The Impact of Tumor Necrosis Factor-α and Interleukin-1β Levels and Polymorphisms on Long-Term Stroke Outcomes

2017 ◽  
Vol 79 (1-2) ◽  
pp. 38-44 ◽  
Author(s):  
Ju-Wan Kim ◽  
Man-Seok Park ◽  
Joon-Tae Kim ◽  
Hee-Ju Kang ◽  
Kyung-Yeol  Bae ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Stroke Outcomes ◽  
Tnf Α ◽  
Poor Outcomes ◽  
Factor Α ◽  
The Impact ◽  
Necrosis Factor

Background: The accuracy of predictions regarding disability that sets in after stroke could be improved by using blood biomarker measurements. This study aimed to investigate the roles of serum tumor necrosis factor alpha (TNF-α) and interleukin (IL)-1β concentrations and polymorphisms in stroke outcomes. Methods: In total, 286 patients were evaluated at the time of admission and at 2 weeks after stroke, and 222 of these patients (78%) were followed up for 1 year to evaluate the consequences of stroke during both the acute and chronic stages. Stroke outcomes were dichotomized into good and poor using the modified Rankin Scale. Results: The association of TNF-α and IL-1β concentrations and their corresponding genotypes with stroke outcomes was investigated using multivariate logistic regression. Higher TNF-α levels were associated with poor outcomes 1 year after stroke in the presence of the –850T and –308A alleles, and IL-1β levels were associated with poor 1-year stroke outcomes in the presence of the –511T and +3953T alleles. No such associations were found at 2 weeks after stroke. Conclusions: These data provide evidence that serum TNF-α and IL-1β concentrations are related to poor long-term outcomes after stroke in the presence of particular alleles.

Tumor Necrosis Factor-α Production-Enhancing Properties of Novel Adamantylalkylthio Derivatives of Some Heterocyclic Compounds

2005 ◽  
Vol 60 (4) ◽  
pp. 471-475 ◽  
Author(s):  
Barbara Orzeszko ◽  
Tomasz Świtaj ◽  
Anna B. Jakubowska-Mućka ◽  
Witold Lasek ◽  
Andrzej Orzeszko ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Heterocyclic Compounds ◽  
Tumor Necrosis ◽  
The Novel ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Factor Α ◽  
Derivatives Of ◽  
Necrosis Factor

Certain adamantylated heterocycles were previously shown to enhance the secretion of tumor necrosis factor alpha (TNF-α) by murine melanoma cells that have been transduced with the gene for human TNF-α and constitutively expressed this cytokine. The stimulatory potency of those compounds depended, among other factors, on the structure of the linker between the adamantyl residue and the heterocyclic core. In the present study, a series of (1-adamantyl)alkylsulfanyl derivatives of heterocyclic compounds was prepared by alkylation of the corresponding thioheterocyles. Of the novel adamantylalkylthio compounds tested in the aforementioned cell line, 2-(2-adamantan-1-ylethylsulfanyl)- 4-methyl-pyrimidine was found to be the most active

Comparisons of the Effects of Anesthesia and Stress on Release of Tumor Necrosis Factor-α, Leptin, and Nitric Oxide in Adult Male Rats

2001 ◽  
Vol 226 (4) ◽  
pp. 296-300 ◽  
Author(s):  
Claudio A. Mastronardi ◽  
Wen H. Yu ◽  
Samuel M. McCann
Keyword(s):  
Nitric Oxide ◽  
Tumor Necrosis Factor ◽  
Adult Male ◽  
Tumor Necrosis ◽  
Fold Increase ◽  
Male Rats ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Bacterial lipopolysaccharide (LPS) stimulates massive release of tumor necrosis factor-alpha (TNF-α) together with nitric oxide (NO) and a lessor release of leptin. We hypothesized that other types of stress such as that of surgery might also release these cytokines and NO. Adult male rats were anesthetized with ketamine/acepromazine/xylazine anesthesia (90 + 2 + 6 mg/ml, respectively) and an external jugular catheter was inserted for removal of blood samples (0.6 ml) at various times postoperatively. Plasma TNF-α was almost undetectable in decapitated rats and was near zero immediately following the placement of the jugular catheter (time zero [to]). As the rats awakened from anesthesia, there was a rise in TNF-α at 30 min that peaked at 2 hr with a 400-fold increase and then precipitously declined 40-fold to a level still greater than zero at 3 hr. At 6 hr on the following morning, TNF-α values were near zero, but following connection of tubing and withdrawal of the initial blood sample, there was a 100-fold increase 1 hr later, followed by a decline over the next 3 hr. In contrast, plasma [NO3/NO2] from decapitated rats was 117 μM. Values at t0 were decreased and plummeted 4-fold within 30 min, then rose slightly in the ensuing 3 hr. At 6 hr on the next day [NO3/NO2] values were lower than at t0 and declined gradually during the next 4 hr. Leptin gradually declined from pre-operative concentrations, reaching a minimum at 3 hr and its concentration was unaffected by the bleeding stress of the second day. We conclude that release of TNF-α, [NO3/NO2], and leptin are neurally controlled since plasma levels of all three declined as a result of anesthesia. TNF-α secretion was remarkably stress responsive, whereas NO release appeared to be suppressed by the combined operative and bleeding stress, and leptin was stress unresponsive.

