scholarly journals Interleukin 6 (IL-6) and Tumor Necrosis Factor α (TNF-α) Single Nucleotide Polymorphisms (SNPs), Inflammation and Metabolism in Gestational Diabetes Mellitus in Inner Mongolia

2017 ◽  
Vol 23 ◽  
pp. 4149-4157 ◽  
Author(s):  
Jie Zhang ◽  
Haiyi Chi ◽  
Huiying Xiao ◽  
Xiaoyan Tian ◽  
Yilin Wang ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Tumor Necrosis Factor ◽  
Inner Mongolia ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Nucleotide Polymorphisms ◽  
Single Nucleotide ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Associations between tumor necrosis factor-α and lymphotoxin-α polymorphisms and idiopathic recurrent miscarriage

Reproduction ◽  
2008 ◽  
Vol 135 (3) ◽  
pp. 397-403 ◽  
Author(s):  
W Zammiti ◽  
N Mtiraoui ◽  
H Khairi ◽  
J-C Gris ◽  
W Y Almawi ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Recurrent Miscarriage ◽  
Nucleotide Polymorphisms ◽  
Single Nucleotide ◽  
Tnf Α ◽  
Idiopathic Recurrent Miscarriage ◽  
Factor Α ◽  
Lymphotoxin Α ◽  
Necrosis Factor

Heightened expression of tumor necrosis factor (TNF)-α and lymphotoxin-α (LT-α) was associated with pregnancy complications, including idiopathic recurrent miscarriage (RM). Whereas TNF-α and LT-α gene polymorphisms affect serum cytokine concentrations, their contribution to RM is controversial. The single nucleotide polymorphisms (SNPs) TNF-α (−238G/A, −308G/A) and LT-α (+252A/G) were investigated in 350 RM women and 200 control women. Higher frequency of the TNF-α −238A, but not the TNF-α −308A or the LT-α+252G, allele was seen in patients, with comparable frequencies of TNF-α −238G/A, TNF-α −308G/A, and LT-α+252A/G genotypes seen between both groups, except for TNF-α −238G/G, which was lower in patients. Regression analysis confirmed the association of the TNF-α −238G/A SNP with idiopathic RM, and both TNF-α −308A/TNF −238G/LT-α+252Gand TNF-α −308G/TNF-α −238A/LT-α+252Ghaplotypes played a susceptible role in idiopathic RM. TNF-α −238G/A and −238A/A, and LT-α+252G/G genotypes were positively associated only with exclusively early RM. This supports the concept of the association of TNF-α (−238G/A) and LT-α (+252A/G) polymorphic variants in idiopathic RM.

scholarly journals Granuloma Annulare: a Review of the Literature

2020 ◽  
Vol 24 (4) ◽  
pp. 410-415
Author(s):  
Tânia Aguiar Passeti ◽  
Wesley Pascoal Lisboa ◽  
Gabrielle Ellen Rodrigues Grinblat ◽  
Fernando Luiz Affonso Fonseca ◽  
Paulo Ricardo Criado ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Mononuclear Cells ◽  
Granuloma Annulare ◽  
Activation Patterns ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Granuloma annulare (GA) is a form of noninfectious skin granuloma, first described in 1895 as a rash in the form of a ring (annular), with regular, rounded edges. Around 50% of the cases are cured spontaneously within 2 years, however, a percentage of patients suffer from recurrent lesions or persistence for years. The pathogenesis of GA lesions is not well understood, with studies linking its expression to the presence of histocompatibility genes (HLA)-Bw35 or AH8.1 allele. These genes are related to the production of TNF-α (Tumor Necrosis Factor-α) by mononuclear cells. The pathogenesis includes the migration of macrophages to the dermis, the presence of cytokines, late hypersensitivity reaction, defects in regulating the neutrophil chemotaxis and degradation of the connective tissue. Its outbreak may be linked to predisposing factors, such as diabetes mellitus, thyroid changes and viral infectious diseases. The macrophages present in GA lesions may receive stimuli that result in its modulation to M1 or M2 activation patterns. The study of the M1 and M2 modulation mechanism in the lesion is important for an understanding of GA development.   Keywords: Granuloma Annulare. Macrophage. Immunology. Pathogenesis and Modulation.     Resumo O Granuloma Anular (GA) é um tipo de granuloma cutâneo não infeccioso, que foi descrito em 1895, como uma exantema em formato de anel (anular), de bordas regulares e arredondadas. Cerca de 50% dos casos têm cura espontânea em 2 anos, mas parte dos pacientes apresentam recidivas das lesões ou persistência por anos. A patogênese das lesões do GA é pouco conhecida. Estudos relacionam sua expressão à presença de genes de histocompatibilidade (HLA)-Bw35 ou AH8.1, que são relacionados à produção de TNF-α (Tumor necrosis factor - α), pelas células mononucleares. A patogênese também inclui migração de macrófagos para derme, presença de citocinas, reação de hipersensibilidade tardia, defeito na quimiotaxia de neutrófilos e degradação do tecido conectivo. O surgimento das lesões pode estar associado a fatores predisponentes, como diabetes mellitus, alterações tireoidianas e doenças infecciosas virais. Os macrófagos presentes nas lesões de GA podem sofrer estímulos que acarretem sua modulação para os padrões de ativação M1 ou M2. O estudo de tais mecanismo de modulação é importante para a compreensão da instalação e desenvolvimento do GA nos pacientes afetados.   Palavras-chave: Granuloma Anular. Macrófagos. Modulação. Imunologia e Patogênese.

