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Aim To explore whether self‐efficacy has any positive or negative mediating effects between family functioning and quality of life among elders with chronic diseases. Design A cross‐sectional study. Methods Questionnaires were collected from 516 community‐dwelling elderly individuals with chronic diseases using a convenience sampling method. The questionnaires included the Self‐efficacy for Managing Chronic Disease Six‐Item Scale, the Family Adaptation Partnership Growth Affection Resolve Index and the MOS 36‐Item Short Form Health Survey. Results Family functioning and self‐efficacy impacted the quality of life of community‐dwelling elderly individuals with chronic diseases. Family functioning was mediated by self‐efficacy and had an indirect impact on quality of life. The mediating effect accounted for 62.50% of the total effect.

Objective: The aim of this study is to analyze the differences in galanin (GAL) and 5-hydroxytryptamine (5-HT) levels in patients with different subtypes of gastroesophageal reflux disease (GERD) and its correlation with anxiety and depression in patients. Methods: Using the reflux disease questionnaire, 238 patients with GERD were selected as the study group. According to the endoscopic performance, they were divided into the nonerosive reflux disease (NERD) group (114 patients) and the RE group (124 patients). Sixty healthy people were selected as the control group. All research subjects were tested using the self-rating anxiety scale (SAS) and the self-rating depression scale (SDS) to assess the severity of anxiety and depression. The levels of 5-HT and GAL were analyzed using enzyme-linked immunosorbent assay. Results: Compared with the control group, 5-HT level in GERD patients without anxiety and depression was higher (t = 1.97, P < 0.05) and GAL level was lower (t = 1.97, P < 0.05). NERD patients demonstrated more server anxiety (F = 55.92, P < 0.05) and depression problems (F = 36.51, P < 0.05) compared to reflux esophagitis (RE) patients. The 5-HT level was lower (F = 54.53, P < 0.05) and the GAL level was higher (F = 8.00, P < 0.05) in NERD patients compared with the control group. Furthermore, 5-HT level was negatively correlated with SAS (r = −0.789, P < 0.05) and SDS (r = −0.787, P < 0.05) scores; GAL level was positively correlated with SAS (r = 0.688, P < 0.05) and SDS (r = 0.705, P < 0.05) scores; 5-HT and GAL level were negatively correlated (r= −0.744, P < 0.05). Conclusions: 5-HT level is higher and GAL level was lower in GERD patients without anxiety and depression than healthy people; the symptoms of anxiety and depression of NERD patients are more severe compared to those of RE patients; the severity of anxiety and depression was negatively correlated with the level of 5-HT and positively with GAL level.

Early pressure injury (PI) can result in either spontaneous healing (SH) or deterioration into ulcer (DU). However, determining whether PI will progress into SH or DU on the basis of non-blanchable erythema only is difficult. In this study, we constructed two animal PI models to mimic SH and DU injuries and observed haemorrhage by using ultraviolet (UV) photography to develop potential clinical indicators for predicting the progression of early PI. Macroscopy, UV photography, and skin temperature observations were obtained. In the SH group, macroscopic observation showed the erythema was obvious at 0.5 hours after decompression and faded gradually had almost disappeared at 72 hours. In the DU group, the erythema persisted, and an erosion appeared at 24 hours after decompression and expanded at 36 hours. The erythema developed into an obvious ulcer at 48 hours and enlarged at 72 hours. The obvious ulcer found at 48 hours through macroscopic observation was clearly visible at 36 hours with UV photography, and a significant difference in grey values between the two groups was found at as early as 18 hours (P < .05). This study provided evidence showing that UV photography can predict the different progression stages of early PI. Additionally, when combined with the transparent disc method, UV photography also can be used to identify the circulatory disorders of early PI, such as haemorrhage or hyperaemia and even congestion.

