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971.
Although profound hypothermia has been used for decades to protect the human brain from hypoxic or ischemic insults, little is known about the underlying mechanism. We therefore report the first characterization of the effects of moderate (30 degrees C) and profound hypothermia (12 degrees to 20 degrees C) on excitotoxicity in cultured cortical neurons exposed to excitatory amino acids (EAA; glutamate, N-methyl-D-aspartate [NMDA], AMPA, or kainate) at different temperatures (12 degrees to 37 degrees C). Cooling neurons to 30 degrees C and 20 degrees C was neuroprotective, but cooling to 12 degrees C was toxic. The extent of protection depended on the temperature, the EAA receptor agonist employed, and the duration of the EAA challenge. Neurons challenged briefly (5 minutes) with all EAA were protected, as were neurons challenged for 60 minutes with NMDA, AMPA, or kainate. The protective effects of hypothermia (20 degrees and 30 degrees C) persisted after rewarming to 37 degrees C, but rewarming from 12 degrees C was deleterious. Surprisingly, however, prolonged (60 minutes) exposures to glutamate unmasked a temperature-insensitive component of glutamate neurotoxicity that was not seen with the other, synthetic EAA; this component was still mediated via NMDA receptors, not by ionotropic or metabotropic non-NMDA receptors. The temperature-insensitivity of glutamate toxicity was not explained by effects of hypothermia on EAA-evoked [Ca2+]i increases measured using high- and low-affinity Ca2+ indicators, nor by effects on mitochondrial production of reactive oxygen species. This first characterization of excitotoxicity at profoundly hypothermic temperatures reveals a previously unnoticed feature of glutamate neurotoxicity unseen with the other EAA, and also suggests that hypothermia protects the brain at the level of neurons by blocking, rather than slowing, excitotoxicity. 相似文献
972.
973.
C Svanes E Omenaas JM Heuch LM Irgens A Gulsvik 《Canadian Metallurgical Quarterly》1998,12(6):1366-1370
There is evidence that the origin of obstructive lung disease may be traced back to foetal life. The associations between birth characteristics and asthma symptoms were studied in a random population sample of young Norwegian adults. Respiratory symptoms were recorded in a population-based questionnaire survey. The records of all subjects aged 20-24 yrs were linked with the Medical Birth Registry of Norway. Of 868 subjects born in Norway, there were 690 (79%) responders. The associations between asthma symptoms and birth characteristics were analysed by logistic regression, adjusted for possible confounding factors. Asthma symptoms in young adults were inversely associated with birth weight (odds ratio (OR)wheeze=0.82; 95% confidence interval (CI)=0.69-0.96x500 g increase in birth weight(-1))), and after adjustment for gestational age, birth length, parity and maternal age (ORwheeze=0.69; 95% CI=0.50-0.95x500 g increase in birth weight(-1)). The association did not vary according to adult smoking habits or atopic status and remained when premature and low weight births were excluded (ORwheeze=0.73; 95% CI=0.60-0.90x500 g increase in birth weight(-1)). The association was consistent for all asthma symptoms. Adjusted for birth weight, asthma symptoms were further associated with low gestational age, high birth length and low maternal age. In a random sample of young adults, asthma symptoms were strongly associated with low birth weight, an association driven by the full-term births within the normal birth weight range. The findings show that the risk for adult asthma is partly established early in life and suggest that poor intrauterine growth is involved in the aetiology of asthma. 相似文献
974.
We have isolated and characterized the Saccharomyces cerevisiae PTR3 gene by functional complementation of a mutant deficient for amino acid-inducible peptide transport. PTR3 is predicted to encode a protein of 678 amino acids that exhibits no similarity to any other protein in the database. Deletion of the PTR3 open reading frame pleiotropically reduced the sensitivity to toxic peptides and amino acid analogues. Initial rates of radiolabelled dipeptide uptake demonstrated that elimination of PTR3 resulted in the loss of amino acid-induced levels of peptide transport. PTR3 was required for amino acid-induced expression of PTR2, the gene encoding the dipeptide/tripeptide transport protein, but was not necessary for nitrogen catabolite repression of peptide import or PTR2 expression. It was determined that PTR3 also modulates expression of BAP2, the gene encoding the branched-amino acid permease. Furthermore, we present genetic evidence that suggests that PTR3 functions within a novel regulatory pathway that facilitates amino acid induction of the PTR system. 相似文献
975.
We retrospectively reviewed the cases of seventy-two consecutive patients who had a lumbar discectomy, between 1950 and 1983, when they were sixteen years of age or younger. There were forty boys and thirty-two girls. At the time of the lumbar discectomy, twelve patients (17 per cent) also had a spinal arthrodesis. The mean duration of follow-up was 27.8 years (range, twelve to forty-five years). Twenty patients (28 per cent) had one reoperation or more, with the first reoperation performed at a mean of 9.7 years after the initial discectomy. Fourteen patients had one reoperation, four had two reoperations, one had three, and one had five. Fifty-two patients (72 per cent) did not need a reoperation. At the time of the latest follow-up, forty-eight (92 per cent) of the fifty-two patients either had no pain or had occasional pain related to strenuous activity and fifty-one (98 per cent) could participate in daily activities with no or mild limitations. Survivorship analysis showed that the overall probability that a patient would not need a reoperation was 80 per cent at ten years and 74 per cent at twenty years after the initial operation. With the numbers available for study, we could not show that age, gender, or an arthrodesis performed at the time of the initial operation were risk factors for a reoperation. We could not detect a difference, with respect to pain or the level of activity, between the patients who had had an arthrodesis at the initial operation and those who had not or between those who had a coexisting structural abnormality of the lumbar spine and those who did not. 相似文献
976.
