Augmented cardiac growth hormone signaling contributes to cardiomyopathy following genetic disruption of the cardiomyocyte circadian clock

Circadian clocks regulate numerous biological processes, at whole body, organ, and cellular levels. This includes both hormone secretion and target tissue sensitivity. Although growth hormone (GH) secretion is time-of-day-dependent (increased pulse amplitude during the sleep period), little is known regarding whether circadian clocks modulate GH sensitivity in target tissues. GH acts in part through induction of insulin-like growth factor 1 (IGF1), and excess GH/IGF1 signaling has been linked to pathologies such as insulin resistance, acromegaly, and cardiomyopathy. Interestingly, genetic disruption of the cardiomyocyte circadian clock leads to cardiac adverse remodeling, contractile dysfunction, and reduced lifespan. These observations led to the hypothesis that the cardiomyopathy observed following cardiomyocyte circadian clock disruption may be secondary to chronic activation of cardiac GH/IGF1 signaling. Here, we report that cardiomyocyte-specific BMAL1 knockout (CBK) mice exhibit increased cardiac GH sensitivity, as evidenced by augmented GH-induced STAT5 phosphorylation (relative to littermate controls) in the heart (but not in the liver). Moreover

Impact of obesity on day-night differences in cardiac metabolism

An intrinsic property of the heart is an ability to rapidly and coordinately adjust flux through metabolic pathways in response to physiologic stimuli (termed metabolic flexibility). Cardiac metabolism also fluctuates across the 24-hours day, in association with diurnal sleep-wake and fasting-feeding cycles. Although loss of metabolic flexibility has been proposed to play a causal role in the pathogenesis of cardiac disease, it is currently unknown whether day-night variations in cardiac metabolism are altered during disease states. Here, we tested the hypothesis that diet-induced obesity disrupts cardiac diurnal metabolic flexibility , which is normalized by time-of-day-restricted feeding. Chronic high fat feeding (20-wk)-induced obesity in mice, abolished diurnal rhythms in whole body metabolic flexibility, and increased markers of adverse cardiac remodeling (hypertrophy, fibrosis, and steatosis). RNAseq analysis revealed that 24-hours rhythms in the cardiac transcriptome were dramatically altered during obesity; only 22% of rhythmic transcripts in control hearts were unaffected by obesity. However, day-night differences in cardiac substrate oxidation were essentially identical in control and high fat fed mice. In contrast, day-night differences in both cardiac triglyceride synthesis and lipidome were abolished during obesity. Next, a subset of obese mice (induced by 18-wks ad libitum high fat feeding) were allowed access to the high fat diet only during the 12-hours dark (active) phase, for a 2-wk period. Dark phase restricted feeding partially restored whole body metabolic flexibility, as well as day-night differences in cardiac triglyceride synthesis and lipidome. Moreover, this intervention partially reversed adverse cardiac remodeling in obese mice. Collectively, these studies reveal diurnal metabolic inflexibility of the heart during obesity specifically for nonoxidative lipid metabolism (but not for substrate oxidation), and that restricting food intake to the active period partially reverses obesity-induced cardiac lipid metabolism abnormalities and adverse remodeling of the heart

Abdominal emergencies performed in general surgery department

Background: Abdominal surgical emergencies constitute a significant portion of a surgeon’s clinical experience and often present with diagnostic and treatment challenges. The present study evaluated various abdominal emergencies performed in general surgery department. Materials & Methods: 158 patients undergone abdominal emergencies performed in general surgery department of both genderswere enrolled. Parameters such as organ system involved, operation performed, initial diagnosis in the emergency room, final diagnosis, and outcome of treatment was recorded. Results: Out of 158 patients, males were 90 and females were 68. Surgeries were performed on liver in 12, lung in 5, small bowel in 27, pancreas in 10, stomach in 20, biliaryin15,rectumin 8, hernia in 19, esophagus in 4, spleen in 12, appendix in 17 and ovaries in 9 patients. Postoperative complications were abscess in 24, bleeding in 15, anastomotic leaks in 5 and anastomotic perforationsin 2. Mortality seen in patients undergoing surgery for small bowel in 5, pancreas in 2, stomach in 4, biliary in 3, rectumin 1, hernia in 1, spleen in 2 and appendix in 1. Conclusion: Common involved organs were liver, lung, small bowel, pancreas, stomach, biliary, rectum, hernia, esophagus, spleen, appendix and ovaries

Early enteral nutrition versus parenteral nutrition after resection of esophageal cancer

