scholarly journals PROFIL TUMOR NECROSIS FACTOR (TNF-α) BERDASARKAN INDEKS MASSA TUBUH (IMT) PADA MAHASISWA FAKULTAS KEDOKTERAN UNSRAT ANGKATAN 2014

2015 ◽  
Vol 3 (2) ◽  
Author(s):  
Ivander A. Supit ◽  
Damajanty H. C. Pangemanan ◽  
Sylvia R. Marunduh
Keyword(s):  
Body Mass Index ◽  
Tumor Necrosis Factor ◽  
Body Mass ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Α Level ◽  
Necrosis Factor

Abstract: Tumor Necrosis Factor alpha (TNF-α) is one of the pleiotrophic cytokines that plays a role in the inflammatory process, initiates and activates polymorphonuclears (PMNs), therefore the PMNs can reach the infection site. This study aimed to determine the profile of TNF-α based on body mass index (BMI) among the students of the Faculty of Medicine Unsrat batch 2014. This was a survey study with a cross sectional design. The study population was students of the Faculty of Medicine University of Sam Ratulangi Manado batch 2014. The results showed that samples with BMI 18-18.9 had an average TNF-α level of 69.48 pg/ml; samples with BMI 19-19.9 had an average TNF-α level of 78.04 pg/ml; samples with BMI 20-20.9 had an average TNF-α level of 61.94 pg/ml; samples with BMI 21-21.9 had an average TNF-α level of 64.37 pg/ml; and samples with BMI 22-22.9 had the highest average level of TNF-α which was 78.65 pg/ml. Conclusion: In this study, all students with normal body mass index (BMI) had normal levels of TNF-α, which was 10-100 pg/ml.Keywords: TNF-α, immune system, body mass index (BMI)Abstrak: Tumor necrosis factor alpha (TNF-α) adalah salah satu sitokin pleiotropik yang berperan dalam proses inflamsi, menginisiasi polymorphonuclear (PMN) dan mengaktivasinya sehingga PMN dapat mencapai tempat infeksi. Penelitian ini bertujuan untuk mengetahui profil TNF-α berdasarkan indeks massa tubuh (IMT) pada mahasiswa Fakultas Kedokteran Unsrat angkatan 2014. Jenis penelitian bersifat survei dengan rancangan potong lintang. Populasi penelitian ialah mahasiswa Fakultas Kedokteran Unsrat angkatan 2014. Hasil penelitian memperlihatkan bahwa sampel dengan IMT 18-18,9 memiliki nilai rerata kadar TNF-α 69,48 pg/ml; sampel dengan IMT 19-19,9 memilki nilai rerata kadar TNF-α 78,04 pg/ml; sampel dengan IMT 20-20,9 memiliki nilai rerata kadar TNF-α 61,94 pg/ml; sampel dengan IMT 21-21,9 memiliki nilai rerata kadar TNF-α 64,37 pg/ml; dan sampel dengan IMT 22-22,9 memiliki nilai rerata TNF-α tertinggi yaitu 78,65 pg/ml. Simpulan: Pada penelitian ini, semua mahasiswa Fakultas Kedokteran Unsrat angkatan 2014 dengan IMT normal memiliki kadar TNF-α normal, yaitu 10-100 ml/pg.Kata kunci: TNF-α, sistem imun, indeks massa tubuh (IMT)

scholarly journals Korelasi Tingkat Depresi dengan Kadar Tumor Necrosis Factor-Alpha (TNF-α) pada Penderita Asma Bronkial Tidak Terkontrol

2017 ◽  
Vol 3 (2) ◽  
pp. 74
Author(s):  
Muhammad Ali Apriansyah ◽  
Rudi Putranto ◽  
Eddy Mart Salim ◽  
Hamzah Shatri
Keyword(s):  
Tumor Necrosis Factor ◽  
Bronchial Asthma ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Enzyme Linked Immunosorbent Assay ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Α Level ◽  
Necrosis Factor

