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Query: UMLS:C0155339 (Brown)
 12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has long been known that severe food deprivation disrupts the estrous cycle. One of the main problems with behavioral tasks that use food for reinforcement is the requirement that the animal be food deprived. This manipulation could be problematic in studies using female animals, since it may interfere with the estrous cycle of the animals. The purpose of the present study was to investigate: (1) the effect of mild food deprivation on four different strains of rats, (2) factors in the food deprivation procedure that could affect the estrous cycle, and (3) the possible effect of enriched diets during food deprivation on the estrous cycle. A comparison of the estrous cycle in four different rat strains revealed differences in the reliability of the estrous cycle even before the onset of food deprivation. Fischer, Long-Evans, and Sprague-Dawley rats all showed reliable cycle patterns. This was not the case for Brown Norway rats. During food deprivation, the cycle of the Fischer rats was disrupted, whereas the Long-Evans and Sprague-Dawley animals continued to cycle. Both the rate of weight loss and the percent of ad libitum body weight were related to cessation of the estrous cycle. However, enriching an animal's diet with sugar or oil additives delayed the disruption of the estrous cycle. Additionally, animals resumed cycling when returned to ad libitum weight levels. The present findings suggest that when animals need to be food deprived, preference should be given to using Long-Evans or Sprague-Dawley rats. If Fischer rats must be used, they should not be deprived below 90-95% of their ad libitum body weight. Strategies for future food deprivation studies are discussed, as well as a comparison of the effects of mild and severe food deprivation.
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PMID:Effects of mild food deprivation on the estrous cycle of rats. 1149 59

Oxidative stress appears relevant to asthma. Therefore, the effects of the antioxidant taurine (oral, 1 and 3 mmol x kg(-1) x day(-1) for 7 days before challenge) were examined on antigen-induced responses in sensitized Brown-Norway rats. Taurine did not reduce the bronchospasm produced by aerosol antigen but prevented airway hyperreactivity to 5-hydroxytryptamine (5-HT) at 24 h after antigen exposure, and reduced the eosinophils (from 0.178+/-0.038x10(6) to 0.044+/-0.014x10(6)* and 0.048+/-0.013x10(6)* cells ml(-1) in antigen and antigen+taurine 1 or 3 mmol x kg(-1), respectively; *P<0.05 vs. antigen), lipid hydroperoxides, and Evans blue dye extravasation in bronchoalveolar lavage fluid. Taurine levels in bronchoalveolar lavage fluid from antigen-challenged rats were higher than control values but treatment with taurine failed to further increase these levels. In conclusion, oral taurine showed beneficial effects in an in vivo model of experimental asthma, which confirm and extend the previous positive findings obtained in other models of lung injury.
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PMID:Effects of taurine on pulmonary responses to antigen in sensitized Brown-Norway rats. 1171 49

Oxidative stress appears to be relevant to asthma pathogenesis. Therefore, the effectiveness of the antioxidant N -acetylcysteine was examined on antigen-induced pulmonary responses in sensitized Brown-Norway rats. N -acetylcysteine (oral, 1 mmol kg(-1)per day for 7 days before challenge) did not reduce the immediate bronchospasm that followed aerosol antigen exposure but prevented airway hyperreactivity to 5-hydroxytryptamine at 24 h after antigen challenge, and reduced the eosinophils (from 0.178 +/- 0.038 in the absence to 0.064 +/- 0.020 x10(6)cells ml(-1)in the presence of N -acetylcysteine;P< 0.05), and Evans blue dye extravasation in bronchoalveolar lavage fluid. Taurine levels in bronchoalveolar lavage fluid from antigen-challenged rats were higher than control values but treatment with N -acetylcysteine failed to further increase these augmented levels. In conclusion, oral N -acetylcysteine showed beneficial effects in an in vivo model of experimental asthma, which confirm and extend the previous positive findings obtained in other models of lung injury.
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PMID:Effectiveness of oral N -acetylcysteine in a rat experimental model of asthma. 1184 26

