scholarly journals The Rheumatology Drugs for COVID-19 Management: Which and When?

2021 ◽  
Vol 10 (4) ◽  
pp. 783
Author(s):  
Fabiola Atzeni ◽  
Ignazio Francesco Masala ◽  
Javier Rodríguez-Carrio ◽  
Roberto Ríos-Garcés ◽  
Elisabetta Gerratana ◽  
...  
Keyword(s):  
English Language ◽  
Multidisciplinary Approach ◽  
Intravenous Immunoglobulins ◽  
Cochrane Library ◽  
Immunomodulatory Drugs ◽  
Antiviral Therapies ◽  
Tnf Α ◽  
Large Heterogeneity ◽  
Necrosis Factor ◽  
Game Changer

Introduction: While waiting for the development of specific antiviral therapies and vaccines to effectively neutralize the SARS-CoV2, a relevant therapeutic strategy is to counteract the hyperinflammatory status, characterized by an increase mainly of interleukin (IL)-1β, IL-2, IL-6, IL-7, IL-8, and tumor necrosis factor (TNF)-α, which hallmarks the most severe clinical cases. ‘Repurposing’ immunomodulatory drugs and applying clinical management approved for rheumatic diseases represents a game-changer option. In this article, we will review the drugs that have indication in patients with COVID-19, including corticosteroids, antimalarials, anti-TNF, anti-IL-1, anti-IL-6, baricitinib, intravenous immunoglobulins, and colchicine. The PubMed, Medline, and Cochrane Library databases were searched for English-language papers concerning COVID-19 treatment published between January 2020 and October 2020. Results were summarized as a narrative review due to large heterogeneity among studies. In the absence of specific treatments, the use of immunomodulatory drugs could be advisable in severe COVID-19 patients, but clinical outcomes are still suboptimal. An early detection and treatment of the complications combined with a multidisciplinary approach could allow a better recovery of these patients.

scholarly journals A meta-analysis of tumor necrosis factor-α-308 G>A polymorphism in gastric cancer

2020 ◽  
Vol 14 (3) ◽  
pp. 91-96
Author(s):  
Xin Jiang ◽  
Niyaz Ahmad Naikoo ◽  
Shuowei Gao
Keyword(s):  
Gastric Cancer ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
English Language ◽  
Meta Analysis ◽  
Recessive Model ◽  
Case Control Studies ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

AbstractBackgroundGastric cancer (GC) is the common cause of cancer-related deaths worldwide and inflammation represents the early phases in the GC.ObjectiveTo review the tumor necrosis factor (TNF)-α-308 G>A (GG, GA, and AA) in GC by meta-analysis studies for any differences in TNF-α-308 G>A gene polymorphisms.MethodsCase–control studies published from 2003 to 2017 were identified by searching PubMed, EMASE, and the Internet with the English language. The analysis published on TNF-α-308 G>A polymorphism was analyzed and a limited number of articles were included in the present study. TNF-α-308 G>A from 4,157 patients and 5,185 healthy controls was evaluated. Studies were evaluated using Cochrane Q-test and publication bias was evaluated by constructing funnel plots.ResultsOverall, TNF-α-308 GA genotype showed significant association [P < 0.0001, odds ratio (OR), 95% confidence interval (CI) = 0.82 (0.74–0.91)]. However, meta-analysis of TNF-α-308 genotypes (GG, GA, AA, and GA + AA) between GC patients and controls showed nonsignificant association with GC [P > 0.05, recessive model: OR = 1.38, 95% CI: 1.15–1.66; dominant model: OR = 1.23, 95% CI: 1.09–1.39; (G/A) vs. (G/G): OR = 1.15, 95% CI: 1.02–1.28; (A/A) vs. (G/G): OR = 1.44, 95% CI: 1.19–1.73]. Analysis stratified by ethnicity showed same results in Asian and Caucasian populations.ConclusionsResults revealed nonsignificant association of TNF-α-308 genotypes (GG, GA, AA, and GA + AA) and GC. TNF-α-308GA genotype showed significant association whereas homozygous genotype AA did not show association with GC risk.

Molecular Mechanisms of Curcumin in Neuroinflammatory Disorders: A Mini Review of Current Evidences

2019 ◽  
Vol 19 (3) ◽  
pp. 247-258 ◽  
Author(s):  
Mahsa Hatami ◽  
Mina Abdolahi ◽  
Neda Soveyd ◽  
Mahmoud Djalali ◽  
Mansoureh Togha ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
English Language ◽  
Molecular Mechanisms ◽  
Randomized Clinical Trials ◽  
Mitochondrial Dynamics ◽  
Nuclear Factor Κb ◽  
General Term ◽  
Neuroinflammatory Disease ◽  
Tnf Α ◽  
Factor Α