Pendahuluan. Prevalensi depresi hamper mencapai 50% pada pasien yang berobat di pelayanan tertier klinik asma. Tumor Necrosis Factor-Alpha (TNF-α) telah diketahui sebagai sitokin pro-inflamasi yang berperan penting dalam mekanisme patogenesis sejumlah penyakit inflamasi kronik, termasuk asma bronkial dan depresi. Belum ada data penelitian mengenai hal tersebut di Indonesia.Metode. Penelitian ini merupakan studi cross sectional yang dilakukan pada 40 pasien asma bronkial tidak terkontrol di alergi imunologi klinik unit rawat jalan Rumah Sakit Umum Pusat (RSUP) Moh Hoesin Palembang selama kurun waktu mulai bulan Juni 2014 sampai dengan Agustus 2014. Asma bronkial tidak terkontrol dinilai dengan menggunakan kuesioner Asthma Control Test (ACT), sedangkan gejala depresi dinilai dengan kuisioner Beck Depression Inventory (BDI). Konfirmasi diagnosis depresi dilakukan dengan kriteria dari Diagnostic and Statistical Manual for Psychiatry-IV Text Revision (DSMIV TR)/ International Code Diagnose 10 (ICD-10). Sementara itu, kadar TNF-α serum diukur dengan metode quantitative enzyme-linked immunosorbent assay (ELISA).Hasil. Nilai median tingkat depresi dan TNF-α serum pada penelitian ini adalah 16 (10 – 45) dan 4,09 (1,29 – 19,57) pg/mL.Tidak didapatkan korelasi yang bermakna secara statistik antara tingkat depresi dan kadar TNF-α (r = -0,265, p = 0,098).Simpulan. Tidak didapatkan korelasi yang bermakna antara tingkat depresi dengan kadar TNF-α pada penderita asma bronkial tidak terkontrol.Kata Kunci: asma bronkial tidak terkontrol, kadar TNF-α, Tingkat depresi The Correlation of Depression Level with Tumor Necrosis Factor-Alpha (TNF-α) Concentration in Uncontrolled Bronchial Asthma PatientsIntroduction. Depression occurs at high rates in people with chronic diseases, including bronchial asthma, with the prevalence of depression approaches 50% in tertiary care asthma clinic. Tumor necrosis factor alpha (TNF-α) is known to play a critical role in the pathogenic mechanism of a number of chronic inflammatory disease, including bronchial asthma and depression. There has not been any research data on the subject in Indonesia. The objective of this study was to investigate the correlation between depressive level and TNF-α level in uncontrolled bronchial asthma. Methods. This was a cross sectional study conducted in 40 patients with uncontrolled bronchial asthma at the allergy immunology clinic outpatient of Dr Moh Hoesin Hospital Palembang, during June 2014 until August 2014. Uncontrolled bronchial asthma was assessed using the Asthma Control Test (ACT) questionnaire, whereas depressive symptoms were assessed by Beck Depression Inventory (BDI) questionnaire, and diagnosis was confirmed by the criteria of the Diagnostic and Statistical Manual for Psychiatry-IV Text Revision (DSM-IV TR) / International Code Diagnose 10 (ICD-10). Serum levels of TNF-α was measured by the method of quantitative enzyme-linked immunosorbent assay (ELISA). Results. The median value of the level of depression and serum TNF- α in this study were 16 (10 - 45) and 4.09 (1.29 - 19.57) pg/mL. There was no significant correlation between depressive level and TNF-α level ( r = -0.265 , p = 0.098 ). Conclusions. There was no significant correlation between depressive level and TNF-α level in uncontrolled bronchial asthma Keywords: depressive level, TNF-α level, uncontrolled asthma bronchial

scholarly journals Association of tumor necrosis factor-alpha -308 G/A and -238 G/A polymorphism with diabetic retinopathy: a systematic review and updated meta-analysis.

