Objective:To investigate the effects of acute sleep deprivation (ASD) on hippocampal glucose metabolism and neuroinflammation in rat models.Methods:Twenty SD rats (10 males and 10 females) were divided into four groups (five in each group) by random sampling method: female ASD group, male ASD group, female control group, and male control group. Among them, the ASD group constructed the ASD model. After 72h sleep deprivation, all rats underwent 18F-FDG and N, N-diethyl-2-(2-(4-(2- 18F-fluoroethoxy)phenyl)-5, 7-dimethylpyrazolo[1, 5-a]pyrimidin-3-yl)acetamide ( 18F-DPA-714) microPET/CT brain imaging in 2d to compare the changes of 18F-FDG and 18F-DPA-714 SUV mean in the hippocampus of rats. Brain histopathology, immunohistochemistry and immunofluorescence staining were detected in rats. Independent-sample t test was used to analyze the data. Results:18F-FDG imaging showed the hippocampal SUV mean between ASD group and control group (female: 4.11±0.35 vs 1.89±0.28; male: 3.43±0.47 vs 2.02±0.54) were statistically significant ( t values: 9.65, 3.92, P values: <0.001, 0.002). 18F-DPA-714 imaging showed the hippocampal SUV mean between ASD group and control group (females: 0.28±0.01 vs 0.28±0.02; male: 0.26±0.02 vs 0.31±0.04) were not statistically significant ( t values: -0.18, -2.24, P values: 0.859, 0.056). The 18×10 3 translocator protein (TSPO) immunohistochemistry showed the expression in the hippocampal region of the brain between ASD group and control group (female: 0.19±0.02 vs 0.19±0.01; male: 0.21±0.01 vs 0.20±0.01) were not statistically different ( t values: -0.48, -1.67, P values: 0.651, 0.139). Immunofluorescence staining showed that microglial cytosol in the hippocampal region of the brain decreased after 72h of ASD, and the protrusion points and surrounding branches were significantly reduced. Conclusion:Increased hippocampal glucose metabolism in rats is observed after 72 h of ASD without significant neuroinflammation.

Objective:To investigate the effects of acute sleep deprivation (ASD) on hippocampal glucose metabolism and neuroinflammation in rat models.Methods:Twenty SD rats (10 males and 10 females) were divided into four groups (five in each group) by random sampling method: female ASD group, male ASD group, female control group, and male control group. Among them, the ASD group constructed the ASD model. After 72h sleep deprivation, all rats underwent 18F-FDG and N, N-diethyl-2-(2-(4-(2- 18F-fluoroethoxy)phenyl)-5, 7-dimethylpyrazolo[1, 5-a]pyrimidin-3-yl)acetamide ( 18F-DPA-714) microPET/CT brain imaging in 2d to compare the changes of 18F-FDG and 18F-DPA-714 SUV mean in the hippocampus of rats. Brain histopathology, immunohistochemistry and immunofluorescence staining were detected in rats. Independent-sample t test was used to analyze the data. Results:18F-FDG imaging showed the hippocampal SUV mean between ASD group and control group (female: 4.11±0.35 vs 1.89±0.28; male: 3.43±0.47 vs 2.02±0.54) were statistically significant ( t values: 9.65, 3.92, P values: <0.001, 0.002). 18F-DPA-714 imaging showed the hippocampal SUV mean between ASD group and control group (females: 0.28±0.01 vs 0.28±0.02; male: 0.26±0.02 vs 0.31±0.04) were not statistically significant ( t values: -0.18, -2.24, P values: 0.859, 0.056). The 18×10 3 translocator protein (TSPO) immunohistochemistry showed the expression in the hippocampal region of the brain between ASD group and control group (female: 0.19±0.02 vs 0.19±0.01; male: 0.21±0.01 vs 0.20±0.01) were not statistically different ( t values: -0.48, -1.67, P values: 0.651, 0.139). Immunofluorescence staining showed that microglial cytosol in the hippocampal region of the brain decreased after 72h of ASD, and the protrusion points and surrounding branches were significantly reduced. Conclusion:Increased hippocampal glucose metabolism in rats is observed after 72 h of ASD without significant neuroinflammation.