scholarly journals Low Levels of Tumor Necrosis Factor-α will Prevent Periodontitis Exacerbation in Type 2 Diabetes Mellitus

2022 ◽  
Author(s):  
Titiek Berniyanti ◽  
Gilang Rasuna Sabdho Wening ◽  
Retno Palupi ◽  
Dini Setyowati ◽  
Cindy Ramadhan Putri
Keyword(s):  
Diabetes Mellitus ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Treatment Needs ◽  
Type 2 Dm ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Abstract Objectives Diabetes mellitus (DM) is a major risk factor for periodontitis. Susceptibility to periodontitis increases approximately three times in people with DM. There is a clear relationship between the degree of hyperglycemia and the severity of periodontitis. This study aimed to analyze the reduction of tumor necrosis factor-α (TNF-α) in diabetics who came for periodontitis examination to prevent exacerbations. Materials and Methods This was an analytic observational study using a cross-sectional approach at health centers in Surabaya, Indonesia. Measurement of periodontal status used the community periodontal index of treatment needs by measuring bleeding at probing and pocket depth. TNF-α was measured using enzyme-linked immunosorbent assay, and behavior and lifestyle using a questionnaire. Statistical Analysis The Kolmogorov–Smirnov test was performed to identify data normality (p < 0.05). A nonparametric test was used to measure the degree of association between different characteristics and the incidence of periodontitis in type 2 DM patients with and without periodontitis. Spearman's test was done to examine the correlation between TNF-α level and severity of periodontitis in diabetics. The significant level was at p <0.05. Results There was a correlation between age, predisposing factors, reinforcing factors, drug consumption, and TNF-α levels in patients with type 2 DM and the incidence of periodontitis. Conclusions Poor glycemic control can induce oxidative stress on the gingiva, thereby aggravating damage to periodontal tissue. An important factor in preventing periodontitis for type 2 DM patients is controlling blood sugar levels through regular consumption of drugs and regular maintenance of oral cavity health. Knowledge is a predisposing factor that affects adherence of people with type 2 DM to consuming drugs regularly, which can be strengthened by family support. These will ultimately play a role in reducing TNF-α levels.

scholarly journals Polymorphisms of the tumor necrosis factor-α gene promoter predict for outcome after thalidomide therapy in relapsed and refractory multiple myeloma

Blood ◽  
2002 ◽  
Vol 100 (6) ◽  
pp. 2263-2265 ◽  
Author(s):  
Kai Neben ◽  
Joannis Mytilineos ◽  
Thomas M. Moehler ◽  
Astrid Preiss ◽  
Alwin Kraemer ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Gene Promoter ◽  
Nucleotide Polymorphisms ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Abstract Thalidomide (Thal) is a drug with antiangiogenic, anti-inflammatory, and immunomodulatory properties that was found to inhibit the production of tumor necrosis factor-α (TNF-α) in vitro. We studied single nucleotide polymorphisms at positions −308 and −238 of the TNF-α gene promoter and measured the corresponding TNF-α cytokine levels in 81 patients (pts) with refractory and relapsed multiple myeloma (MM) who were treated with Thal. In myeloma pts carrying the TNF-238A allele (n = 8), we found a correlation with higher pretreatment TNF-α levels in peripheral blood (P = .047). After Thal administration, this TNF-238A group had a prolonged 12-month progression-free and overall survival of 86% and 100% versus 44% and 84% (P = .003 andP = .07) in pts with the TNF-238G allele, respectively. These findings suggest that regulatory polymorphisms of the TNF-α gene can affect TNF-α production and predict the outcome after Thal therapy, particularly in those MM pts who are genetically defined as “high producers” of TNF-α.

scholarly journals Polymorphisms of the tumor necrosis factor-α gene promoter predict for outcome after thalidomide therapy in relapsed and refractory multiple myeloma

Blood ◽  
2002 ◽  
Vol 100 (6) ◽  
pp. 2263-2265 ◽  
Author(s):  
Kai Neben ◽  
Joannis Mytilineos ◽  
Thomas M. Moehler ◽  
Astrid Preiss ◽  
Alwin Kraemer ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Gene Promoter ◽  
Nucleotide Polymorphisms ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Thalidomide (Thal) is a drug with antiangiogenic, anti-inflammatory, and immunomodulatory properties that was found to inhibit the production of tumor necrosis factor-α (TNF-α) in vitro. We studied single nucleotide polymorphisms at positions −308 and −238 of the TNF-α gene promoter and measured the corresponding TNF-α cytokine levels in 81 patients (pts) with refractory and relapsed multiple myeloma (MM) who were treated with Thal. In myeloma pts carrying the TNF-238A allele (n = 8), we found a correlation with higher pretreatment TNF-α levels in peripheral blood (P = .047). After Thal administration, this TNF-238A group had a prolonged 12-month progression-free and overall survival of 86% and 100% versus 44% and 84% (P = .003 andP = .07) in pts with the TNF-238G allele, respectively. These findings suggest that regulatory polymorphisms of the TNF-α gene can affect TNF-α production and predict the outcome after Thal therapy, particularly in those MM pts who are genetically defined as “high producers” of TNF-α.

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