To examine the preventive effect of heat preconditioning (HPC) on intraoperatively acquired pressure ulcers (IAPU) in surgical patients and explore the mechanisms of HPC on pressure injury (PI) in rat skin. We generated a skin PI model using hairless rats and treated these rats with HPC. Skin injury size was measured and the expression of heat shock proteins (HSPs) in the skin were examined by real-time RT PCR, Western blotting, and immunohistochemical staining. For human studies, 118 surgical patients were randomly divided into HPC and control groups. We measured sacral skin temperature, sacral pressure and compared the PI prevalence rate. HPC treatment significantly reduced both area(p =0.007, p =0.007, p =0.012) and incidence (p=0.025, p =0.019, p =0.012) of PI in rats on the second, third and fourth days. HSP27 expression was increased in HPC group. Immunohistochemical staining showed that HSP27 was distributed in all types of dermal cells with increase in basal cells. In human studies, HPC treatment increased sacral temperature (p. The incidence of IAPUs was significantly decreased by 75% in HPC group. HPC can reduce the incidence of PI in both experimental animals and humans. Beneficial effects of HPC were possibly mediated by upregulation of HSP27.

Objective: The aim of this study is to investigate the mediating effect of self-efficacy between diabetes-related distress and self-management in empty-nest elderly patients with type 2 diabetes mellitus (T2DM). Methods: A total of 347 empty-nest elderly patients with T2DM from Jiangsu Province Hospital of Chinese Medicine and Affiliated Hospital of Yangzhou University were investigated by a self-designed General Information Questionnaire, the Self-efficacy for diabetes, the Diabetes Distress Scale, and the summary of diabetes self-care activities. Diabetes-related distress and diabetes self-management were tested for correlation analysis with self-efficacy. Meditational analyses were conducted to test the hypothesized mediating effects of diabetes self-efficacy as an intervention variable between diabetes distress and self-management. Results: About 68.59% of patients suffered from diabetes-related distress. The results of bivariate correlations revealed that self-efficacy was negatively correlated with diabetes-related distress (r =–0.627, P < 0.01) and positively correlated with self-management (r = 0.356, P < 0.01). The relationship effects of diabetes distress on self-management were fully mediated by self-efficacy. Conclusions: Diabetes-related distress prevails in empty-nest elderly patients with T2DM. Self-efficacy plays a mediate role between diabetes-related distress and self-management. Psychological intervention is contributed to reducing diabetes-related distress.

The risk factors for secondary stomach carcinogenesis after distal gastrectomy have not been evaluated in detail.Using gastrointestinal endoscopy, we examined 112 patients who had undergone gastrectomy. Biopsy specimens were taken from the stoma and the upper corpus mucosa in the remnant stomach to examine the associations among Helicobacter pylori (H.pylori) infection, bile reflux, and the expressions of interleukin-8 (IL-8), cyclo-oxygenase-2 (COX-2), and trefoil factor family 1 (TFF1) genes in the stomach mucosa.The IL-8 levels in the corpus mucosa were significantly higher in the H.pylori-positive patients than in the H.pylori-negative patients (P = 0.015). The IL-8 levels were significantly higher in the stomal mucosa than in the corpus mucosa in the H.pylori-positive patients (P = 0.047). The COX-2 levels in the corpus mucosa tended to be higher in the H.pylori-positive patients, but these levels were not significantly different in the stoma mucosa. The COX-2 levels in the corpus were significantly higher after Billroth II (BII) anastomosis than after Billroth I (BI) anastomosis (P = 0.041). TFF1 expression in the stoma was higher in the H.pylori-positive patients than in the H.pylori-negative patients, but the difference was not significant.Both H.pylori infection and bile reflux increased IL-8 levels after BI anastomosis. Furthermore, COX-2 levels were higher after BII than after BI anastomosis. These indicators will become useful not only as biomarkers to predict the degree of inflammation in the stomach mucosa, but also as surrogate biomarkers to predict the risk of secondary stomach carcinogenesis in the remnant stomach mucosa.

