Which one predicts mortality better? Hemogram and ST elevation myocardial infarction.

OBJECTIVE: The aim of this study was to determine the effectiveness of hematological parameters measured at the moment of admission to the emergency room in predicting in-hospital mortality and to determine cut-off values of strongly predictive values. SUBJECTS AND METHODS: The study began with approval of the ethics committee. In total, 1,929 patients over 18 years of age, whose date could be obtained, were included in the study. From the hemogram parameters, white blood cells (WBC), red cell distribution width, mean platelet volume, and ratio of neutrophils to lymphocytes (NLR) values were determined and recorded. CK-MB and high-sensitive Troponin T values were recorded as cardiac markers. For statistical analysis, "SPSS for Windows Version 21" package program was used. FINDINGS: About 71.7% (n = 1384) of the patients were male and 28.3% (n = 545) of the patients were female. About 92.5% of the patients (n = 1785) were discharged from the hospital, whereas the remaining 144 patients (7.5%) were exitus in the hospital. When the efficacy of hematological parameters and cardiac markers in predicting mortality was examined by receiver operating charecteristics analysis, NLR was found to be the strongest predictor (area under the curve [AUC], 0.772, standard deviation [SD] = 0.022, 95% confidence interval [CI]). It was found that the WBC value came in second place after NLR as a strong predictor of mortality (AUC, 0.749, SD = 0.024, % 95 CI). CONCLUSION: The use of predictors for the prediction of mortality for ST elevation myocardial infarction patients is of great importance for faster implementation of treatment modalities. We found that WBC and especially NLR values obtained with a simple method can be used as powerful predictors.

Changes in kidney tissue and effects of erythropoietin after acute heart failure.

Impairment of cardiac function causes renal damage. Renal failure after heart failure is attributed to hemodynamic derangement including reduced renal perfusion and increased venous pressure. One mechanism involves apoptosis and is defined as cardiorenal syndrome type 1. Erythropoietin (EPO) is a cytokine that induces erythropoiesis under hypoxic conditions. Hypoxia inducible factor 1 alpha (HIF-1α) plays a regulatory role in cellular response to hypoxia. Protective effects of EPO on heart, kidney and nervous system are unrelated to red blood cell production. We investigated early changes in and effects of EPO on renal tissues of rats with myocardial infarction by morphology and immunohistochemistry. Coronary artery ligation was used to induce myocardial infarction in Wistar rats. Group 1 comprised sham operated rats; groups 2, 3 and 4 included rats after coronary artery ligation that were sacrificed 6 h after ligation and that were treated with saline, 5,000 U/kg EPO or 10,000 U/kg EPO, respectively; group 5 included rats sacrificed 1 h after ligation. Group 2 showed increased renal tubule damage. Significantly less tubule damage was observed in EPO treated groups. EPO and EPO receptor (EPO-R) immunostaining intensities increased slightly for group 5 and became more intense for group 2. EPO and EPO-R immunostaining was observed in the interstitial area, glomerular cells and tubule epithelial cells of EPO treated groups. HIF-1α immunostaining was observed in collecting tubules in the medulla only in group 2. Caspase-3 immunostaining is an indicator of apoptosis. Caspase-3 staining intensity decreased in renal medulla of EPO treated groups. EPO treatment may exert a protective effect on the renal tissues of patients with cardiorenal syndrome.

Histopathological changes in rat pancreas and skeletal muscle associated with high fat diet induced insulin resistance.

The effects of a high fat diet on the development of diabetes mellitus, insulin resistance and secretion have been widely investigated. We investigated the effects of a high fat diet on the pancreas and skeletal muscle of normal rats to explore diet-induced insulin resistance mechanisms. Forty-four male Wistar rats were divided into six groups: a control group fed standard chow, a group fed a 45% fat diet and a group fed a 60% fat diet for 3 weeks to measure acute effects; an additional three groups were fed the same diet regimens for 8 weeks to measure chronic effects. The morphological effects of the two high fat diets were examined by light microscopy. Insulin in pancreatic islets was detected using immunohistochemistry. The homeostasis model assessment of insulin resistance index and insulin staining intensity in islets increased significantly with acute administration of high fat diets, whereas staining intensity decreased with chronic administration of the 45% fat diet. Islet areas increased significantly with chronic administration. High fat diet administration led to islet degeneration, interlobular adipocyte accumulation and vacuolization in the pancreatic tissue, as well as degeneration and lipid droplet accumulation in the skeletal muscle tissue. Vacuolization in the pancreas and lipid droplets in skeletal muscle tissue increased significantly with chronic high fat diet administration. We suggest that the glucolipotoxic effects of high fat diet administration depend on the ratio of saturated to unsaturated fatty acid content in the diet and to the total fat content of the diet.

Acute-phase reactants and cytokines in ischemic stroke: do they have any relationship with short-term mortality?

