scholarly journals Soluble TNF-Like Weak Inducer of Apoptosis as a New Marker in Preeclampsia: A Pilot Clinical Study

2016 ◽  
Vol 2016 ◽  
pp. 1-5 ◽  
Author(s):  
Zeynep Kayaoglu Yildirim ◽  
Abdullah Sumnu ◽  
Neslihan Bademler ◽  
Elif Kilic ◽  
Gulay Sumnu ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Pregnant Women ◽  
Tumor Necrosis ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Elisa Kit ◽  
Pilot Clinical Study ◽  
Clinical Consequences ◽  
Necrosis Factor

Introduction. All findings of preeclampsia appear as the clinical consequences of diffuse endothelial dysfunction. Soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) was recently introduced as a TNF related cytokine in various inflammatory and noninflammatory disorders. sTWEAK was found to be related to endothelial dysfunction in patients with chronic kidney disease. In our study we aimed to compare sTWEAK levels in women with preeclampsia to corresponding levels in a healthy pregnant control group.Materials and Methods. The study was undertaken with 33 patients with preeclampsia and 33 normal pregnant women. The concentration of sTWEAK in serum was calculated with an enzyme linked immunosorbent assay (ELISA) kit.Results. Serum creatinine, uric acid, LDH levels, and uPCR were significantly higher in the patient group compared to the control group. sTWEAK levels were significantly lower in preeclamptic patients (332 ± 144 pg/mL) than in control subjects (412 ± 166 pg/mL) (p=0.04).Discussion. Our study demonstrates that sTWEAK is decreased in patients with preeclampsia compared to healthy pregnant women. There is a need for further studies to identify the role of sTWEAK in the pathogenesis of preeclampsia and to determine whether it can be regarded as a predictor of the development of preeclampsia.

scholarly journals Association of C1q/TNF-related protein-1 (CTRP1) serum levels with coronary artery disease

2019 ◽  
Vol 47 (6) ◽  
pp. 2571-2579 ◽  
Author(s):  
Linhui Shen ◽  
Shuhong Wang ◽  
Yuan Ling ◽  
Wei Liang
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Multiple Logistic Regression Analysis ◽  
Serum Levels ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Artery Disease ◽  
Necrosis Factor

Objective Complement C1q tumor necrosis factor-related proteins (CTRPs), belonging to the CTRP superfamily, are extensively involved in regulating metabolism and the immune-inflammatory response. The inflammatory process is linked to the pathogenesis of coronary artery disease (CAD). Here, we investigated the association of serum levels of CTRP1 with CAD. Methods Study participants were divided into two groups according to the results of coronary angiography: a control group (n = 63) and a CAD group (n = 76). The concentrations of serum CTRP1 and inflammatory cytokines were determined by enzyme-linked immunosorbent assay. Further analysis of CTRP1 levels in individuals with different severities of CAD was conducted. The CAD severity was assessed by Gensini score. Results Serum levels of CTRP1 were significantly higher in CAD patients than in controls (17.24 ± 1.07 versus 9.31 ± 0.56 ng/mL), and CTRP1 levels increased with increasing severity of CAD. CTRP1 levels were positively correlated with concentrations of tumor necrosis factor-α and interleukin-6. Multiple logistic regression analysis showed that CTRP1 was significantly associated with CAD. Conclusions Our data showed close associations of serum CTRP1 levels with the prevalence and severity of CAD, indicating that CTRP1 can be regarded as a novel and valuable biomarker for CAD.

Role of Tumor Necrosis Factor and Interleukin-1 in Endotoxin-Induced Middle Ear Effusions

1997 ◽  
Vol 106 (8) ◽  
pp. 633-639 ◽  
Author(s):  
Jiri Prazma ◽  
Rudolph J. Triana ◽  
Steven S. Ball ◽  
C. G. Dean Dais ◽  
Harold C. Pillsbury
Keyword(s):  
Tumor Necrosis Factor ◽  
Middle Ear ◽  
Rat Model ◽  
Tumor Necrosis ◽  
Otitis Media With Effusion ◽  
Interleukin 1 ◽  
Enzyme Linked Immunosorbent Assay ◽  
Novel Approach ◽  
Necrosis Factor