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) exposure during gestation has revealed reproductive anomalies in rat offspring, including inconclusive reports of stunted mammary development in females (Brown et al., 1998, Carcinogenesis 19, 1623-1629; Lewis et al., 2001, TOXICOL: Sci. 62, 46-53). The current studies were designed to examine mammary-gland development in female offspring exposed in utero and lactationally to TCDD, and to determine a critical exposure period and cellular source of these effects. Long-Evans rats were exposed to 1 microg TCDD/kg body weight (bw) or vehicle on gestation day (GD) 15. TCDD-exposed females sacrificed on postnatal days (PND) 4, 25, 33, 37, 45, and 68 weighed significantly less than control litter mates, and peripubertal animals exhibited delayed vaginal opening and persistent vaginal threads, yet did not display altered estrous cyclicity. Mammary glands taken from TCDD-exposed animals on PND 4 demonstrated reduced primary branches, decreased epithelial elongation, and significantly fewer alveolar buds and lateral branches. This phenomenon persisted through PND 68 when, unlike fully developed glands of controls, TCDD-exposed rats retained undifferentiated terminal structures. Glands of offspring exposed to TCDD or oil on gestation days 15 and 20 or lactation days 1, 3, 5, and 10 were examined on PND 4 or 25 to discern that GD 15 was a critical period for consistent inhibition of epithelial development. Experiments using mammary epithelial transplantation between control and TCDD-exposed females suggested that the stroma plays a major role in the retarded development of the mammary gland following TCDD exposure. Our data suggest that exposure to TCDD prior to migration of the mammary bud into the fat pad permanently alters mammary epithelial development in female rat offspring.
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PMID:Persistent abnormalities in the rat mammary gland following gestational and lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). 1196 Dec 17

Enzymatic retinyl ester hydrolysis is a key reaction for maintaining cellular retinol homeostasis. The ability of naftidrofuryl and erythromycin to inhibit retinol liberation by retinyl ester hydrolase (REH) in vitro suggests an ability to interfere with vitamin A metabolism in vivo, particularly during hepatic processing. To address this question, systemic and local response to these agents were studied in Brown Norway (BN) and Long-Evans (LE) rats. The study was conducted in two parts: a drug-loading phase and a washout phase. Analysis of variance of the time course changes in plasma retinol during the post-treatment period (Days 10-18) showed rat strain (p < 0.04) and time (p < 0.001; strain-by-time interactive effect, p < 0.001) to be significant factors, but drug exposure (p = 0.19) was not significant. Endpoints included hepatic REH activity, size and composition of the liver vitamin A stores, and retinoid content of the kidneys. Rats recovering from naftidrofuryl dosing demonstrated a lower REH activity than did animals recovering from erythromycin treatment (p < 0.009). The major side effect of erythromycin is vitamin A accumulation in the liver (p < 0.001) and reductions in retinol reserves (p < 0.02) were among the consequences of naftidrofuryl treatment. In the kidney of LE rats, there were higher concentrations of vitamin A (p < 0.003) secondary to naftidrofuryl exposure. Together our data suggest that clinically achievable concentrations of the drugs, given as a continuous infusion, produce aberrations in vitamin A metabolism.
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PMID:Vitamin A metabolism is altered in brown Norway and long-Evans rats infused with naftidrofuryl or erythromycin intravenously. 1221 58

The objective of this study was to determine if 1) the full employment-unemployment rate, or natural unemployment rate, changed between 1954-79 differentially for various subgroups in the US population; 2) minimum wage laws and unemployment compensation impacted differentially on subgroups in the population; and 3) there were structural shifts in the determinants of unemployment and labor force participation rates among subgroups. The 6 subgroups investigated were white and nonwhite teenagers, white and nonwhite females, and white and nonwhite males. Trends and cycles in unemployment were analyzed using regression techniques and basic time series models, and structural changes in the unemployment rate were analyzed by using a technique developed by Brown, Durbin, and Evans to test for change in estimated regression coefficients. Results indicated that the natural unemployment rate in the US increased from 4.70% to 5.14% between 1959-79. This increase was due in part to the unemployment rate increases observed among different subgroups in the population, and expecially among teenagers. In 1979 the unemployment rates among teenagers were 13.6% for whites and 28.72% for nonwhites. Respective rates in 1979 for white and nonwhite adult females were 4.20% and 9.98%, and for white and nonwhite adult males they were 2.78% and 6.36%. Other findings were 1) increases in minimum wage had a positive impact on the nonwhite teenagers' jobless rates, no effect on the white teenager jobless rate, and a negative impact on the adult unemployment rate; 2) increased unemployment compensation was positively associated with higher jobless rates for adult males and nonwhite teenagers; 3) the jobless rate was not significantly related to changes between 1954-79 in the proportion of different age, sex, and race groups in the population; and 4) structural shifts in the determinants of unemployment were observed for secondary workers only. Tables provided the results of the regression analysis, estimates of unemployment rates, by race, sex, and age for 1959, 1969, and 1979, and labor force composition and employment rates by race, sex, and age for 1954 and 1981.
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PMID:Cyclical and noncyclical unemployment differences among demographic groups. 1226 7

