scholarly journals The Effects of Obesity on Local and Circulating Levels of Tumor Necrosis Factor-α and Interleukin-6 in Patients with Chronic Periodontitis

2015 ◽  
Vol 7 (1) ◽  
pp. 7-14 ◽  
Author(s):  
Oğuz Kose ◽  
Varol Canakcı ◽  
Cenk Fatih Canakcı ◽  
Abdulkadir Yıldırım ◽  
Eda Kermen ◽  
...  
Keyword(s):  
Chronic Periodontitis ◽  
Tumor Necrosis ◽  
Serum Levels ◽  
Normal Weight ◽  
Control Group ◽  
Tnf Α ◽  
Factor Α ◽  
Circulating Levels ◽  
Necrosis Factor ◽  
Control Group Group

Background and aims. The aim of this study was to evaluate the possible effects of obesity on the local (salivary) and systemic TNF-α and IL-6 levels in patients with chronic periodontitis (CP). Materials and methods. This study included 88 subjects assigned to four groups of 22 subjects each, as follows: group O+P+ (patients with obesity and CP), group O-P+ (patients with normal weight and CP), group O+P- (periodontally healthy patients with obesity), and the control group, group O-P- (periodontally healthy patients with normal weight). Serum and salivary samples were obtained a week before the recording of clinical periodontal parameters. Local and systemic TNF-α and IL-6 levels were determined biochemically. Results. In serum and saliva, both TNF-α and IL-6 levels were the lowest in O-P- group (P < 0.05). The highest TNF-α and IL-6 levels were observed in O+P+ group, while only IL-6 levels were statistically significant (P < 0.05). Conclusion. Obesity upregulated the salivary and serum levels of TNF-α and IL-6. In patients with periodontitis, who were also obese, the serum and saliva levels of IL-6 were significantly high. Obesity might play a destructive and provocative role in the pathogenesis of periodontitis by negatively affecting IL-6 levels.

Effect of Hypothermia on Serum Myelin Basic Protein and Tumor Necrosis Factor-α in Neonatal Hypoxic-Ischemic Encephalopathy

2021 ◽  
Author(s):  
Qiuli Wang ◽  
Hongyan Lv ◽  
Sujing Wu ◽  
Junxia Song ◽  
Junqin Li ◽  
...  
Keyword(s):  
Tumor Necrosis ◽  
Basic Protein ◽  
Serum Levels ◽  
Control Group ◽  
Tnf Α ◽  
Hypothermia Group ◽  
Neurodevelopmental Impairment ◽  
Factor Α ◽  
Ischemic Encephalopathy ◽  
Necrosis Factor

Objective Multiple randomized controlled trials have shown that hypothermia is a safe and effective treatment for neonatal moderate or severe hypoxic-ischemic encephalopathy (HIE). The neuroprotective mechanisms of hypothermia need further study. The aim of this study was to investigate the effect of hypothermia on the serum levels of myelin basic protein (MBP) and tumor necrosis factor-α (TNF-α) as well as neurodevelopmental outcomes in neonatal HIE. Study Design Eighty-five neonates with moderate-to-severe HIE were divided into a hypothermia group (n = 49) and a control group (n = 36). Serum levels of MBP and TNF-α within 6 hours after birth and after 3 days of treatment were determined by enzyme-linked immunosorbent assay, and neurodevelopmental outcome at the age of 12 to 15 months was assessed by using the Gesell development scale. Results After 3 days of treatment, serum levels of MBP and TNF-α in the control group were not significantly different from levels before treatment (p > 0.05), and serum levels of MBP and TNF-α in the hypothermia group were significantly lower than levels before treatment (p < 0.05). Serum levels of MBP and TNF-α were significantly negatively correlated with developmental quotient (DQ; r =  − 0.7945, p = 0.0000; r =  − 0.7035, p = 0.0000, respectively). Serum levels of MBP and TNF-α in neurodevelopmentally impaired infants were significantly higher than those in infants with suspected neurodevelopmental impairment and those in neurodevelopmentally normal infants (both p < 0.01). The rate of reduction of neurodevelopmental impairment was higher among infants in the hypothermia group than among those in the control group (χ2 = 16.3900, p < 0.05). Conclusion Hypothermia can reduce serum levels of MBP and TNF-α in neonates with HIE. Inhibiting the release of TNF-α may be one of the mechanisms by which hypothermia protects the myelin sheath. Key Points

Importance of Markers of Sepsis in Surgical Patients

2018 ◽  
Vol 84 (6) ◽  
pp. 1058-1063 ◽  
Author(s):  
Marek Smolár ◽  
Ivana Dedinská ◽  
Michal Hošala ◽  
Július Mazúch ◽  
L'Udovit Laca
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Serum Levels ◽  
Control Group ◽  
Risk Of Death ◽  
Significant Difference ◽  
Important Position ◽  
Factor Α ◽  
Necrosis Factor ◽  
Septic Condition