In a rat model, we investigated the role of tumor necrosis factor (TNF) and interleukin-1 (IL-1) in endotoxin-induced middle ear effusions (MEEs). After the eustachian tube was obstructed, the middle ear was transtympanically injected with 35μL of either 1) 1 mg/ mL lipopolysaccharide (LPS); 2) LPS and 100 μg TNF binding protein (TNFbp); 3) LPS and 1 μg IL-1 receptor antagonist (IL-1ra); or 4) LPS, TNFbp, and IL-1ra. Every 2 hours, the fluid within the middle ear was collected, and the quantity of albumin in the fluid, an index of vascular leakage, was determined by enzyme-linked immunosorbent assay. After 6 hours, the middle ear was fixed for histologic analysis. The TNFbp significantly attenuated vascular extravasation into the middle ear. The IL-1ra did not significantly alter effusion development. These results indicate that TNF, but not IL-1, is a mediator of LPS-induced MEE. Therefore, TNFbp may represent a novel approach to the treatment of otitis media with effusion.

scholarly journals Inhibitory Activity ofFicus deltoideavar.trengganuensisAqueous Extract on Lipopolysaccharide-Induced TNF-αProduction from Microglia

2017 ◽  
Vol 2017 ◽  
pp. 1-7
Author(s):  
Huiling Wang ◽  
Sharmili Vidyadaran ◽  
Mohamad Aris Mohd Moklas ◽  
Mohamad Taufik Hidayat Baharuldin
Keyword(s):  
Tumor Necrosis ◽  
Therapeutic Potential ◽  
Immunocytochemical Staining ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Blank Control Group ◽  
Ficus Deltoidea ◽  
Bv2 Cells ◽  
Set Up ◽  
Necrosis Factor

Objective. To explore the effect ofFicus deltoidea(FD) aqueous extracts on the release of tumor necrosis factor-α(TNF-α), the expression of CD40, and the morphology of microglial cells in lipopolysaccharide- (LPS-) activated BV2 cells.Methods. The cytotoxicity of FD extract was assessed by MTS solution. BV2 cells were divided into 5 experimental groups, intervened, respectively, by FD (4 mg/mL) and LPS + FD (0, 1, 2, and 4 mg/mL). Besides, a blank control group was set up without any intervention. TNF-αrelease was assessed by enzyme linked immunosorbent assay (ELISA). The expression of CD40 was examined by flow cytometry. Immunocytochemical staining was used to show the morphology of BV2 cells.Results. FD extract of different concentrations (1, 2, and 4 mg/mL) had no significant toxic effects on the BV2 cells. FD suppressed the activation of microglia in morphology and reduced TNF-αproduction and expression of CD40 induced by LPS.Conclusion. FD extract has a therapeutic potential against neuroinflammatory diseases.

scholarly journals Role of inflammation and iron exchange disorders in progression of liver cirrosis

2021 ◽  
Vol 38 (1) ◽  
pp. 38-45
Author(s):  
I. A. Bulatova ◽  
A. P. Shchekotova ◽  
S. V. Paducheva
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Clinical Manifestations ◽  
Control Group ◽  
Necrosis Factor Alpha ◽  
Inflammatory Protein ◽  
Factor Alpha ◽  
Necrosis Factor

Objective. To assess the role of the main pathogenetically significant molecules, including tumor necrosis factor alpha (TNF-) and transferrin, as an inflammatory protein, in the progression of chronic diffuse liver diseases (CDLD). Material and methods. The study involved 86 patients with cirrhosis of the liver (LC) of viral, alcoholic and mixed etiology. Inflammatory parameters were studied, including tumor necrosis factor alpha (TNF-), indicators of iron metabolism, -fetoprotein (AFP), vasculoendothelial growth factor (VEGF), and functional liver biochemical tests. The control group consisted of 70 persons. Results. It was revealed that the LC severity class is interrelated with the clinical manifestations of the disease, the severity of biochemical syndromes as well as a significant increase in the concentration of -globulins, CRP, the amount of TNF- up to 3.5 (2.64.7) pg/ ml (p 0.001) and ferritin up to 325.8 (209; 401) ng / ml (p 0.001) compared to the control group. An increase in TNF- and ferritin as inflammatory protein in LC confirms the growth of the activity of inflammation in the liver and correlates with other parameters involved in the pathogenesis of LC: with VEGF, as a marker of endothelial dysfunction, which is involved in the activation of fibrosis and neoangiogenesis, and AFP, reflecting regeneration processes in the liver. Conclusions. The progression of liver damage in cirrhosis is based primarily on the secondary inflammation caused by portal hypertension with the entry of intestinal antigens and toxins into the central bloodstream. At the same time, the perverse circle of the development of the disease is closed.