Although clinical diabetes mellitus is obviously a high risk factor for myocardial infarction, there is disagreement about the sensitivity of ischemic injury of an infarcted myocardium in experimental studies. The present study evaluated the influences of different durations of hyperglycemia on ischemic and reperfusion injuries of the myocardium, and focused on extracellular signal-regulated kinase 1/2 (ERK1/2), which plays an important role in the intracellular signaling pathway and is reported to be associated with myocardial protection against heart injury. Short- and long-term hyperglycemias were induced in rats by streptozotocin (STZ) injection and the rats were examined 4 (4WDM) and 20 weeks (20WDM) after the treatment. Ischemia and reperfusion were induced by occlusion and reperfusion (I/R) of the left coronary artery (LCA). I/R-induced infarct size was determined using triphenyltetrazolium chloride (TTC) staining. After 20 weeks of STZ treatment (20WDM+I/R), the infarct size in the rat heart increased by 65.2 +/- 4.3%, whereas after 4 weeks of STZ treatment (4WDM+I/R), the infarct size decreased compared with the time-matched I/R group (43.1 +/- 3.6% and 59.5 +/- 5.6%, respectively). The number of dead myocytes including necrotic and apoptotic cells was determined using horseradish peroxidase (HRP) and terminal deoxynucleotide nick-end labeling (TUNEL) methods. The number of dead myocytes decreased in the 4WDM+I/R group, while the number of dead myocytes increased markedly in the 20WDM+I/R group, compared with the time-matched I/R group. The increment of ERK1/2 phosphorylation in the 4WDM group and the slight enhancement of this phosphorylation by I/R treatment were observed by western blotting. However, in the 20WDM group, the level of ERK1/2 phosphorylation reduced by approximately 1/3 compared with the time-matched control group; moreover, I/R treatment did not enhance the phosphorylation level. This study demonstrated that short- and long-term hyperglycemias exert opposite influences on ischemic myocardial injury, and these contradictory influences may depend on an ERK1/2-mediated intracellular signaling pathway.

Background —The mitochondrial K ATP (mitoK ATP ) channel has been shown to confer short- and long-term cardioprotection against prolonged ischemia via protein kinase C (PKC) signaling pathways. However, the exact association between PKC or its isoforms and mitoK ATP channels has not yet been clarified. The present study tested the hypothesis that the activity and translocation of PKC to the mitochondria are important for cardiac protection elicited by mitoK ATP channels. Methods and Results —PKC was downregulated by prolonged (24-hour) treatment with phorbol 12-myristate 13-acetate (4 μg/kg body weight) before subsequent experiments in rats. Langendorff-perfused rat hearts were subjected to 40 minutes of ischemia followed by 30 minutes of reperfusion. Effects of PKC downregulation on the activation of mitoK ATP channels and other interventions on hemodynamic, biochemical, and pathological changes were assessed. Subcellular localization of PKC isoforms by Western blot analysis and immunocytochemistry demonstrated that PKC-α and PKC-δ were translocated to the sarcolemma and that PKC-δ was translocated to the mitochondria after diazoxide treatment. In hearts treated with diazoxide (80 μmol/L), a significant improvement in cardiac function and an attenuation of cell injury were observed. In PKC-downregulated hearts, protection was abolished because mitoK ATP channels could not be activated by diazoxide. Conclusions —These data suggest that PKC activation is required for the opening of mitoK ATP channels during protection against ischemia and that this effect is linked to isoform-specific translocation of PKC-δ to the mitochondria.

Lumican belongs to the small leucine-rich proteoglycan family and has an important role in the regulation of corneal and dermal collagen fiber assembly. Recently, lumican mRNA was found in the heart and its high expression was reported during wound healing of the cornea. In the present study, the expression and role of lumican in fibrosis of an ischemic and reperfused rat heart were examined. The expression level of lumican mRNA increased in the ischemic and reperfused rat heart and was highest on the fourth week. Lumican protein existed in the forms of core protein and proteoglycan in the control rat heart. The amount of lumican in the form of proteoglycan increased, and that as the form glycoprotein was newly detected in the ischemic and reperfused rat heart on the fourth week. In the control heart, lumican was weakly expressed in the collagen fibers of the perivascular area, but it was expressed strongly in many capillary endothelial cells in the ischemic lesion on day 1. After 3 days, lumican was localized in collagen fibers and in the fibroblasts of fibrotic lesions. A few myocardial cells close to the ischemic lesion expressed lumican mRNA. Lumican is considered to play an important role in the fibrillogenesis of the ischemic and reperfused rat heart.

