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Aims: The aim of this study was to investigate the relationship between resting energy expenditure (REE) based on equation estimation and renal outcomes in patients with diabetes kidney disease (DKD). Methods: A total of 124 patients were enrolled from a retrospective cohort of Type 2 Diabetes mellitus (T2DM) patients with biopsy-proven DKD. Renal outcome defined as End-Stage Renal Disease (ESRD). To compare the predictive ability of different REE estimation equations on ESRD. Patients' REE was assessed according to the estimating equation with the best predictive power, and then the relationship between REE and ESRD risk was fitted using a restricted cubic spline curve (RCS) plot and REE cutoff values were obtained. Grouping using cutoff values, and ultimately evaluate the relationship between REE and the risk of ESRD using a Multivariate Cox regression model. Results: The strongest predictive validity for renal outcomes was the NDCKD-equation. The patients were divided into the higher-REE group (n = 78) and the lower-REE group (n = 46), based on the cutoff value. During the follow-up, 30 of 124 patients (24.2%) proceeded to ESRD. Multivariate Cox regression models showed that the risk of ESRD in patients with lower REE was 6.08 times increased compared with that in those with higher REE (HR = 6.08; 95% CI, 1.28-28.80, p = 0.023). Conclusion: These findings suggested that the lower REE was an independent risk factor for unfavorable renal outcomes in patients with DKD. [ABSTRACT FROM AUTHOR]

Background Endoplasmic reticulum (ER) stress and autophagy each play important roles in hepatocyte cell injury. We hypothesized that gene expression of C/EBP-homologous protein (CHOP) and the BH3 proteins Bcl2-interacting mediator of cell death (BIM) and BH3-interacting domain death agonist (BID) are involved in a complex interplay that regulates ER stress-induced autophagy and cell death. Materials and methods Hepatocytes were cultured from lean Zucker rats. Confluent hepatocytes were incubated with single or combined small interfering RNA for CHOP, BIM, and/or BID for 24 h providing gene inhibition. Incubation with tunicamycin (TM) for another 24 h stimulated ER stress. Quantitative real-time polymerase chain reaction determined the expression levels of CHOP, BIM, and BID. Immunostaining with microtubule-associated protein 1 light chain 3 measured autophagy activity. Trypan blue exclusion determined the cell viability. Results TM treatment increased the messenger RNA levels of CHOP and BIM but decreased the messenger RNA levels of BID. TM increased autophagy and decreased cell viability. Individual inhibition of CHOP, BIM, or BID protected against autophagy and cell death. However, simultaneous treatment with any combination of CHOP, BIM, and BID small interfering RNAs reduced autophagy activity but increased cell death independent of ER stress induction. [ABSTRACT FROM AUTHOR]

Converging lines of evidence show that a sizable subset of autism-spectrum disorders (ASDs) is charac-terized by increased blood levels of serotonin (5-hydroxytryptamine, 5-HT), yet the mechanistic link between these two phenomena remains unclear. The enzymatic degradation of brain 5-HT is mainly mediated by monoamine oxidase (MAO)A and, in the absence of this enzyme, by its cognate isoenzyme MAOB. MAOA and A/B knockout (KO) mice display high 5-HT levels, particularly during early devel-opmental stages. Here we show that both mutant lines exhibit numerous behavioural hallmarks of ASDs, such as social and communication impairments, perseverative and stereotypical responses, behavioural inflexibility, as well as subtle tactile and motor deficits. Furthermore, both MAOA and A/B KO mice displayed neuropathological alterations reminiscent of typical ASD features, including reduced thickness of the corpus callosum, increased dendritic arborization of pyramidal neurons in the prefrontal cortex and disrupted microarchitecture of the cerebellum. The severity of repetitive responses and neuropathological aberrances was generally greater in MAOA/B KO animals. These findings suggest that the neurochemical imbalances induced by MAOA deficiency (either by itself or in conjunction with lack of MAOB) may result in an array of abnormalities similar to those observed in ASDs. Thus, MAOA and A/B KO mice may afford valuable models to help elucidate the neurobiological bases of these disorders and related neuro-developmental problems. [ABSTRACT FROM AUTHOR]

Selective serotonin reuptake inhibitors (SSRIs), such as citalopram (CTM), have been widely prescribed for major depressive disorder, not only for adult populations, but also for children and pregnant mothers. Recent evidence suggests that chronic SSRI exposure in adults increases serotonin (5-HT) levels in the raphe system and decreases norepinephrine (NE) locus ceruleus (LC) neural activity, suggesting a robust opposing interaction between these two monoamines. In contrast, perinatal SSRI exposure induces a long-lasting downregulation of the 5-HT-raphe system, which is opposite to that seen with chronic adult treatment. Therefore, the goal of the present investigation was to test the hypothesis that perinatal CTM exposure (20 mg/kg/d) from postnatal day 1 (PN1) to PN10 leads to hyperexcited NE-LC circuit function in adult rats (>PN90). Our single-neuron LC electrophysiological data demonstrated an increase in spontaneous and stimulus-driven neural activity, including an increase in phasic bursts in CTM-exposed animals. In addition, we demonstrated a corresponding immunoreactive increase in the rate-limiting catalyzing catecholamine enzyme (tyrosine hydroxylase) within the LC and their neocortical target sites compared to saline controls. Moreover, these effects were only evident in male exposed rats, suggesting a sexual dimorphism in neural development after SSRI exposure. Together, these results indicate that administration of SSRIs during a sensitive period of brain development results in long-lasting alterations in NE-LC circuit function in adults and may be useful in understanding the etiology of pervasive developmental disorders such as autism spectrum disorder. [ABSTRACT FROM AUTHOR]

