Study a level of TNF-α and INF-Ƴ in patients with Type I and II Diabetes Mellitus in Diayla governorate

2017 ◽  
Vol 13 (3) ◽  
pp. 196-207
Author(s):  
Mohammed Abdul-Daim Saleh ◽  
◽  
Shahrazad Ahmed Khalaf
Keyword(s):  
Type I ◽  
2021 ◽  
Vol 12 ◽  
Author(s):  
Shaimaa Nasr Amin ◽  
Nivin Sharawy ◽  
Nashwa El Tablawy ◽  
Dalia Azmy Elberry ◽  
Mira Farouk Youssef ◽  
...  

Diabetes mellitus (DM) is a multisystem endocrine disorder affecting the brain. Mesenchymal stem cells (MSCs) pretreated with Melatonin have been shown to increase the potency of MSCs. This work aimed to compare Melatonin, stem cells, and stem cells pretreated with Melatonin on the cognitive functions and markers of synaptic plasticity in an animal model of type I diabetes mellitus (TIDM). Thirty-six rats represented the animal model; six rats for isolation of MSCs and 30 rats were divided into five groups: control, TIDM, TIDM + Melatonin, TIDM + Stem cells, and TIDM + Stem ex vivo Melatonin. Functional assessment was performed with Y-maze, forced swimming test and novel object recognition. Histological and biochemical evaluation of hippocampal Neuroligin 1, Sortilin, Brain-Derived Neurotrophic Factor (BDNF), inducible nitric oxide synthase (iNOS), toll-like receptor 2 (TLR2), Tumor necrosis factor-alpha (TNF-α), and Growth Associated Protein 43 (GAP43). The TIDM group showed a significant decrease of hippocampal Neuroligin, Sortilin, and BDNF and a significant increase in iNOS, TNF-α, TLR2, and GAP43. Melatonin or stem cells groups showed improvement compared to the diabetic group but not compared to the control group. TIDM + Stem ex vivo Melatonin group showed a significant improvement, and some values were restored to normal. Ex vivo melatonin-treated stem cells had improved spatial working and object recognition memory and depression, with positive effects on glucose homeostasis, inflammatory markers levels and synaptic plasticity markers expression.


2019 ◽  
Vol 2 (21) ◽  
pp. 22-27
Author(s):  
A. A. Tarasov ◽  
M. A. Gordeeva ◽  
S. I. Davydov ◽  
E. A. Reznikova ◽  
A. R. Babaeva

The article presents the results of a cluster analysis of the contribution of immune inflammationmarkers and endothelial dysfunction (ED) to the cardiovascular complicationsfrequency and severity in cohorts of patients with asymptomatic atherosclerosis (AAS), coronary artery disease (CAD), tyepe 2 diabetes mellitus (T2DM) and metabolic syndrome (MS) during 3 years of prospective observation. A comparative analysis of the spectrum of the examined markers was performed depending on the stage of the development of the disease, the presence of T2DM and the MS. It was revealed that the greatest contribution to the cardiovascular complications development in AAS is provided by such circulating markers of ED and immune inflammation as ET-1, IL-1β, TNF-α, total autoantibodies to type I and III collagen (a-Coll) and to Chondroitine-sulfate (a-ChS). With IHD, the greatest contribution is provided by ET-1, eNOs, antibodies a-Coll and also IL-6 and vWf.In T2DM patients without CAD, a profile of markers associated with the high rate of adverse events includes ET-1, eNOs, IL-6, a-Coll and antibodies against hyaluronic acid (a-HA). In a cohort of patients with chronic CAD in the setting of T2DM, a profile of markers associated with the development of adverse events includes vWf, TNF-α, as well as the level of eNOs, IL-6, a-Coll, a-HA and CRP. In the cases of AAS without concomitant MS, the greatest contribution is due to the increase in the level of ET-1, vWf, a-Coll and a-ChS content; in the presence of MS — IL-1β, TNF-α, a-Coll, anti-ChS, anti-HA and CRP. In CAD without MS profile of markers associated with the development of adverse events, includes ET-1, eNOs and a-HA, the presence of the MS — a-Coll, ET-1 and IL-6 levels.


The last few decades has seen monumental strides in both technologic and scientific advances and discoveries in the field of diabetic research. This review article discusses the background behind Type I Diabetes Mellitus (T1DM), how it is an autoimmune condition with a molecular origin dysfunction before presenting discussion on recently discovered concepts. The article explores the role that stem cells play in diabetic treatment beginning with graft harvesting before discussion of newly discovered stem cells in the spleen and what that means for treatment. Tumor necrosis factor alpha (TNF- α) is believed to play a role in therapeutic options for diabetics, as there is reason to believe that TNF-α is capable of inducing apoptosis in selectively autoreactive CD8+ T-cells and data behind utilizing TNF agonists is illustrated. Ultrasensitive c-peptide assays shed light on the true functional status of islet β cells and conclude that the decline in function occurs over decades and not months as was previously thought. All these concepts and discoveries pave the way for future clinical trials and the discovery of more curative diabetic treatment options.


2019 ◽  
Vol 3 (25) ◽  
pp. 43-45
Author(s):  
I. I. Krukier ◽  
V. V. Avrutskaya ◽  
A. A. Grigoriants ◽  
A. S. Degtyaryova ◽  
A. A. Nikashina ◽  
...  

Objective of research was to study the production of serum and placental cytokines and relaxin in women with a physiological pregnancy (45) and complicated by type I diabetes mellitus (42). The research material was the placenta and serum of pregnant women, in which determined the level of cytokines TNF-α, TGF-β, IL-1β and relaxin. It has been shown that the cytokine-producing function of the placenta plays an important role in the development of that organ, and systemic production of cytokines and relaxin is of key importance in the development of endothelial dysfunction syndrome. Early diagnosis of complications in pregnant women with type 1 diabetes will make it possible to start etiopathogenetic therapy in a timely manner and makes it possible to perform adequate obstetric tactics of labor.


2007 ◽  
Vol 2 (04) ◽  
Author(s):  
N Kyriakopoulos ◽  
C Gavala ◽  
I Georgantis ◽  
S Patiakas ◽  
S Tsitlakidou ◽  
...  

Diabetes ◽  
1984 ◽  
Vol 33 (4) ◽  
pp. 394-400 ◽  
Author(s):  
G. Bolli ◽  
P. De Feo ◽  
S. De Cosmo ◽  
G. Perriello ◽  
G. Angeletti ◽  
...  

Diabetes ◽  
1987 ◽  
Vol 36 (11) ◽  
pp. 1286-1291 ◽  
Author(s):  
P. Vardi ◽  
S. A. Dib ◽  
M. Tuttleman ◽  
J. E. Connelly ◽  
M. Grinbergs ◽  
...  

Diabetes ◽  
1990 ◽  
Vol 39 (3) ◽  
pp. 369-375 ◽  
Author(s):  
M. M. Landgraf-Leurs ◽  
C. Drummer ◽  
H. Froschl ◽  
R. Steinhuber ◽  
C. Von Schacky ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document