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171.
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Summary Conventional and molecular cytogenetic analyses of three murine cancer cell lines that had been induced in male athymic mice by the injection of three different human prostate cancer cell lines revealed selective amplification of the Y chromosome. In particular, analysis of metaphase and interphase nuclei by fluorescence in situ hybridization (FISH) with the mouse Y chromosome-specific DNA painting probe revealed the presence of various numbers of Y chromosomes, ranging from one to eight, with a large majority of nuclei showing two copies (46.5–60.1%). In Interphase nuclei, the Y chromosomes showed distinct morphology, allowing identification irrespective of whether the preparations were treated for 15 min or for 5 h with Colcemid, a chemical known to cause chromosome condensation. However, FISH performed on human lymphocyte cultures with chromosome-specific DNA painting probes other than the Y chromosome did not reveal condensed chromosome morphology in interphase nuclei even after 12 h of Colcemid treatment. Our FISH results indicate that (1) the Y chromosome is selectively amplified in all three cell lines; (2) the mouse Y chromosome number is comparable in both interphase and metaphase cells; (3) the Y chromosome number varies between one and eight, with a large majority of cells showing two or three copies in most interphase nuclei; (4) the condensation of the Y chromosome is not affected by the duration of Colcemid treatment but by its inherent DNA constitution; and (5) the number of copies of the Y chromosome is increased and retained not only in human prostate tumor cell lines but also in murine tumors induced by these prostate tumor cell lines.  相似文献   
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BACKGROUND AND AIM: Low birth-weight is known to be associated with an increase in cardiovascular risk similar to that seen with major environmental risk factors, such as cigarette smoking or hypertension. Much epidemiological evidence has linked low birth-weight with hypertriglyceridaemia. METHOD: We measured aortic wall thickness by ultrasonography and lipid profile in 40 newborn babies with intrauterine growth restriction and 40 controls. RESULTS: Maximum and mean aortic intima-media thickness were significantly higher in the babies with intrauterine growth retardation (0.58 +/- 0.06, 0.52 +/- 0.03 mm, respectively) than in controls (0.44 +/- 0.05, 0.40 +/- 0.03 mm, p < 0.0001, p < 0.0001, respectively), more so after adjustment for birth-weight (maximum intima-media thickness: 0.23 +/- 0.03 mm/kg vs. 0.12 +/- 0.02 mm/kg, p < 0.0001; mean intima-media thickness: 0.21 +/- 0.02 mm/kg vs. 0.11 +/- 0.01 mm/kg, p < 0.0001). Serum triglyceride levels were significantly higher in the intrauterine growth retardation group (48.9 +/- 14.8 mg/dl) compared with the control group (32.5 +/- 9.8 mg/dl, p < 0.0001). The mean body mass index, prepregnancy weight, weight gain during pregnancy, maternal LDL cholesterol level and, height of the mothers were significantly lower in the intrauterine growth retardation group compared with the control group. For maximum aIMT, significant associations included the ponderal index (p = <0.01), length (p = 0.01) and serum triglyceride levels of infants (p = 0.02). CONCLUSION: Newborn babies with growth restriction have significant maximum aortic thickening with hypertriglyceridaemia, suggesting that prenatal events might predispose to later cardiovascular risk.  相似文献   
175.
Carbonic anhydrase (CA; EC 4.2.1.1) is used for remedial purposes for several years, as there is significant focus on expanding more new activators (CAAs) and high affinity inhibitors. Alzheimer′s disease and other similar ailments such as dementia and vascular dementia with Lewy bodies reduce cholinergic activity in the important areas involved in cognition and memory. Prevalent drugs for the symptomatic therapy of dementia are significant in increasing the associated cholinergic deficiency by inhibiting acetylcholinesterase (AChE). These six‐membered carbocycles showed nice inhibitory action against AChE and human carbonic anhydrase (hCA) II and I isoforms. The hCA I, II, and AChE were efficiently inhibited by these molecules, with Ki values in the range of 6.70–35.85 nM for hCA I, 18.77–60.84 nM for hCA II, and 0.74–4.60 for AChE, respectively.  相似文献   
176.
