Do industrial robots reduce carbon intensity? The role of natural resource rents and corruption control.

Although the research on the impact of robotics on carbon emissions is increasing, there are still relatively few studies on the impact of robots on carbon intensity from the perspective of natural resources and corruption. In order to fill in the research gaps, panel data from 66 countries between 1993 and 2018 are collected, and linear and nonlinear panel regression approaches are developed. Natural resource rent and corruption control are used as threshold variables, robot penetration is used as explanatory variables, and carbon emission intensity is the explained variable. The results of the linear model show that robot penetration is negatively correlated with carbon emission intensity, which means that robot penetration reduces carbon emission intensity. The results of the nonlinear model show that when natural resource rents and corruption control are used as thresholds, the relationship between robot penetration and carbon emission intensity presents a U shape and an inverted U shape, respectively. Specifically, the threshold for natural resource rents is 4.7%. When the natural resource rent is lower than this threshold, the robot penetration rate reduces the carbon emission intensity, but when the natural resource rent is higher than this threshold, the robot penetration rate increases the carbon emission intensity. The threshold value of corruption control is -0.4349. When the corruption control is lower than this threshold, the robot penetration rate increases the carbon emission intensity. If the corruption control is higher than this threshold, the robot reduces the carbon emission intensity. Finally, policy recommendations for better use of robotics to reduce carbon emission intensity are put forward from the perspective of natural resource rent and corruption control.

The Role of Osteocalcin in Placental Function in Gestational Diabetes Mellitus.

Evidence for the role of osteocalcin in glucose metabolism is increasing. The aim of this study was to examine the associations between osteocalcin and gestational diabetes mellitus. Thirteen discovery study subjects and 76 reduplication study subjects were recruited from the Maternal and Child Health Hospital Guangxi Zhuang Autonomous Region from May 2018 to August 2018. Total osteocalcin and biochemical indices of maternal serum and umbilical vein serum were analyzed. Placental tissue samples were used for transcriptome sequencing. For the discovery study subjects, the total osteocalcin concentration in umbilical vein serum was significantly higher than that in maternal serum and umbilical artery serum (55.32 ng/mL ± 17.37 vs. 12.06 ng/mL ± 5.42 [P < 0.001] vs. 38.31 ng/mL ± 11.52 [P < 0.01]), suggesting that trophoblasts may synthesize osteocalcin. In a reduplication subject study, the gestational diabetes mellitus group had lower umbilical vein serum total osteocalcin (51.46 ng/mL ± 24.29 vs. 67.00 ng/mL ± 25.33, P = 0.008), lower adiponectin (1099.72 µg/L ± 102.65 vs. 1235.85 µg/L ± 94.63, P < 0.001). Spearman's correlation analysis showed that umbilical vein serum total osteocalcin levels were closely correlated with leptin (r = -0.456, P = 0.007). A coexpression model of the placental RNA sequence was constructed. Two modules were correlated with osteocalcin, and the Gene ontology pathways of these modules were rich in glucose and lipid metabolism. In conclusion, the placenta may synthesize osteocalcin by itself, and a lower osteocalcin level in umbilical vein serum is associated with gestational diabetes mellitus.

Effects of Adiponectin on T2DM and Glucose Homeostasis: A Mendelian Randomization Study.

PURPOSE: The associations of adiponectin with type 2 diabetes mellitus (T2DM), glucose homeostasis (including ß-cell function index (HOMA-ß), insulin resistance (HOMA-IR), fasting insulin (FI) and fasting glucose (FG)) have reported in epidemiological studies. However, the previous observational studies are prone to biases, such as reverse causation and residual confounding factors. Herein, a Mendelian Randomization (MR) study was conducted to determine whether causal effects exist among them. MATERIALS AND AND METHODS: Two-sample MR analyses and multiple sensitivity analyses were performed using the summary data from the ADIPOGen consortium, MAGIC Consortium, and a meta-analysis of GWAS with a considerable sample of T2DM (62,892 cases and 596,424 controls of European ancestry). We got eight valid genetic variants to predict the causal effect among adiponectin and T2DM and glucose homeostasis after excluding the probable invalid or pleiotropic variants. RESULTS: Adiponectin was not associated with T2DM (odds ratio (OR) = 1.004; 95% confidence interval (CI): 0.740, 1.363) when using MR Egger after removing the invalid SNPs, and the results were consistent when using the other four methods. Similar results existed among adiponectin and HOMA-ß, HOMA-IR, FI, FG. CONCLUSION: Our MR study revealed that adiponectin had no causal effect on T2DM and glucose homeostasis and that the associations among them in observational studies may be due to confounding factors.