Exposure to prolonged unpredictable light impairs spatial memory via induction of oxidative stress and tumor necrosis factor-alpha in rats

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Oluwaseun S. Faborode ◽  
Issa O. Yusuf ◽  
Paschal O. Okpe ◽  
Ann O. Okudaje ◽  
Samuel A. Onasanwo
Keyword(s):  
Oxidative Stress ◽  
Object Recognition ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Light Exposure ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

Abstract Objectives The human body physiology rapidly changes and adapt to several environmental stimuli, including light. Abnormal artificial light exposures have been shown to affect sleep cycle, cognition, and mood. Although studies have reported inconsistent effects of short-term or constant long-term light exposures, human exposures to artificial lights occur at varying, unpredictable times and duration daily. Here, we studied the effects of long-term unpredictable light exposure on learning, memory, oxidative status, and associated cytokines in rats. Methods Artificial lighting was provided using an array of white light-emitting diodes coupled to a microcontroller that switches them on or off at unpredictable times and duration (light intensity = 200 ± 20 lx). Within the last eight days of 40 days exposure, animals were subjected to open field test, Morris water maze, and novel object recognition behavioral paradigms. Brain levels of malondialdehyde (MDA), superoxide dismutase (SOD), catalase, reduced glutathione (GSH), glutathione S-transferase (GST), tumor necrosis factor-alpha (TNF-α), and vascular endothelial growth factor (VEGF) were assayed. Results Exposed rats showed impaired spatial learning and memory (p<0.05), but no changes in object recognition memory or locomotor activity. Oxidative stress analyses also revealed significant changes in the concentrations of MDA, SOD, catalase, and GSH levels (p<0.05), not GST. Similarly, there was an increased TNF-α expression (p<0.05), not VEGF. Conclusions We conclude that oxidative stress is involved in memory impairment in rats exposed to prolonged unpredictable lights, which again suggests the detrimental effects of extended light exposure on the nervous system.

scholarly journals Tumor Necrosis Factor-α sebagai Prediktor Terjadinya Anemia pada Ibu Hamil di Wilayah Endemis Malaria

2015 ◽  
Vol 9 (3) ◽  
pp. 288
Author(s):  
Rostika Flora ◽  
Mukni Mukni ◽  
Bina Melvia Girsang ◽  
Sigit Purwanto
Keyword(s):  
Tumor Necrosis Factor ◽  
Malaria Infection ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Α Level ◽  
Factor Α ◽  
Necrosis Factor ◽  
Pregnant Mothers