"The structural change model of the demographic transition developed by Easterlin and others is explored empirically by applying the Brown, Durbin and Evans test of structural change to annual data from the transitions of Sweden, Norway, England and Wales, and Finland. The evidence strongly supports the structural change model over traditional models (based on gradual changes in explanatory variables), indicating a supply response of fertility to declining illness and death during the early stages of transition, and a demand response to the death of children during the latter stages, when families are likely to have achieved desired size."
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PMID:An econometric test of structural change in the demographic transition. 1226 83

A sequence variation in the pigment epithelial protein RPE65 has been shown to correlate with RPE65 protein levels, rhodopsin regeneration kinetics and light damage susceptibility in different mouse strains. Here, we tested whether such a correlation can also be found in rats. We examined four rat strains for RPE65 protein levels and the Rpe65 gene sequence. In two strains, we additionally determined Rpe65 mRNA levels, rhodopsin regeneration and light damage susceptibility (LDS).RPE65 protein levels were higher in Lewis and Brown Norway rats compared to Wistar and Long Evans. The albino strains Wistar and Lewis were investigated further. Lewis had higher Rpe65 mRNA levels than Wistar. Sequence analysis of the coding region of the Rpe65 cDNA revealed no relevant sequence variations in the two strains. Content and regeneration of rhodopsin were comparable in both strains. However, Wistar rats were more susceptible to light damage than Lewis. We conclude that lower RPE65 protein levels in Wistar may have been caused by decreased gene expression and not by a sequence variation as suggested for mice. In rats, RPE65 may not be a limiting factor for rhodopsin regeneration. Since LDS in rats did not directly correlate with RPE65 protein levels and rhodopsin regeneration, other yet unidentified (genetic) factors may account for the susceptibility differences observed in rats.
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PMID:Light damage susceptibility and RPE65 in rats. 1238 88

Mutations in the gene encoding seipin cause Berardinelli-Seip congenital lipodystrophy 2, with symptoms including near-absence of adipose tissue and altered glucose tolerance. Radiation hybrid analysis localized the seipin gene (Bscl2) in rat to a major quantitative trait locus in rat chromosome 1 linked to glucose intolerance in the Goto-Kakizaki (GK) rat model of Type 2 diabetes. We determined the genomic organization of Bscl2 and screened coding exons and flanking intron sequences for mutations in GK, Wistar and Brown Norway rats, as well as in the Otsuka Long-Evans Tokushima Fatty (OLETF) diabetic rat. Two silent single nucleotide polymorphisms that were identified also were found in non-diabetic rat strains. We conclude that mutations in the gene for seipin are unlikely to contribute to diabetes in GK and OLETF rats.
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PMID:Localization, cDNA sequence and genomic organization of the rat seipin gene (Bscl2) and sequence analysis in inbred rat models of Type 2 diabetes mellitus. 1258 44

The role of the arterial sympathetic innervation in cerebrovascular pathology was investigated in new experimental models using Brown Norway (BN) and Long-Evans (LE) rats. The BN rat is susceptible to intracerebral hemorrhage (ICH) within the cerebral cortex when rendered hypertensive whereas the LE rat is prone to cerebral aneurysms (CAs) in arteries of the circle of Willis with hypertension and carotid ligation. Noradrenaline (NA) content, determined by high performance liquid chromatography (HPLC), was lower both in the caudal and cerebral arteries in the BN than in the LE rat. Denervation of cerebral arteries by superior cervical ganglionectomy did not increase ICH lesion incidence in BN hypertensive rats. A possible link between the level of caudal artery NA content and the occurrence of ICH lesions and CAs was studied in rats from two distinct BNXLE crosses: back-cross (BC) rats (F1XBN) and F2 rats (F1XF1) which respectively display, with hypertension and carotid ligation, a high incidence of either ICH lesions or CAs. In BC rats, the level of caudal artery NA content was not related to ICH lesion occurrence. However, in F2 rats a low caudal artery NA content was associated with a high incidence of ruptured CAs. Thus, a low arterial sympathetic innervation may participate in mechanisms leading to rupture of CAs.
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PMID:Arterial sympathetic innervation and cerebrovascular diseases in original rat models. 1264 15


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