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

In our companion paper (Le Calvez et al., 1998), the levels of distortion product otoacoustic emissions (DPOAE) were collected in the ears of CD1 mice with progressive degeneration of cochlear outer hair cells (OHC). Their comparison to standard functional measurements such as auditory-evoked brainstem responses (ABR) showed that CD1 ears could be classified as normal or impaired in a frequency-specific manner using DPOAE levels. The present work reports how DPOAE phases and levels of young CD1 mice were affected by varying the frequency ratio of eliciting stimuli at frequencies f1 and f2. Normally hearing CBA/J mice served as controls. The rate of phase change of DPOAE when f1 was varied and f2 was fixed allowed the group delay of DPOAE to be derived. The changes of DPOAE levels during this procedure disclosed bandpass characteristics that several reports (Fahey and Allen, 1986; Brown and Gaskill, 1990) assumed to be the reflection of important features of cochlear micromechanics, possibly in relation to the coupling of OHCs to the tectorial membrane. Group delays became significantly shorter when ABR thresholds exceeded 40 dB elevation. The bandpass filter characteristics strikingly depended on auditory function so that the optimal ratio f2/f1 progressively shifted from 1.24 to 1.50 or more when hearing loss increased. A difference was also noted between CD1 ears whose ABR thresholds were not yet increased and control CBA/J (optimal ratio 1.20). Scanning electron microscopy disclosed a variety of often minor OHC lesions that were only roughly correlated with cochlear function. However, the presence of abnormalities in the reticular lamina associated with early changes of DPOAE fine structure as a function of f2/f1 supported the hypothesis of some involvement of micromechanical features in the bandpass filter characteristics of DPOAE. The sensitivity of their measurement in pathological situations is potentially interesting.
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PMID:CD1 hearing-impaired mice. II. Group latencies and optimal f2/f1 ratios of distortion product otoacoustic emissions, and scanning electron microscopy. 966 30

The in vivo effects of adriamycin (ADR) on the mouse and rat embryos are well described in the literature. However, there is a lack of knowledge about the in vitro effects of ADR. The aim of this study was to investigate the effects of ADR on the developing mouse embryo and to identify a dose of ADR, which could be used for further studies of ADR effects in vitro. CD1 mouse embryos were collected at day 8.5 post conception. They were cultured in the presence of different doses of ADR (0, 125, 250, 375 and 500 microM). After 24 h, the culture was stopped and the embryos (n = 77) were scored morphologically using the Brown-Fabro scoring system and the mean score for each organ was calculated. Dose-response plots were generated and the effective dose 50 (ED50) for each organ was identified from the plots. The effects of ADR on the developing embryo were found to be dose related and there is a dose-response relationship in most of the plots. The dose-response plots were found to be parallel for some organs. A dose of 250 microM ADR was identified as the appropriate dose for further in vitro studies. The effects of ADR on the embryos were dose related and there is a dose-response relationship in most of the developing systems. The presence of parallel dose-response plots for some regions is suggestive of similar mechanism of action of ADR on these regions. A dose of 250 microM of ADR was identified for the first time in the literature and could be used for further studies of the effects of ADR on the mouse foregut in vitro.
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PMID:In vitro effects of adriamycin: a dose-response study. 1721 89

Brown adipose tissue (BAT) generates heat during adaptive thermogenesis through a combination of oxidative metabolism and uncoupling protein 1-mediated electron transport chain uncoupling, using both free-fatty acids and glucose as substrate. Previous rat-based work in 1942 showed that prolonged partial fasting followed by refeeding led to a dramatic, transient increase in glycogen stores in multiple fat depots. In the present study, the protocol was replicated in male CD1 mice, resulting in a 2000-fold increase in interscapular BAT (IBAT) glycogen levels within 4-12 hours (hr) of refeeding, with IBAT glycogen stores reaching levels comparable to fed liver glycogen. Lesser effects occurred in white adipose tissues (WAT). Over the next 36 hr, glycogen levels dissipated and histological analysis revealed an over-accumulation of lipid droplets, suggesting a potential metabolic connection between glycogenolysis and lipid synthesis. 24 hr of total starvation followed by refeeding induced a robust and consistent glycogen over-accumulation similar in magnitude and time course to the prolonged partial fast. Experimentation demonstrated that hyperglycemia was not sufficient to drive glycogen accumulation in IBAT, but that elevated circulating insulin was sufficient. Additionally, pharmacological inhibition of catecholamine production reduced refeeding-induced IBAT glycogen storage, providing evidence of a contribution from the central nervous system. These findings highlight IBAT as a tissue that integrates both canonically-anabolic and catabolic stimulation for the promotion of glycogen storage during recovery from caloric deficit. The preservation of this robust response through many generations of animals not subjected to food deprivation suggests that the over-accumulation phenomenon plays a critical role in IBAT physiology.
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PMID:Refeeding-induced brown adipose tissue glycogen hyper-accumulation in mice is mediated by insulin and catecholamines. 2386 10