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Exploring economic, scalable, and highly efficient carbon materials for the oxygen reduction reaction (ORR) is of great significance to a variety of renewable energy conversion and storage technologies. Herein, we directly convert soya peptone as a carbon precursor to a series of mesoporous nanocarbon-based materials for the ORR via a one-step pyrolysis process combined with the help of ZnCl2 as an activator. Benefiting from the effective chemical activation effect during carbonization, the optimal electrocatalysts possess mesoporous structures and high surface area (>1000 m2 g−1) which favor fast mass transport, electron transfer, and exposure of abundant active sites. Remarkably, the electrocatalysts show a comparable ORR catalytic performance, excellent stability, and superior methanol tolerance, comparable to the commercial Pt/C catalyst. Thus, soya peptone biomass derived carbon materials are surely helpful for providing a new space to develop ORR electrocatalysts.

Nowadays, bacterial resistance has continued to be a troublesome issue caused by the abuse of antibiotics, and it is the paramount difficulty in resolving the bacterial proliferation and infection. In this study, fresh lotus leaf was treated with Zn

The design and preparation of highly efficient and durable electrocatalysts for the oxygen reduction reaction (ORR) and the oxygen evolution reaction (OER) is essential due to their applications in many green energy conversion devices, such as fuel cells and rechargeable metal–air batteries. Herein, we report a Co/Co9S8 composite catalyst, which is coupled with reduced graphene oxide (rGO) and multi-walled carbon nanotubes (MWCNTs) via a combined hydrothermal reaction with a calcination method. Benefiting from the unique porous scaffold structures and synergistic interactions between rGO/MWCNT and Co/Co9S8, the electrocatalyst (Co/Co9S8/rGO/MWCNT-800) exhibits high electrochemical activity for the ORR, showing a four-electron oxygen reduction pathway with an onset potential of 0.946 V (vs. RHE) in alkaline medium. Meanwhile, the electrocatalyst shows high electrochemical stability, excellent selectivity and methanol tolerance over the commercial Pt/C. It also exhibits good overall oxygen electrode activity (ΔE = EOER,10 − EORR,1/2 of 890 mV). The present work highlights a potential general strategy for developing carbon-based transition metal sulfide nanocomposites as cathodes with better performance in the ORR/OER.

A graphene quantum dots (GQDs) and horse radish peroxidase (HRP) hybrid system was designed for the sensing of alkaline phosphatase (ALP) activity and inhibitor screening. We found that the photoluminescence (PL) intensity of GQDs could be quenched efficiently in the presence of phenol, H2O2 and HRP. Moreover, ALP could hydrolyze disodium phenyl phosphate (DPP) to produce phenol, and also could result in the photoluminescence quenching of GQDs. The decrease in the PL intensity was linear to the activity of ALP in the concentration range of 0.02 - 0.8 U/L, with a detection limit of 0.008 U/L. The proposed GQDs/HRP hybrid system was successfully applied to ALP determination in human serum samples. The inhibition study was further analyzed, and Na3VO4 (as an ALP inhibitor) showed a clear inhibition effect. The results suggest that the GQDs/HRP hybrid system has good potential applications for the assay of ALP activity and inhibitors screening in related biochemical fields.

This work analyzes the suboptimal health (subhealth) status of Chinese software programmers in 2017 and reveals its major causes. By using the Chinese subhealth evaluation scale (CSHES), programmers from China were invited to participate in the designed survey. On the basis of the analysis of the programmer's score in terms of the CSHES, the data were processed with a logistic regression model and analyzed to reveal the major causes of subhealth. The data analysis results show that the Chinese programmers' subhealth issue in 2017 is mainly induced by metabolic disorders, depression, pressure, satisfaction, and the quality of their sexual life. Through this survey based on a data-mining study, Chinese programmers can clearly understand their own health status through their own subhealth characterization, discover their own possible causes of subhealth status, develop a healthy lifestyle in accordance with the corresponding symptoms, and improve their health level.

In this contribution, a high-performance bifunctional electrocatalyst composed of Co/Co2P nanoparticles encapsulated in nitrogen and phosphorus co-doped carbon nanotubes (NPCNTs) has been synthesized via a mechanochemistry-pyrolysis approach. The Schottky effect of metal-semiconductor heterojunction affords a built-in electric field at the interfaces to enhance electron transport, whereas the intertwined structure of one-dimensional (1D) NPCNTs facilitates the mass transfer of reactants and intermediates. Therefore, the as-prepared Co/Co2P@NPCNTs catalyst exhibits outstanding bifunctional ORR/OER activities, which are superior to those of commercial Pt/C and RuO2. It can also deliver a high power density and cycling life when used as the cathode for rechargeable ZABs. Theoretical calculation confirms that the spontaneous electron transport from Co to Co2P enables an up-shifted d-band center of Co/Co2P heterojunctions, which is beneficial for the intermediate adsorption in electrocatalytic process.