Sepsis, severe sepsis, and septic shock represent a serious medicinal and general social problem and still maintain an important position among the present issues in the basic and clinical research. In the prospective analysis of patients satisfying the criteria of septic condition, we determined serum levels of bioparameters in three consecutive days from the first signs of sepsis depending on the stage or advancement of the septic condition. We determined the most significant parameter/parameters which are able to determine the stage of sepsis or to predict patient's death. In the group of 68 patients, all monitored biomarkers showed significant difference in serum concentrations versus the control group (P = 0.001). The strongest positive connection between the seriousness of sepsis and serum level is in case of procalcitonin. Predictor of mortality (r = -0.468; P = 0.001), transferrin (r = -0.506; P = 0.003), and tumor necrosis factor-α (r = 0.939; P = 0.001). Our results show that the monitored parameters (procalcitonin, C-reactive protein, tumor necrosis factor-a, and interleukin 6) have strong correlations between the serum levels and the stage of disease. Examination of at least one cytokine in normal clinical practice might lead to better interpretation of the patient's condition, determining the risk of death.

The change of proinflammatory cytokine tumor necrosis factor α level in the use of meloxicam in rat model of osteoarthritis

2019 ◽  
Vol 30 (6) ◽  
Author(s):  
Junaidi Khotib ◽  
Naning Windi Utami ◽  
Maria Apriliani Gani ◽  
Chrismawan Ardianto
Keyword(s):  
Tumor Necrosis Factor ◽  
Rat Model ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Control Group ◽  
Treatment Groups ◽  
Tnf Α ◽  
Α Level ◽  
Factor Α ◽  
Necrosis Factor

Abstract Background Osteoarthritis (OA) is a chronic disease in the joints. One of the proinflammatory cytokines that is thought to have a major role in the inflammatory process, the emergence of pain, and cartilage damage in OA is tumor necrosis factor α (TNF-α). Meloxicam is a nonsteroidal anti-inflammatory drug class of drugs that is relatively selective in inhibiting the activity of cyclooxygenase 2 (COX-2) formation. This study is conducted to prove the change in TNF-α level in the use of meloxicam with model in animals suffering from OA. Methods The OA rat model was induced with sodium monoiodoacetate intra-articularly. Rats were divided into 5 groups: negative control group, positive control group, and treatment groups with various doses of meloxicam. Hyperalgesia effect was evaluated using a warm plate test, and TNF-α level was determined using enzyme-linked immunosorbent assay. Results The treatment groups that received meloxicam at a dose of 1.0, 3.0, or 10.0 mg/kg body weight (BW) did not show significant differences in rat knee joint diameter (p = 0.99), but showed a significant difference in sensitivity to heat stimulation (p = 0.02) compared to the control group. Osteoarthritis rats experienced a significant reduction in TNF-α level after being given meloxicam at a dose of 10 mg/kg BW compared with the control group. This shows that the 10 mg/kg BW of meloxicam is a potential dose in reducing the TNF-α level in OA rat models. Conclusions Based on these data, it can be concluded that the inhibition of pain and the development of OA by meloxicam in animal models may be assigned to a decreased level of TNF-α.

scholarly journals Application of Dexmedetomidine in Cardiopulmonary Bypass Prefilling

Dose-Response ◽  
2020 ◽  
Vol 18 (3) ◽  
pp. 155932582093976 ◽  
Author(s):  
Li Wang ◽  
Shaowei Wang ◽  
Zhen Xing ◽  
Fulong Li ◽  
Jinliang Teng ◽  
...  
Keyword(s):  
Cardiopulmonary Bypass ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Serum Levels ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Anesthesia Induction ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Objective: The purpose of this study was to explore the application of dexmedetomidine (Dex) in cardiopulmonary bypass. Methods: A total of 60 patients undergoing elective cardiopulmonary bypass were divided into control (C) group and Dex group. In the Dex group, appropriate amount of Dex was added into the membrane lung prefilling solution before anesthesia induction, while those in control group were given normal saline. The levels of mean arterial pressure (MAP) and heart rate (HR) at different times were measured. The levels of cardiac troponin I (CTNI), malondialdehyde (MDA), interleukin 6 (IL-6), and tumor necrosis factor α (TNF-α) at different points (T0/T1/T2/T3/T4) in both groups were measured by enzyme-linked immunosorbent assay kits. Results: The intraoperative and postoperative levels of MAP and HR in the 2 groups were significantly lower than those preoperatively ( P < .05). The levels of MAP and HR in the Dex group were significantly lower than those of the C group ( P < .05). The levels of CTNI/MDA/IL-6/TNF-α at different points in both groups were significantly higher than those at T0 ( P < .05). The serum levels of CTNI, MDA, IL-6, and TNF-α in the Dex group at T1/T2/T3/T4 were significantly lower than those in the C group ( P < .05). The rate of arrhythmia in the Dex group was significantly lower than that in the C group ( P < .05). Conclusion: Dexmedetomidine has a stable effect in cardiopulmonary priming solution.