Ibu hamil yang berada di daerah endemis malaria sangat rentan terhadap infeksi malaria selama kehamilan. Gejala malaria pada kelompok ini sering asimptomatik atau bahkan tidak terdeteksi sama sekali karena adanya efek imunitas protektif melalui infeksi yang berulang. Adanya peningkatan kadar tumor necrosis factor-alpha (TNF-α) dapat dijadikan indikator terjadinya infeksi malaria. TNF-α berperan penting dalam respons imun pada malaria akut yang menghambat terjadinya eritropoesis. Penelitian ini bertujuan untuk mengetahui hubungan antara kadar TNF-α dengan kejadian anemia pada ibu hamil didaerah endemik malaria vivax. Penelitian ini menggunakan desain potong lintang, dilakukan pada bulan Januari - Februari 2014 di lima wilayah kerja puskesmas Kota Bengkulu. Sampel penelitian adalah ibu hamil di daerah endemis malaria vivax yang diambil secara accidental sampling. Dilakukan pengambilan darah untuk pemeriksaan mikroskopis malaria, kadar TNF-α dan kadar hemoglobin (Hb). Hasil penelitian menunjukkan seluruh ibu hamil memiliki riwayat pernah terinfeksi malaria vivax, walaupun hasil pemeriksaan slide negatif. Terjadi peningkatan kadar TNF- α dengan rerata 6,90 ± 2,48 pg/mL dan penurunan kadar Hb dengan rerata 9,75 ± 0,88 g%. Uji korelasi Spearman didapatkan korelasi negatif yang kuat (r = -0,734) dan bermakna (nilai p < 0,05) antara Kadar TNF-α dengan kadar Hb. Terdapat hubungan yang bermakna antara kadar TNF-α dengan kejadian anemia.Tumor Necrosis Factor-α as Predictor of Anemia Occurrence among Pregnant Mothers in Malaria-Endemic AreasPregnant mothers living in malaria - endemic area are very susceptible to malaria infection during pregnancy. Malaria symptoms in this group are often asymptomatic or even not detected at all due to protective immunity effect through repeated infections. Any elevation of tumor necrosis factor-alpha (TNF-α) level can be used as indicator of malaria infection. TNF-α takes an important role in immune response on acute malaria that hinders occurence eritropoesis process. This study aimed to find out relations between TNF-α level and anemia occurrence among pregnant women living in malaria vivax - endemic areas. The study used cross-sectional design conducted on January to February 2014 in five working areas in Bengkulu city. Sample of study was pregnant mothers in malaria vivax - endemic areas which was taken through accidental sampling. Blood was taken for malaria-microscopic examination, TNF-α and haemoglobine (Hb) level. The results showed that all of pregnant mothers have malaria vivax - infected record, although slide examination showed negative result. Any TNF-α level elevation with average 6.90 ± 2.48 pg/mL and decrease of Hb level with average 9.75 ± 0.88 g%. Spearman correlation test showed strong negative correlation (r = -0.734) and significant (p value < 0.05) between TNF-α level and Hb level. There was significant relation between TNF-α level and anemia occurrence.

scholarly journals Recombinant Tumor Necrosis Factor Alpha Does Not Inhibit the Growth of African Trypanosomes in Axenic Cultures

2002 ◽  
Vol 70 (4) ◽  
pp. 2210-2214 ◽  
Author(s):  
Hiroshi Kitani ◽  
Samuel J. Black ◽  
Yoshio Nakamura ◽  
Jan Naessens ◽  
Noel B. Murphy ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Culture Conditions ◽  
Necrosis Factor Alpha ◽  
African Trypanosomes ◽  
Tnf Α ◽  
Factor Alpha ◽  
The Impact ◽  
Necrosis Factor

ABSTRACT Mice whose tumor necrosis factor alpha (TNF-α) genes were disrupted developed higher levels of parasitemia than wild-type mice following infection with Trypanosoma congolense IL1180 or T. brucei brucei GUTat3.1, confirming the results of earlier studies. To determine whether TNF-α directly affects the growth of these and other bloodstream forms of African trypanosomes, we studied the effects of recombinant mouse, human, and bovine TNF-α on the growth of two isolates of T. congolense, IL1180 and IL3338, and two isolates of T. brucei brucei, GUTat3.1 and ILTat1.1, under axenic culture conditions. The preparations of recombinant TNF-α used were biologically active as determined by their capacity to kill L929 cells. Of five recombinant TNF-α lots tested, one lot of mouse TNF-α inhibited the growth of both isolates of T. brucei brucei and one lot of bovine TNF-α inhibited the growth of T. brucei brucei ILTat1.1 but only at very high concentrations and without causing detectable killing of the parasites. The other lots of mouse recombinant TNF-α, as well as human TNF-α, did not affect the growth of any of the test trypanosomes even at maximal concentrations that could be attained in the culture systems (3,000 to 15,000 U of TNF-α/ml of medium). These results suggest that exogenously added recombinant TNF-α generally does not inhibit the growth of African trypanosomes under the culture conditions we used. The impact of TNF-α on trypanosome parasitemia may be indirect, at least with respect to the four strains of trypanosomes reported here.

scholarly journals The characterization of tumor necrosis factor alpha (TNF-α), its role in cancerogenesis and cardiovascular system diseases and possibilities of using this cytokine as a molecular marker

2017 ◽  
Vol 13 ◽  
pp. 1-8 ◽  
Author(s):  
Beniamin Grabarek ◽  
Martyna Bednarczyk ◽  
Urszula Mazurek
Keyword(s):  
Tumor Necrosis Factor ◽  
Molecular Marker ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Inflammatory Diseases ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
The Impact ◽  
Necrosis Factor

