Cell Death-Inducing DNA Fragmentation Factor Alpha-Like Effector A (CIDEA) V115F (G>T) Polymorphism Associated with Obesity and Metabolic Alterations in Brazilian Obese Children and Adolescents

2011 ◽  
pp. P3-403-P3-403
Author(s):  
Simone Magalhaes Diniz ◽  
Sophie Deram ◽  
Isabel Guazzelli ◽  
Eliana Frazzatto ◽  
Thais Arthur ◽  
...  
Keyword(s):  
Cell Death ◽  
Children And Adolescents ◽  
Dna Fragmentation ◽  
Obese Children ◽  
Metabolic Alterations ◽  
Factor Alpha

Isoflurane Pretreatment Inhibits Cytokine-induced Cell Death in Cultured Rat Smooth Muscle Cells and Human Endothelial Cells

2002 ◽  
Vol 97 (1) ◽  
pp. 24-32 ◽  
Author(s):  
Manuela J. M. de Klaver ◽  
Lee Manning ◽  
Lisa A. Palmer ◽  
George F. Rich
Keyword(s):  
Cell Death ◽  
Smooth Muscle ◽  
Cell Survival ◽  
Dna Fragmentation ◽  
Interleukin 1 ◽  
Vascular Endothelial Cell ◽  
Blue Staining ◽  
Vascular Endothelial ◽  
Necrosis Factor Alpha ◽  
Factor Alpha

Background Anesthetics are protective during ischemic-reperfusion injury and associated inflammation; therefore, the authors hypothesized that anesthetic pretreatment may provide protection in culture from cytokine-induced cell death. Methods Rat vascular smooth muscle (VSM) cell and human umbilical vascular endothelial cell (HUVEC) cultures were used to determine whether pretreatment with 30 min of isoflurane decreases cell death from tumor necrosis factor alpha (TNF-alpha), interleukin 1 (IL-1 beta), and interferon (IFN-gamma) alone or in combination. Cell survival and viability were determined by trypan blue staining and cell proliferation assay, as well as by DNA fragmentation assays. The roles of protein kinase C (PKC) and adenosine triphosphate-sensitive potassium (K(ATP)) channels in mediating isoflurane (and halothane) protection were evaluated with the antagonists staurosporine or glibenclamide in cytokine- and also hydrogen peroxide (H(2)O(2))-induced cell death. Results Pretreatment with 1.5% isoflurane immediately prior to cytokine exposure increased cell survival and viability from cytokines by 10-60% for 24, 48, 72, and 96 h in VSMs and up to 72 h in HUVECs. DNA fragmentation (TUNEL) was also attenuated by isoflurane. Isoflurane was equally effective in VSMs at 0.75, 1.5, and 2.5%, whereas in HUVECs, 1.5 and 2.5% were more effective than 0.75%. In VSMs, isoflurane administered 1 h prior to or simultaneously with cytokines was also effective, whereas isoflurane 2 h prior to cytokines was less effective, and either 4 h prior to or 30 min after cytokines was not effective. In both cytokine- and H(2)O(2)-induced cell death, isoflurane and halothane pretreatment were equally protective, and staurosporine and glibenclamide attenuated the protective effect. Conclusions Thirty minutes of isoflurane attenuates cytokine-induced cell death and increases cell viability in VSMs for 96 h and in HUVECs for 72 h. Isoflurane must be administered less than 2 h prior to or simultaneously with the cytokines to be protective. These initial inhibitor studies suggest involvement of PKC and K(ATP) channels in isoflurane and halothane protection against both cytokine- and H(2)O(2)-induced cell death of VSMs and HUVECs.

The 19-kilodalton adenovirus E1B transforming protein inhibits programmed cell death and prevents cytolysis by tumor necrosis factor alpha

1992 ◽  
Vol 12 (6) ◽  
pp. 2570-2580
Author(s):  
E White ◽  
P Sabbatini ◽  
M Debbas ◽  
W S Wold ◽  
D I Kusher ◽  
...  
Keyword(s):  
Cell Death ◽  
Tumor Necrosis Factor ◽  
Programmed Cell Death ◽  
Dna Fragmentation ◽  
Tumor Necrosis ◽  
Tnf Alpha ◽  
Necrosis Factor Alpha ◽  
Transforming Activity ◽  
Factor Alpha ◽  
Necrosis Factor

The adenovirus E1A and E1B proteins are required for transformation of primary rodent cells. When expressed in the absence of the 19,000-dalton (19K) E1B protein, however, the E1A proteins are acutely cytotoxic and induce host cell chromosomal DNA fragmentation and cytolysis, analogous to cells undergoing programmed cell death (apoptosis). E1A alone can efficiently initiate the formation of foci which subsequently undergo abortive transformation whereby stimulation of cell growth is counteracted by continual cell death. Cell lines with an immortalized growth potential eventually arise with low frequency. Coexpression of the E1B 19K protein with E1A is sufficient to overcome abortive transformation to produce high-frequency transformation. Like E1A, the tumoricidal cytokine tumor necrosis factor alpha (TNF-alpha) evokes a programmed cell death response in many tumor cell lines by inducing DNA fragmentation and cytolysis. Expression of the E1B 19K protein by viral infection, by transient expression, or in transformed cells completely and specifically blocks this TNF-alpha-induced DNA fragmentation and cell death. Cosegregation of 19K protein transforming activity with protection from TNF-alpha-mediated cytolysis demonstrates that both activities are likely the consequence of the same function of the protein. Therefore, we propose that by suppressing an intrinsic cell death mechanism activated by TNF-alpha or E1A, the E1B 19K protein enhances the transforming activity of E1A and enables adenovirus to evade TNF-alpha-dependent immune surveillance.

scholarly journals The 19-kilodalton adenovirus E1B transforming protein inhibits programmed cell death and prevents cytolysis by tumor necrosis factor alpha.