Assessment Causality in Associations Between Serum Uric Acid and Risk of Schizophrenia: A Two-Sample Bidirectional Mendelian Randomization Study.

PURPOSE: Although increasing lines of evidence showed associations between serum uric acid (UA) levels and schizophrenia, the causality and the direction of the associations remain uncertain. Thus, we aimed to assess whether the relationships between serum UA levels and schizophrenia are causal and to determine the direction of the association. PATIENTS AND METHODS: Two-sample bidirectional Mendelian randomization (MR) analyses and various sensitivity analyses were performed utilizing the summary data from genome-wide association studies within the Global Urate Genetics Consortium and the Psychiatric Genomics Consortium. Secondary MR analyses in both directions were conducted within summary data using genetic risk scores (GRSs) as instrumental variables. RESULTS: Three MR methods provided no causal relationship between serum UA and schizophrenia. Furthermore, GRS approach showed similar results in the three MR methods after adjustment for heterogeneity. By contrast, inverse variance weighted method, weighted median and GRS approach suggested a causal effect of schizophrenia risk on serum UA after adjustment for heterogeneity (per 10-symmetric percentage increase in schizophrenia risk, beta: -0.039, standard error (SE): 0.013, P = 0.003; beta: -0.036, SE: 0.018, P = 0.043; beta: -0.039, SE: 0.013, P = 0.002; respectively). Moreover, in both directions' analyses, the heterogeneity and sensitivity tests suggested no strong evidence of bias due to pleiotropy. CONCLUSION: Schizophrenia may causally affect serum UA levels, whereas the causal role of serum UA concentrations in schizophrenia was not supported by our MR analyses. These findings suggest that UA may be a useful potential biomarker for monitoring treatment or diagnosis of schizophrenia rather than a therapeutic target for schizophrenia.

Oil tea improves glucose and lipid levels and alters gut microbiota in type 2 diabetic mice.

Oil tea has traditionally been used in minority populations in China for treating various ailments in traditional Chinese medicine. Individually, green tea and ginger, which are the main ingredients of oil tea, have demonstrated antidiabetic effects; however, whether oil tea exerts antidiabetic effects remains unknown. In addition, aberrant gut microbiota structure is associated with diabetic status, and research indicates that there may be beneficial effects of tea on gut microbiota. Therefore, we hypothesized that oil tea exerts antidiabetic effects and induces alteration in gut microbiota. To test our hypothesis, we first examined the nutrition composition of oil tea. Then, db/db mice were randomly divided into 3 groups and orally gavaged with saline, metformin, and oil tea for 8 weeks. Fasting blood glucose (FBG), oral glucose tolerance test (OGTT), and lipid levels were tested during the experiment. 16S rRNA genes were sequenced and changes in gut microbiota in response pre/post treatment were examined. Our experiments showed that oil tea contains high concentrations of tea polyphenols (246.35 mg/100 g) and [6]-gingerol (2.98 mg/100 g). It appeared that oil tea treatment significantly suppressed the postprandial blood glucose elevation and lowered the levels of FBG, total cholesterol, triglycerides, and LDL-cholesterol (P < .05). The composition of gut microbiota changed significantly in response to oil tea treatment, Lachnospiraceae were significantly enriched (q < 0.05, LDA score> 3.5). Redundancy analysis identified 155 oil tea-modulating family level phylotypes, where Lachnospiraceae significantly correlated with FBG, total cholesterol, and LDL-cholesterol (P < .05). Our findings demonstrate that oil tea improved glucose and lipid levels and modulated gut microbiota in db/db mice.