Methods: This study enrolled 40 patients with AIS, 20 patients with congenital scoliosis (CS), and 20 patients with spinal degenerative disease (SDD). All patients underwent open posterior surgery in our hospital, and a paravertebral muscle (multifidus muscle) biopsy was performed intraoperatively. This study included many indexes that describe muscle, especially dystrophin staining. The above pathological results were compared among the AIS, CS, and SDD groups. The correlation between the Cobb angle and Nash–Moe classification and the above pathological results was analyzed in patients with AIS. Results: Significant reductions in the dystrophin staining of dystrophin-1 (p<0.001), dystrophin-2 (p<0.001), and dystrophin-3 (p<0.001) were observed in the AIS group than in the CS and SDD groups. The higher the Nash–Moe classification in the AIS group, the more significant the loss of dystrophin-2 (p=0.042) in the convex paraspinal muscles. Additionally, a significantly positive correlation was observed between the reductions of dystrophin-2 on the concave side of the AIS group and Cobb angle (p=0.011). Conclusions Dystrophin protein deficiency in the paraspinal muscles plays a crucial role in AIS formation and progression. The severity of scoliosis in patients with AIS is correlated with the extent of dystrophin loss in the paravertebral muscles. Therefore, dystrophin dysfunction may be relevant to AIS occurrence and development.

Methods: This study enrolled 40 patients with AIS, 20 patients with congenital scoliosis (CS), and 20 patients with spinal degenerative disease (SDD). All patients underwent open posterior surgery in our hospital, and a paravertebral muscle (multifidus muscle) biopsy was performed intraoperatively. This study included many indexes that describe muscle, especially dystrophin staining. The above pathological results were compared among the AIS, CS, and SDD groups. The correlation between the Cobb angle and Nash–Moe classification and the above pathological results was analyzed in patients with AIS. Results: Significant reductions in the dystrophin staining of dystrophin-1 (p<0.001), dystrophin-2 (p<0.001), and dystrophin-3 (p<0.001) were observed in the AIS group than in the CS and SDD groups. The higher the Nash–Moe classification in the AIS group, the more significant the loss of dystrophin-2 (p=0.042) in the convex paraspinal muscles. Additionally, a significantly positive correlation was observed between the reductions of dystrophin-2 on the concave side of the AIS group and Cobb angle (p=0.011). Conclusions Dystrophin protein deficiency in the paraspinal muscles plays a crucial role in AIS formation and progression. The severity of scoliosis in patients with AIS is correlated with the extent of dystrophin loss in the paravertebral muscles. Therefore, dystrophin dysfunction may be relevant to AIS occurrence and development.

Methods: This study enrolled 40 patients with AIS, 20 patients with congenital scoliosis (CS), and 20 patients with spinal degenerative disease (SDD). All patients underwent open posterior surgery in our hospital, and a paravertebral muscle (multifidus muscle) biopsy was performed intraoperatively. This study included many indexes that describe muscle, especially dystrophin staining. The above pathological results were compared among the AIS, CS, and SDD groups. The correlation between the Cobb angle and Nash–Moe classification and the above pathological results was analyzed in patients with AIS. Results: Significant reductions in the dystrophin staining of dystrophin-1 (p<0.001), dystrophin-2 (p<0.001), and dystrophin-3 (p<0.001) were observed in the AIS group than in the CS and SDD groups. The higher the Nash–Moe classification in the AIS group, the more significant the loss of dystrophin-2 (p=0.042) in the convex paraspinal muscles. Additionally, a significantly positive correlation was observed between the reductions of dystrophin-2 on the concave side of the AIS group and Cobb angle (p=0.011). Conclusions Dystrophin protein deficiency in the paraspinal muscles plays a crucial role in AIS formation and progression. The severity of scoliosis in patients with AIS is correlated with the extent of dystrophin loss in the paravertebral muscles. Therefore, dystrophin dysfunction may be relevant to AIS occurrence and development.

