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This paper deals with an initial boundary value problem for a class of nonlinear wave equation with nonlinear damping and source terms whose solution may blow up in finite time. An explicit lower bound for blow up time is determined by means of a differential inequality argument if blow up occurs. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Zhejiang University: Science B is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Purpose: Serum complement C3 has been shown to contribute to the incidence of type 2 diabetes (T2D), but how serum complement C3 affects islet β-cell function throughout the course of T2D is unclear. This study explored whether serum complement C3 is independently associated with changes in islet β-cell function over time in patients with T2D. Methods: Serum complement C3 was measured, and endogenous β-cell function was evaluated by area under the C-peptide curve (AUCcp) during an oral glucose tolerance test (OGTT) in 411 patients with T2D at baseline from 2011 to 2015. Next, 347 of those patients with available data were pooled for a final follow-up analysis from 2014 to 2018. Changes in islet β-cell function at follow-up were evaluated by AUCcp percentage changes (ΔAUCcp%). In addition, other possible clinical risks for diabetes were also examined. Results: The 347 patients included in the analysis had a diabetes duration of 4.84 ± 3.63 years at baseline. Baseline serum complement C3 (baseline C3) levels were positively correlated with baseline natural logarithm of AUCcp (lnAUCcp) (n = 347, r = 0.288, p < 0.001), and baseline C3 was independently associated with baseline lnAUCcp (β = 0.17, t = 3.52, p < 0.001) after adjustment for baseline glycemic status and other clinical confounders by multivariate liner regression analysis. Compared with the baseline values, complement C3 changes (ΔC3) and ΔAUCcp% was –0.15 ± 0.28 mg/ml and –17.2 ± 18.4%, respectively, at a follow-up visit 4.57 ± 0.78 years later. Moreover, ΔC3 was positively correlated with ΔAUCcp% (n = 347, r = 0.302, p < 0.001). Furthermore, each 0.1 mg/ml increase in ΔC3 was associated with a higher ΔAUCcp% (1.41% [95% CI, 0.82–2.00%]) after adjusting for changes in glycemic status and other clinical confounders at follow-up. Conclusions: In addition to serum complement C3 being independently associated with islet β-cell function at baseline, its changes were also independently associated with changes in islet β-cell function over time in patients with T2D. [ABSTRACT FROM AUTHOR]

Loss-aversion behaviors reflect individuals' personal preference bias when they meet uncertainties and measure the potential gains and losses of the uncertain situations before making a decision. Such behaviors are common and well documented in daily life; one example is irrational financial investments. The exact neural mechanisms for these loss-aversion behaviors have been widely discussed. In this study, we explored the neural mechanisms of loss-aversion behaviors by using voxel-based morphometry of brain regions based on two datasets. In the behavioral analysis, the degree of individual behavioral loss aversion was measured. Voxel-based morphometry analysis revealed positive correlations between the degree of individual behavioral loss aversion and grey matter volume in the superior frontal gyrus, which may be crucial neural structures for individual loss-aversion behaviors. [ABSTRACT FROM AUTHOR]

Recurrent spontaneous abortion (RSA) is a common health problem that affects 1–5% of women in reproductive age. Plenty of studies have indicated that microRNAs (miRNAs) are involved in the occurrence of miscarriage. MiR-93 has a wide range of functions in mammalian tissues and plays an important role in many diseases especially for cancers. However, it remains unknown whether miR-93 is associated with human RSA. In this report, clinical samples revealed that miR-93 expression was significantly elevated in the villi tissues of RSA patients. Upregulation of miR-93 inhibited human trophoblast cells HTR-8/SVneo cell proliferation, migration, and invasiveness, but promoted cell apoptosis in vitro. Conversely, the downregulation of miR-93 reversed these effects. Bcl-2 like protein 2 (BCL2L2), a potential target gene of miR-93, was inversely correlated with miR-93 expression in the villi of clinical samples. Furthermore, the luciferase reporter system demonstrated that miR-93 directly downregulated the expression of BCL2L2 by binding a specific sequence of its 3′-untranslated region (3′UTR). Collectively, these data strongly suggest that miR-93 regulates trophoblast cell proliferation, migration, invasive, and apoptosis by targeting BCL2L2 expression and is involved in the pathogenesis of RSA. [ABSTRACT FROM AUTHOR]