Susceptibility to different diseases among related species, such as coho salmon (Oncorhynchus kisutch), rainbow trout (Oncorhyncus mykiss) and Atlantic salmon (Salmo salar), is variable. The prominence of these species in aquaculture warrants investigation into sources of this variability to assist future disease management. To develop a better understanding of the basis for species variability, several important non-specific humoral parameters were examined in juvenile fish of these three economically important species. Mucous protease, alkaline phosphatase and lysozyme, as well as plasma lysozyme activities and histological parameters (epidermal thickness and mucous cell density, and size) were characterized and compared for three salmonids: rainbow trout, Atlantic salmon and coho salmon. Rainbow trout had a thicker epidermis and significantly more mucous cells per cross-sectional area than the other two species. Rainbow trout also had significantly higher mucous protease activity than Atlantic salmon and significantly higher lysozyme (plasma and mucus) activities than coho and Atlantic salmon, in seawater. Atlantic salmon, on the other hand, had the lowest activities of mucous lysozyme and proteases, the thinnest epidermal layer and the sparsest distribution of mucous cells, compared with the two other salmonids in seawater. Only coho salmon had sacciform cells. Atlantic and coho salmon had higher mucous lysozyme activities in freshwater as compared to seawater. There was no significant difference between mucous lysozyme activities in any of the three species reared in freshwater; however, rainbow trout still had a significantly higher plasma lysozyme activity compared with the other two species. All three species exhibited significantly lower mucous alkaline phosphatase and protease activities in freshwater than in seawater. Our results demonstrate that there are significant histological and biochemical differences between the skin and mucus of these three salmonid species, which may change as a result of differing environments. Variation in these innate immune factors is likely to have differing influences on each species response to disease processes.  相似文献   
177.
AIM: Weill-Marchesani syndrome (WMS) is a rare systemic disorder with both autosomal recessive and dominant inheritances. Accumulation of reactive oxygen species such as O2*-, H2O2 and OH* causes lipid peroxidation (LPO), whereas antioxidant enzymes (superoxide dismutase (SOD), glutathione peroxidase (GSHPx)) mediate defence against oxidative stress. Excess tumour necrosis factor (TNF)-alpha and NO* react with O2*- and cause further antioxidant depletion with an increase in mutation frequency by H2O2. This study investigated the levels of SOD, GSHPx, catalase (CAT), TNF-alpha, NO and LPO in patients with WMS. METHODS: A group of 10 WMS patients (four males, six females; age, 26.5+/-19.0 years) and 10 age-matched and sex-matched controls (five males, five females; age, 27.3+/-18.2 years) were included. Serum TNF-alpha levels were determined by a spectrophotometer technique using immulite chemiluminescent immunometric assay. Malondialdehyde (MDA) was determined in plasma; CAT in red blood cells (RBCs), and SOD and GSHPx in both plasma and RBCs. Total serum NO* levels were evaluated by Griess reaction. RESULTS: Mean levels of TNF-alpha (8.3+/-0.6 pg/ml) in WMS patients were significantly (p<0.001) higher than controls (4.3+/-0.2 pg/ml). Plasma MDA levels in patients and controls were 5.4+/-0.8 and 1.8+/-0.6 micromol/l, respectively, and the difference was significant (p=0.0002). SOD and GSHPx activities were significantly lower in both RBCs and plasma of WMS than in controls (RBC-SOD, 3981.9+/-626.6 versus 5261.6+/-523.0 U/g haemoglobin (Hb), p=0.0005; plasma-SOD, 529.4+/-49.3 versus 713.4+/-55.7 U/g protein, p=0.0002; RBC-GSHPx, 682.7+/-42.0 versus 756.5+/-47.6 U/g Hb, p=0.0011; plasma-GSHPx, 107.3+/-15.0 versus 131.4+/-19.7 U/g protein, p=0.0113). In addition, serum NO (NO*-2 + NO*-3) levels were also significantly (p = 0.0002) increased in WMS patients (54.4+/-5.7 versus 26.9+/-6.7 micromol/l). RBC-CAT levels were similar between groups (125.6+/-21.3 versus 131.0+/-21.5 k/g Hb, p = 0.8798). CONCLUSIONS: The elevated LPO, TNF-alpha and NO* with decreased antioxidant enzyme activities indicated impaired antioxidative defence mechanisms with an oxidative injury and cell toxicity in WMS patients. The use of multiple antioxidants and free radical scavengers might be helpful in this genetic disorder.  相似文献   
178.
Fifty-two healthy Swiss Male Albino rats aged two mo were used in this study. They were divided into four groups: control (C), diabetic (D), cadmium (Cd), and diabetic+Cd (D+Cd) groups. Diabetic condition was induced in D and D+Cd groups by administration of alloxane (5 mg/100 g). After this treatment, CD and D+Cd groups were injected with CdCl2 ip (2 mg/kg/wk). At the end of the 2-mo experimental period, thiobarbituric acid reactive substances (TBARS), plasma and erythrocyte selenium (SE), plasma ceruloplasmin (Cp), and vitamin E (vit E) were determined in four groups of rats. The erythrocyte Se was lower in the experimental groups than in the controls. Plasma Se was significantly decreased in the D and D+Cd groups compared with the control group. Plasma Cp was unaltered. Plasma vit E was significantly decreased in Cd group in comparison with the C, D, and D+Cd groups.  相似文献   
179.