Timely knowing glucose level helps diabetic patients to manage the disease, including decisions about food, physical activity and medication. This study compared two continuous glucose monitoring systems in conscious and moving-free nonhuman primates (NHPs, Macaca fascicularis). Each normoglycemic or diabetic monkey was implanted with one Dexcom G4 Platinum subcutaneously or one HD-XG glucose sensor arterially for glucose monitoring. The glucose levels measured by both telemetry devices significantly correlated with the glucometer readings. The data of oral glucose tolerance test (oGTT) showed that the glucose levels measured by either Dexcom G4 Platinum or HD-XG transmitter were very similar to glucometer readings. However, compared to HD-XG transmitter or glucometer, Dexcom G4 Platinum detected a decreased glucose peak of ivGTT with approximately 10 min delay due to interstitial glucose far behind blood glucose change. Our data showed the advantages of the telemetry systems are: (1) consecutive data collection (day and night); (2) no bleeding; (3) no anesthesia (moving freely); (4) recording natural response without physical restriction and stress; (5) less labor intensity during ivGTT and other tests; (6) quick outcomes without lab tests. This article summarized and compared the differences of the general characteristics of two continuous glucose monitoring systems in diabetic research.

A novel multifunctional semiconducting polymer dot (Pdots)/pyrogallic acid (PA) system was successfully established for fluorescence sensing of urea, urease, and pesticides. The Pdots/PA system was pH controllable, emitting strong fluorescence at pH 6.0. However, in an alkaline environment, PA transformed into its quinone structure, which is an efficient fluorescence quencher, resulting in fluorescence quenching of the Pdots/PA system. Furthermore, urea was hydrolyzed in the presence of urease, releasing hydroxyl groups that transformed PA into its quinone structure, resulting in fluorescence quenching of the Pdots/PA system. Therefore, a sensitive detection method for urea and urease was developed. The limits of detection for urea and urease were 0.02 mM and 0.08 U L−1, respectively. Pesticides, such as dimethoate, were able to inhibit the urease activity, resulting in recovery of the fluorescence intensity of the Pdots/PA system. Therefore, the fluorescence turn-on detection of pesticides could be also achieved. A satisfactory result was obtained when using the system to detect pesticides in fruit and vegetable samples.

A facile fluorescence turn-on approach for the detection of l -ascorbic acid (AA) and alkaline phosphatase (ALP) activity was designed based on graphene quantum dots (GQDs). It is found that the fluorescence intensity of GQDs can be efficiently quenched by para-benzoquinone (BQ). And a turn-on fluorescence signal can be observed if BQ is reduced by AA. In addition, ALP can hydrolyze l -ascorbic acid-2-phosphate (AAP) to produce AA, which also results in the recovery of the GQDs fluorescence. The recovered fluorescence intensity of GQDs was proportional to the concentration of AA or ALP in the concentration ranges of 5.0 × 10−7 to 2.0 × 10−5 mol/L and 1.0–90 U/L, respectively. The detection limit for AA and ALP were 2.0 × 10−7 mol/L and 0.45 U/L. The established method showed a high selectivity for ALP activity compared with other interference components. Furthermore, the detection system as a fluorescence probe has great potential in the development of sensors for widely detecting various analytes with AA producing process.

In this paper, a simple and specific graphene quantum dots (GQDs)-based fluorescent biosensor adopted for the determination of glucose based on the combination of the enzyme-coupled method and fluorescence quenching mechanism is demonstrated. Glucose was oxidized by the enzyme glucose oxidase (GOx), forming hydrogen peroxide (H 2 O 2 ) via the catalysis by horseradish peroxidase (HRP). H 2 O 2 was then employed to oxidize phenol to quinone, which led to effective quenching effect in the GQDs&ndash, GOx&ndash, HRP&ndash, phenol system. By optimizing the reaction conditions of the GQDs-enzyme system, a linear relationship between the concentration of glucose and the fluorescence intensity over a range of 0.2&ndash, 10 &mu, mol/L was obtained. The limit of detection for glucose is 0.08 &mu, mol/L. The present biosensor for the determination of glucose showed satisfactory reproducibility and accuracy in human serum samples. Since the enzymes have high specificity and unique affinity to the certain substance, the enzyme-coupled system promises a sensitive way for further detection of those chemicals which could be oxidized by enzymes and generated H 2 O 2 or glucose. GQDs and other fluorescent materials coupled with several enzymes can be applied to extensive sensing field.