Introduction: To determine the clinical efficacy and economic value of insulin lispro 25-Prandilin 25 vs. insulin lispro 25-Humalog mix 25 in treatment of newly diagnosed type 2 diabetes mellitus (T2DM) by a continuous glucose monitoring system (CGMS).Methods: This was a single-center, randomized, case-crossover clinical trial. Participants were randomly allocated to two groups and underwent two kinds of insulin lispro 25 treatment separated by a 1-day washout period. In total, 81 patients with newly diagnosed T2DM with hemoglobin A1c (HbA1c) above 9% were hospitalized and randomly divided to receive Prandilin 25/Humalog mix 25 or Humalog mix 25/Prandilin 25 treatment. All participants were subjected to metformin therapy simultaneously. Glycemic control was reached after 7-8 days Prandilin 25 or Humalog mix 25 treatment; each patient received continuous glucose monitoring (CGM) for 5 consecutive days (from day 1 to day 5). On day 3 of CGM performance, Prandilin 25 treatment was switched to Humalog mix 25 treatment at the same dosage or vice versa. Parameters representing glycemic variability (GV) and postprandial glucose excursions, including 24-h mean blood glucose (24hMBG), 24-h standard deviation of blood glucose (24hSDBG), 24-h mean amplitude of glycemic excursion (24hMAGE), large amplitude of glycemic excursion (LAGE), incremental area under the curve (AUC) for different glucose levels, and postmeal relative areas under the CGM curve (AUCpp) for 1-4 h of each meal, were calculated for each patient.Results: No significant differences were found in the 24hMAGE, 24hMBG, 24hSDBG, LAGE, mean 1-h preprandial blood glucose and the incidence of hypoglycemia between the Prandilin 25 treatment group and Humalog mix 25 treatment group. Similarly, there were no between-treatment differences for AUC and time when blood glucose was below 3.9 mmol/l, between 3.9 mmol/l and 10.0 mmol/l, or above 10.0 mmol/l. Further analysis showed the AUCpp for 1-4 h of each meal for two kinds of treatments were similar. However, the mean estimated cost of Prandilin 25 was only 85% of Humalog mix 25 in one treatment course.Conclusion: Prandilin 25 is non-inferior in clinical efficacy compared with Humalog mix 25. In view of the significant difference in the cost of the two kinds of insulin lispro 25, Prandilin 25 is a much more cost-effective anti-diabetes drug for management of T2DM.Trial Registration: Chinese Clinical Trial Register identifier, ChiCTR1800015829. [ABSTRACT FROM AUTHOR]

Purpose: High-normal thyrotropin (TSH) is related to reduced insulin sensitivity and may contribute to glycemic disorders in diabetes. We investigated the relationship between normal serum TSH levels and glycemic variability in euthyroid type 2 diabetic patients.Methods: A total of 432 newly diagnosed type 2 diabetic patients with euthyroid function and normal serum TSH levels were recruited between March 2013 and February 2017. Insulin sensitivity was evaluated by the Matsuda index (ISIMatsuda) following a 75-g oral glucose tolerance test. Multiple glycemic variability indices, including the mean amplitude of glycemic excursions (MAGE), mean of daily differences (MODD), and standard deviation of glucose (SD), were calculated from glucose data obtained with a continuous glucose monitoring system. Average glucose accessed by 24-h mean glucose (24-h MG) was also calculated.Results: A normal serum TSH level was positively correlated with MAGE, MODD, SD, and 24-h MG (r = 0.206, 0.178, 0.186, and 0.132, respectively, p < 0.01). After adjusting for somatometric parameters, lipid profiles, ISIMatsuda, and HbA1c via multiple linear regression analysis, mean differences [B(95% CI)] in MAGE, MODD, SD, and 24-h MG between the patients in the lowest and highest quartiles of TSH levels were 0.128(0.031, 0.226), 0.085(0.022, 0.148), 0.039(0.001, 0.078), and 0.002(−0.264, 0.267) mmol/L, respectively. High-normal TSH was independently associated with MAGE, MODD, and SD, but not 24-h MG.Conclusions: High-normal serum TSH is a significant additional risk factor for increased glycemic variability in type 2 diabetic patients. [ABSTRACT FROM AUTHOR]

Purpose: Diabetic peripheral neuropathy (DPN), a common microvascular complication of diabetes, is linked to glycaemic derangements. Glycaemic variability, as a pattern of glycaemic derangements, is a key risk factor for diabetic complications. We investigated the association of glycaemic variability with DPN in a large-scale sample of type 2 diabetic patients.Methods: In this cross-sectional study, we enrolled 982 type 2 diabetic patients who were screened for DPN and monitored by a continuous glucose monitoring (CGM) system between February 2011 and January 2017. Multiple glycaemic variability parameters, including the mean amplitude of glycaemic excursions (MAGE), mean of daily differences (MODD), standard deviation of glucose (SD), and 24-h mean glucose (24-h MG), were calculated from glucose profiles obtained from CGM. Other possible risks for DPN were also examined.Results: Of the recruited type 2 diabetic patients, 20.1% (n = 197) presented with DPN, and these patients also had a higher MAGE, MODD, SD, and 24-h MG than patients without DPN (p < 0.001). Using univariate and multiple logistic regression analyses, MAGE and conventional risks including diabetic duration, HOMA-IR, and hemoglobin A1c (HbA1c) were found to be independent contributors to DPN, and the corresponding odds ratios (95% confidence interval) were 4.57 (3.48-6.01), 1.10 (1.03-1.17), 1.24 (1.09-1.41), and 1.33 (1.15-1.53), respectively. Receiver operating characteristic analysis indicated that the optimal MAGE cutoff value for predicting DPN was 4.60 mmol/L; the corresponding sensitivity was 64.47%, and the specificity was 75.54%.Conclusions: In addition to conventional risks including diabetic duration, HOMA-IR and HbA1c, increased glycaemic variability assessed by MAGE is a significant independent contributor to DPN in type 2 diabetic patients. [ABSTRACT FROM AUTHOR]

