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排序方式: 共有1080条查询结果,搜索用时 15 毫秒
91.
92.
K D Bagshawe K Sharma P J Southall J A Boden G M Boxer T A Patridge P Antoniw R B Pedley 《The British journal of radiology》1991,64(757):37-44
We report uptake of a thymidine analogue 125-Iodine-5-iodo-2'-deoxyuridine (125IUdR) by nude mice bearing human xenografts of choriocarcinoma or colonic cancer. When 125IUdR was given alone, uptake by intestinal tissues was 5-10 times greater than by the tumours as measured by tissue gamma counting. This ratio was reversed when hydroxyurea or cytosine arabinoside were used as inhibitors of ribonucleotide reductase and were given in combination with 5-fluorouracil or methotrexate to inhibit thymidine synthesis shortly before injecting 125IUdR. Counting the radioactivity in tissues removed 24 hours after 125IUdR gave tumour to highest normal tissue ratios of up to 15:1, but the corresponding nuclear grain counts, which is probably a more reliable indicator of selective uptake into DNA, were in excess of 100:1. The addition of unlabelled IUdR to the regimen only reduced the uptake of 125IUdR when given in relatively large amounts. For this approach to be exploited it is concluded that the tumour must be resistant at the cell level to the inhibitor of DNA synthesis either de novo or as a result of prior exposure to it. This inhibitor can then be used to block uptake of the potentially toxic nucleoside analogue by normal renewal tissues while it is taken up by the resistant cancer cells. By inhibiting synthesis of the corresponding normal nucleosides with inhibitors to which the cancer cells are not resistant, incorporation of the toxic analogues into tumour DNA was enhanced. Although 125IUdR is a convenient agent for exploring this approach and is highly cytotoxic when incorporated in DNA, the clinical potential of reverse role chemotherapy probably lies with the development of toxic non-radioactive nucleoside analogues. 相似文献
93.
Guenther Boden 《Journal of investigative medicine》2004,52(6):375-378
Reviewed are data on gluconeogenesis (GNG) and glycogenolysis (GL) obtained in healthy volunteers and diabetic patients with newer, quantitative methods. Specifically addressed are effects of overnight and prolonged fasting, of acute changes in serum insulin and plasma free fatty acid (FFA) levels, as well as acute changes of combined FFA and insulin levels on GNG and GL in nondiabetic subjects and of abnormalities in GNG and GL in patients with type 1 and type 2 diabetes. 相似文献
94.
Hepatic and renal metabolism before and after portasystemic shunts in patients with cirrhosis. 总被引:1,自引:0,他引:1 下载免费PDF全文
O E Owen M A Mozzoli F A Reichle T H Kreulen R S Owen G Boden M Polansky 《The Journal of clinical investigation》1985,76(3):1209-1217
Hepatic cirrhosis with portal hypertension and gastroesophageal hemorrhage is a disease complex that continues to be treated by surgical portasystemic shunts. Whether or not a reduction or diversion of portal blood flow to the liver adversely affects the ability of the liver to maintain fuel homeostasis via gluconeogenesis, glycogenolysis, and ketogenesis is unknown. 11 patients with biopsy-proven severe hepatic cirrhosis were studied before and after distal splenorenal or mesocaval shunts. Hepatic, portal, and renal blood flow rates and glucose, lactate, pyruvate, glycerol, amino acids, ketone bodies, free fatty acids, and triglyceride arteriovenous concentration differences were determined to calculate net precursor-product exchange rates across the liver, gut, and kidney. The study showed that hepatic contribution of glucose and ketone bodies and the caloric equivalents of these fuels delivered to the blood was not adversely affected by either a distal splenorenal or mesocaval shunt. In addition to these general observations, isolated findings emerged. Mesocaval shunts reversed portal venous blood and functionally converted this venous avenue into hepatic venous blood. The ability of the kidney to make a substantial net contribution of ketone bodies to the blood was also observed. 相似文献
95.