Objective: Neuroinflammatory disease is a general term used to denote the progressive loss of neuronal function or structure. Many neuroinflammatory diseases, including Alzheimer’s, Parkinson’s, and multiple sclerosis (MS), occur due to neuroinflammation. Neuroinflammation increases nuclear factor-κB (NF-κB) levels, cyclooxygenase-2 enzymes and inducible nitric oxide synthase, resulting in the release of inflammatory cytokines, such as interleukin-6 (IL-6), interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). It could also lead to cellular deterioration and symptoms of neuroinflammatory diseases. Recent studies have suggested that curcumin (the active ingredient in turmeric) could alleviate the process of neuroinflammatory disease. Thus, the present mini-review was conducted to summarize studies regarding cellular and molecular targets of curcumin relevant to neuroinflammatory disorders. Methods: A literature search strategy was conducted for all English-language literature. Studies that assessed the various properties of curcuminoids in respect of neuroinflammatory disorders were included in this review. Results: The studies have suggested that curcuminoids have significant anti- neuroinflammatory, antioxidant and neuroprotective properties that could attenuate the development and symptom of neuroinflammatory disorders. Curcumin can alleviate neurodegeneration and neuroinflammation through multiple mechanisms, by reducing inflammatory mediators (such as TNF-α, IL-1β, nitric oxide and NF-κB gene expression), and affect mitochondrial dynamics and even epigenetic changes. Conclusion: It is a promising subject of study in the prevention and management of the neuroinflammatory disease. However, controlled, randomized clinical trials are needed to fully evaluate its clinical potential.

scholarly journals Anti-Inflammatory Effect of Simonsinol on Lipopolysaccharide Stimulated RAW264.7 Cells through Inactivation of NF-κB Signaling Pathway

Molecules ◽  
2020 ◽  
Vol 25 (16) ◽  
pp. 3573
Author(s):  
Lian-Chun Li ◽  
Zheng-Hong Pan ◽  
De-Sheng Ning ◽  
Yu-Xia Fu
Keyword(s):  
Nitric Oxide ◽  
Signaling Pathway ◽  
Morphological Changes ◽  
Raw264.7 Cells ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Oxide Synthase ◽  
Necrosis Factor

Simonsinol is a natural sesqui-neolignan firstly isolated from the bark of Illicium simonsii. In this study, the anti-inflammatory activity of simonsinol was investigated with a lipopolysaccharide (LPS)-stimulated murine macrophages RAW264.7 cells model. The results demonstrated that simonsinol could antagonize the effect of LPS on morphological changes of RAW264.7 cells, and decrease the production of nitric oxide (NO), tumor necrosis factor α (TNF-α), and interleukin 6 (IL-6) in LPS-stimulated RAW264.7 cells, as determined by Griess assay and enzyme-linked immunosorbent assay (ELISA). Furthermore, simonsinol could downregulate transcription of inducible nitric oxide synthase (iNOS), TNF-α, and IL-6 as measured by reverse transcription polymerase chain reaction (RT-PCR), and inhibit phosphorylation of the alpha inhibitor of NF-κB (IκBα) as assayed by Western blot. In conclusion, these data demonstrate that simonsinol could inhibit inflammation response in LPS-stimulated RAW264.7 cells through the inactivation of the nuclear transcription factor kappa-B (NF-κB) signaling pathway.

#50 Gestational exposure of tumor necrosis factor-α (TNF-α) inhibitor drugs

2019 ◽  
Vol 88 ◽  
pp. 149-150 ◽  
Author(s):  
Erkoseoglu Ilknur ◽  
Kadioglu Mine ◽  
Cavusoglu Irem ◽  
Sisman Mulkiye ◽  
Aran Turhan ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Gestational Exposure ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

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 Accuracy of Pulse Oximetry in the Presence of Fetal Hemoglobin—A Systematic Review

Children ◽  
2021 ◽  
Vol 8 (5) ◽  
pp. 361
Author(s):  
Ena Pritišanac ◽  
Berndt Urlesberger ◽  
Bernhard Schwaberger ◽  
Gerhard Pichler
Keyword(s):  
Pulse Oximetry ◽  
Neonatal Intensive Care ◽  
English Language ◽  
Arterial Oxygen Saturation ◽  
Fetal Hemoglobin ◽  
Arterial Oxygen ◽  
Cochrane Library ◽  
Preterm Neonates ◽  
Neonatal Blood ◽  
The Impact

Continuous monitoring of arterial oxygen saturation by pulse oximetry (SpO2) is the main method to guide respiratory and oxygen support in neonates during postnatal stabilization and after admission to neonatal intensive care unit. The accuracy of these devices is therefore crucial. The presence of fetal hemoglobin (HbF) in neonatal blood might affect SpO2 readings. We performed a systematic qualitative review to investigate the impact of HbF on SpO2 accuracy in neonates. PubMed/Medline, Embase, Cumulative Index to Nursing & Allied Health database (CINAHL) and Cochrane library databases were searched from inception to January 2021 for human studies in the English language, which compared arterial oxygen saturations (SaO2) from neonatal blood with SpO2 readings and included HbF measurements in their reports. Ten observational studies were included. Eight studies reported SpO2-SaO2 bias that ranged from −3.6%, standard deviation (SD) 2.3%, to +4.2% (SD 2.4). However, it remains unclear to what extent this depends on HbF. Five studies showed that an increase in HbF changes the relation of partial oxygen pressure (paO2) to SpO2, which is physiologically explained by the leftward shift in oxygen dissociation curve. It is important to be aware of this shift when treating a neonate, especially for the lower SpO2 limits in preterm neonates to avoid undetected hypoxia.

Sign in / Sign up

Export Citation Format

Share Document