Dietary self-efficacy: determinant of compliance behaviours and biochemical outcomes in haemodialysis patients

Background. Despite the diversity of proposed theories, researchers are still unable to fully explain dietary compliance behaviours of dialysis patients. Dietary self-efficacy, a concept less studied in dialysis, has been linked to positive compliance outcomes in the chronic illness literature. Therefore, the aim of the present research was to determine how dietary self-efficacy is related to selected biochemical markers and self-reported behavioural outcomes in haemodialysis patients. Methods. 107 subjects participated in a cross-sectional study. Four questionnaires assessed dietary self-efficacy, compliance attitudes and behaviours, and staff-patient relationships. Laboratory outcomes were retrospectively obtained from patients' medical records and averaged for the previous 6 months. Results. Of the behavioural measures, only dietary self-efficacy was associated with laboratory outcomes. Dietary self-efficacy was also positively related to staff-patient relationships and to patients' self-reported assessment of compliance behaviours. Women had greater dietary self-efficacy than men. The number of family members living with the respondent was inversely related to dietary self-efficacy. Conclusions. Results indicated that dietary self-efficacy determined both behaviours and laboratory outcomes. Patients with greater dietary self-efficacy had lower serum potassium and weight gain, showed favourable compliance attitudes and behaviours toward prescribed regimens and fostered better relationships with staff. Based on these findings we recommend an experimental approach to clarify whether maximizing dietary self-efficacy efforts is without psychological burden to patients and whether the positive effect of increased dietary self-efficacy is maintained in long-term dialysis patient

Bidirectional Relationship Between Reduced Blood pH and Acute Pancreatitis: A Translational Study of Their Noxious Combination

Acute pancreatitis (AP) is often accompanied by alterations in the acid-base balance, but how blood pH influences the outcome of AP is largely unknown. We studied the association between blood pH and the outcome of AP with meta-analysis of clinical trials, and aimed to discover the causative relationship between blood pH and AP in animal models. PubMed, EMBASE, and Cochrane Controlled Trials Registry databases were searched from inception to January 2017. Human studies reporting systemic pH status and outcomes (mortality rate, severity scores, and length of hospital stay) of patient groups with AP were included in the analyses. We developed a new mouse model of chronic metabolic acidosis (MA) and induced mild or severe AP in the mice. Besides laboratory blood testing, the extent of pancreatic edema, necrosis, and leukocyte infiltration were assessed in tissue sections of the mice. Thirteen studies reported sufficient data in patient groups with AP (n = 2,311). Meta-analysis revealed markedly higher mortality, elevated severity scores, and longer hospital stay in AP patients with lower blood pH or base excess (P < 0.001 for all studied outcomes). Meta-regression analysis showed significant negative correlation between blood pH and mortality in severe AP. In our mouse model, pre-existing MA deteriorated the pancreatic damage in mild and severe AP and, vice versa, severe AP further decreased the blood pH of mice with MA. In conclusion, MA worsens the outcome of AP, while severe AP augments the decrease of blood pH. The discovery of this vicious metabolic cycle opens up new therapeutic possibilities in AP

Ferritin Light Chain Confers Protection Against Sepsis-Induced Inflammation and Organ Injury

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Adverse Impact of Diet-Induced Hypercholesterolemia on Cardiovascular Tissue Homeostasis in a Rabbit Model: Time-Dependent Changes in Cardiac Parameters

The present study evaluates a hypothesis that diet-related hypercholesterolemia increases oxidative stress-related burden to cardiovascular tissue, resulting in progressively increased mortality, along with deterioration of electrophysiological and enzymatic function in rabbit myocardium. New Zealand white rabbits were divided into four groups, defined as follows: GROUP I, cholesterol-free rabbit chow for 12 weeks; GROUP II, cholesterol-free chow, 40 weeks; GROUP III, chow supplemented with 2% cholesterol, 12 weeks; GROUP IV, chow supplemented with 2% cholesterol, 40 weeks. At the 12 and 40 weeks time points, animals in each of the aforementioned cohorts were subjected to echocardiographic measurements, followed by sacrifice. Significant deterioration in major outcome variables measured in the present study were observed only in animals maintained for 40 weeks on 2% cholesterol-supplemented chow, with much lesser adverse effects noted in animals fed high cholesterol diets for only 12 weeks. It was observed that rabbits receiving high cholesterol diets for 40 weeks exhibited significantly increased mortality, worsened ejection fraction and general deterioration of cardiac functions, along with increased atherosclerotic plaque formation and infarct size. Additionally, myocardium of GROUP IV animals was observed to contain lower levels of heme oxygenase-1 (HO-1) and cytochrome c oxidase III (COX III) protein relative to the controls

