and lower anterior crowding was analyzed using receiver operating characteristic (ROC) curves. Results: Ankyloglossia was significantly associated with mandibular development and lower anterior crowding (P<0.05). The case group showed significantly lower values for the lingual frenulum length, simplified HATLFF score, SNB angle, and Co-Gn, while the ANB angle and lower anterior crowding index were significantly higher compared to the normal group (P<0.05). The lingual frenulum length and simplified HATLFF score were negatively correlated with the ANB angle and lower anterior crowding index, and positively correlated with the SNB angle and Co-Gn (P<0.05). ROC curve analysis indicated that the area under the curve (AUC) for the simplified HATLFF score, and ankyloglossia in predicting mandibular development deficiency and lower anterior crowding was greater than 0.700, demonstrating good diagnostic value. Conclusion A significant correlation exists between ankyloglossia and both mandibular development deficiency and lower anterior crowding.

Objective To explore whether the cognitive function of central obese mice is decreased by affecting the expression of brain-derived neurotrophic factor(BDNF)in hippocampus.Methods Healthy mice at the neonatal stage were divided into normal group and model group at random.To obtain the obese models,model group mice were injected at cervical subcutaneous with 10％L-monosodium glutamate(MSG;3 mg·g-1·d-1)for 5 days.The normal group was injected with the same dose of 0.9％NaCl.In addition,mice were removed according to the requirements.Finally,we got 8 mice in each group.The following parameters were compared:body weight,Lee's index and levels of the serum lipid.The BDNF expression levels in hippocampal tissue were measured using western blotting.Results At the 8th weekend,the body weight of the model and normal groups was(49.01±2.47)and(41.27±3.28)g;the Lee's indexes were(357.14±9.24)and(330.15±7.37)g1/3·cm-1;triglyceride levels were(1.37±0.52)and(0.73±0.31)mmol·L-1;total cholesterol levels were(2.98±0.18)and(1.98±0.30)mmol·L-1;low-density lipoprotein levels were(0.31±0.03)and(0.24±0.02)mmol·L-1;high-density lipoprotein levels were(2.70±0.15)and(1.98±0.40)mmol·L-1;the differences were statistically significant(P＜0.05,P＜0.01),which were consistent with the characteristics of the central obesity model.The BDNF protein expression levels in the hippocampus of the model and normal groups were 6.02 x 104±626.53 and 7.04 x 104±1 440.81,which has statistically significant(P＜0.01).Conclusion The cognitive function of central obese mice may be decreased by down-regulating the expression of BDNF in hippocampus.

Fibromyalgia syndrome （FMS） is a refractory， chronic non-articular rheumatic disease characterized by widespread pain throughout the body， for which there are no satisfactory therapeutic drugs or options. There are rich Chinese medical therapies， and some non-drug therapies， such as acupuncture， Tai Chi， and Ba-Duan-Jin， have shown satisfactory efficacy and safety and definite advantages of simultaneously adjusting mind and body. FMS is taken as a disease responding specifically to traditional Chinese medicine （TCM） by the National Administration of Traditional Chinese Medicine in 2018. In order to clarify the research progress in FMS and the clinical advantages of TCM/integrated Chinese and Western medicine， the China Academy of Chinese Medicine organized a seminar for nearly 20 experts in Chinese and Western medicine， including rheumatology， psychology， acupuncture and moxibustion， and encephalopathy， with the topic of difficulties in clinical diagnosis and treatment of FMS and advantages of TCM and Western medicine. The recommendations were reached on the difficulties in early diagnosis and solutions of FMS， mitigation of common non-specific symptoms， preferential analgesic therapy， TCM pathogenesis and treatment advantages， and direction of treatment with integrated Chinese and Western medicine. FMS is currently facing the triple dilemma of low early correct diagnosis， poor patient participation， and unsatisfactory benefit from pure Western medicine treatment. To solve the above problems， this paper suggests that rheumatologists should serve as the main diagnostic force of this disease， and they should improve patient participation in treatment decision-making， implement exercise therapy， and fully utilize the holistic and multidimensional features of TCM， which is effective in alleviating pain， improving mood， and decreasing adverse events. In addition， it is suggested that FMS treatment should rely on both TCM and Western medicine and adopt multidisciplinary joint treatment， which is expected to improve the standard of diagnosis and treatment of FMS in China.