Abstract: Diabetes mellitus is one of risk factors of cardiovascular diseases including atherosclerosis. Whether and how diabetes promotes the formation of unstable atherosclerotic plaque is not fully understood. Here, we show that streptozotocin-induced type 1 diabetes reduced collagen synthesis, leading to the formation of unstable atherosclerotic plaque induced by collar placement around carotid in apolipoprotein E knockout (Apoe−/−) mice. These detrimental effects of hyperglycemia on plaque stability were reversed by metformin in vivo without altering the levels of blood glucose and lipids. Mechanistically, we found that high glucose reduced the phosphorylated level of AMP-activated protein kinase alpha (AMPKα) and the transcriptional activity of activator protein 2 alpha (AP-2α), increased the expression of miR-124 expression, and downregulated prolyl-4-hydroxylase alpha 1 (P4Hα1) protein expression and collagen biosynthesis in cultured vascular smooth muscle cells. Importantly, these in vitro effects produced by high glucose were abolished by AMPKα pharmacological activation or adenovirus-mediated AMPKα overexpression. Further, adenovirus-mediated AMPKα gain of function remitted the process of diabetes-induced plaque destabilization in Apoe−/− mice injected with streptozotocin. Administration of metformin enhanced pAP-2α level, reduced miR-124 expression, and increased P4Hα1 and collagens in carotid atherosclerotic plaque in diabetic Apoe−/− mice. We conclude that streptozotocin-induced toxic diabetes promotes the formation of unstable atherosclerotic plaques based on the vulnerability index in Apoe−/− mice, which is related to the inactivation of AMPKα/AP-2α/miRNA-124/P4Hα1 axis. Clinically, targeting AMPKα/AP-2α/miRNA-124/P4Hα1 signaling should be considered to increase the plaque stability in patients with atherosclerosis.Key messages: Hyperglycemia reduced collagen synthesis, leading to the formation of unstable atherosclerotic plaque induced by collar placement around carotid in apolipoprotein E knockout mice.Hyperglycemia destabilizes atherosclerotic plaque in vivo through an AMPKα/AP-2α/miRNA-124/P4Hα1-dependent collagen synthesis.Metformin functions as a stabilizer of atherosclerotic plaque to reduce acute coronary accent. [ABSTRACT FROM AUTHOR]

Rationale: Environmental enrichment (EE) could influence brain plasticity and behavior in rodents. Whether the early EE may predispose individuals to a particular social hierarchy in the social dominance tube test (SDTT) at adulthood is still unknown. Objective: The present study directly investigated the influence of EE on competitive success in the SDTT among adult rats. Methods: Male rats were maintained in EE from postnatal days 21 to 35. Social dominance behavior was determined by SDTT, competitive food foraging test, and mate preference test at adulthood. IBA-1 expression in the hypothalamus was examined using immunohistochemistry and western blot. Results: EE rats were prone to become submissive during a social encounter with standard environment (SE) rats in the SDTT. No difference was found in food foraging in the competitive food foraging test between SE and EE rats. Male EE rats were more attractive than the SE to the female rats in the mate preference test. IBA-1 expression was found to be decreased in the hypothalamus of EE rats compared to SE group. Infusion of a microglia inhibitor reduced percentage of forward in SE rats in the SDTT. Infusion of DNA methyltransferase inhibitor prevented the development of subordinate status in EE rats and restored the expression of IBA-1 in the hypothalamus. Conclusions: The results suggest that early EE did not lead to reduced social hierarchy in the male rat. However, EE caused a reduction in the percentage of forward in the SDTT, which might be associated with reduced number of microglia in the hypothalamus. [ABSTRACT FROM AUTHOR]