Induction of endogenous tumor necrosis factor-α: suppression of centrally stimulated gastric motility

1999 ◽  
Vol 276 (1) ◽  
pp. R59-R68 ◽  
Author(s):  
Gerlinda E. Hermann ◽  
C. Amy Tovar ◽  
Richard C. Rogers
Keyword(s):  
Tumor Necrosis Factor ◽  
Gastric Motility ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Gastric Stasis ◽  
Intravenous Injections ◽  
Tnf Α ◽  
Factor Α ◽  
Circulating Levels ◽  
Necrosis Factor

Gastric stasis is frequently seen in conjunction with critical infectious illness, chronic inflammatory disorders, radiation sickness, and carcinogenesis. These conditions are associated with elevated circulating levels of the cytokine tumor necrosis factor-α (TNF-α). The present studies examined the relationship between endogenously produced TNF-α and the central neural mechanisms that augment gastric motility. Systemic lipopolysaccharide (LPS) was employed to induce TNF-α production in thiobutabarbital-anesthetized rats. Sixty minutes after intravenous LPS injection, gastric motility could not be stimulated by a potent centrally acting gastrokinetic stimulant, thyrotropin-releasing hormone (TRH). This failure to elicit gastric motility via central mechanisms coincided with high circulating levels of TNF-α. However, intravenous injections of bethanecol, a peripherally acting cholinergic agonist with direct gastrokinetic effects, were still able to elicit normal increases in gastric motility in the presence of TNF-α and LPS. Therefore, the inability to stimulate gastric motility via central TRH could not be attributed to the direct inhibitory effects of either LPS or TNF-α on the stomach. If the production of endogenous TNF-α was suppressed via the use of urethan as the anesthetic agent, then intravenous injections of LPS were no longer effective in suppressing gastric motility. Thus these effects on gastric motility are not directly attributable to LPS nor are they due to direct effects on the gastric smooth muscle. Our previous study demonstrated that microinjection of femtomole quantities of TNF-α in the brain stem dorsal vagal complex (DVC) can modulate gastric motility. This central TNF-α effect on gastric motility was dose dependent and required an intact vagal efferent pathway. The results from these two studies suggest that systemically produced TNF-α may gain access to the DVC to modulate gastric function.

Serum levels of interleukin 6 and tumor necrosis factor-α in hyperthyroid patients before and after propylthiouracil treatment

1995 ◽  
Vol 132 (6) ◽  
pp. 668-672 ◽  
Author(s):  
Ismail Çelik ◽  
Sema Akalin ◽  
Tomris Erbaş
Keyword(s):  
Tumor Necrosis Factor ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Serum Levels ◽  
Graves Disease ◽  
Tnf Α ◽  
Factor Α ◽  
Hyperthyroid Patients ◽  
Necrosis Factor

Çelik I, Akalin S, Erbaş T. Serum levels of interleukin 6 and tumor necrosis factor-α in hyperthyroid patients before and after propylthiouracil treatment. Eur J Endocrinol 1995;132:668–72. ISSN 0804–4643 Contrary to the usual inhibitory role of tumor necrosis factor-α (TNF-α) thyroid metabolism, it also has specific stimulatory effects in autoimmune thyroid disorders, including induction of HLA class II antigen-presenting cell—T cell interaction. Despite high intrathyroidal concentrations, various studies were not able to demonstrate high serum levels of TNF-α in patients with Graves' disease. To investigate this discrepancy we determined TNF-α and interleukin 6 (IL-6) levels in 25 hyperthyroid patients who responded to propylthiouracil treatment (16 with Graves' disease and nine with toxic multinodular goiter) and compared them with the levels found in euthyroid patients with simple diffuse goiter (n = 15) and normal healthy controls (n = 15). Median IL-6 levels were high in both Graves' disease and toxic multinodular goiter patients before propylthiouracil treatment (23 and 26.5 pg/ml, respectively). After restoring euthyroidism there was a statistically significant decline to near-normal levels (3 and 10 pg/ml, respectively). On the other hand, median serum TNF-α levels were high only in Graves' disease patients (20 pg/ml) and could not be normalized with antithyroid medication (20 pg/ml) compared to that of controls (5 pg/ml). Tumor necrosis factor-α, but not IL-6, was found to be high in the sera of Graves' disease patients when euthyroid, which may be due to an ongoing antigen–antibody interaction, a feature of autoimmune attack. It remains to be determined whether the degree of TNF-α and/or IL-6 elevation will be a predictor of disease recurrence. Ismail Çelik, Section of Oncology, Dept. of Medicine, Hacettepe University Institute of Oncology, Ankara 06100, Turkey

scholarly journals TINGGINYA KADAR TUMOR NECROSIS FACTOR-α (TNF-α) PLASMA PADA MENCIT BUNTING YANG TERINFEKSI PLASMODIUM BERGHEI BERHUBUNGAN KUAT DENGAN KADAR HEMOGLOBIN YANG RENDAH TETAPI TIDAK BERHUBUNGAN DENGAN BERAT BADAN JANIN RENDAH

