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81.
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Although retrograde and anterograde degeneration studies have provided important information concerning brain stem afferents to the fastigal nucleus (FN), these data may be incomplete and should be confirmed by axonal transport methods. Attempts were made to inject horseradish peroxidase (HRP) unilaterally into the FN in a series of adult cats. Animals were perfused with dextran and a fixative solution of paraformaldehyde and glutaraldehyde in 0.1 M phospate buffer. Representative sections were treated by the Graham and Karnovsky ('66) method. Selective HRP injections in one FN resulted in retrograde transport of the marker to Purkinje cells of the ipsilateral vermis and distinctive appendages of the contralateral medial accessory olivary (MAO) nucleus (nucleus beta and the dorso-medial cell column). Retrograde transport of the label was found bilaterally in cells of the medial (MVN) and inferior (IVN) vestibular nuclei, in cell group x and in the nucleus prepositus (PP). Labeled vestibular neurons, most numerous in MVN, were identified in dorsal, caudal and lateral regions, with a slight ipsilateral preponderance. Only a few neurons in caudal, dorsal and lateral regions of the IVN were labeled and none of these included cells of group f. Labeled cells in the caudal third of PP were greatest ipsilaterally. Rostral and caudal injections of FN labeled smaller numbers of cells in MVN, IVN, cell group x and PP. HRP injections of FN and portions of lobules VIII and IX resulted in bilateral retrograde labeling of larger numbers of cells in MVN, IVN and cell group x, and ipsilateral labeling of cells in group y and the interstitial nucleus of the vestibular nerve. Injections of HRP into basal folia of lobules V and VI resulted in retrograde transport of the marker to cells of the medial and dorsal accessory olivary nuclei contralaterally, and to cells of the ipsilateral accessory cuneate nucleus. Transport of label injected into portions of the pyramis was detected in parts of the contralateral MAO and bilaterally in parts of the pontine and reticulotegmental nuclei. This study suggests that the principal afferents of the fastigial nucleus arise from: (1) Purkinje cells of the ipsilateral vermis, (2) restricted portions of the contralateral MAO (nucleus beta and dorsomedial cell column), (3) portions of the MVN and IVN (bilaterally) and (4) caudal parts of the PP. Secondary vestibular inputs to the fastigial nucleus probably are relayed mainly by Purkinje cells in the cerebellar cortex.  相似文献   
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This study examined the neuroprotective effects and possible hepatotoxicity of (-)-epigallocatechin gallate (EGCG) in a rat model of transient focal cerebral ischemia. Male Sprague-Dawley rats (265-295 g) were treated with either 50 mg kg(-1) of EGCG or saline, i.p., immediately post-ischemia and every day thereafter, in a middle cerebral artery occlusion model of stroke. Sacrifice occurred 72 h post-ischemia and 2,3,5-triphenyltetrazolium chloride staining was used to quantify neuronal infarction. Hepatotoxicity was determined by taking blood samples for plasma alanine aminotransferase (ALT) activity. Spleen, kidney, liver and testes wet weights were also recorded. Total infarct volume was significantly (P<0.05) reduced in the EGCG-treated group as compared to controls. Analysis of the mean infarct area showed a significant (P<0.05) decrease in slices 6 and 7 in the EGCG-treated group. No significant differences were found in organ weights or ALT levels between treatment groups. Our findings, in part, validate and extend previous observations illustrating that 50 mg kg(-1), i.p. EGCG is non-toxic and neuroprotective. However, we also found that EGCG treatment appreciably increased (>50%) the number of animals that developed an intracerebral hemorrhage. We therefore conclude that 50 mg kg(-1) EGCG is not a viable intervention for the acute treatment of cerebral ischemia, as it is likely to increase the risk of intracerebral hemorrhaging.  相似文献   
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BACKGROUND: Chronic, hypointense black holes (BHs) are recognized as a sign of permanent damage in patients with multiple sclerosis. Although the effects of interferon beta-1b in reducing the formation of new BHs are established, it is not clear whether the drug may reduce BH duration after these lesions are formed. OBJECTIVE: To analyze the effects of interferon beta-1b in reducing the duration of T1 BHs in patients with multiple sclerosis. DESIGN: Patients were clinically assessed and imaged monthly over a 36-month natural history phase and 36-month therapy phase. Numbers of contrast-enhanced lesions and newly formed BHs were counted on each scan. Each BH was counted until it was no longer seen. SETTING: Outpatient service of the Neuroimmunology Branch at the National Institutes of Health, Bethesda, Md. PATIENTS: Six patients with relapsing-remitting multiple sclerosis were included. One patient did not form any BHs during the therapy phase. Analyses were performed on the remaining 5 individuals. INTERVENTIONS: Interferon beta-1b at the dosage of 8 million international units every other day. MAIN OUTCOME MEASURES: Number and duration (in months) of newly formed BHs. RESULTS: Rate of BH accumulation decreased with treatment (P = .01), but Kaplan-Meier models revealed that the duration of BHs did not shorten (chi2(1) = 2.47, P = .12). CONCLUSIONS: Interferon beta-1b reduces the frequency of new BH formation but does not appear to decrease their duration in time. Analyses with larger patient cohorts are needed to confirm these preliminary findings.  相似文献   
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Neural classification of lung sounds using wavelet coefficients   总被引:6,自引:0,他引:6  
Electronic auscultation is an efficient technique to evaluate the condition of respiratory system using lung sounds. As lung sound signals are non-stationary, the conventional method of frequency analysis is not highly successful in diagnostic classification. This paper deals with a novel method of analysis of lung sound signals using wavelet transform, and classification using artificial neural network (ANN). Lung sound signals were decomposed into the frequency subbands using wavelet transform and a set of statistical features was extracted from the subbands to represent the distribution of wavelet coefficients. An ANN based system, trained using the resilient back propagation algorithm, was implemented to classify the lung sounds to one of the six categories: normal, wheeze, crackle, squawk, stridor, or rhonchus.  相似文献   
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Purpose