1992 ◽  
Vol 12 (6) ◽  
pp. 2570-2580 ◽  
Author(s):  
E White ◽  
P Sabbatini ◽  
M Debbas ◽  
W S Wold ◽  
D I Kusher ◽  
...  
Keyword(s):  
Cell Death ◽  
Tumor Necrosis Factor ◽  
Programmed Cell Death ◽  
Dna Fragmentation ◽  
Tumor Necrosis ◽  
Tnf Alpha ◽  
Necrosis Factor Alpha ◽  
Transforming Activity ◽  
Factor Alpha ◽  
Necrosis Factor

The adenovirus E1A and E1B proteins are required for transformation of primary rodent cells. When expressed in the absence of the 19,000-dalton (19K) E1B protein, however, the E1A proteins are acutely cytotoxic and induce host cell chromosomal DNA fragmentation and cytolysis, analogous to cells undergoing programmed cell death (apoptosis). E1A alone can efficiently initiate the formation of foci which subsequently undergo abortive transformation whereby stimulation of cell growth is counteracted by continual cell death. Cell lines with an immortalized growth potential eventually arise with low frequency. Coexpression of the E1B 19K protein with E1A is sufficient to overcome abortive transformation to produce high-frequency transformation. Like E1A, the tumoricidal cytokine tumor necrosis factor alpha (TNF-alpha) evokes a programmed cell death response in many tumor cell lines by inducing DNA fragmentation and cytolysis. Expression of the E1B 19K protein by viral infection, by transient expression, or in transformed cells completely and specifically blocks this TNF-alpha-induced DNA fragmentation and cell death. Cosegregation of 19K protein transforming activity with protection from TNF-alpha-mediated cytolysis demonstrates that both activities are likely the consequence of the same function of the protein. Therefore, we propose that by suppressing an intrinsic cell death mechanism activated by TNF-alpha or E1A, the E1B 19K protein enhances the transforming activity of E1A and enables adenovirus to evade TNF-alpha-dependent immune surveillance.

Neurophysiological correlatives of eating behavior in obese children and adolescents

2006 ◽  
Vol 37 (06) ◽  
Author(s):  
N Utzig ◽  
K Wagner ◽  
M Jagdhuhn ◽  
C Schröder ◽  
H Hirschfeld ◽  
...  
Keyword(s):  
Children And Adolescents ◽  
Eating Behavior ◽  
Obese Children

Effectiveness of a Multidisciplinary Lifestyle Intervention to Reduce Obesity among Children and Adolescents

2020 ◽  
Vol 35 (2) ◽  
pp. 111-118
Author(s):  
Md Rizwanul Ahsan ◽  
Sabrina Makbul ◽  
Probir Kumar Sarkar
Keyword(s):  
Body Composition ◽  
Body Weight ◽  
Children And Adolescents ◽  
Physical Performance ◽  
Cardiometabolic Risk ◽  
Dietary Habits ◽  
Obese Children ◽  
Height Ratio ◽  
Waist To Height Ratio ◽  
Family Based

Background: Now a days unhealthy lifestyle primarily responsible for the dramatic increase obesity among children and adolescents. Objective: The purpose of the study is to see the effects of a multidisciplinary lifestyle intervention to reduce obese children and adolescents. The main outcome was cardiometabolic risk based on the waist-to-height ratio (WHTR) measurement. Secondary outcomes were (1) changes in body composition; (2) adherence to a Mediterranean diet; and (3) physical performance. Methods: The study involved 64 overweight/obese children or adolescents conducted at Dhaka Shishu Hospital from October 2017 to September 2018. The intervention was multidisciplinary including nutrition, exercise, and psychological aspects based on a family-based approach; it was delivered for six months for children and three months for adolescents. Before and after the intervention, several anthropometric measures height, body weight, body mass index (BMI), waist circumference, and body composition, cardiometabolic risk index waist-to-height ratio (WHTR), and dietary habits of the participants and their families were evaluated. In addition, a set of functional motor fitness tests was performed to evaluate physical performance measures. Results: After the intervention both children and adolescents showed a significant reduction in body weight, BMI, waist circumference, fat mass, and WHTR index and an improvement of fat-free mass, adherence to the Mediterranean diet, and physical fitness performance. Conclusion: A short term family-based multidisciplinary approach is effective in ameliorating the health status, dietary habits, and physical performance in children and adolescents. DS (Child) H J 2019; 35(2) : 111-118

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