BACKGROUND:Apoptosis of islet cel s is closely related to the long-term hyperglycemia-and hyperlipemia-induced injuries. OBJECTIVE:To observe the effect of Shizidaiping formula on the apoptosis and insulin secretion in MIN6 cel s under the high glucose and lipid environment, and to explore the protective effect of Shizidaiping formula and the related apoptosis mechanism. METHODS:MIN6 cel s were divided into normal, model, melbine, low-, medium-and high-dose Shizidaiping formula groups. The cel activity was examined by cel counting kit-8, the insulin secretion was measured by ELISA, the rate of apoptosis was measured by Annexin V-FITC&PI and the expression levels of MEK1/2, ERK1/2 and p-ERK1/2 were examined by western blot assay. RESULTS AND CONCLUSION:Shizidaiping formula significantly improved MIN6 cel activity under high glucose and lipid condition (P<0.05), decreased early cel apoptosis, increased the level of insulin stimulated by low glucose in cel supernatant (P<0.05), and improved the expression levels of MEK1/2, ERK1/2 and p-ERK1/2 (P<0.05). These results suggest that Shizidaiping formula can protect islet cel s from hyperglycemia and hyperlipemia damage by improving the activity of MIN6 cel s, reducing the insulin secretion and inhibiting the apoptosis of pancreaticβcel s in MIN6 cel s.

Dermatomyofibroma is a benign and rare proliferation of myofibroblasts and fibroblasts of the skin.Dermatomyofibroma commonly locates at the shoulder and neck of young adults and adolescents.Other frequently affected anatomic sites are upper arms,thigh,chest wall,back,axillary region and abdomen.Herein,we reported a case of dermatomyofibroma occurred in the nasion.The asymptomatic firm nodule and histopathological features were consistent with dermatomyofibroma.Immunohistochemically,the tumor cells expressed vimentin,HHF35 and α-smooth muscle actin (α-SMA).The patient was followed up for 2 years after excision of the tumors and recurrences were not observed.

Objectives To analyze the changes of serum complement C1q level in patients with metabolic syndrome (MS) and investigate whether it is associated with lipid metabolism and glycometabolism. Methods In a cross-sectional study, the subjects were selected as the patients and healthy people who went to the second xiangya hospital of central south university from July 2017 to June 2018. A total of 152 MS patients were enrolled and another 90 healthy subjects were enrolled as control group. Anthropometry parameters such as body mass index (BMI), systolic blood pressure (SBP), diastolic blood pressure (DBP) were measured. Serum concentrations of C1q and other biochemical indexes including blood glucose (GLU), triglycerides (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C) were measured in all groups. The correlations between C1q and these parameters were analyzed by spearman's rho test and the clinical value of C1q in predicting MS was further evaluated by stepwise multiple linear regression analysis. Results MS group had higher serum C1q levels (244.34±62.66) mg/L compared with the control group (202.37±35.92) mg/L (t=-6.250, P=0.000). C1q levels (244.34±62.66) mg/L were positively associated with TG levels [2.34(1.89, 3.62)] mmol/L (r=0.245, P=0.001), TC levels (4.91±1.26) mmol/L (r=0.398, P=0.000), LDL-C levels (3.23±1.03) mmol/L (r=0.325, P=0.000) in MS group, While C1q levels (258.92±69.59)mg/L were positively associated with SBP (144.76 ± 22.94) mmHg (r=0.388, P=0.018), TG levels [2.65(1.87, 3.82)] mmol / L (r=0.482, P=0.003), TC levels (5.18±1.31) mmol/L (r=0.529,P=0.001) in MS patients with obesity. The stepwise multiple regression analysis showed that TG levels were independently correlated with serum C1q levels both in MS patients (β=0.302, P=0.000) and in MS patients with obesity (β=0.653, P=0.000) after adjusting for age, gender and other biochemical markers. Conclusions MS patients had higher C1q levels than healthy subjects and serum C1q levels were closely positive related to harmful lipid profiles. Serum TG level was an independent influencing factor of serum C1q in MS patients.

