Transcript levels of 4 genes in umbilical cord blood are predictive of later autism development: a longitudinal follow-up study.

BACKGROUND: Over recent decades, autism spectrum disorder (ASD) has been of increasing epidemiological importance, given the substantial increase in its prevalence; at present, clinical diagnosis is possible only after 2 years of age. In this study, we sought to develop a potential predictive model for ASD screening. METHODS: We conducted a longitudinal follow-up study of newborns over 3 years. We measured transcript levels of 4 genes (superoxide dismutase-2 [SOD2], retinoic acid-related orphan receptor-α [RORA], G protein-coupled estrogen receptor-1 [GPER], progesterone receptor [PGR]), 2 oxidative stress markers and epigenetic marks at the RORA promoter in case-control umbilical cord blood mononuclear cell (UCBMC) samples. RESULTS: We followed 2623 newborns; we identified 41 children with ASD, 63 with delayed development and 2519 typically developing children. We matched the 41 children with ASD to 41 typically developing children for UCBMC measurements. Our results showed that children with ASD had significantly higher levels of H3K9me3 histone modifications at the RORA promoter and oxidative stress in UCBMC than typically developing children; children with delayed development showed no significant differences. Children with ASD had significantly lower expression of SOD2, RORA and GPER, but higher PGR expression than typically developing children. We established a model based on these 4 candidate genes, and achieved an area under the curve of 87.0% (standard deviation 3.9%) with a sensitivity of 1.000 and specificity of 0.854 to predict ASD in UCBMC. LIMITATIONS: Although the gene combinations produced a good pass/fail cut-off value for ASD evaluation, relatively few children in our study sample had ASD. CONCLUSION: The altered gene expression in UCBMC can predict later autism development, possibly providing a predictive model for ASD screening immediately after birth.

Application of the Improved Clustering Algorithm in Operating Room Nursing Recommendation under the Background of Medical Big Data.

The nursing work in the operating room has the characteristics of long time, strong technicality, and heavy work, which have an important influence on the quality of the operation. Operating room nursing recommendations based on data mining technology can solve a series of practical problems in clinical nursing and nursing management. This paper selects the clustering algorithm in commonly used data mining technology as the research object and actually analyzes the impact of this algorithm in operating room nursing recommendations. At this stage, there is little research on data mining technology in the field of nursing in China. This paper aims to provide new ideas for the field of nursing research by exploring the actual application in the field of nursing.

Puerarin ameliorates hyperglycemia in HFD diabetic mice by promoting ß-cell neogenesis via GLP-1R signaling activation.

BACKGROUND: Diabetes is characterized by ß-cell loss and dysfunction. A strategy for diabetes treatment is to promote new ß-cell formation. Puerarin is an isoflavone from the root of Pueraria lobata (Willd.) Ohwi. Our previous study demonstrated puerarin could ameliorate hyperglycemia in diabetic mice. However, related mechanisms and potential roles of puerarin in ß-cell neogenesis have not been elucidated. PURPOSE: The present study aims to investigate whether anti-diabetic effect of puerarin is dependent on promoting ß-cell neogenesis via GLP-1R signaling activation. METHODS: A high-fat diet (HFD) induced diabetic mouse model was applied to investigate effects of puerarin in vivo, exendin-4 (GLP-1R agonist) and metformin were used as positive controls. Moreover, related mechanisms and GLP-1R downstream signal transduction were explored in isolated cultured mouse pancreatic ductal cells. RESULTS: Puerarin improved glucose homeostasis in HFD diabetic mice significantly. Markers of new ß-cell formation (insulin, PDX1 and Ngn3) were observed in pancreatic ducts of HFD mice treated by puerarin. Of note, efficacy of puerarin in vivo was suppressed by GLP-1R antagonist exendin9-39, but enhanced by exendin-4 respectively. In cultured mouse pancreatic ductal cells, puerarin induced expressions of insulin and PDX1, upregulated GLP-1R expression and activated ß-catenin and STAT3 subsequently. Expressions of insulin and PDX1 in ductal cells could be blocked by exendin9-39, or ß-catenin inhibitor ICG001, or JAK2 inhibitor AG490. CONCLUSION: These data clarified puerarin ameliorated hyperglycemia of HFD mice via a novel mechanism involved promoting ß-cell neogenesis. Our finding highlights the potential value of puerarin developing as an anti-diabetic agent.

Salidroside, A Natural Antioxidant, Improves ß-Cell Survival and Function via Activating AMPK Pathway.

Aim: The enhanced oxidative stress contributes to progression of type 2 diabetes mellitus (T2DM) and induces ß-cell failure. Salidroside is a natural antioxidant extracted from medicinal food plant Rhodiola rosea. This study was aimed to evaluate protective effects of salidroside on ß-cells against diabetes associated oxidative stress. Methods and Results: In diabetic db/db and high-fat diet-induced mice, we found salidroside ameliorated hyperglycemia and relieved oxidative stress. More importantly, salidroside increased ß-cell mass and ß-cell replication of diabetic mice. Mechanism study in Min6 cells revealed that, under diabetic stimuli, salidroside suppressed reactive oxygen species production and restore mitochondrial membrane potential (ΔΨm) via reducing NOX2 expression and inhibiting JNK-caspase 3 apoptotic cascade subsequently to protect ß-cell survival. Simultaneously, diabetes associated oxidative stress also activated FOXO1 and triggered nuclear exclusion of PDX1 which resulted in ß-cell dysfunction. This deleterious result was reversed by salidroside by activating AMPK-AKT to inhibit FOXO1 and recover PDX1 nuclear localization. The efficacy of salidroside in improving ß-cell survival and function was further confirmed in isolated cultured mouse islets. Moreover, the protective effects of salidroside on ß-cells against diabetic stimuli can be abolished by an AMPK inhibitor compound C, which indicated functions of salidroside on ß-cells were AMPK activation dependent. Conclusion: These results confirmed beneficial metabolic effects of salidroside and identified a novel role for salidroside in preventing ß-cell failure via AMPK activation. Our finding highlights the potential value of Rhodiola rosea as a dietary supplement for diabetes control.