The inflammatory process is directly associated with secretion of cytokines, e.g. tumor necrosis factor alpha (TNF-α). This molecule is one of the 22 proteins which belong to TNF family and is secreted mainly by: macrophages, monocytes, T lymphocyte and mast cells. The biological effects of TNF-α is possible through binding this cytokine to specific receptors – TNFR1 and TNFR2. The large number of reports provides that this cytokine plays extremely important role in cancers and cardiovascular disease – two groups of inflammatory diseases. Unfortunately, these diseases are the main cause of death in spite of advances in medicine and increasing public awareness of prevention. It is believed that better understanding both molecular potential of this cytokine and the impact in cancerogenesis and others inflammatory diseases may cause using TNF-α as a molecular marker in these diseases and will make it possible to observe the effects of anti-inflammatory therapy. It will be able to cause a drop in the incidence of these diseases and better monitoring of them.

scholarly journals Tumor necrosis factor-α induces a biphasic change in claudin-2 expression in tubular epithelial cells: role in barrier functions

2015 ◽  
Vol 309 (1) ◽  
pp. C38-C50 ◽  
Author(s):  
Yasaman Amoozadeh ◽  
Qinghong Dan ◽  
Jenny Xiao ◽  
Faiza Waheed ◽  
Katalin Szászi
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Mrna Levels ◽  
Tnf Α ◽  
Biphasic Effect ◽  
Early Increase ◽  
Factor Α ◽  
The Impact ◽  
Necrosis Factor

The inflammatory cytokine tumor necrosis factor-α (TNF-α) is a pathogenic factor in acute and chronic kidney disease. TNF-α is known to alter expression of epithelial tight junction (TJ) proteins; however, the underlying mechanisms and the impact of this effect on epithelial functions remain poorly defined. Here we describe a novel biphasic effect of TNF-α on TJ protein expression. In LLC-PK1 tubular cells, short-term (1–6 h) TNF-α treatment selectively elevated the expression of the channel-forming TJ protein claudin-2. In contrast, prolonged (>8 h) TNF-α treatment caused a marked downregulation in claudin-2 and an increase in claudin-1, -4, and -7. The early increase and the late decrease in claudin-2 expression involved distinct mechanisms. TNF-α slowed claudin-2 degradation through ERK, causing the early increase. This increase was also mediated by the EGF receptor and RhoA and Rho kinase. In contrast, prolonged TNF-α treatment reduced claudin-2 mRNA levels and promoter activity independent from these signaling pathways. Electric Cell-substrate Impedance Sensing measurements revealed that TNF-α also exerted a biphasic effect on transepithelial resistance (TER) with an initial decrease and a late increase. Thus there was a good temporal correlation between TNF-α-induced claudin-2 protein and TER changes. Indeed, silencing experiments showed that the late TER increase was at least in part caused by reduced claudin-2 expression. Surprisingly, however, claudin-2 silencing did not prevent the early TER drop. Taken together, the TNF-α-induced changes in claudin-2 levels might contribute to TER changes and could also play a role in newly described functions of claudin-2 such as proliferation regulation.

scholarly journals Association between five types of Tumor Necrosis Factor-α Gene Polymorphism and Hepatocellular Carcinoma Risk: A Meta-Analysis

2020 ◽  
Author(s):  
Citrawati Dyah Kencono Wungu ◽  
Fis Citra Ariyanto ◽  
Gwenny Ichsan Prabowo ◽  
Soetjipto Soetjipto ◽  
Retno Handajani
Keyword(s):  
Hepatocellular Carcinoma ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Meta Analysis ◽  
Random Effect ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Α ◽  
The Relationship ◽  
Necrosis Factor

Abstract Background: Research focusing on the relationship between five types of tumor necrosis factor-alpha (TNF-α) SNPs and the risk of hepatocellular carcinoma (HCC) were still controversial. Hereby, we performed a meta-analysis to determine the association between TNF-α promoter SNPs: -1031 T/C, -863 C/A, -857 C/T, -308 G/A, and -238 G/A with HCC risk. Methods: We interrogated articles from journal database: PubMed, Pro-Quest, EBSCO, Science Direct, and Springer to determine the relationship between five types of SNPs in TNF-α gene with HCC risk. RevMan 5.3 software was used for analysis in fixed/random effect models. Results: This meta-analysis included 23 potential articles from 2004-2018 with 3,237 HCC cases and 4,843 controls. We found that SNP -863 C/A were associated with a significantly increased HCC risk (A vs C, OR=1.31, 95% CI=1.03-1.67). Similar results were obtained in -857 C/T (TT/CT vs CC, OR=1.31, 95% CI=1.06-1.62), -308 G/A (AA vs GG, OR=3.14, 95% CI=2.06-4.79), and -238 G/A (AA vs GG, OR=3.87, 95% CI=1.32-11.34). While no associations were observed between SNP TNF-α -1031 T/C and HCC risk.Conclusions: The present meta-analysis showed that TNFα SNPs -863C/A, -857 C/T, -308 G/A, and -238 G/A were associated with the risk of HCC.

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