Background: Esophagectomy for esophageal cancer is one of the most invasive procedures among gastrointestinal surgeries, and patients undergoing esophagectomy are unable to gain nutrition by mouth within the first few days after surgery. The present study compared early enteral nutrition versus parenteral nutrition after resection of esophageal cancer. Materials & Methods: 52 cases of esophageal cancer of both genders were divided into EEN group and PNgroup. Each group Comprised of 26 each. Factors such as site of lesion, pathologic stage, time to first fecal passage, post-operative albumin infusion, differences of serum albumin value, hospital stay, systematic inflammatory response syndrome (SIRS) duration and mortality was recorded. Results: Group I comprised of 18 males and 8 females and group II 14 males and 12 females. Site of lesions was upper thoracic in 12and 11, middle thoracic in 9 and 10 and lower thoracic in 5 and 5 in group I and group II respectively. Pathologic stage was 0 seen in 1 and 2, I in 4 and 6, II in 12 and 10, III in 6 and 6 and IV in 3 and 2 in group I and group II respectively. Preoperative adjuvant therapy was neoadjuvant in 15 and 16 and chemoradiotherapy in 11 and 10 in group I and group II respectively. The mean preoperative serum albumin (g/L) was 33.5 and 34.2, first fecal passage (day) was 2.7 and 3.8, hospital stay (day) was 16.2 and 18.7, albumin infusion (g) was 30.5 and 40.3, SIRS duration (day) was 3.4 and 4.7 and in-hospital mortality was seen in 1 and 2 in group I and group II respectively. The difference was significant (P< 0.05). Conclusion: Early EN is safe, economic, and superior for promoting early recovery of intestinal movement

Effect of Chronic Western Diets on Non-Alcoholic Fatty Liver of Male Mice Modifying the PPAR-γ Pathway via miR-27b-5p Regulation

Western diets contribute to metabolic diseases. However, the effects of various diets and epigenetic mechanisms are mostly unknown. Here, six week-old C57BL/6J male and female mice were fed with a low-fat diet (LFD), high-fat diet (HFD), and high-fat high-fructose diet (HFD-HF) for 20 weeks. We determined that HFD-HF or HFD mice experienced significant metabolic dysregulation compared to the LFD. HFD-HF and HFD-fed male mice showed significantly increased body weight, liver size, and fasting glucose levels with downregulated PPARγ, SCD1, and FAS protein expression. In contrast, female mice were less affected by HFD and HFD-HF. As miR-27b contains a seed sequence in PPARγ, it was discovered that these changes are accompanied by male-specific upregulation of miR-27b-5p, which is even more pronounced in the HFD-HF group (p < 0.01 vs. LFD) compared to the HFD group (p < 0.05 vs. LFD). Other miR-27 subtypes were increased but not significantly. HFD-HF showed insignificant changes in fibrosis markers when compared to LFD. Interestingly, fat ballooning in hepatocytes was increased in HFD-fed mice compared to HFD-HF fed mice, however, the HFD-HF liver showed an increase in the number of small cells. Here, we concluded that chronic Western diet-composition administered for 20 weeks may surpass the non-alcoholic fatty liver (NAFL) stage but may be at an intermediate stage between fatty liver and fibrosis via miR-27b-5p-induced PPARγ downregulation

Single walled carbon nanotubes decorated vanadyl phthalocyanine composite for electrochemical oxygen reduction in fuel cells

821-825Vanadyl phthalocyanine (VOPc) has been immobilized on single walled carbon nanotubes by the adsorption process and characterized using UV-vis spectroscopy, infrared spectroscopy and X-ray diffraction techniques. Electrochemical characterization of VOPc immobilized SWCNTs (SWCNTs-VOPc) has been done by coating an aqueous colloid of SWCNTs-VOPc on glassy carbon electrode (represented as GC/SWCNTs-VOPc). GC/SWCNTs-VOPc exhibits a pair of peaks at –265 and –97 mV (at 20 mV s-1 in 0.1 M H2SO4) due to the characteristic redox process, VIV/III of VOPc. Further, electrocatalytic reduction of oxygen is analysed using GC/SWCNTs-VOPc electrode by cyclic voltammetry. GC/SWCNTs-VOPc electrode efficiently reduces oxygen in 0.1 M H2SO4 with a low onset potential of 0.16 V. Also, GC/SWCNTs-VOPc exhibits significant storage stability, retaining 91% of its original catalytic reduction current after 10 days storage at room temperature in air and dry conditions