Aural vertigo frequently encountered in the otolaryngology department of traditional Chinese medicine （TCM） mainly involves peripheral vestibular diseases of Western medicine， such as Meniere's disease， benign paroxysmal positional vertigo， vestibular neuritis， and vestibular migraine， being a hot research topic in both TCM and Western medicine. Western medical therapies alone have unsatisfactory effects on recurrent aural vertigo， aural vertigo affecting the quality of life， aural vertigo not relieved after surgery， aural vertigo with complex causes， and children's aural vertigo. The literature records and clinical practice have proven that TCM demonstrates unique advantages in the treatment of aural vertigo. The China Association of Chinese medicine sponsored the "17th youth salon on the diseases responding specifically to TCM： Aural vertigo" and invited vertigo experts of TCM and Western medicine to discuss the difficulties and advantages of TCM diagnosis and treatment of aural vertigo. The experts deeply discussed the achievements and contributions of TCM and Western medicine in the diagnosis and treatment of aural vertigo， the control and mitigation of the symptoms， and the solutions to disease recurrence. The discussion clarified the positioning and advantages of TCM treatment and provided guidance for clinical and basic research on aural vertigo.

Based on the theory of "controlling channels and collaterals"， this paper expounds the role of channels and collaterals system in the recurrence and metastasis of gastric cancer after surgery， and puts forward the prevention and treatment idea of warming the yang qi of channels and collaterals to consolidate the essence， and removing the stasis and blockage of channels and collaterals to clear the source. In the process of pattern differentiation and treatment， attention should be paid to the influence of surgery and cold medicinals on the yang qi of middle jiao. The yang qi of middle jiao should be supplemented to warm yang and strengthen vessels to prevent chuanshe （metastasis）； the channels and collaterals with pathogens should be opened to remove its stasis and blockage， and the cancer toxin should be attacked to clear the source and flow， and also the cancer toxin should be given a way out to prevent its accumulation and carcinogenesis； At the same time， envoy medicinals should be given to guide the effects of other herbs to specific channels， so as to induce the medicinals to reach the internal organs through the meridians； to achieve the organic combination of macroscopic differentiation and microscopic differentiation， and the organic combination of zang-fu pattern differentiation and channel pattern differentiation， and it is also a further extension of the treatment method of consolidating the root and clearing up the source， in the hope that it can provide reference for the pattern differentiation and treatment of recurrence and metastasis of gastric cancer after surgery.

Objective:To describe the prevalence of food allergy among children aged 0-5 years in China and to explore related influencing factors.Methods:Multistage stratified random sampling method was used to collect data from 275 surveillance sites of the China National Nutrition and Health Survey of Chinese children and lactating mothers programs in 31 provinces (autonomous regions and municipalities) of China in 2016-2017. A total of 70 107 participants aged 0-5 years were included in this study. The study collected information of participants' demographic characteristics and food allergies by face-to-face questionnaire. The prevalence of food allergy was analyzed, using the complex data weighting method. The logistic regression models were used to analyze the influencing factors related to food allergy.Results:The overall prevalence of self-reported food allergy among children aged 0-5 years was 4.81%. Prevalence rates in infants aged 0-5 months, and 6-23 months and preschool children aged 2-5 years were 0.81%, 4.68% and 5.26%, respectively. The results of logistic analysis showed that there was a significantly positive correlation between factors including children from 6 months to 5 years old, urban area, southwest area, first-born, mothers with college education or above, and the prevalence of food allergy in children. Shrimp, poultry eggs, crab shellfish, fruit, milk and fish appeared the common allergic foods in children aged 0-5 years, with prevalence rates of self-reported food allergy as 1.55%, 1.25%, 0.99%, 0.97%, 0.87% and 0.86%, respectively. The proportion of single food allergy in children with allergies was 69.85%.Conclusions:Among children aged 0-5 years, the prevalence of self-reported food allergy increases with age, in China. Foods that is prone to allergies include fish, shrimp, crab, shellfish, poultry eggs, milk and fruits, etc. Most allergies were only caused by single food in children, under observation.

