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61.
F Zindy H Soares KH Herzog J Morgan CJ Sherr MF Roussel 《Canadian Metallurgical Quarterly》1997,8(11):1139-1150
In situ hybridization of mouse embryo sections demonstrated expression of mRNAs encoding two polypeptide inhibitors (p18INK4c and p19INK4d) of cyclin D-dependent kinase (CDK) 4 and CDK6 in the central nervous system. No expression of two other INK4 members, p16INK4a and p15INK4b, was observed. The p19INK4d and p18INK4c proteins formed complexes with either CDK4 or CDK6 in a temporal pattern consistent with the results of in situ hybridization. Expression of INK4c was observed at embryonic day 13.5 in neuroepithelial zones of the developing brain, being restricted to dividing neuroblasts but absent from differentiating postmitotic neurons. In the neocortex, p18INK4c was expressed precisely at those developmental stages when neuroblasts switch from a symmetric to an asymmetric pattern of cell division with concomitant increases in their G1 interval. INK4d RNA was detected from embryonic day 11.5 onward, at higher levels than INK4c and with a distinctly different spatial and temporal pattern. Marked INK4d expression was seen in dorsal root ganglia, spinal cord, and focally throughout the brain, but primarily in postmitotic neurons. Neural expression of INK4d continued postnatally into adulthood in postmitotic cells of the dentate gyrus, the pyramidal layer of the hippocampus, and in discrete regions of the cerebral cortex, cerebellum, thalamus, and brainstem. Downregulation of p19INK4d in the dentate gyrus after kainic acid-induced seizures indicated that its expression could also be modified in nondividing cells by excitotoxic stress. Therefore, p19INK4d may contribute to maintaining the quiescent state, acting as a buffer to prevent reactivation of cyclin D-dependent kinases in terminally differentiated cells. 相似文献
62.
In patients with Wolff-Parkinson-White syndrome the accessory pathway may participate in various tachyarrhythmias thereby influencing symptoms and prognosis. Atrial fibrillation occurs in 10 to 32% of patients and may have life-threatening consequences by precipitating ventricular fibrillation in patients with rapid conduction due to an accessory pathway with short anterograde refractory period (< 250 ms). Pathogenesis of atrial fibrillation in the WPW syndrome and therapeutic options are reviewed in this presentation. Spontaneous degeneration of atrioventricular reentrant tachycardia has been reported to represent the most frequent mode of initiation of atrial fibrillation during electrophysiologic study (up to 64% of episodes). Hemodynamic changes during tachycardia may lead to increased sympathetic tone, hypoxemia or increased tension of the atrial wall, thus, triggering atrial fibrillation. Induction of reentrant tachycardia during electrophysiologic study also has shown to be strongly correlated to its clinical prevalence and is inducible in up to 77% of patients with atrial fibrillation. The pathogenesis and high incidence of atrial fibrillation in patients with WPW syndrome is related to presence and functional properties of the accessory pathway. After surgical excision or catheter ablation more than 90% of patients are free of this arrhythmia. Anterograde conduction properties of the pathway appear to be more important than retrograde properties. High incidence of atrial fibrillation is related to short anterograde refractory periods, and of note, this arrhythmia is rare (3%) in patients with concealed pathways. With intracardiac recordings, Jackman et al. could demonstrate atrial fibrillation due to micro-reentry originating in accessory pathway networks.(ABSTRACT TRUNCATED AT 250 WORDS) 相似文献
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Senior nursing students described their interactions with faculty in a journal writing assignment. These interactions were categorized by the ethical perspectives of justice, autonomy, beneficence, and caring. An ethical analysis of faculty-student interactions is a strategy that may help nursing faculty and students understand differing perceptions about their relationships. 相似文献
65.
BACKGROUND: We have previously observed a potentiation of the metabolic response to cachectin/tumor necrosis factor (TNF) by total parenteral nutrition (TPN) but not in anorexic orally fed animals. We hypothesized that nutritional status might affect TNF clearance kinetics. METHODS: We compared the clearance of a bolus of labeled TNF in TPN-fed animals given sufficient nutrients to grow called weight-gaining rats (WGR) with those given 50% of the WGR called weight-losing rats (WLR) and with orally fed rats (OFR). Data were analyzed using a two-compartment open system model and by linear systems analysis. RESULTS: The data from both types of analysis indicator that although metabolic clearance was similar, WGR had a slower fractional TNF clearance rate (FCR) as well as a larger volume of distribution than WLR or OFR. Further analysis showed that an increased proportion of the total mass of TNF resided in a plasma-associated compartment in WGR compared with WLR and OFR. In addition, WGR had reduced uptake of labeled TNF by the kidney. CONCLUSION: The data suggest that nutrition support influences either the distribution of TNF or the FCR, resulting in a greater retention in the plasma-associated compartment with intact absolute removal rates. This study has important implications concerning the type of nutrition support provided to the critically ill patient because our data suggest that clinical states with increased circulating TNF levels may be adversely affected by currently available nutritional practices. 相似文献
66.
LB Corbeil RP Gogolewski I Kacskovics KH Nielsen RR Corbeil JL Morrill R Greenwood JE Butler 《Canadian Metallurgical Quarterly》1997,61(3):207-213
AIMS/BACKGROUND: To characterise clinically a large kindred segregating retinitis pigmentosa and sensorineural hearing impairment in an autosomal dominant pattern and perform genetic linkage studies in this family. Extensive linkage analysis in this family had previously excluded the majority of loci shown to be involved in the aetiologies of RP, some other forms of inherited retinal degeneration, and inherited deafness. METHODS: Members of the family were subjected to detailed ophthalmic and audiological assessment. In addition, some family members underwent skeletal muscle biopsy, electromyography, and electrocardiography. Linkage analysis using anonymous microsatellite markers was performed on DNA samples from all living members of the pedigree. RESULTS: Patients in this kindred have a retinopathy typical of retinitis pigmentosa in addition to a hearing impairment. Those members of the pedigree examined demonstrated a subclinical myopathy, as evidence by abnormal skeletal muscle histology, electromyography, and electrocardiography. LOD scores of Zmax = 3.75 (theta = 0.10), Zmax = 3.41 (theta = 0.10), and Zmax = 3.25 (theta = 0.15) respectively were obtained with the markers D9S118, D9S121, and ASS, located on chromosome 9q34-qter, suggesting that the causative gene in this family may lie on the long arm (q) of chromosome 9. CONCLUSIONS: These data indicate that the gene responsible for the phenotype in this kindred is located on chromosome 9 q. These data, together with evidence that a murine deafness gene is located in a syntenic area of the mouse genome, should direct the research community to consider this area as a candidate region for retinopathy and/or deafness genes. 相似文献
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介绍了在红外系统中,采用步进电机作为扫描机构驱动元件,以D/A数模转换器作细分方式的定频脉宽调制驱动方式,实现微机控制下的扫描机的构步距均匀稳定,满足红外系统分辨率的要求。 相似文献
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