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21.
Transgenic Research - 相似文献
22.
Whole body exposure of rats to microwaves emitted from a cell phone does not affect the testes 总被引:7,自引:0,他引:7
Dasdag S Zulkuf Akdag M Aksen F Yilmaz F Bashan M Mutlu Dasdag M Salih Celik M 《Bioelectromagnetics》2003,24(3):182-188
The objective of this study was to investigate the effects of radiofrequency radiation emitted from cellular phones on the lipid composition, malondialdehyde concentration, p53 immune reactivity, sperm count, morphology, histological structure of testes, and on rectal temperature of rats exposed to microwave radiation emitted from cellular phones. Sixteen Spraque-Dawley rats were separated into two groups of eight, sham exposed (control) and experimental. The rats were confined in plexiglas cages specially designed for this study, and cellular phones were placed 0.5 cm under the cages. For the experimental group, cellular phones were activated 20 min per day (7 days a week) for 1 month. For the control group, the cellular phones were placed beneath the cages for 20 min a day, but the phones were turned off. Rectal temperatures were measured weekly. For 250 mW radiated power, the whole body average SAR (rms) is 0.52 W/kg and 1 g averaged peak SAR (rms) is 3.13 W/kg. The Mann-Whitney U-test was used for statistical comparisons of groups. No statistically significant alteration in any of the endpoints was noted. This study found no evidence suggesting an adverse effect of cell phone exposure on measures of testicular function or structure. 相似文献
23.
Salih HR Kosowski SG Haluska VF Starling GC Loo DT Lee F Aruffo AA Trail PA Kiener PA 《Journal of immunology (Baltimore, Md. : 1950)》2000,165(5):2903-2910
Members of the TNF superfamily, including Fas, Fas ligand, and CD40, have been shown to be expressed on tumor cells. In the studies described in this work, we report that another family member, the ligand for 4-1BB (CD137), is expressed on various human carcinoma cell lines, on cells of solid tumors derived from these cell lines, and cells obtained from human tumors. Expression of 4-1BB ligand (4-1BBL) mRNA was detected by both RT-PCR and Northern blot analysis, and expression of 4-1BBL protein was detected by Western blot analysis of whole cell lysates and by FACS analysis of tumor cells and cell lines. Incubation of tumor cells with a 4-1BB-Ig fusion protein led to the production of IL-8 by the cells, demonstrating that the 4-1BBL is functionally active and signals back into the tumor cells. Furthermore, 4-1BBL expressed on the carcinoma cells functioned as a costimulatory molecule for the production of cytokines (most notably IFN-gamma) in cocultures of T cells and tumor cells. These findings suggest that 4-1BBL expressed on carcinoma cells may significantly influence the outcome of a T cell-tumor cell interaction. 相似文献
24.
Fulya Tekşen Bekir Sitki Şayli Ahmet Aydin Ahmet Sayal Aşkin Işimer 《Biological trace element research》1998,63(2):123-127
Down syndrome is the most common cause of mental retardation, affecting 1 in 700–800 liveborn infants. Although numerous biochemical
abnormalities accompanying the syndrome have not yet been completely clarified, the antioxidant defense system enzymes have
shown to be altered due to increased gene dosage on chromosome 21 and overproduction of superoxide dismutase (SOD-1 or Cu/Zn
SOD). The purpose of this study was to investigate the activities of SOD-1 and glutathione peroxidase (GSH-Px) enzymes and
the levels of their cofactors zinc (Zn), copper (Cu) and selenium (Se) in plasma of 20 Down syndrome patients.
In comparison with age and sex-matched controls (n=15), plasma GSH-Px, SOD, and Cu levels were significantly decreased in the patient group, but Zn and Se concentrations remained
unchanged.
This study was presented as a poster in 29th Annual Meeting of European Society of Human Genetics held in Genoa in May, 1997. 相似文献
25.
Ranbir Chander Sobti Nega Berhane Salih Abedule Mehedi Rupinder Kler Seyed Ali Hosseini Vijish Kuttiat Ajay Wanchu 《Molecular biology reports》2010,37(1):317-324
Various efforts made to stop the deadly epidemic of HIV since its discovery in 1983 remain unsuccessful and this virus still
continues to claim the lives of millions of individuals every year. The viral effect in the cell is complicated and the overall
disease outcome is the result of interaction between a few viral proteins and complex host immune response. Because it has
been reported that XPG (Xeroderma pigementesum group G) gene does play a role in reducing UV induced apoptosis and participate in Nucleotide Excision
Repair (NER) process of DNA damage, it was hypothesized that polymorphism in this gene may have a role in HIV 1 disease progression
to AIDS. The aim of the present study, therefore, was to find out the association between XPG gene polymorphism and its effect on the rate of HIV 1 disease progression to AIDS. 300 HIV seropositive cases and an equal
number of age and sex matched controls were recruited for the study from north Indian population. The PCR-RFLP method was
utilized to genotype 600 study subject for the XPG Asp
1104
His gene polymorphism. There was significant difference in the frequency of the His/His variant genotype (OR 1.95, 95% CI = 1.93–3.63, P = 0.04) between cases and controls indicating a probable role of this gene in host viral interactions. 相似文献
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Tellioglu AT Menevse GT Uregen SE 《Plastic and reconstructive surgery》2007,119(3):1120-1; author reply 1122
30.
Dajani R Sanlioglu S Zhang Y Li Q Monick MM Lazartigues E Eggleston T Davisson RL Hunninghake GW Engelhardt JF 《American journal of physiology. Gastrointestinal and liver physiology》2007,292(1):G242-G252
TNF-alpha influences morbidity and mortality during the course of endotoxemia. However, the complex pleiotropic functions of TNF-alpha remain poorly understood. We evaluated how hepatic induction of NF-kappaB and TNF-alpha influence survival and hepatocellular death in a lethal murine model of endotoxic shock. Using dominant-negative viral vectors to inhibit the IKK complex, we demonstrate through this study that the liver is a major source of TNF-alpha during the course of lethal endotoxemia and that IKKbeta (but not IKKalpha) is predominantly responsible for activating NF-kappaB and TNF-alpha in the liver after LPS administration. Using TNF-alpha knockout mice and hepatic-specific inhibition of IKKbeta, we demonstrate that the status of TNF-alpha and NF-kappaB balances necrotic and apoptotic fates of hepatocytes in the setting of endotoxemia. In the presence of TNF-alpha, inhibiting hepatic IKKbeta resulted in increased survival, reduced serum proinflammatory cytokines, and reduced hepatocyte necrosis in response to a lethal dose of endotoxin. In contrast, inhibiting hepatic IKKbeta in TNF-alpha knockout mice resulted in decreased survival and increased caspase 3-mediated hepatocyte apoptosis after endotoxin challenge, despite a reduced proinflammatory cytokine response. In the presence of TNF-alpha, NF-kappaB-dependent hepatocellular necrosis predominated, while in the absence of TNF-alpha, NF-kappaB primarily influenced apoptotic fate of hepatocytes. Changes in JNK phosphorylation after LPS challenge were also dynamically affected by both IKKbeta and TNF-alpha; however, this pathway could not solely explain the differential outcomes in hepatocellular fates. In conclusion, our studies demonstrate that induction of NF-kappaB and TNF-alpha balances protective (antiapoptotic) and detrimental (proinflammatory) pathways to determine hepatocellular fates during endotoxemia. 相似文献