Objective To investigate the role of SIRT1/autophagy pathway in mediating the regulatory effect of lncRNA SOX2OT on 5-fluorouracil(5-FU)resistance in cholangiocarcinoma cells.Methods HCCC-9810 cells were used to construct a 5-FU-resistant cell model(HCCC-9810/5-FU cells),and the expression levels of lncRNA SOX2OT and SIRT1 mRNA and the protein expressions of SIRT1,Beclin1,LC3 and P62 were detected with qRT-PCR and Western blotting.The effects of transfection with a SOX2OT mimic on drug resistance and cell migration of HCCC-9810/5-FU cells were detected using CCK-8 assay and wound healing assay,and the changes in expressions of SOX2OT,SIRT1,Beclin1,LC3 and P62 were detected.Rescue experiment was performed by co-transfection of HCCC-9810/5-FU cells with both a SOX2OT-overexpressing plasmid and si-SIRT1 to confirm the role of SIRT1 in SOX2OT-mediated regulation of 5-FU resistance.A RNA pulldown assay was used to verify the targeted binding between SOX2OT and SIRT1.Results The proliferation of HCCC-9810 cells was significantly inhibited after treatment with different concentrations of 5-FU(P<0.05).The 5-FU-resistant cells showed significantly increased protein expressions of SIRT1,Beclin1 and p62,an increased LC3Ⅱ/LC3Ⅰ ratio,and enhanced expressions of SIRT1 mRNA and SOX2OT(P<0.05).Transfection of the resistant cells with SOX2OT mimic significantly enhanced cell migration and increased the protein expressions of SIRT1,Beclin1 and p62,the LC3Ⅱ/LC3Ⅰratio,and expression levels of SIRT1 mRNA and SOX2OT(P<0.05),and these changes were obviously attenuated by SIRT1 knockdown,which also resulted in lowered 5-FU resistance of the cells without significantly affecting the expression level of SOX2OT(P>0.05).RNA pulldown assay suggested that SOX2OT could directly bind to SIRT1.Conclusion LncRNA SOX2OT enhances 5-FU resistance in HCCC-9810 cells by promoting autophagy through up-regulating SIRT1 expression.

Objective To compare the effect of palliative mitral valve surgeries and medication therapies for secondary non-ischemic mitral regurgitation. Methods The clinical data of patients with non-ischemic functional mitral regurgitation treated in our hospital between 2009 and 2019 were retrospectively analyzed. Patients with a left ventricular ejection fraction (LVEF)＜40% underwent a dobutamine stress test, and a positive result was determined when the LVEF improved by more than 15% compared to the baseline value. Positive patients were divided into a surgery group and a medication group. The surgery group underwent surgical mitral valve repair or replacement, while the medication group received simple medication treatment. Follow-up on survival and cardiac function status through outpatient or telephone visits every six months after surgery, and patients underwent cardiac ultrasound examination one year after surgery. The main research endpoint was a composite endpoint of all-cause death, heart failure readmission, and heart transplantation, and the differences in cardiac function and cardiac ultrasound parameters between the two groups were compared. Results Ultimately 41 patients were collected, including 28 males and 13 females with an average age of 55.5±11.1 years. Twenty-five patients were in the surgery group and sixteen patients in the medication group. The median follow-up time was 16 months, ranging 1-96 months. The occurrence of all-cause death in the surgery group was lower than that in the medication group (HR=0.124, 95%CI 0.024-0.641, P=0.034). The difference between the two groups was not statistically significant in the composite endpoint (HR=0.499, 95%CI 0.523-1.631, P=0.229). The New York Heart Association (NYHA) grade of the surgery group was better (NYHA Ⅰ-Ⅱ accounted for 68.0% in the surgury group and 18.8% in the medication group, P<0.01) as well as the grade of mitral valve regurgitation (87.5% of the patients in the medication group had moderate or above regurgitation at follow-up, while all the patients in the surgery group had moderate below regurgitation, P<0.01). There was no statistical difference in preoperative and follow-up changes in echocardiograph parameters between the two groups (P＞0.05). Conclusion For non-ischemic functional mitral regurgitation, if the cardiac systolic function is well reserved, mitral valve surgery can improve survival and quality of life compare to simple medication therapy.

Objective To investigate the role of SIRT1/autophagy pathway in mediating the regulatory effect of lncRNA SOX2OT on 5-fluorouracil(5-FU)resistance in cholangiocarcinoma cells.Methods HCCC-9810 cells were used to construct a 5-FU-resistant cell model(HCCC-9810/5-FU cells),and the expression levels of lncRNA SOX2OT and SIRT1 mRNA and the protein expressions of SIRT1,Beclin1,LC3 and P62 were detected with qRT-PCR and Western blotting.The effects of transfection with a SOX2OT mimic on drug resistance and cell migration of HCCC-9810/5-FU cells were detected using CCK-8 assay and wound healing assay,and the changes in expressions of SOX2OT,SIRT1,Beclin1,LC3 and P62 were detected.Rescue experiment was performed by co-transfection of HCCC-9810/5-FU cells with both a SOX2OT-overexpressing plasmid and si-SIRT1 to confirm the role of SIRT1 in SOX2OT-mediated regulation of 5-FU resistance.A RNA pulldown assay was used to verify the targeted binding between SOX2OT and SIRT1.Results The proliferation of HCCC-9810 cells was significantly inhibited after treatment with different concentrations of 5-FU(P<0.05).The 5-FU-resistant cells showed significantly increased protein expressions of SIRT1,Beclin1 and p62,an increased LC3Ⅱ/LC3Ⅰ ratio,and enhanced expressions of SIRT1 mRNA and SOX2OT(P<0.05).Transfection of the resistant cells with SOX2OT mimic significantly enhanced cell migration and increased the protein expressions of SIRT1,Beclin1 and p62,the LC3Ⅱ/LC3Ⅰratio,and expression levels of SIRT1 mRNA and SOX2OT(P<0.05),and these changes were obviously attenuated by SIRT1 knockdown,which also resulted in lowered 5-FU resistance of the cells without significantly affecting the expression level of SOX2OT(P>0.05).RNA pulldown assay suggested that SOX2OT could directly bind to SIRT1.Conclusion LncRNA SOX2OT enhances 5-FU resistance in HCCC-9810 cells by promoting autophagy through up-regulating SIRT1 expression.