Gastrointestinal (GI) dysmotility occurs frequently in full-term infants with gastroschisis (GS). Although controversial, preterm delivery of infants with GS has been advocated to prevent the development of GI dysmotility, and understanding the etiology of gestational-related bowel injury may lead to prenatal therapies. Using a fetal rabbit model, the authors assessed in vivo and in vitro GI motility in preterm GS fetuses.

Methods

On gestation day 24 (term, 31), surgery was performed in maternal rabbits and GS induced in fetuses, whereas control fetuses underwent sham procedures. On gestation day 29, both groups of fetuses received ultrasound-guided intragastric injection of fluorescein and colored microspheres. Two hours after injection, fetuses were delivered by cesarean section and stomach and small intestine harvested intact. “GI motility” was calculated as the distance traveled by fluorescein divided by total length. In vitro studies of fetal gastric muscle strips contractility responses to bethanechol, a cholinergic agonist, were assessed in an organ bath system. Data were analyzed as paired and unpaired t tests and expressed as means ± SEM.

Results

GS reduced fetal body weight and intestinal length compared with controls (28.4 ± 1.4 v. 33.5 ± 1.5 g, 36.9 ± 1.8 v. 25.9 ± 1.2 cm; P < .05, respectively). Fetuses with GS showed markedly reduced in vivo GI motility (51.4 ± 2.9 v 24.8 ± 2.7%; P < .05) and in vitro gastric contractile tension (769 ± 53 v 396 ± 26 mNcm2; P < .05).

Conclusions

GI exposure to amniotic fluid reduces intestinal motility and gastric contractility functions in the preterm rabbit fetus. The results suggest that GS-associated impairment of GI neuromuscular functions occurs in utero, before term, and may be responsive to manipulation of amniotic fluid content or other therapeutic interventions.  相似文献   
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