Prediction of Survival in Patients with Non-Hodgkin’s Lymphoma: Role of Tumor Necrosis Factor Ligand-Receptor and Extracellular Protein Kinase A.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 4737-4737
Author(s):  
Chul Won Choi ◽  
Soo-Young Yoon ◽  
Hwa Jung Sung ◽  
In Keun Choi ◽  
Seok Jin Kim ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Tumor Necrosis Factor ◽  
Protein Kinase A ◽  
Patient Group ◽  
Tumor Necrosis ◽  
Extracellular Protein ◽  
Control Group ◽  
Necrosis Factor ◽  
Kinase A

Abstract Backgrounds: The International Prognostic Index (IPI) is the most commonly used survival parameter for patients with Non-Hodgkin’s lymphoma (NHL). To investigate an another factor to predict survival, we studied the role of tumor necrosis factor receptor with molecular weight of 75 kd (p75-R-TNF) and extracellular protein kinase A (ECPKA). TNF has a central role in inflammatory processes, and its receptor is constitutively found in the circulation and is elevated in a variety diseases. The cAMP-dependent protein kinase (PKA) is critically involved in the regulation of metabolism, cell growth and differentiation, and gene expression. PKA is a predominantly intracellular enzyme, but it has been shown that cancer cells of various cell types excrete PKA into the conditioned medium. This extracellular form i.e., ECPKA is known to be upregulated in the serum of cancer patients as compared with normal serum. The aim of this prospective study was to evaluate p75-R-TNF and ECPKA as feasible prognostic factors for patients with NHL. Methods: From October 2003 to May 2005, chemotherapy-naive patients with NHL who were planned to receive CEOP-B or R-CHOP chemotherapy at Guro Hospital, Korea University were enrolled. Blood sampling for p75-R-TNF and ECPKA was done before chemotherapy initiation and was stored at −70°C until the assay. The level of p75-R-TNF was measured using ELISA kit. ECPKA was measured by RIA method. A total of 20 serum samples from normal people were used as control. Results: A total of 45 patients were enrolled. The male to female ratio was 22:23, and the median age was 58 years old (range: 29–87). Indolent histologic type and aggressive type were 4 and 41 patients, respectively. Twenty-two patients were limited stage (stage I, II) and 23 patients were advanced stage (stage III, IV). The level (mean±SD) of p75-R-TNF was 1066.6±1174.9 pg/ml for patient group and that of control group was 678.2±312.4 pg/ml. ECPKA activity of patient group was 87.6±21.1 mU/ml as compared with 40.6±21.5 mU/ml in control group. During the median follow-up period of 8.5 months, 12 patients died and 33 patients were alive. As a result of univariate analysis, serum albumin (p=0.005), hemoglobin (p=0.054), the IPI score [0–2 vs 3–5] (p=0.006), occurrence of febrile neutropenia (p=0.01), and level of p75-R-TNF (p=0.003) were significantly associated with survival. By logistic regression testing, p75-R-TNF level was identified as an independent predictive factor for survival (p=0.037). Median survival of patients with elevated p75-R-TNF (cutoff: 678.2 pg/ml) was 10.5 months. For patients with p75-R-TNF < 678.2 pg/ml, median value was not reached yet. Conclusions: This study indicates that in addition to the IPI, high baseline levels of p75-R-TNF can predict the survival of patients with NHL. The levels of ECPKA were elevated in patient group than those of normal controls, but its level could not predict the prognosis.

scholarly journals The Role of Endothelial Dysfunction Markers in Pregnant Women with Chorion Detachment, Included in the Program of Auxiliary Reproductive Technologies

2017 ◽  
Vol 24 (3) ◽  
Author(s):  
Natalya Lytvyn
Keyword(s):  
Endothelial Dysfunction ◽  
Pregnant Women ◽  
Reproductive Function ◽  
Reproductive Technologies ◽  
The Body ◽  
Control Group ◽  
Vitro Fertilization ◽  
Endothelin 1

