Weak Inducer Of Apoptosis Levels Research Articles

Sclerostin and TNF-related weak inducer of apoptosis: can they be important in the patients with glomerulonephritis?

Sclerostin is a protein produced by osteocytes, kidneys, and vascular cells and has many effects on kidney and vascular structures. Soluble TNF-related weak inducer of apoptosis is a proinflammatory cytokine that may cause glomerular and tubular injury and increase sclerostin expression. This study aimed to investigate serum sclerostin and soluble TNF-related weak inducer of apoptosis levels in patients with glomerulonephritis and the effects they may be associated with. This cross-sectional study included 93 patients, 63 of whom were glomerulonephritis and 30 were healthy controls. Serum sclerostin, soluble TNF-related weak inducer of apoptosis, and 24-h urinary protein excretion were measured, and pulse wave velocity was calculated for arterial stiffness. Serum sclerostin and soluble TNF-related weak inducer of apoptosis were higher in glomerulonephritis patients than in the control group, and serum sclerostin and soluble TNF-related weak inducer of apoptosis levels were correlated with both proteinuria and pulse wave velocity. In addition, in the regression analysis, serum sclerostin and soluble TNF-related weak inducer of apoptosis levels were found to be independent predictors of proteinuria in patients with glomerulonephritis. This is the first study to show that serum sclerostin and soluble TNF-related weak inducer of apoptosis are elevated in glomerulonephritis patients, and these two markers correlate with arterial stiffness and proteinuria in these patients. Considering the effects of sclerostin and soluble TNF-related weak inducer of apoptosis in patients with glomerulonephritis, we think these mechanisms will be the target of both diagnosis and new therapies.

Serum tumor necrosis factor-like weak inducer of apoptosis levels are elevated in schizophrenia

Objective:The purpose of this study was to assess serum Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) concentrations to determine whether changes in patients with schizophrenia could have etiopathogenetic importance. Since very little research has addressed the connection between the inflammatory marker TWEAK and schizophrenia, we wanted to examine alterations of TWEAK and investigate the possible correlation between clinical symptomatology and serum concentrations.Methods:A total of 45 schizophrenia patients and 40 healthy controls were included in this study. The Positive Symptom Assessment scale and the Negative Symptom Assessment scale were administered to determine symptom severity. Venous blood samples were collected and serum TWEAK levels were measured.Results:Serum TWEAK levels were significantly higher in the schizophrenia group than the control group, independently of potential confounders, including sex, age, body mass index and smoking status.Conclusion:The results indicate that TWEAK is elevated in schizophrenia patients, which could deepen our understanding of the role of inflammation in the pathogenesis of schizophrenia.

The Diagnostic Value of Stweak in Acute Ischemic Stroke

Background:Considering the critical role of early diagnosis and management of acute ischemic stroke, biomarkers that can reliable assist in the diagnosis are still needed. These biomarkers should rapidly analyze, have high specificity for brain damage, and be available in the emergency settings for early diagnosis and exclusion of other conditions that mimic acute ischemic stroke. Soluble tumor necrosis factor-like weak inducer of apoptosis, a protein involved in the regulation of several biological functions, could be a potential acute ischemic stroke biomarker.Aims:To investigate the diagnostic value of soluble tumor necrosis factor-like weak inducer of apoptosis in patients with acute ischemic stroke and examine the relationship between ischemic area volume determined at diffusion-weighted magnetic resonance imaging and soluble tumor necrosis factor-like weak inducer of apoptosis.Study Design:A prospective, case-control study.Methods:This case-control prospective study included 36 patients with acute ischemic stroke and 36 healthy volunteers. Information on age, sex, presence of chronic disease, neurological examination findings, times of presentation to the emergency department after acute ischemic stroke, soluble tumor necrosis factor-like weak inducer of apoptosis levels, ischemic area volumes at diffusion-weighted magnetic resonance imaging, and 6-month mortality rates after stroke were recorded. The results were analyzed on SPSS 22.0 software (SPSS Inc., Chicago, IL, USA), and p<0.05 was considered statistically significant.Results:A soluble tumor necrosis factor-like weak inducer of apoptosis cut-off value of 995.5 pg/mL exhibited a sensitivity of 80.5% and a positive predictive value of 82.5% with an area under the curve of 0.84 (95% confidence interval: 0.74-0.94; p<0.001). The mean soluble tumor necrosis factor-like weak inducer of apoptosis levels in the acute ischemic stroke group (1968.08±1441.99 μg/L) were significantly higher than those in the control group (704.81±291.72 μg/L) (p<0.001). No correlation was observed between soluble tumor necrosis factor-like weak inducer of apoptosis levels and ischemic area volume measured at diffusion-weighted magnetic resonance imaging (r=-0.008; p=0.07). The mean ischemic area volume was 505.68±381.10 and 60.96±80.89 mm3 in the nonsurviving and surviving patients, respectively (p=0.002).Conclusion:Soluble tumor necrosis factor-like weak inducer of apoptosis can be used in the diagnosis of acute ischemic stroke. However, it is inconclusive in estimating ischemic area volume and early mortality following acute ischemic stroke. Ischemic area volume measured at diffusion-weighted magnetic resonance imaging is a marker of poor prognosis and can be used in predicting early mortality.