Purpose: Patients with obesity and type 2 diabetes (T2D) are more susceptible to the occurrence of nonalcoholic fatty liver disease (NAFLD)/steatohepatitis (NASH). Although liver biopsy is still reviewed as a gold standard for the diagnosis, due to its invasiveness, high cost and variable readouts, it has limited application in large scale clinical investigation and long term following up the therapeutic benefits. This study was to apply a clinically used noninvasive echography to quantitatively evaluate the NAFLD/NASH model in dysmetabolic nonhuman primates. Method: Noninvasive echography with computer-assisted imaging analysis was used to quantify hepatic pathological changes in 36 cynolmolgus monkeys at different dysmetabolic stage. Result: Both hepatic/renal echo-intensity ratio (H/R=1.69 ± 0.12 vs 1.36 ± 0.09) and hepatic echo-intensity attenuation rate (HA=25.7 ± 5.7 vs 12.0 ± 3.2 kHz/cm) were significantly higher in obese (n=14) compared to control (n=22) monkeys, which were highly correlated with multiple metabolic risks such as obese, hyperlipidemia and liver fibrosis indices including body mass index (BMI), Alanine/Aspartate Transaminase (AST/ALT) and diabetes (BARD) score, fibrosis-4 (FIB4), AST to platelet ratio index (APRI), etc. Postmortem examination of liver biopsy tissue revealed liver pathology resembling human NAFLD/NASH and higher triglycerides (245 ± 26 vs 101 ± 32 mg/100 g tissue) in diabetic than control monkeys. Conclusion: The data demonstrate for the first time that obese, dysmetabolic and diabetic monkeys can develop NAFLD/NASH assembling to human disease. The noninvasive and quantitative echography along with the nonhuman primate model can be used as a powerful translational tool for following-up disease progression, and evaluation of novel therapies for NAFLD/NASH both clinically and pre-clinically.

Effects of betatrophin on β-cell proliferation and insulin secretion have been reported controversially in rodent studies. This study was to investigate the dynamic changes of betatrophin and its potential effect on β-cell function in non-human primates (NHPs). Blood betatrophin levels in naturally developed diabetes cynomolgus monkeys (n=65) significantly correlated with their body weights and blood glucose levels in the females (n=20) and with insulin and C-peptide levels in the males (n=45). Liver expression of betatrophin mRNA was markedly higher in spontaneously developed diabetes monkeys than in normoglycemic ones. Its liver expression correlated well with islet size and insulin content in normoglycemic cynomolgus monkeys and also well in spontaneously hyperglycemic (>200 mg/ dL) cynomolgus monkeys with high blood insulin level, but not well in those with very low blood insulin content. Both blood glucose and betatrophin increased dramatically in normoglycemic rhesus monkeys (n=7) after streptozocin (STZ) administration. Blood insulin initially increased on day 1 after STZ dosing and then decreased dramatically. Two NHPs with blood glucose back to ~80 mg/mL on day 14 after STZ injection showed recovery of insulin secretion. In another two STZ-treated NHPs with blood glucose >250 mg/dL, apparent proliferation of both β-cells and non-β- cells was observed in their islets. The rest NHPs with more completed β-cell destruction after STZ dosing showed much higher blood glucose (>300 mg/dL) with very low insulin and no obvious β-cell proliferation. Our results indicate that NHP liver expresses abundant betatrophin mRNA. As its levels correlated well with islet size and insulin content in some diabetic NHPs, it might play a role in β-cell proliferation. Our data are consistent with the clinical finding of the elevation of circulating betatrophin in patients with type 2 diabetes. In addition, betatrophin-enhanced β-cell proliferation seems requiring a minimal base level of pancreatic β-cells and islets.