Androgenetic alopecia is a distinctive condition associated with genetic factors and effect of androgens, usually adversely affects the appearance and mental health of patients. This review summarizes research progress in the pathogenesis, diagnosis, evaluation and clinical treatment of androgenetic alopecia in 2020.

Humans ; Infant ; Biliary Atresia/diagnosis* ; Choledochal Cyst/diagnosis* ; RNA, Circular ; Diagnosis, Differential

Effective response to the aging of China′s population bears on the overall development of the country and the well-being of hundreds of millions of people. From the elderly social participation, intelligent media use and calm better death as the entry point actively promote healthy aging, happy aging through the community nursing, information nursing, hospice care and other perspectives. Nursing has always adhered to the people-centered, social reality needs as the guidance. It is expected to provide reference for improving the welfare construction of the broad masses of people represented by the elderly and facilitating the all-round promotion of the Healthy China strategy.

INTRODUCTION: The impact of noninvasive follicular thyroid neoplasm with papillary-like nuclear features (NIFTP) on the risk of malignancy (ROM) in fine-needle aspiration cytology (FNAC) per The Bethesda System for Reporting Thyroid Cytopathology has not been well reported in Singapore. METHODS: We retrospectively identified 821 thyroid nodules with preoperative FNAC from 788 patients out of 1,279 consecutive thyroidectomies performed between January 2010 and August 2016 in a tertiary general hospital in Singapore. Possible cases of NIFTP were reviewed for reclassification and the impact of NIFTP on ROM was analysed. RESULTS: The incidence of NIFTP was 1.2% (10 out of 821). If NIFTP is considered benign, ROM in Bethesda I through VI were 8.6%, 3.5%, 26.3%, 20.0%, 87.7%, 97.0% versus 8.6%, 4.2%, 28.1%, 26.7%, 89.2% and 100% if NIFTP is considered malignant. Eight patients with NIFTP had follow-up of 15 to 110 months. One had possible rib metastasis as evidenced by I131 uptake but remained free of structural or biochemical disease during a follow-up period of 110 months. None had lymph node metastasis at presentation, nor locoregional or distant recurrence. CONCLUSION Classifying NIFTP as benign decreased ROM in Bethesda II through VI, but the benignity of NIFTP requires more prospective studies to ascertain. The impact of NIFTP on ROM in our institution also appears to be lower than that reported in the Western studies.
Adenocarcinoma, Follicular/epidemiology* ; Humans ; Prospective Studies ; Retrospective Studies ; Singapore/epidemiology* ; Thyroid Neoplasms/epidemiology*

Increased intestinal barrier permeability, leaky gut, has been reported in patients with autism. However, its contribution to the development of autism has not been determined. We selected dextran sulfate sodium (DSS) to disrupt and metformin to repair the intestinal barrier in BTBR T⁺tf/J autistic mice to test this hypothesis. DSS treatment resulted in a decreased affinity for social proximity; however, autistic behaviors in mice were improved after the administration of metformin. We found an increased affinity for social proximity/social memory and decreased repetitive and anxiety-related behaviors. The concentration of lipopolysaccharides in blood decreased after the administration of metformin. The expression levels of the key molecules in the toll-like receptor 4 (TLR4)-myeloid differentiation factor 88 (MyD88)-nuclear factor kappa B (NF-κB) pathway and their downstream inflammatory cytokines in the cerebral cortex were both repressed. Thus, "leaky gut" could be a trigger for the development of autism via activation of the lipopolysaccharide-mediated TLR4-MyD88-NF-κB pathway.
Mice ; Animals ; NF-kappa B ; Myeloid Differentiation Factor 88/metabolism* ; Lipopolysaccharides/pharmacology* ; Toll-Like Receptor 4/metabolism* ; Autistic Disorder/metabolism* ; Signal Transduction/physiology*