Secretion of VEGF-165 has unique characteristics, including shedding from the plasma membrane

Vascular endothelial growth factor (VEGF) is a critical regulator of endothelial cell differentiation and vasculogenesis during both development and tumor vascularization. VEGF-165 is a major form that is secreted from the cells via a poorly characterized pathway. Here we use green fluorescent protein- and epitope-tagged VEGF-165 and find that its early trafficking between the endoplasmic reticulum and the Golgi requires the small GTP-binding proteins Sar1 and Arf1 and that its glycosylation in the Golgi compartment is necessary for efficient post-Golgi transport and secretion from the cells. The relative temperature insensitivity of VEGF secretion and its Sar1 and Arf1 inhibitory profiles distinguish it from other cargoes using the "constitutive" secretory pathway. Prominent features of VEGF secretion are the retention of the protein on the outer surface of the plasma membrane and the stimulation of its secretion by Ca(2+) and protein kinase C. Of importance, shedding of VEGF-165 from the cell surface together with other membrane components appears to be a unique feature by which some VEGF is delivered to the surroundings to exert its known biological actions. Understanding VEGF trafficking can reveal additional means by which tumor vascularization can be inhibited by pharmacological interventions

Effects of long-term, low and high dose beta-carotene treatment in Zucker diabetic fatty rats: the role of HO-1

Abstract: Nowadays, there is a growing interest in compounds derived from plants as potential raw materials for drug development. One of the most studied compounds is beta-carotene (BC). Several clinical studies can be found investigating the cardiovascular effects of BC, however, all these results are controversial. There is increasing body of evidence showing that beside the well-known antioxidant properties, under strong oxidative circumstances BC could become prooxidant either. In this study we investigated the effects of long term, low- and high-dose BC treatment in ischemic/reperfused (ISA/REP) hearts isolated from zucker diabetic fatty (ZDF) rats. The animals were treated with various daily doses of BC for 4 weeks, and then hearts were isolated and subjected to 30 min of global ischemia (ISA) followed by 120 min of reperfusion (REP). Blood glucose levels were measured before, after two weeks and at the end of the treatment. In isolated hearts myocardial function was registered. At the end of reperfusion period infarctract size (IS) and heme oxygenase-1 (HO-1) expression were measured. The results show that low dose of BC treatment significantly improved postischemic recovery, which was reflected in a decreased IS. Interestingly, when BC was applied at high concentration, the observed protective effects were lost. Although, BC treatment increased HO-1 expression, we did not observe a better heart function and/or decreased IS in the high dose treated group. The glucose tolerance test showed concentration independent decrease in blood glucose levels. Our results suggest that long-term, low-dose BC treatment could be effective in the treatment of type-2-diabetes and related cardiovascular disease

Atorvastatin prevents hypoxia-induced inhibition of endothelial nitric oxide synthase expression but does not affect heme oxygenase-1 in human microvascular endothelial cells

Beneficial cardiovascular effects of statins, the inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, are particularly assigned to the modulation of inflammation. Endothelial nitric oxide synthase (eNOS) and heme oxygenase-1 (HO-1) are listed among the crucial protective, anti-inflammatory genes in the vasculature. Here we show that atorvastatin at pharmacologically relevant concentration (0.1 mu M) enhanced the expression of eNOS in human microvascular endothelial cells (HMEC-1). Moreover, atorvastatin prevented hypoxia-induced decrease in eNOS expression. However, in the same cells atorvastatin was ineffective in modulation of HO-1 protein level. Therefore, we suggest that the protective effect of statins at their pharmacological concentrations is not mediated by enhancement of HO-1 activity, but may involve eNOS. (c) 2006 Elsevier Ireland Ltd. All rights reserved