2013 ◽  
Vol 2 (1) ◽  
pp. 51-64
Author(s):  
Yuliyanik Yuliyanik
Keyword(s):  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Placental Tissue ◽  
Control Group ◽  
Study Group ◽  
Low Weight ◽  
Tnf Α ◽  
Pregnant Mice ◽  
Factor Α ◽  
Necrosis Factor

Malaria infection in pregnancy may increase the morbidity and mortality of both mother and fetus. In pregnant women, it can lead to severe anemia, cerebral malaria, pulmonary edema, renal failure and even death, while in the fetus it can cause abortion, premature birth, low birth weight, and fetal death. Elevated levels of tumor necrosis factor-α(TNF-α ) is associated with low birth weight and anemia in pregnant women. This study was conducted to measure the levels of TNF-α in plasma and placental tissue, and hemoglobin levels as well as fetal weight to determine the relationship between them in P. berghei infected pregnant mice and normal pregnant mice. Seventeen BALB/c mice used in this study were divided into two groups, those were the study group (9 pregnant mice infected with P. berghei) and control group (8 pregnant mice not infected with P. berghei). Level of TNF-α were measured using Enzyme Linked Immunosorbent assay (R&D Systems, catalog A00B MT). Hemoglobin levels were determined using flowcytometri, whereas fetal weight were performed with Mettler analytical balance AE 50. T-test statistical analysis showed that the levels of TNF-α in plasma and placental tissue in study group were higher than control group (p=0.000, p=0.034). Hemoglobin levels in the study group were lower than control group (p=0.025). Fetal weights were also lower in fetuses of infected mice than fetuses of uninfected mice (p=0.002). Pearson correlation test showed increasing plasma levels of TNF-α in infected P. berghei pregnant mice were related with the decreasing levels of Hb, (r=-0.748; p=0.020,), whereas levels of placental TNF-α were not associated with hemoglobin level (p=0.337). Both plasma and placental levels of TNF-α were not associated with the incidence of fetal low weight (p=0.380, and p=0.365). It can be concluded that the increased levels of TNF-α is associated with decreased levels of hemoglobin (Hb), but not associated with fetal low weight.

scholarly journals Incidence of Toxoplasmosis in Psoriasis Patients and Possible Correlation with Tumor Necrosis Factor-α

2020 ◽  
Vol 17 (1(Suppl.)) ◽  
pp. 0214
Author(s):  
Entsar J. Saheb ◽  
Yasser A.H Al-Issa ◽  
Israa Salim Mussa ◽  
Khawla H. Zghair
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Control Group ◽  
City Hospital ◽  
Tnf Α ◽  
Medical City ◽  
Positive Rate ◽  
Factor Α ◽  
Necrosis Factor

            Toxoplasma gondii is an opportunistic parasite in immune-compromised persons. The prevalence of toxoplasmosis in psoriasis patients is investigated. In addition, the treatment effect on psoriasis patients infected with toxoplasmosis through evaluating Tumor Necrosis Factor-α (TNF-α) cytokine levels is studied. Blood samples were collected from 130 individuals who involved 60 control samples and 70 samples with psoriasis. They attended Medical City Hospital in Baghdad province from October 2017 - February 2018. Then, the anti- T. gondii antibodies (IgM and IgG) and TNF- α in the sera were determined via the enzyme linked immune-sorbent assay. The highest rate of anti-Toxoplasma IgG was in psoriasis patients before treatment, it was 45 (64.29%) compared with the control which was 33 (55.00%), while the highest sero-positive rate of T. gondii IgM in the control group was 14 (23.33%) compared with patients with psoriasis 10 (14.29%). The highest rate of toxoplasmosis was in the age group (21-30) years in psoriasis patients which was 14 (31.82%). In addition, the TNF- α levels in psoriatic patients before treatment were 180.2±2.2 µg/ml, and after treatment were 223.3±41.1 µg/ml compared with the healthy control group 90.5±1.9 µg/ml. These findings suggest that incidental rate of toxoplasmosis is higher in psoriasis patients. Thus, the incidental rate of toxoplasmosis could be considered as an indication to the high risk of psoriasis.

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