The aim of this work was to determine the protective effects of intraperitoneally administrated vitamin E and Se on total lipid, total cholesterol, and fatty acid composition of rat liver and muscle tissues. Total lipid content of muscle tissue in Se and combination groups decreased as compared to the control group. However, the level of total lipid in the liver tissues was seen to decrease only in the combination group (P < 0.05). While the amount of total cholesterol in liver tissue was lower (P < 0.05) in the vitamin E and combination groups, the amount of total cholesterol in muscle tissue decreased (P < 0.05) in the combination group. The amount of linoleic acid in muscle tissue slightly decreased (P < 0.05), whereas the eicosenoic and eicosatrienoic acid amounts significantly increased (P < 0.01, P < 0.001) in the vitamin E group as compared to the control group. The amounts of most fatty acid decreased (P < 0.05) in the combination group. The proportions of eicosenoic, eicosatrienoic, and total polyunsaturated fatty acid (PUFA) within the total fatty acid were higher (P < 0.05) in vitamin E group, whereas these fatty acids proportions were lower (P < 0.05) in the Se group. Although the proportions of palmitic, linolenic, and total saturated fatty acids were low (P < 0.05), oleic and total unsaturated fatty acid proportions were higher (P < 0.05) in the combination group than in the control group. The amount of palmitic acid and total saturated fatty acid in liver tissue decreased (P < 0.01 and P < 0.05, respectively) in the vitamin E and combination groups. However, the amount of linoleic acid only decreased (P < 0.05) in the combination group. The amount of PUFA was slightly higher (P < 0.05) in vitamin E. The proportions of stearic acid and linoleic acid decreased (P < 0.05) both in the Se and combination groups. However, the proportions of eicosatrienoic, ω 6, and PUFA were slightly higher (P < 0.05) in the vitamin E group, but total saturated fatty acid proportion significantly decreased (P < 0.01) in both the vitamin E and combination groups. In conclusion, the level of total lipid and cholesterol in muscle and liver tissues were reduced by administrating vitamin E and Se together. Additionally, the fatty acid synthesis in the muscle and liver tissues was decreased by this process. However, it was observed that the protective effect of intraperitoneally administrated vitamin E was higher than Se on fatty acid composition in muscle and liver tissues. J. Cell. Biochem. 64:233–241. © 1997 Wiley-Liss, Inc.  相似文献   
180.
The present study was aimed to examine the effects of 3-week zinc and melatonin administration on testicular tissue injury and serum Inhibin-B levels caused by unilateral testicular torsion–detorsion in rats. The study was performed on 60 Wistar Albino-type adult male rats. The animals were allocated to 6 groups in equal numbers. 1. Control; 2. Sham; 3. Ischemia–reperfusion; 4. Zinc + ischemia–reperfusion; 5. Melatonin + ischemia–reperfusion; 6. Zinc + melatonin + ischemia–reperfusion. Zinc and melatonin were administered before ischemia–reperfusion at doses of 5 and 3 mg/kg respectively, by intraperitoneal route for a period of 3 weeks. Testicular torsion–detorsion procedures consisted of ischemia for 1 h and then reperfusion for another hour of the left testis. Blood and testicular tissue samples were collected to analyze erythrocyte and tissue GSH and plasma and tissue MDA, Inhibin-B levels. The highest erythrocyte and testis GSH values were found in zinc, melatonin, and zinc + melatonin groups (p < 0.001). Torsion–detorsion group has significantly lower erythrocyte GSH levels and higher plasma MDA values (p < 0.001). Serum inhibin-B and spermatogenic activity levels in the torsion–detorsion group were also significantly lower than those in the other groups (p < 0.001). However, zinc-, melatonin-, and melatonin + zinc-supplemented groups have higher inhibin-B and spermatogenetic activity (p < 0.001). The results of the study show that zinc, melatonin, and melatonin + zinc administration partially restores the increased oxidative stress, as well as the reduced inhibin-B and spermatogenic activity levels in testes ischemia–reperfusion in rats. Suppressed inhibin-B levels in the testicular tissue may be a marker of oxidative stress.  相似文献   
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