BACKGROUND: Congenital scoliosis (CS) is a complex spinal malformation of unknown etiology with abnormal bone metabolism. Fibroblast growth factor 23 (FGF23), secreted by osteoblasts and osteocytes, can inhibit bone formation and mineralization. This research aims to investigate the relationship between CS and FGF23. METHODS: We collected peripheral blood from two pairs of identical twins for methylation sequencing of the target region. FGF23 mRNA levels in the peripheral blood of CS patients and age-matched controls were measured. Receiver operator characteristic (ROC) curve analyses were conducted to evaluate the specificity and sensitivity of FGF23. The expression levels of FGF23 and its downstream factors fibroblast growth factor receptor 3 (FGFr3)/tissue non-specific alkaline phosphatase (TNAP)/osteopontin (OPN) in primary osteoblasts from CS patients (CS-Ob) and controls (CT-Ob) were detected. In addition, the osteogenic abilities of FGF23-knockdown or FGF23-overexpressing Ob were examined. RESULTS: DNA methylation of the FGF23 gene in CS patients was decreased compared to that of their identical twins, accompanied by increased mRNA levels. CS patients had increased peripheral blood FGF23 mRNA levels and decreased computed tomography (CT) values compared with controls. The FGF23 mRNA levels were negatively correlated with the CT value of the spine, and ROCs of FGF23 mRNA levels showed high sensitivity and specificity for CS. Additionally, significantly increased levels of FGF23, FGFr3, OPN, impaired osteogenic mineralization and lower TNAP levels were observed in CS-Ob. Moreover, FGF23 overexpression in CT-Ob increased FGFr3 and OPN levels and decreased TNAP levels, while FGF23 knockdown induced downregulation of FGFr3 and OPN but upregulation of TNAP in CS-Ob. Mineralization of CS-Ob was rescued after FGF23 knockdown. CONCLUSIONS Our results suggested increased peripheral blood FGF23 levels, decreased bone mineral density in CS patients, and a good predictive ability of CS by peripheral blood FGF23 levels. FGF23 may contribute to osteopenia in CS patients through FGFr3/TNAP / OPN pathway.
Humans ; Osteopontin/genetics* ; Alkaline Phosphatase/metabolism* ; Receptor, Fibroblast Growth Factor, Type 3/metabolism* ; Scoliosis/genetics* ; Osteoblasts/metabolism* ; Calcinosis ; RNA, Messenger/metabolism* ; Bone Diseases, Metabolic/metabolism* ; Fibroblast Growth Factors/genetics*

Polycystic ovary syndrome (PCOS) is a common gynecological endocrine disease, mostly associated with menstrual disorders, obesity, anovulation, etc., and 50%-70% with insulin resistance (IR), its pathogenesis is still unclear. Gut microbiota is a microecosystem involved in the occurrence and development of diseases as an environmental factor. A number of studies have shown that gut microbiota is closely related to the occurrence of PCOS. This paper summarizes the correlation between gut microbiota and IR-PCOS, and summarizes the mechanism of gut microbiota in IR-PCOS through low-grade inflammation, oxidative stress, DNA methylation and glucolipid metabolism, so as to provide new ideas for clinical diagnosis and treatment.

Polycystic ovary syndrome (PCOS) is a common gynecological endocrine disease, mostly associated with menstrual disorders, obesity, anovulation, etc., and 50%-70% with insulin resistance (IR), its pathogenesis is still unclear. Gut microbiota is a microecosystem involved in the occurrence and development of diseases as an environmental factor. A number of studies have shown that gut microbiota is closely related to the occurrence of PCOS. This paper summarizes the correlation between gut microbiota and IR-PCOS, and summarizes the mechanism of gut microbiota in IR-PCOS through low-grade inflammation, oxidative stress, DNA methylation and glucolipid metabolism, so as to provide new ideas for clinical diagnosis and treatment.

This study aimed to investigate the protective effect of total alkaloids(TA)and one of the active components, neotuberostemonine, of Stemona tuberosa on bleomycin-induced pulmonary fibrosis in mice and to explore the mechanism by fibroblasts model. The bleomycin-induced mice were orally administered with TA(60 mg/kg)and neotuberostemonine(10, 20 mg/kg), with prednisone(6. 67 mg/kg)as a positive control. The anti-fibrotic effects were assessed by hydroxyproline content, TGF-β1 level, inflammatory score, collagen deposition and the expression of α-SMA in the lung tissues. The results revealed that TA and neotuberostemonine could significantly ameliorate the inflammation and injury, and attenuate the hydroxyproline content and collagen deposition. Moreover, neotuberostemonine treatment markedly down-regulated the α-SMA level and TGF-β1 content in bleomycin-injured mice lungs. The in vitro experiments showed that neotuberostemonine inhibited the expression of α-SMA induced by TGF-β1 in a dose-dependent manner, indicating that suppression on differentiation of fibroblasts to myofibroblasts may be one of the mechanisms for neotuberostemonine against pulmonary fibrosis.

Objective To investigate the relationship between the polymorphisms of angiotensin Ⅱ receptor gene and the risk of primary aldosteronism (PA).Methods Polymerase chain reaction -restriction fragment length polymorphism (PCR -RFLP)was used to examine the 1 1 66A /C polymorphism of AT1 R gene and 1 675A /G poly-morphism of AT2R gene in 85 patients with PA and 1 00 healthy controls.Results There was no significant difference of AT1 R 1 1 66A /C genotypes (AA,AC,CC)and allele (A and C)frequency among patients and controls (χ2 =0.430,P =0.806).There was obvious difference of AT2R 1 675A /G genotypes (AA,AG,GG)and allele (A and G) frequency among two groups (χ2 =6.1 21 ,P =0.01 3).The G allele was higher than A allele in PA group (χ2 =6.767,P =0.009).Conclusion Homogenic mutation of 1 675A /G site in AT2R gene may be one of risk factors of PA.