BACKGROUND: Many unknown risk factors play a role in the etiopathogenesis of stroke. The appearance of inflammatory cells within the damaged tissue after cerebral ischemia suggests that an inflammatory response may play a role in stroke pathogenesis. In our study, we examined whether an association exists between the acute-phase reactants and the levels of cytokines, the volume and diameter of the stroke, and short-term mortality in patients who were diagnosed as acute ischemic a stroke after admission to the Emergency Department. PATIENTS AND METHODS: A total of 50 consecutive patients who applied to the Emergency Service with acute ischemic stroke were enrolled in the study. Their stroke volume were calculated and serum samples were obtained as soon as they arrived into the Emergency Service. The patients were evaluated according to the Glasgow Coma Scale (GCS) and National Institutes of Health Stroke Scale (NIHSS). RESULTS: There was no significant correlations between stroke volume and levels of cytokine and acute-phase reactants in dead patient group or in living patient group. A correlation and statistical significance was found between stroke volume and hospital stay time in living patient group. In addition, GCS and NIHSS scores were correlated with stroke volume and was found a significant statistically. CONCLUSIONS: Scales such as GKS and NIHHS, which evaluate the functional state of patients, are the best indicators for defining prognosis in our daily practices. In addition, we found a positive correlation between levels of CRP (C reactive protein) and prognosis. However, we did not observe a statistically significant correlation between prognosis and other acute-phase reactants such as TNF-alpha, IL-6, IL-8, IL-10, fibrinogen, and leukocytes.

Autoimmunity to uroplakin II causes cystitis in mice: a novel model of interstitial cystitis.

BACKGROUND: The pathophysiology of interstitial cystitis (IC) is unknown. Deficits in urothelial cell layers and autoimmune mechanisms may play a role. OBJECTIVE: To examine whether immunization of mice with recombinant mouse uroplakin II (rmUPK2), a bladder-specific protein, would provoke an autoimmune response sufficient to create an IC phenotype. DESIGN, SETTING, AND PARTICIPANTS: RmUPK2 complementary DNA was generated, transferred into a bacterial expression vector, and the generated protein was purified. Eight-week-old SWXJ female mice were immunized with rmUPK2 protein via subcutaneous injection of 200µg of rmUPK2 protein in 200µl of an emulsion. MEASUREMENTS: Mice were euthanized 5 wk after immunization. Axillary and inguinal lymph node cells were tested for antigen-specific responsiveness and cytokine production, serum isotype antibody titers against rmUPK2 were determined, and gene expression of inflammatory mediators was measured in the bladder and other organs. For functional analysis, mice were placed in urodynamic chambers for 24-h micturition frequency and total voided urine measurements. RESULTS AND LIMITATIONS: Immunization with rmUPK2 resulted in T-cell infiltration of the bladder urothelium and increased rmUPK2-specific serum antibody responses in the experimental autoimmune cystitis (EAC) mice models compared with controls. The ratio of bladder to body weight was increased in EAC mice. Quantitative reverse transcriptase polymerase chain reaction analysis showed elevated gene expression of tumor necrosis factor α, interferon γ, interleukin (IL)-17A, and IL-1ß in bladder urothelium but not in other organs. Evaluation of 24-h micturition habits of EAC mice showed significantly increased urinary frequency (p<0.02) and significantly decreased urine output per void (p<0.021) when compared with control mice. CONCLUSIONS: Our study showed that a bladder-specific autoimmune response sufficient to induce inflammation and EAC occurs in mice following immunization with rmUPK2. EAC mice displayed significant evidence of urinary frequency and decreased urine output per void. Further phenotype characterization of EAC mice should include evidence for pain and/or afferent hypersensitivity, and evidence of urothelial cell layer damage.

Bladder dysfunction in mice with experimental autoimmune encephalomyelitis.

The vast majority of patients with multiple sclerosis (MS) develop bladder control problems including urgency to urinate, urinary incontinence, frequency of urination, and retention of urine. Over 60% of MS patients show detrusor-sphincter dyssynergia, an abnormality characterized by obstruction of urinary outflow as a result of discoordinated contraction of the urethral sphincter muscle and the bladder detrusor muscle. In the current study we examined bladder function in female SWXJ mice with different defined levels of neurological impairment following induction of experimental autoimmune encephalomyelitis (EAE), an animal model of central nervous system inflammation widely used in MS research. We found that EAE mice develop profound bladder dysfunction characterized by significantly increased micturition frequencies and significantly decreased urine output per micturition. Moreover, we found that the severity of bladder abnormalities in EAE mice was directly related to the severity of clinical EAE and neurologic disability. Our study is the first to show and characterize micturition abnormalities in EAE mice thereby providing a most useful model system for understanding and treating neurogenic bladder.

[Splenic trauma and treatments. Haseki Educational and Research Hospital Surgical Department survey of the feasibility of surgery for splenic trauma]. / Dalak yaralanmalari ve tedavisi haseki egitim ve arastirma hastanesi acil cerrahi servisinde dalak yaralanmalarinda uygulanan cerrahi girisimler.

184 patients were admitted with splenic injuries, between 1992 and 1998. 131 (71%) patients were male and 53 (29%) patients were female. The average age of patients were 20.4 years. There were 176 (95%) blunt and 8 (5%) penetrating injuries. The management of our cases involved splenectomy in 164 (89%), splenorraphy in 12 (7%) and partial splenectomy in 8 (4%). 172 (93%) of the operated patients had isolated splenic injuries and 12 (7%) concomitant organ injuries. The lenght of hospital stay of splenectomies; partial splenectomy and splenorraphy were 7.9, 7 and 6 days respectively. The complication rate of splenectomy, partial splenectomies; and splenorraphy after the operation were 3 (2%), 1 (0.5%) and 0. No deaths occurred as a result of splenic injury and operation.