An urgent medical and social problem is the restoration of reproductive function of womenwho suffer from infertility, which became possible due to auxiliary reproductive technologies. Women with induced pregnancy make thegroup of a high-risk on miscarriage, due to interrelated processes –immunological disorders and endothelial dysfunction that occur in the body of pregnant women after the use of extracorporal fertilization programs, and can lead to the chorion detachment and the formation of subchorionic hematomas.The purpose of the study is to determine the role of endothelial dysfunction as one of the leading factors that determine the development of a local non-progressive chorion detachment in infertile patients included in the program of auxiliary reproductive technologies.Materials and methods. We have examined 130 pregnant women, who were divided into groups: the control group included 30 women, whose pregnancy occurred in the natural cycle and with uncomplicated gestational course; the main group – 50 patients with induced pregnancy and risk factors of the occurrence of chorion detachment, who wereperformed the proposed pre-gravidapreparation; the comparative group – 50 pregnant women who received a standard scheme of pregnancy management before and after in-vitro fertilization. A general clinical examination, ultrasound examination, homocysteine level determination, endothelin-1 and nitrogen oxide metabolites were performed.Results. In women included into the program of auxiliary reproductive technologies with local chorion detachment were recorded changes of vascular endothelial function with a possible increase in endothelin-1 production and a decrease of the nitric oxidesynthesis. During the induced pregnancy with the presence of subchorionic hematoma, an increase of the level of endothelium-damaging factor of homocysteine was noted.Conclusions.This study identifies the parameters that reflect the main links of endothelial dysfunction and can be used as markers of local chorion detachment.

scholarly journals The Role of High Concentration of Resistin in Endothelial Dysfunction Through Induction of Proinflammatory Cytokines Tumor Necrosis Factor-alpha (TNF-alpha), Interleukin-6 (IL-6) and Chemokin Monocyte Chemotactic Protein-1 (MCP-1)

2009 ◽  
Vol 1 (2) ◽  
pp. 24
Author(s):  
Anna Meiliana ◽  
Ilhamjaya Patellongi ◽  
Andi Wijaya
Keyword(s):  
Endothelial Dysfunction ◽  
Tumor Necrosis Factor ◽  
Proinflammatory Cytokines ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
High Concentration ◽  
Chemotactic Protein ◽  
Tnf Α ◽  
Necrosis Factor

BACKGROUND: Many previous studies have reported that central obesity is related to inflammation and endothelial dysfunction. It has also been reported that resistin can induce proinflammatory cytokines TNF-α and IL-6, which can result in endothelial dysfunction, although the role of resistin in human remains unclear. The aim of this study was to assess the role of resistin in influencing the proinflammatory cytokines TNF-α, IL-6, and chemokin MCP-1 in nondiabetic, central obese individuals. Results of this study are hoped to be useful to make a strategy for early prevention of endothelial dysfunction especially in obese individuals.METHOD: This was a cross-sectional study on 73 non diabetic obese male subjects (waist circumferences >90 cm). Resistin, hs-TNF-α, IL-6, MCP-1, VCAM-1 were assessed by ELISA. Statistical analysis was performed using SPSS for Windows v.11.5 with significance p<0.05. The correlations among biomarkers were assessed using Spearman’s Rho test.RESULTS: The study results showed a significant correlation between resistin and TNF-α (r=0.274, p<0.005), and a significant correlation between TNF-α and IL-6 (r=0.430, p<0.001). It was found that high concentration of resistin caused the concentration of TNF-α , IL-6 and MCP-1 to increase, and affected the increase of VCAM-1 (p=0.0030), A significant correlation between waist circumference and inflammation (hsCRP, r=0.296, p<0.005; IL-6, r=0.374, p<0.001 and HOMA IR, r=0.331, p<0.001) was also found.CONCLUSION: This study showed that the role of resistin in endothelial dysfunction occurred at a high concentration of resistin through induction of proinflammatory cytokines TNF-α, IL-6, and chemokin MCP-1. We suggest that inflammation in obesity starts with a positive feedback loop mechanism between resistin and TNF-α.KEYWORDS: obesity, inflammation, adipocytokines, resistin, tumor necrosis factor-α, interleukin-6, monocyte chemotactic protein-1, vascular cell adhesion molecule–1

Sign in / Sign up

Export Citation Format

Share Document