Objective:To investigate the protective effect of folic acid on melanocytes under oxidative stress.Methods:The normal human melanocyte cell line (PIG1) was cultured in vitro and divided into 5 groups to receive corresponding treatments: control group (normal culture for 48 hours without other treatment), H 2O 2 treatment group (normal culture for 24 hours followed by the treatment with 1 mmol/L H 2O 2 for another 24 hours), and 3 folic acid pretreatment groups (pretreatment with folic acid at concentrations of 50, 125, and 250 μmol/L for 24 hours followed by the treatment with 1 mmol/L H 2O 2 for another 24 hours). The cell viability was assessed using the cell counting kit 8 (CCK8) assay, the intracellular melanin content was measured by the sodium hydroxide solubilization method, cell apoptosis rates were detected by annexin V-fluorescein isothiocyanate/propidium iodide double staining, levels of intracellular reactive oxygen species (ROS) were detected using the fluorescent probe CM-H2DCFDA, the mitochondrial membrane potential was determined using the fluorescent probe JC-1, and the mitochondrial ultrastructure was observed by transmission electron microscopy. Comparisons among multiple groups were performed using one-way analysis of variance, and multiple comparisons were performed using Tukey test. Results:Compared with the control group, the H 2O 2 treatment group showed decreased cell viability (83.62% ± 3.77% vs. 99.99% ± 5.06%, P = 0.031), intracellular melanin content (68.48% ± 4.17% vs. 100.11% ± 2.30%, P < 0.001) and mitochondrial membrane potential (2.96 ± 0.26 vs. 5.86 ± 0.56, P = 0.002), but increased cell apoptosis rate (16.35% ± 1.20% vs. 6.45% ± 1.34%, P = 0.001) and intracellular ROS level (138.98% ± 2.74% vs. 100.00% ± 0.64%, P = 0.004). Compared with the H 2O 2 treatment group, the 125-μmol/L and 250-μmol/L folic acid pretreatment groups showed increased cell viability (106.21% ± 6.34%, 101.64% ± 6.77%, respectively; both P < 0.05) and intracellular melanin content (77.24% ± 3.85%, 88.34% ± 2.65%, respectively; both P < 0.05) ; the 50-μmol/L, 125-μmol/L and 250-μmol/L folic acid pretreatment groups all showed decreased cell apoptosis rates (9.40% ± 0.99%, 9.00% ± 1.13%, 6.50% ± 0.28%, P = 0.007, 0.005, 0.001, respectively) ; the 125-μmol/L and 250-μmol/L folic acid pretreatment groups showed decreased intracellular ROS levels (112.99% ± 4.21%, 101.36% ± 10.60%, P = 0.023, 0.005, respectively), but increased mitochondrial membrane potential (4.93 ± 0.25, 5.67 ± 0.35, P = 0.012, 0.003, respectively). Transmission electron microscopy showed damaged mitochondrial ultrastructure in melanocytes in the H 2O 2 treatment group, characterized by a substantial number of vacuolated mitochondria, intimal swelling, and reduced ridges, compared with the control group; compared with the H 2O 2 treatment group, the 250-μmol/L folic acid pretreatment group exhibited decreased degree of mitochondrial damage, manifesting as reduced mitochondrial vacuolization, clearer mitochondrial ultrastructure, and slight swelling of mitochondrial ridges. Conclusion:Folic acid could reduce the oxidative stress level in melanocytes, thus protecting melanocytes from oxidative stress.