FJ Meiland JA Danse JF Wendte JM Kegel LJ Gunning-Schepers 《Canadian Metallurgical Quarterly》1998,29(6):285-291
The distribution, morphological features, and postnatal development of parvalbumin (PV) immunoreactive neurons in the main olfactory bulb (MOB) of the house musk shrew, Suncus murinus, were studied to report for the first time on PV positive bulbar interneurons in the order Insectivora. In adult animals, PV neurons are distributed in the glomerular layer (GL), the external plexiform layer (EPL), the internal plexiform layer (IPL) and the granule cell layer (GCL) of the MOB. These neurons were identified as a subpopulation of periglomerular cells and perinidal cells [Alonso et al., 1995] in the GL and at the GL-EPL border, respectively, and as bipolar and multipolar neurons in the EPL and four types of the interneurons (horizontal cells, Cajal cells, Golgi cells, and bitufted cells) in the layers deeper than the mitral cell layer. During development of PV neurons, neurons exhibiting extremely faint PV immunoreactivity first appeared in the GCL at postnatal day 14 and increased markedly in number and intensity of their PV immunoreactivity from postnatal days 14 to 28. At postnatal day 21, PV neurons were identified as periglomerular cells in the GL, perinidal cells at the GL-EPL border, and morphologically unidentifiable neurons in the EPL, IPL and GCL. At postnatal day 28, PV neurons exhibited a nearly adult pattern with respect to distribution and structural features. The present results strongly suggest that a wide variety of PV positive neurons in the MOB of the house musk shrew may develop postnatally. 相似文献
977.
Kindling is widely accepted as a model of chronic epilepsy as well as a model of plasticity in the nervous system. Conventional kindling studies have used infrequent stimuli (separated by many hours) to establish a fully kindled state in which enhanced responses (kindled motor seizures and protracted afterdischarges) are consistently triggered by stimuli that initially did not elicit such responses. The enhanced responses occur even after a prolonged stimulus-free interval. Whereas the establishment of a kindled state with traditional stimulus protocols takes several weeks, our previous work showed that kindling could take place much more quickly when the interstimulus interval was set at 30 min (rapid kindling). In this report we tested whether rapid kindling protocols share with traditional kindling protocols the ability to establish a fully kindled state. Using different stimulus protocols involving recurrent hippocampal seizures, we characterized two types of kindling. 'Rapid kindling' developed over hours, but was transient, with a decay rate of a few days so that a fully kindled state did not persist. In contrast, 'slow kindling' developed over several weeks and was enduring, apparently permanent, being associated with a fully kindled state. These findings suggest that, while having certain similarities, the two types of kindling arise from dissimilar mechanisms. The existence of these two types of kindling has implications for epileptogenesis in humans. Moreover, the protocols developed in this work provide a useful means to control for the effects of seizures that are not related to mechanisms underlying a fully kindled state. 相似文献
978.
979.
To clarify whether vitamin E enhances the pharmacologic effect of warfarin, we completed a double-blind clinical trial in which 21 subjects taking chronic warfarin therapy were randomized to receive either vitamin E or placebo. None of the subjects who received vitamin E had a significant change in the international normalized ratio, and thus it appears that vitamin E can safely be given to patients who require chronic warfarin therapy. 相似文献
980.
Treadmill exercise activates the hypothalamic-pituitary-adrenal axis and evokes metabolic responses proportional to exercise intensity and duration. To determine whether glucocorticoid administration would alter humoral and metabolic regulation during exercise, we administered 4 mg dexamethasone (DEX) or placebo to 11 normal, moderately trained men (19-42 yr old) in a double blinded random fashion 4 h before high intensity intermittent treadmill running. Plasma levels of ACTH, cortisol, arginine vasopressin (AVP), lactate, and glucose were measured before, during, and after exercise. A wide range of ACTH responses were seen in the DEX-treated group and arbitrarily defined as two subsets of individuals according to their responses to dexamethasone: DEX nonsuppressors and DEX suppressors. Exercise-induced increases in heart rate and circulating concentrations of cortisol, AVP, lactate, and glucose were all significantly greater (P < 0.05) in nonsuppressors (n = 4) compared to suppressors (n = 7) after both placebo and DEX administration. Interestingly, heart rate, AVP, and lactate responses were unaltered by DEX alone in both groups. In summary, this study demonstrates that normal individuals exhibit differential neuroendocrine and metabolic responses to exercise and pituitary/adrenal suppression after pretreatment with DEX. These findings reflect marked individual differences in the stress response to exercise that may derive from or lead to differential glucocorticoid negative feedback sensitivity in humans. 相似文献