Clinical significance of serum interleukin-8 and soluble tumor necrosis factor-like weak inducer of apoptosis levels in patients with diabetic nephropathy.

Aims/IntroductionRecent studies suggest that chronic inflammatory responses are important in the development of diabetic nephropathy (DN). Various inflammatory and angiogenesis molecules affect the pathogenesis and progression of DN. Inflammation damages the microcirculation and causes kidney damage. In the present study, we studied changes in interleukin‐8 (IL‐8) and soluble tumor necrosis factor‐like weak inducer of apoptosis (sTWEAK) levels in patients with DN, and investigated the clinical significance of these two inflammatory factors.Materials and MethodsParticipants were categorized into healthy controls (n = 30) and patients with type 2 diabetes mellitus (n = 124). The type 2 diabetes mellitus group was further subdivided into the normoalbuminuria (n = 34), microalbuminuria (MAU ; n = 46,) and proteinuria (MaAU; n = 44,) groups. Patients with DN were included in the MAU and MaAU groups. Total cholesterol, triglyceride, low‐density lipoprotein cholesterol, glycosylated hemoglobin, fasting blood glucose, 2‐h postprandial blood glucose, blood urea nitrogen, serum creatinine, 24‐h urine microalbumin, IL‐8 and sTWEAK levels were measured. Logistic regression was used to analyze the factors associated with proteinuria.ResultsIn the healthy controls, normoalbuminuria, MAU and MaAU groups, we found that IL‐8 levels increased, whereas sTWEAK levels decreased (P < 0.05). IL‐8 might be an independent risk factor and serum sTWEAK a protective factor for MAU and MaAU. Serum levels of sTWEAK, IL‐8 and microalbumin were significantly correlated in the MAU and MaAU groups.ConclusionsSerum IL‐8 and sTWEAK levels might be markers that can be used for an early diagnosis of DN.

P.3.b.046 - Comparison of serum tumor necrosis factor-like weak inducer of apoptosis levels in patients with schizophrenia and healthy control subjects

P.3.b.046 - Comparison of serum tumor necrosis factor-like weak inducer of apoptosis levels in patients with schizophrenia and healthy control subjects

P.3.b.021 - Comparison of serum tumor necrosis factor-like weak inducer of apoptosis levels in patients with schizophrenia and healthy control subjects

P.3.b.021 - Comparison of serum tumor necrosis factor-like weak inducer of apoptosis levels in patients with schizophrenia and healthy control subjects

Polycystic Ovary Syndrome and Increased Soluble Tumor Necrosis Factor Like Weak Inducer of Apoptosis Levels Are Independent Predictors of Dyslipidemia in Youth