A series of Ag/TiO-NaY (TY) composite adsorbents were successfully prepared and characterized by X-ray diffraction (XRD), Fourier transform infrared (FTIR) spectroscopy, BET, scanning electron microscopy (SEM) and X-ray photoelectron spectroscopy (XPS) techniques. The effects of TiO and Ag contents on the structure and desulfurization performance of NaY zeolite were studied. The results show that anatase phase is the main form of TiO in AgTY adsorbent, and the Y-zeolite framework remained unchanged. AgTY with 6 wt % of Ag and 50 wt % of TiO exhibited the best desulfurization performance with the effluent volume of 63.2 mL/g at 10 mg/L sulfur breakthrough level (desulfurization rate of 95%). The benzothiophene (BT) removal performance of the various adsorbents follows the order: NaY < TiO < TY-50 < AgTY-50-6. The equilibrium data were modeled by Langmuir and Freundlich equations. The Langmuir model can describe well the adsorption isotherms of BT over AgTY. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Zhejiang University: Science B is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Maternal hyperglycemia in gestational diabetes mellitus (GDM), especially hyperglycemic excursions, is associated with increased risks of adverse pregnancy outcomes. Continuous glucose monitoring (CGM) system (CGMS) is better than intermittent self-measurements in detecting detailed glucose profiles on the magnitude and duration of glucose fluctuations. Hyperglycemia resulted from impaired β cell function. This study analyzed the characteristics of glycemic variability in GDM with 24-28 gestational weeks and its association with β cell function. Thirty GDM with 24-28 gestational weeks (GDM group) were included in this study, and 20 normal gestational women (NGW group) and 20 normal glucose regulation non-pregnant women (NGRW group) were set as controls. The three groups were monitored using the CGMS for consecutive 72 h. The parameters of glycemic variability included the standard deviation of blood glucose (SDBG), mean of continuous 24-h blood glucose (MBG), mean amplitude of glycemic excursions (MAGEs), and mean of daily differences (MODDs). Homeostasis model assessments were applied to access the insulin resistance (HOMA-IR). The early insulinogenic index (ΔI30/ΔG30) and the area under the curve of insulin (AUCI180) derived from 75-g oral glucose tolerance test were applied to evaluate the early-phase insulin secretion and second-phase insulin secretion, respectively. After CGM, MAGE and MBG value increased progressively from NGRW, NGW to GDM group ( p < 0.05); MODD and SDBG values of GDM group were all higher than those of NGRW and NGW groups ( p < 0.05), but there are no differences in MODD and SDBG between NGRW and NGW groups ( p > 0.05). After comparison of β cell function, ΔI30/ΔG30 decreased progressively from NGRW, NGW to GDM group ( p < 0.05); HOMA-IR and AUCI180 increased progressively from NGRW, NGW to GDM group ( p < 0.05). MAGE value was correlated with ΔI30/ΔG30 and HOMA-IR in GDM group ( r = −0.78 and 0.65, respectively, p < 0.05). Multiple linear stepwise regression analysis showed that ΔI30/ΔG30 and HOMA-IR were the independent factors of MAGE ( β = −0.61, 0.34, respectively, p < 0.05). Glycemic variability in GDM was higher than in normal pregnant women, and glycemic variability evaluated by MAGE correlates well with impaired early-phase insulin secretion in GDM. Further large-scale studies are needed to formulate treatment strategies to make up for the impaired early-phase insulin secretion and flat glycemic variability, and analyze the association between pregnancy outcomes improvement and glycemic variability remission in GDM. [ABSTRACT FROM AUTHOR]

Previous studies suggested patients with bipolar depressive disorder (BDd) or unipolar depressive disorder (UDd) have cerebral metabolites abnormalities. These abnormalities may stem from multiple sub-regions of gray matter in brain regions. Thirteen BDd patients, 20 UDd patients and 20 healthy controls (HC) were enrolled to investigate these abnormalities. Absolute concentrations of 5 cerebral metabolites (glutamate-glutamine (Glx), N-acetylaspartate (NAA), choline (Cho), myo-inositol (mI), creatine (Cr), parietal cortex (PC)) were measured from 4 subregions (the medial frontal cortex (mPFC), anterior cingulate cortex (ACC), posterior cingulate cortex (PCC), and parietal cortex (PC)) of gray matter. Main and interaction effects of cerebral metabolites across subregions of gray matter were evaluated. For example, the Glx was significantly higher in BDd compared with UDd, and so on. As the interaction analyses showed, some interaction effects existed. The concentrations of BDds' Glx, Cho, Cr in the ACC and HCs' mI and Cr in the PC were higher than that of other interaction effects. In addition, the concentrations of BDds' Glx and Cr in the PC and HCs' mI in the ACC were statistically significant lower than that of other interaction effects. These findings point to region-related abnormalities of cerebral metabolites across subjects with BDd and UDd. [ABSTRACT FROM AUTHOR]