Background Diabetes is one of the major risk factors for cardiomyopathy and heart failure with reduced ejection fraction (EF) and highly associated with left ventricular (LV) dysfunction in human. This study aimed 1) to noninvasively assess cardiac function using echocardiography; 2) to test the hypothesis that like diabetic human, cardiac function may also be compromised; in spontaneously developed obese, dysmetabolic and diabetic nonhuman primates (NHPs). Methods Cardiovascular functions were measured by noninvasive echocardiography in 28 control, 20 dysmetabolic/pre-diabetic and 41 diabetic cynomolgus monkeys based on fasting blood glucose and other metabolic status. Results The LV end-systolic volume (ESV) was higher while end-diastolic volume (EDV, 12 ± 5.7 mL) and EF (63 ± 12.8 %) significantly lower in the diabetic compared to control (14 ± 7 mL and 68 ± 9.8 %) group, respectively. The E/A ratio of LV trans-mitral peak flow rate during early (E) over late (A) diastole was significantly lower in the diabetic (1.19 ± 0.45) than control (1.44 ± 0.48) group. E-wave deceleration time (E DT) was prolonged in the diabetic (89 ± 41 ms) compared to control (78 ± 26 ms) group. Left atrial (LA) maximal dimension (LADmax) was significantly greater in the diabetic (1.3 ± 0.17 cm) than control (1.1 ± 0.16 cm) group. Biochemical tests showed that total cholesterol and LDL were significant higher in the diabetic (167 ± 63 and 69 ± 37 mg/dL) than both pre-diabetic (113 ± 37 and 41 ± 23 mg/dL) and control (120 ± 28 and 41 ± 17 mg/dL) groups, respectively. Multivariable logistic regression analysis demonstrated that LV systolic (reduced EF) and diastolic (abnormal E/A ratio) dysfunctions are significantly correlated with aging and hyperglycemia. Histopathology examination of the necropsy heart revealed inflammatory infiltration, cardiomyocyte hypertrophy and fragmentation, indicating the myocardial ischemia and remodeling which is consistent with the LV dysfunction phenotype. Conclusions Using noninvasive echocardiography, the present study demonstrated for the first time that dysmetabolic and diabetic NHPs are associated with LV systolic (increased ESV, decreased EF, etc.) and diastolic (decreased EDV and E/A ratio, prolonged E DT, etc.) dysfunctions, accompanied by LA hypertrophic remodeling (increased LADmax), the phenotypes similarly to those found in diabetic patients. Thus, spontaneously developed dysmetabolic and diabetic NHPs is a highly translatable model to human diseases not only in the pathogenic mechanisms but also can be used for testing novel therapies for cardiometabolic disorders.

Obesity is viewed as one of the most serious public health issues of this century, which is likely due to economic growth, urbanization, modernization, life-style change and decreased physical activity. In 2013, the American Medical Association classified obesity as a disease. Sustained excessive accumulation of body fat to the extent, such as overweight or obesity, can reduce life expectancy and increase health risks, particularly heart disease and type 2 diabetes. Cardiovascular, diabetes and other health problems of obesity have been studied for many decades. Inflammation, mitochondrial dysfunction, hyperinsulinemia, lipotoxicity, medical and others, such as genetic background and aging, may result in obesity. However, the underlying precise mechanisms have yet to be elucidated further. Various obesity animal models have been used and induced for obesity research and therapy. To better understand the pathophysiology of human obesity, corpulent nonhuman primates (NHPs) are useful models due to resembling humans, not only physiologically but in eating habits (bored-eat). NHP obesity models have been developed and used for delineating molecular and cellular mechanisms and for testing new novel therapies, which provides critical pre-clinic information for drug discovery. We recently published the data obtained from naturally occurring diabetes NHPs. This article summarizes the data collected from a large scale of naturally occurring and high calorie (fat) diet (HCD)-induced obesity monkeys housed in our facility. Manuscript for another NHP model, streptozocin-induced diabetes, developed in our facility will follow lately.

Insulin-resistant diabetes (Type 2 diabetes mellitus, T2DM) is one of the main comorbidities of obesity and is the most common form of diabetes. T2DM and obesity dynamically influence each other and often escalate patients’ other health issues. Cardiovascular, renal and other health consequences of obesity and diabetes have been studied for several decades. However, the underlying precise mechanisms and interactions of obesity and insulin-resistant diabetes have yet to be elucidated further. It has been recognized that sustained greater energy intake than expenditure is the main cause of obesity that can potentially lead to insulin resistance and diabetes due to excessive fat accumulation. To better understand the pathophysiology of human obesity and diabetes, nonhuman primate (NHP) models have been used for research to delineate molecular and cellular mechanisms because of the similarity of the metabolic diseases between NHP and humans. Also, NHP models have been well used for testing new novel therapies, which provides critical pre-clinic information for drug discovery. This article summarizes the data collected from a large scale of the naturally occurring diabetes monkeys housed in our facility. Manuscripts for other NHP models, such as diet-induced dyslipidemia and dysglycemia and streptozocin-induced diabetes, developed in our facility will follow lately.