Background/Aims: Dyslipidemia is common in women with polycystic ovary syndrome (PCOS) irrespective of age. Our aim was to investigate soluble tumor necrosis factor like weak inducer of apoptosis (sTWEAK), a cardiovascular risk marker in PCOS, and to determine if it is associated with dyslipidemia in youth. Methods: A prospective-observational study was carried out including 35 PCOS patients and 35 healthy controls. Serum sTWEAK levels were measured using commercially available kits. Multiple logistic regression analysis was then performed to verify the statistically significant differences in the possible predictors of dyslipidemia. Results: Serum sTWEAK levels and the percentage of women with dyslipidemia were significantly higher in the PCOS group (p = 0.024 and p < 0.001, respectively). Participants were further divided into 2 subgroups based on the presence of dyslipidemia. The percentage of women with PCOS was significantly higher in the dyslipidemic group when compared with controls; 70.7 vs. 20.7%, respectively (p < 0.001). Multiple logistic regression analysis revealed that both the presence of PCOS (OR 7.924, 95% CI 2.117-29.657, p = 0.002) and increased levels of sTWEAK (>693 pg/ml; OR 3.810, 95% CI 1.075-13.501, p = 0.038) were independently associated with dyslipidemia. Conclusions: Increased levels of both sTWEAK and PCOS were found to be independently associated with dyslipidemia in youth.

The Relationship between Soluble Tumor Necrosis Factor-like Weak Inducer of Apoptosis Levels and Cardiac Functions in Peritoneal Dialysis Patients

Tumor necrosis factor (TNF)-like weak inducer of apoptosis (sTWEAK) levels has been reported to be decreased in patients on hemodialysis (HD) and patients with heart failure. We aimed to study the relationship between sTWEAK levels and cardiac functions in peritoneal dialysis (PD) patients. This cross-sectional study was carried out on patients on chronic PD programs for more than three months. Patients aged under 18 or over 80 years, patients with overt cardiac disease, overt hypervolemia, active systemic infection, malignancy, peritonitis within the last month were excluded. The patient group was compared with the control group including healthy adults aged 24–61 years. Fifty-two PD patients were included in the study (mean age: 52.7±15.4 years; female/male ratio: 30/22). The corresponding data of the control group were 41.3±10.7 years and 17/14. There was no statistically significant difference between demographic parameters of the groups except age. The mean sTWEAK level of the patient and the control groups were similar (564±17 pcg/ml vs 535±126 pcg/ml, p=0.419). No correlation was detected between any of the demographic variables and sTWEAK levels. Among the echocardiographic parameters, only ejection fraction was found to be correlated negatively with sTWEAK levels. Patients with ischemic heart disease (IHD) and heart failure had significantly higher sTWEAK levels compared with the patients without these diseases. With linear regression analysis, only age and the presence of heart failure were found to be the independent determinants of sTWEAK levels. Level of sTWEAK is significantly high in PD patients with heart failure and IHD. sTWEAK may be a marker of cardiac functions in PD patients.

Serum TNF‐Related and Weak Inducer of Apoptosis Levels in Septic Shock Patients

Capillary permeability is a tightly regulated feature of microcirculation in all organ beds. In sepsis, this feature is fundamentally altered. We have previously reported elevated levels of angiopoietin-2 in patients with septic shock, and have investigated tumor necrosis factor (TNF)-related and weak inducer of apoptosis (TWEAK), which mediates both angiogenesis and inflammation, in those patients. Enzyme-linked immunoassay was used to measure serum TWEAK levels in 20 patients with septic shock, all of whom were treated by direct hemoperfusion with a polymyxin B-immobilized fiber column (DHP-PMX), and in 20 non-septic controls. The TWEAK levels were higher in patients with septic shock (192.8 ± 230.5 pg/mL) than in controls (84.1 ± 28.7 pg/mL, P = 0.043). Between 11 survivors and 10 non-survivors, there was no significant difference in the serum TWEAK levels before the DHP-PMX therapy. During DHP-PMX therapy, however, the serum TWEAK levels were significantly increased in non-survivors (142.2 ± 88.1 pg/mL to 399.0 ± 307.1 pg/mL, P = 0.022). There was a significant correlation between the serum TWEAK levels and white blood cell counts (r = 0.393, P < 0.001), platelet counts (r = 0.418, P < 0.001), or serum CRP levels (r = 0.259, P = 0.029), but there was no correlation between the serum TWEAK levels and blood pressure. The serum TWEAK levels were also correlated with the ratio of angiopoietin-2 to -1 (r = 0.464, P < 0.001). TWEAK may be a suitable marker of disease severity and mortality in septic patients, and TWEAK levels may be associated with vascular permeability via angiopoietin balance.