For clarifying the influence of fresh acid and residual acid on the corrosion performance of tubing materials and the adaptability of materials in an acid fracturing environment in a certain oil field， the corrosion damage development trend， pitting sensitivity in the whole process of acidizing and corrosion morphology characteristics of P110 and C110 tubing materials under different conditions were analyzed by corrosion weight loss method and three-dimensional stereo optical microscope observation， and the acidizing corrosion inhibitor was optimized.Results showed that as the acidification temperature of fresh acid gradually increased， the degree of material corrosion tends to increased.When the temperature was ≥180 ℃， the average corrosion rate of C110 was vcorr ＝127.7 g/(m2·h)， while the average corrosion rate of P110 was vcorr ＝407.0 g/(m2·h)， which is much higher than the index requirement.When the simulated fresh acid temperature was 100 ℃，pitting nucleation occurred on the material surface.As the temperature increased， the pitting sensitivity gradually increased.In the residual acid environment at ultra-high temperature of 180 ℃， both C110 and P110 materials suffered extremely severe corrosion.Furthermore， the corrosion inhibitor in the acidizing fluid component was obviously ineffective under high temperature conditions， resulting in serious corrosion damage to the pipes in the residual acid flowback environment.The optimized modified manene alkali acidizing corrosion inhibitor significantly slowed down the corrosion rate of the material through the formation of a multilayer adsorption film， and the corrosion inhibition rate was 89.4%in a high temperature fresh acid environment at 180 ℃.

Described herein are findings in a 58-year-old man in whom necropsy disclosed origin of the left vertebral artery (or the arteria thryoidea ima) directly from the aortic arch. No functional consequences resulted. Study of previous publications disclosed the frequency of this anomaly in adults to be approximately 3.5%. Dissection has been reported to be more frequent in the left vertebral artery when it arises directly from the aorta than when it arises from the left subclavian artery. [ABSTRACT FROM AUTHOR]

We describe an aortic arch anomaly consisting of the origin of the left subclavian artery as the fourth branch and the right subclavian artery as the first branch off the aortic arch with crisscrossing of these two arteries anterior to the trachea without clinical consequences. This anomaly, to our knowledge, has not been reported previously. [ABSTRACT FROM AUTHOR]

Background: Disturbance of circadian rhythm leads to abnormalities in bile acid (BA) and lipid metabolism, and it is of great significance to explore the relationship between them. This study explored the effects of circadian dysregulation on the rhythms of intestinal BA metabolism. Method: Period circadian clock 1/period circadian clock 2 (Per1/Per2) double gene knockout (DKO) and wildtype (WT) male C57BL/6 mice were fed with a control or high-fat diet for 16 weeks. We measure plasma parameters of mice. Pathological changes including those in liver and intestine were detected by hematoxylin and eosin (H&E) and oil O staining. Western blot was used to detect the intestinal core rhythm protein clock circadian regulator (CLOCK), nuclear receptor subfamily 1, group D, member 1 (REV-ERBα), Farnesoid X receptor (FXR), Small heterodimer partner (SHP), and Fibroblast growth factor 15 (FGF15) expressions. We analyzed the bile acid and intestinal flora profile in the mice intestine tissues by BA-targeted metabolomics detection and high-throughput sequencing. Results: Rhythmic chaos affected lipid metabolism and lipid accumulation in mice liver and intestine, and diurnal fluctuations of plasma triglycerides (TGs) were absent in normal-feeding DKO mice. The normal circadian fluctuations of the CLOCK and REV-ERBα observed in wild mice disappeared (normal diet) or were reversed (high-fat diet) in DKO mice. In WT mice intestine, total BA and conjugated BA were affected by circadian rhythm under both normal and high-fat diets, while these circadian fluctuations disappeared in DKO mice. Unconjugated BA seemed to be affected exclusively by diet (significantly increased in the high-fat group) without obvious fluctuations associated with circadian rhythm. Correlation analysis showed that the ratio of conjugated/unconjugated BA was positively correlated with the presence of Bacteroidetes and displayed a circadian rhythm. The expression levels of BA receptor pathway protein FXR, SHP, and FGF15 were affected by the ratio of conjugated/unconjugated BA. Conclusion: Bacteroidetes-related diurnal changes to intestinal ratios of conjugated/unconjugated BA have the potential to regulate diurnal fluctuations in liver BA synthesis via FXR-FGF15. The inverted intestinal circadian rhythm observed in DKO mice fed with a high-fat diet may be an important reason for their abnormal circadian plasma TG rhythms and their susceptibility to lipid metabolism disorders. [ABSTRACT FROM AUTHOR]