Objective To analyze the effect and molecular mechanism of phellodendron amurense in the treatment of liver injury based on network pharmacology,and to verify the relevant prediction targets and the protective effect of phellodendron amurense extract-Phellodendron amurense polysaccharide on immune liver injury through mice.Methods TCMSP and Swiss target prediction databases were used to retrieve and screen phellodendron amurenses active components and action targets,and then obtain disease-related targets on GeneCards and OMIM websites,and take compounds and disease intersection targets for protein interaction.Analysis,GO biological function and KEGG signaling pathway enrichment analysis,followed by molecular docking of compounds and key target proteins,and finally established a mouse liver injury model induced by Daodou protein A(Con A)to explore the mechanism of phellodendron amurense extract in the treatment of liver injury.Results 37 active ingredients were screened.The key targets for their treatment were tumor necrosis factor α(TNF-α),serine/threonine protein kinase 1(AKT1),signal transduction and transcription activation factor 3(STAT3),epidermal growth factor receptor(EGFR)anditin.Enzyme 3(CASP3)and other enrichment analysis showed that phellodendron amurense might play a protective role in protecting the liver through molecular mechanisms such as positive regulation of MAPK cas-cade reaction,oxidative stress response and regulatory PI3K-Akt signaling pathway,lipid and atherosclerosis.Ani-mal experiments had found that the gastric treatment of phellodendron amurense polysaccharide could improve the activity of superoxide dismutase(SOD)and catalase(CAT)in liver tissue,reduce the levels of serum alkaline phosphatase(ALP),aspartate aminotransferase(AST)and malonaldehyde(MDA)in liver tissue,and regulate serum inflammatory factor while the expression of intercitin(IL)-6,IL-1 β,tumor necrosis factor α(TNF-α),ac-tivated the expression of transforming growth factor β1(TGF-β1),and reduced TNF-α mRNA expression in liver tissue.Conclusion Phellodendron amurense can intervene in lipid and atherosclerosis pathways by acting on tar-gets such as TNF-α,AKT1,STAT3,EGFR and CASP3 to reduce oxidative stress and inflammatory reactions and achieve liver protection.

The shared decision marking between doctors and patients is a moral requirement，which stems from the basic rights of medical staff to accept patients or their families，such as autonomy，informed consent and choice.In order to achieve the shared decision marking between doctors and patients，medical staff and patients play different roles.The task of medical staff is to introduce professional knowledge and specific experience，provide patients with multiple recommendations for diagnosis and treatment choices，and the task of patients is to choose treatment plans recognized in the shared decision marking based on their understanding of medical and ethical knowledge such as treatment goals，health values，and basic rights.From the ethical perspective，based on the shared decision marking between doctors and patients，this study deeply analyzes its ethical significance.Centering on the basic requirements of ethics，this study explores various practical models such as the doctor-patient joint participation model，the doctor-patient-family joint participation model，the doctor-nurse-patient joint participation model，the high-risk case conversation model of medical intervention，and the multidisciplinary team collaboration model from multiple perspectives and depths，to further promote the implementation of the shared decision marking between doctors and patients and to provide some reference basis.

Hyperpolarization-activated cyclic nucleotide-gated(HCN)channels are widely expressed in the central and peripheral nervous systems.They can generate hyperpolarization-activated current(Ih)that regulates the resting membrane potential and excitability of neurons.Furthermore,it can affect the precise processing and con-duction of hearing,which plays a crucial role in the accurate analysis of temporal information.Therefore,through the review of HCN channel structure and distribution,as well as electrophysiological effects,the role and mecha-nism of HCN channels in the auditory pathways of the normal and unilateral or bilateral deafness patients will be fur-ther investigated.

Objective To explore the effectiveness of FOCUS-PDCA(find,organise,clarify,understand,select,plan,do,check and act)mode in prevention and treatment of incontinence-associated dermatitis(IAD)in emergency intensive care unit(EICU),and to reduce the incidence of IAD.Methods A pre-post control study design was employed in this study.Inpatients admitted to the EICU of the hospital between 1st January and 31st December 2022 were enrolled as study subjects.A total of 169 patients in EICU between January and June 2022 were assigned as a control group,while 197 patients in EICU between July and December 2022 as an trial group.Patients in the control group received conventional quality management,while those in the trial group were treated with the FOCUS-PDCA mode.The two groups were compared in terms of incidence of IAD,the knowledge,trust and behaviour scores of the nurses,and satisfaction from the communications with nurses before and after implementation of the FOCUS-PDCA mode.Results All patients in the two groups had completed the study.Following the implementation of FOCUS-PDCA mode,patients in the trial group exhibited a significantly decrease in incidence of IAD from 10.06%(trial group)to 1.52%(control group),significant increase of scores on the IAD knowledge,behaviour and satisfaction from communications with the nurses,from(36.07±3.98),(16.56±2.15)and(25.15±5.21),to(38.59±3.72),(18.07±1.66),and(30.67±5.84),respectively(all P<0.05).Conclusion FOCUS-PDCA mode can effectively decrease the incidence of IAD,enhance the IAD knowledge and behaviour of nurses and gain satisfactions from communication with nursing staff and clinical quality,thereby improving therapeutic outcomes.