2020 ◽  
Author(s):  
Wenna Gao ◽  
Ruilin Zhu ◽  
liu yang
Keyword(s):  
Diabetic Retinopathy ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Meta Analysis ◽  
Entire Group ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

Background: Mounting evidence has suggested tumor necrosis factor-alpha (TNF-α) can promote the development of diabetic retinopathy (DR), and TNF-α gene variants may influence DR risk. However, the results are quite different. Objectives: To comprehensively address this issue, we performed the meta-analysis to evaluate the association of TNF-α-308 G/A and -238 G/A polymorphism with DR. Method: Data were retrieved in a systematic manner and analyzed using STATA Statistical Software. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of associations. Allelic and genotypic comparisons between cases and controls were evaluated. Results: For the TNF-α-308 G/A polymorphism, overall analysis suggested a marginal association with DR [the OR(95%CI) of (GA versus GG), (GA + AA) versus GG, and (A versus G) are 1.21(1.04, 1.41), 1.20(1.03, 1.39), and 1.14(1.01, 1.30), respectively]. And the subgroup analysis indicated an enhanced association among the European population. For the TNF-α-238 G/A polymorphism, there was mild correlation in the entire group [the OR(95%CI) of (GA versus GG) is 1.55(1.14,2.11) ], which was strengthened among the Asian population. Conclusion: The meta-analysis suggested that -308 A and -238 A allele in TNF-α gene potentially increased DR risk and showed a discrepancy in different ethnicities.

scholarly journals Analysis of Subcellular RNA Fractions Revealed a Transcription-Independent Effect of Tumor Necrosis Factor Alpha on Splicing, Mediated by Spt5

2016 ◽  
Vol 36 (9) ◽  
pp. 1342-1353 ◽  
Author(s):  
Gil Diamant ◽  
Tal Eisenbaum ◽  
Dena Leshkowitz ◽  
Rivka Dikstein
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Independent Effect ◽  
Necrosis Factor Alpha ◽  
Pol Ii ◽  
Tnf Α ◽  
Factor Alpha ◽  
Induced Genes ◽  
Necrosis Factor

The proinflammatory cytokine tumor necrosis factor alpha (TNF-α) modulates the expression of many genes, primarily through activation of NF-κB. Here, we examined the global effects of the elongation factor Spt5 on nascent and mature mRNAs of TNF-α-induced cells using chromatin and cytosolic subcellular fractions. We identified several classes of TNF-α-induced genes controlled at the level of transcription, splicing, and chromatin retention. Spt5 was found to facilitate splicing and chromatin release in genes displaying high induction rates. Further analysis revealed striking effects of TNF-α on the splicing of 25% of expressed genes; the vast majority were not transcriptionally induced. Splicing enhancement of noninduced genes by TNF-α was transient and independent of NF-κB. Investigating the underlying basis, we found that Spt5 is required for the splicing facilitation of the noninduced genes. In line with this, Spt5 interacts with Sm core protein splicing factors. Furthermore, following TNF-α treatment, levels of RNA polymerase II (Pol II) but not Spt5 are reduced from the splicing-induced genes, suggesting that these genes become enriched with a Pol II-Spt5 form. Our findings revealed the Pol II-Spt5 complex as a highly competent coordinator of cotranscriptional splicing.

scholarly journals HSP70 Induction by ING Proteins Sensitizes Cells to Tumor Necrosis Factor Alpha Receptor-Mediated Apoptosis

2006 ◽  
Vol 26 (24) ◽  
pp. 9244-9255 ◽  
Author(s):  
Xiaolan Feng ◽  
Shirin Bonni ◽  
Karl Riabowol
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Kinase Inhibitor ◽  
Heat Shock Gene ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Primary Fibroblasts ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT ING proteins affect apoptosis, growth, and DNA repair by transducing stress signals such as DNA damage, binding histones, and subsequently regulating chromatin structure and p53 activity. p53 target genes, including the p21 cyclin-dependent kinase inhibitor and Bax, an inducer of apoptosis, are regulated by ING proteins. To identify additional targets downstream of p33ING1 and p32ING2, cDNA microarrays were performed on phenotypically normal human primary fibroblasts. The 0.36% of genes affected by ING proteins in primary fibroblasts were distinct from targets seen in established cells and included the HSP70 heat shock gene, whose promoter was specifically induced >10-fold. ING1-induced expression of HSP70 shifted cells from survival to a death pathway in response to tumor necrosis factor alpha (TNF-α), and p33ING1b protein showed synergy with TNF-α in inducing apoptosis, which correlated with reduced NF-κB-dependent transcription. These findings are consistent with previous reports that HSP70 promotes TNF-α-mediated apoptosis by binding I-κΒ kinase gamma and impairing NF-κB survival signaling. Induction of HSP70 required the amino terminus of ING1b but not the plant homeodomain region that was recently identified as a histone binding domain. Regulation of HSP70 gene expression by the ING tumor suppressors provides a novel link between the INGs and the stress-regulated NF-κB survival pathway important in hypoxia and angiogenesis.