Abstract —Activation of mitochondrial K ATP (mitoK ATP ) channel induces acute ischemic preconditioning (PC) against ischemic injury. The ability of this channel to elicit late PC remains unknown. The present study tests the hypothesis that stimulation of mitoK ATP channel induces late PC via the protein kinase C (PKC) signaling pathway. Rats were subjected to 30 minutes of regional ischemia and 120 minutes of reperfusion (I/R). In other groups, rats were pretreated with diazoxide, a specific opener of the mitoK ATP channel (7 mg/kg, IV), 12, 24, 48, and 72 hours before they were subjected to I/R. A maximum reduction in infarct size was observed after 24 hours (33.3±2.2% versus I/R group, 62.1 ±2.4%). Pretreatment with diazoxide did not reduce the infarct size significantly after 12, 48, and 72 hours (50.2±4.3%, 50.5±4.6%, and 58.2±4.9%) compared with the I/R group. The protection was blocked with 5-hydroxydecanoic acid (5-HD, 5 mg/kg IV), a relatively selective mitoK ATP channel blocker (56.5±2.7%), and chelerythrine (5 mg/kg IV), an effective PKC inhibitor (57.1±3.4%) administered either on the first day before diazoxide pretreatment or 10 minutes before I/R on the second day. Cell necrosis was decreased by ≈50% in the diazoxide preconditioned hearts compared with control I/R hearts. Cell death by apoptosis was also significantly decreased in diazoxide pretreated hearts (3.2%) as compared with I/R (11.3%). In conclusion, activation of mitoK ATP channel with diazoxide produces late PC against reperfusion injury. The effect of mitoK ATP channel appears to be dependent on the PKC-mediated signal pathway.

Extracellular signal-regulated kinase (ERK) 1/2 is an important intracellular proteinase associated with myocardial protection against heart injury. Hyperglycemia was also reported to be highly involved in heart injury by the formation of advanced glycation end products (AGEs) in myocardial protein, resulting in its altered structure and function. However, the effect of this glycation on mitogen-activated protein kinases, particularly ERK1/2, in the myocardium is largely unclarified. In this study, we investigated whether the glycation of an intracellular protein, ERK1/2, would result in ERK1/2-AGEs formation that adversely affects ERK1/2 activation in the rat heart under hyperglycemia. Hyperglycemia was induced by injection of streptozotocin (STZ) and hearts were examined 4 and 20 weeks after STZ treatment. By immunohistochemical staining and Western blotting, it was determined that the level of phosphorylated ERK1/2 in the rat heart under hyperglycemia 20 weeks after STZ treatment decreased markedly by about 50% of that of the time-matched control group, whereas in the case of 4 weeks after STZ treatment, it increased by about 2.7-fold that of the time-matched group. The level of deposition of AGEs in proteins of the myocardium increased significantly depending on the duration of hyperglycemia. Twenty weeks after STZ treatment, two clear bands corresponding to 44- and 42-kDa AGEs were detected by Western blotting; these corresponded to protein sizes of ERK1/2. The immunoprecipitation method further confirmed the formation and the increased intensity of ERK1/2-AGEs in the rat heart under hyperglycemia for 20 weeks. These results demonstrate that long-term hyperglycemia may inhibit ERK1/2 phosphorylation in the myocardium, whereas a short-term (4 weeks) hyperglycemia enhances its phosphorylation. The ERK1/2 phosphorylation under long-term hyperglycemia is very different from that under short-term hyperglycemia. In addition, this inhibition of ERK1/2 activation appears to be dependent on the formation of ERK1/2-AGEs under long-term hyperglycemia, which may be related in part to the etiology of diabetic cardiomyopathy. It also suggests that the formation of AGEs in intracellular enzymes and proteins under hyperglycemia could play important roles in the development of diabetes complications.