Effects of fat on glucose uptake and utilization in patients with non-insulin-dependent diabetes. 总被引:7,自引:1,他引:7 下载免费PDF全文
It was the aim of this study to determine whether FFA inhibit insulin-stimulated whole body glucose uptake and utilization in patients with non-insulin-dependent diabetes. We performed five types of isoglycemic (approximately 11mM) clamps: (a) with insulin; (b) with insulin plus fat/heparin; (c) with insulin plus glycerol; (d) with saline; (e) with saline plus fat/heparin and two types of euglycemic (approximately 5mM) clamps: (a) with insulin; (b) with insulin plus fat/heparin. During these studies, we determined rates of glucose uptake, glycolysis (both with 3[3H] glucose), glycogen synthesis (determined as glucose uptake minus glycolysis), carbohydrate oxidation (by indirect calorimetry) and nonoxidative glycolysis (determined as glycolysis minus carbohydrate oxidation). Fat/heparin infusion did not affect basal glucose uptake, but inhibited total stimulated (insulin stimulated plus basal) glucose uptake by 40-50% in isoglycemic and in euglycemic patients at plasma FFA concentration of approximately 950 and approximately 550 microM, respectively. In isoglycemic patients, the 40-50% inhibition of total stimulated glucose uptake was due to near complete inhibition of the insulin-stimulated part of glucose uptake. Proportional inhibition of glucose uptake, glycogen synthesis, and glycolysis suggested a major FFA-mediated defect involving glucose transport and/or phosphorylation. In summary, fat produced proportional inhibitions of insulin-stimulated glucose uptake and of intracellular glucose utilization. We conclude, that physiologically elevated levels of FFa could potentially be responsible for a large part of the peripheral insulin resistance in patients with non-insulin-dependent diabetes mellitus. 相似文献
96.
Free fatty acids and insulin secretion in humans 总被引:3,自引:0,他引:3
Boden G 《Current diabetes reports》2005,5(3):167-170
Acute increases in plasma levels of long-chain fatty acids raise plasma insulin levels by stimulating insulin secretion or
by decreasing insulin clearance. In normal subjects, longterm elevations of fatty acids also stimulate insulin secretion.
In fact, they increase insulin precisely to the degree needed to compensate for the fatty acid-induced insulin resistance.
In contrast, in individuals who are genetically predisposed to develop type 2 diabetes (prediabetic subjects), the free fatty
acid (FFA) stimulation of insulin secretion is not sufficient to fully compensate for the FFAinduced insulin resistance. Therefore,
obesity, if associated with elevated fatty acid levels, may lead to hyperglycemia in prediabetic but not in normal individuals. 相似文献
97.
Boden JM Fergusson DM Horwood LJ 《Social psychiatry and psychiatric epidemiology》2007,42(11):881-891
This study investigated the relationship between self-esteem in adolescence and later violent offending and hostility via
self- and other-report, examining data from a birth cohort of over 1,000 New Zealand young adults studied to age 25. Lower
levels of self-esteem at age 15 were related to greater risks of violent offending and higher levels of hostility at ages
18, 21, and 25. Adjustment for potentially confounding factors reduced the strength of the associations between self-esteem
at age 15 and both self- and other-reported violent offending and other-reported hostility at ages 18, 21, and 25 to statistically
non-significant levels. The association between self-esteem at age 15 and later self-reported hostility remained statistically
significant, but was small in magnitude. A similar pattern of results were obtained using self-esteem at age 10 as the predictor
variable in place of the age 15 measure. In addition, a persistent association was found between unstable high self-esteem
and self-reported violent offending. The results suggest that self-esteem level plays a limited role in the understanding
of violent behavior. 相似文献
98.
99.
100.
D Altavilla F Squadrito A Bitto F Polito BP Burnett V Di Stefano L Minutoli 《British journal of pharmacology》2009,157(8):1410-1418