Although Type 2 Diabetes Mellitus (T2DM) is well characterized Non-Human Primate (NHP), the phenotypes of diabetic nephropathy, and its molecular mechanisms are not well studied in NHPs. Diabetic nephropathy in cynomolgus macaques with spontaneous dysmetabolism (Pre-DM, n=19) and diabetes (DM, n=20) were compared with normal controls (N, n=11). There were 9 NHPs with albuminuria (>42 mg/day) in the DM (45%), only 1 in Pre-DM and none in N group. The renal function measured by estimated glomerular filtration rate (eGFR) was not significantly different among the 3 groups, indicating that these NHPs were in an early stage of renal disease. From these NHPs, 3 N, 3 Pre-DM without albuminuria and 6 DM with albuminuria were selected for transcriptome analysis of kidney biopsies. There were 95 differentially expressed genes (DEGs) detected amongst the 3 groups, of which, 75DEGs between the N and DM related to diabetic nephropathy; 66 DEGs between the N and Pre-DM related to dysmetabolism without nephropathy; 68 DEGs between N and both Pre-DM & DM related to dsymetabolism; but only 1 nephropathy specific gene (LCT lactase) between the DM with albuminuria (DM) and Pre-DM without albuminuria; only 4 DEGs between the DM with albuminuria and both N & Pre-DM without albuminuria specific to nephropathy. Signaling pathway analysis of the relevant DEGs and encoded proteins highlighted the role of a kidney failure, renal and urological diseases, and inflammatory diseases related network, in which the most pivotal gene in this network is Tumor Necrosis Factor (TNF), indicating that nephropathy is a disease closely related to inflammation and cell death. Thus, the present study was the first detailed characterization of the diabetic nephropathy phenotypes and the kidney histopathological changes in NHPs and provided molecular insights into novel mechanisms of disease progression, potential new drug targets as well as specific diagnostic biomarkers.

Background The α2-adrenoceptor agonist xylazine as an anesthetic has been widely used either alone or in combination with other anesthetics, such as ketamine, in veterinary clinic and research. In the last decade xylazine has been used in drug abusers in certain geographic area. This study investigated the effects of xylazine on blood glucose level and insulin secretion in normoglycemic and insulin-dependent diabetic monkeys. Methods Both adult cynomolgus (n = 10) and rhesus (n = 8) monkeys with either sex were used in the study. Xylazine (1–2 mg/kg) was administrated intramuscularly. Blood glucose, insulin, glucagon and glucagon-like peptide 1 in overnight-fasted monkeys were measured immediately before and after xylazine administration. The hyperinsulinemic-euglycemic clamp method was used in the study for assessing the potential mechanism of xylazine-induced hyperglycemia. Results Xylazine administration increased the blood glucose levels from 58 ± 3 to 108 ± 12 mg/dL in normoglycemic (n = 5, p

Background Quantitation of β-cell function is critical in better understanding of the dynamic interactions of insulin secretion, clearance and action at different phases in the progression of diabetes. The present study aimed to quantify β-cell secretory function independently of insulin sensitivity in the context of differential metabolic clearance rates of insulin (MCRI) in nonhuman primates (NHPs). Methods Insulin secretion rate (ISR) was derived from deconvolution of serial C-peptide concentrations measured during a 5 stage graded glucose infusion (GGI) in 12 nondiabetic (N), 8 prediabetic or dysmetabolic (DYS) and 4 overtly diabetic (DM) cynomolgus monkeys. The characterization of the monkeys was based on the fasting glucose and insulin concentrations, glucose clearance rate measured by intravenous glucose tolerance test, and insulin resistance indices measured in separate experiments. The molar ratio of C-peptide/insulin (C/I) was used as a surrogate index of hepatic MCRI. Results Compared to the N monkeys, the DYS with normal glycemia and hyperinsulinemia had significantly higher basal and GGI-induced elevation of insulin and C-peptide concentrations and lower C/I, however, each unit of glucose-stimulated ISR increment was not significantly different from that in the N monkeys. In contrast, the DM monkeys with β-cell failure and hyperglycemia had a depressed GGI-stimulated ISR response and elevated C/I. Conclusions The present data demonstrated that in addition to β-cell hypersecretion of insulin, reduced hepatic MCRI may also contribute to the development of hyperinsulinemia in the DYS monkeys. On the other hand, hyperinsulinemia may cause the saturation of hepatic insulin extraction capacity, which in turn reduced MCRI in the DYS monkeys. The differential contribution of ISR and MCRI in causing hyperinsulinemia provides a new insight into the trajectory of β-cell dysfunction in the development of diabetes. The present study was the first to use the GGI and C-peptide deconvolution method to quantify the β-cell function in NHPs.