Objective To observe the clinical efficacy and safety of bevacizumab in the treatment of platinum-resistant ovarian cancer,tubal cancer,peritoneal carcinoma cancer.Methods Patients with platinum resistance ovarian cancer,tubal cancer and peritoneal carcinoma cancer treated with bevacizumab were in included into treatment group.Patients with platinum-resistance in ovarian cancer,tubal cancer and peritoneal carcinoma cancer who received docetaxel chemotherapy during the same period were included into control group.The treatment group was given bevacizumab 5 mg·kg-1 by intravenous infusion once every 2 weeks,and the first intravenous infusion lasted for 90 min,with a total of 4 times of chemotherapy.The control group was given docetaxel 70-75 mg·m-2 by intravenous infusion,once every 3 weeks,1 h each time,a total of 4 times of chemotherapy.The clinical efficacy after chemotherapy,the levels of serum squamous cell carcinoma antigen(SCC-Ag),malignant tumor-related substance group(TSGF),cytokeratin 19 fragment(CYFRA21-1),the changes of tumor markers,immune indexes and the occurrence of adverse drug reactions were compared between the two groups.Results There are 70 cases in treatment group and 50 cases in control group.After four rounds of chemotherapy,the total effective rates of treatment group and control group were 47.14％(33 cases/70 cases)and 30.00％(15 cases/50 cases),with statistically significant difference(P＜0.05).After chemotherapy,the SCC-Ag levels in treatment group and control group were(3.10±1.05)and(5.50±1.95)mg·L-1;TSGF levels were(30.20±9.94)and(56.70±10.45)U·mL-1;CYFRA21-1 levels were(1.03±0.45)and(2.10±0.99)mg·L-1;carcinoembryonic antigen(CEA)levels were(66.81±48.74)and(89.18±56.08)ng·mL-1;the tumor markers CA199 were(110.26±51.36)and(124.13±53.80)U·mdL-1;the gastric cancer antigen(CA724)were(14.70±9.72)and(20.54±18.51)U·mL-1;the CD3+levels were(72.45±9.45)％and(67.10±10.25)％;the CD4+levels were(48.49±9.15)％and(39.56±6.77)％;the CD8+levels were(20.18±3.85)％and(24.02±4.45)％,the differences were all statistically significant(all P＜0.05).There was no significant difference in the incidence of adverse drug reactions between the two groups(P＞0.05).Conclusion Bevacizumab is more effective than docetaxel in the treatment of platinum-resistant ovarian cancer,tubal cancer,peritoneal carcinoma cancer.

Aim To investigate whether Linggui Zhugan Decoction ( LGZGD) can inhibit ventricular remodeling and prevent heart failure in rats after myocardial infarction by regulating Nrf2/BNIP3 pathway. Methods The model of heart failure after myocardial infarction was established by left coronary artery ligation in rats. Two weeks after modeling, all rats were randomly divided into model group, LGZGD group, and captopril group. Meanwhile sham operation group was set up. The rats were given continuous intragastric administration with drug or distilled water for 28 days, once a day. The behavioral signs of rats in each group were observed. The cardiac function of rats in each group was examined by echocardiography. Serum BNP and NT-ProBNP content were detected by enzyme -linked immunoassay; The changes of myocardial his-topathological and collagen fibers in rats were detected using sirius staining. The contents of oxidative stress index including ROS, SOD in myocardial tissue of rats in each group were observed by DCFH-DA fluorescent probe and Enzyme-linked immunoassay. The ultra-structure of mitochondria was observed by transmission electron microscopy. Expressions of apoptotic proteins ( mitochondrial CytC, cytoplasmic CytC) were detected by Western blot. Expression of proteins related to the Nrf2/BNIP3 pathway were examined by immunofluorescence and Western blot. Results LGZGD could significantly improve the cardiac function of rats, reduce the contents of BNP and NT-ProBNP, inhibit the excessive deposition of collagen in myocardial interstiti-um, reduce ROS, increase the content of SOD, improve mitochondrial structure damage, up-regulate the expression of Nrf2 and nuclear translocation, and reduce the expression of BNIP3. Conclusions LGZGD can inhibit the ventricular remodeling and prevent the occurrence of heart failure after myocardial infarction. Its pharmacological effects are mainly related to regulating the Nrf2/BNIP3 pathway, activating Nrf2, promoting its nuclear transfer, and further down-regulating BNIP3, protecting mitochondrial function, and reducing cardiomyocyte apoptosis.

Autosomal recessive congenital ichthyosis caused by CERS3 mutations is extremely rare in clinical practice. We recently identified a family of autosomal recessive congenital ichthyosis and performed multigene exome sequencing for hereditary skin diseases to identify causative genes. Mutation analysis revealed compound heterozygous mutations of c.746A>G(from the mother) and exon12 deletion(from the father)in CERS3 were detected in the proband, which were verified by Sanger sequencing and co-segregated with the ichthyosis phenotype in the proband and her parents. These mutations were both reported for the first time. For the treatment, the proband received an oral acitretin capsules of 20 mg once daily. After 3-month follow up, the patient's lesion improved significantly.