scholarly journals Comparative Analysis of Lipopolysaccharide-Induced Tumor Necrosis Factor Alpha Activity in Serum and Lethality in Mice and Rabbits Pretreated with the Staphylococcal Superantigen Toxic Shock Syndrome Toxin 1

2001 ◽  
Vol 69 (11) ◽  
pp. 7169-7172 ◽  
Author(s):  
Martin M. Dinges ◽  
Patrick M. Schlievert
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Host Susceptibility ◽  
Necrosis Factor Alpha ◽  
Lethal Effects ◽  
Tnf Α ◽  
Factor Alpha ◽  
Toxic Shock Syndrome Toxin ◽  
Necrosis Factor

ABSTRACT Host susceptibility to lipopolysaccharide (LPS) is correlated with the levels of circulating tumor necrosis factor alpha (TNF-α) that develop in response to circulating LPS. Mice are resistant, relative to rabbits, to the lethal effects of LPS. This study indicates that mice and rabbits are equally sensitive to the lethal effects of circulating TNF-α but that mice are more resistant than rabbits to the induction of circulating TNF-α by LPS.

scholarly journals Major Outer Membrane Protein Omp25 of Brucella suis Is Involved in Inhibition of Tumor Necrosis Factor Alpha Production during Infection of Human Macrophages

2001 ◽  
Vol 69 (8) ◽  
pp. 4823-4830 ◽  
Author(s):  
Véronique Jubier-Maurin ◽  
Rose-Anne Boigegrain ◽  
Axel Cloeckaert ◽  
Antoine Gross ◽  
Maria-Teresa Alvarez-Martinez ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Macrophage Infection ◽  
Necrosis Factor Alpha ◽  
Human Macrophages ◽  
Tnf Α ◽  
Brucella Suis ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT Brucella spp. can establish themselves and cause disease in humans and animals. The mechanisms by whichBrucella spp. evade the antibacterial defenses of their host, however, remain largely unknown. We have previously reported that live brucellae failed to induce tumor necrosis factor alpha (TNF-α) production upon human macrophage infection. This inhibition is associated with a nonidentified protein that is released into culture medium. Outer membrane proteins (OMPs) of gram-negative bacteria have been shown to modulate macrophage functions, including cytokine production. Thus, we have analyzed the effects of two major OMPs (Omp25 and Omp31) of Brucella suis 1330 (wild-type [WT] B. suis) on TNF-α production. For this purpose, omp25and omp31 null mutants of B. suis(Δomp25 B. suis and Δomp31 B. suis, respectively) were constructed and analyzed for the ability to activate human macrophages to secrete TNF-α. We showed that, in contrast to WTB. suis or Δomp31 B. suis, Δomp25 B. suis induced TNF-α production when phagocytosed by human macrophages. The complementation of Δomp25 B. suis with WT omp25 (Δomp25-omp25 B. suis mutant) significantly reversed this effect: Δomp25-omp25 B. suis-infected macrophages secreted significantly less TNF-α than did macrophages infected with the Δomp25 B. suismutant. Furthermore, pretreatment of WT B. suis with an anti-Omp25 monoclonal antibody directed against an epitope exposed at the surface of the bacteria resulted in substancial TNF-α production during macrophage infection. These observations demonstrated that Omp25 of B. suis is involved in the negative regulation of TNF-α production upon infection of human macrophages.

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