Identification of euglenoid algae that produce ichthyotoxin(s).
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Biomedical subjects
Publications and source records attributed to M Rowan.
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2,5-Hexanedione is a neurotoxic metabolite of hexane. The mechanisms of its neurotoxicity remain unclear. We assessed whether chronic exposure to 2,5-hexanedione affects the glutamate-nitric oxide-cGMP pathway in primary cultures of cerebellar neurons and/or in the cerebellum of rats. Chronic exposure of cultured cerebellar neurons to 2,5-hexanedione (200 microM) reduced by approximately 50% NMDA-induced formation of cGMP. Activation of soluble guanylate cyclase by nitric oxide was reduced by 46%. This treatment reduced the content of neuronal nitric oxide synthase and soluble guanylate cyclase in neurons by 23 and 20%, respectively. In the cerebellum of rats chronically exposed to 2,5-hexanedione (in the drinking water) NMDA-induced formation of cGMP was reduced by 55% as determined by in vivo brain microdialysis. Activation of soluble guanylate cyclase by nitric oxide was reduced by 65%. The content of neuronal nitric oxide synthase and of soluble guanylate cyclase was reduced by 25 and 21%, respectively, in the cerebellum of these rats. The effects are the same in both systems, indicating that cultured neurons are a good model to study the mechanisms of neurotoxicity of 2,5-hexanedione. These results indicate that chronic exposure to 2,5-hexanedione affects the glutamate-nitric oxide-cGMP pathway at different steps both in cultured neurons and in cerebellum of the animal in vivo. The alteration of this pathway may contribute to the neurotoxic effects of 2,5-hexanedione.
A cross-sectional study examined whether there was a difference in endogenous serum sex hormone levels between community-dwelling postmenopausal women with Alzheimer's disease (AD) and healthy controls. Total morning levels of serum estrone, estradiol, androstenedione, testosterone, and cortisol were measured in 52 nondepressed women with AD and 60 postmenopausal women who were neither depressed nor cognitively impaired. Estradiol was undetectable in 35.7% of cases, but detectable hormone was found in 96-100% of cases otherwise. After adjustment for potential confounds, serum levels were significantly higher for estrone (P = 0.0057) and androstenedione (P = 0.02), but not testosterone (P = 0.086) or estradiol (P = 0.59), in subjects with AD. Sex hormone levels did not correlate with cognitive scores in either group. Although the failure to detect estradiol in a third of cases limits the conclusions that can be drawn for this hormone, the possibility that AD is associated with abnormalities in certain serum sex hormone levels should be considered and warrants further research.
Quantitative 2-dimensional and Doppler echocardiography was used to assess the longitudinal effects of angiotensin-converting enzyme inhibition in asymptomatic patients with chronic, severe mitral regurgitation due to mitral valve prolapse. Over a 6-month period, angiotensin-converting enzyme inhibition therapy resulted in significant reductions in left ventricular volumes and mass in association with a minor reduction in regurgitant fraction.
OBJECTIVE: To define qualitative research in terms of its philosophical roots, the questions it addresses, its methods and analyses, and the type of results it can offer. DATA SOURCES: MEDLINE and CINAHL (Cumulative Index to Nursing and Allied Health Literature) databases were searched for the years January 1985 to April 1998. The search strategy consisted of "textword" terms that searched in the "title" field of both databases. Qualitative research and evaluation textbooks in health and the social sciences were also used. QUALITY OF EVIDENCE: The information on qualitative research is based on the most recent and valid evidence from the health and social science fields. MAIN MESSAGE: Qualitative research seeks to understand and interpret personal experience to explain social phenomena, including those related to health. It can address questions that quantitative research cannot, such as why people do not adhere to a treatment regimen or why a certain health care intervention is successful. It uses many methods of data collection, including participant observation, case studies, and interviews, and numerous approaches to data analysis that range from the quasistatistical to the intuitive and inductive. CONCLUSIONS: Qualitative research, a form of research completely different from quantitative research, can provide important insights into health-related phenomena and can enrich further research inquiries.
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We have previously shown that block of high-frequency stimulation (HFS) induced long-term potentiation (LTP) of synaptic transmission in area CA1 by (1S,3S)-1-aminocyclopentane-1,3-dicarboxylic acid (1S,3S-ACPD; 5 microliters of a 20 mM solution), an agonist at group II metabotropic glutamate receptors, did not prevent animals from learning a spatial task. Here we show that the same dose of 1S,3S-ACPD also blocked the induction of HFS-induced LTP of the slope of the excitatory postsynaptic potential and of the amplitude of the population spike in the dentate gyrus. We conclude that HFS-induced LTP in the dentate gyrus is not a good model for memory formation.
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BACKGROUND: The N2 and P3 components of auditory event-related potentials (ERPs) and single-photon emission computed tomographic (SPECT) images are separate independent biological markers of cerebral function and are abnormal in Alzheimer's disease (AD). The relationship between ERP N2 and P3 latencies and regional cerebral perfusion abnormalities in AD is unknown. METHODS: ERP and SPECT data were obtained one week apart in 18 patients with "probable" AD of mild or moderate severity, and 12 healthy age-matched elderly controls. Average premotor frontal, anterior temporal, inferior parietal, and occipital cortical/cerebellar perfusion ratios were calculated from the SPECT data and correlations with ERP N2 and P3 latencies derived for AD and control groups separately. RESULTS: ERP N2 latency was correlated significantly with the average frontal perfusion ratio (r = -.59; p < .009), but correlations with average temporal, parietal, and occipital ratios were nonsignificant in the AD group. Similarly, ERP P3 latency was correlated significantly with the average frontal perfusion ratio (r = -.65; p < .004), but not with the other perfusion ratios in the AD group. In the control group, a partial correlation between the average frontal perfusion ratio and the ERP N2 latency was noted (r = -.52; p < .09), but no other ERP/SPECT correlations approached statistical significance. CONCLUSION: ERP N2 and P3 latency delay in AD is a function of differential frontal lobe hypoperfusion.
BACKGROUND: Current evidence indicates that, on their own, neither flash visual evoked responses (FVEPs) nor event related potentials (ERPs) are sufficiently useful to the clinician in the very early stages of memory dysfunction. However, the possibilities for the combined use of these measures has not been fully explored. METHODS: This study examined the clinical utility of combined FVEP and ERP-P300 component latencies as predictive markers in 16 patients with Alzheimer's disease, 15 patients with depression, and 21 control subjects. RESULTS: There were significant group differences in FVEP P2 latency (P = 0.004) between the controls and both the depressive patients and those with very mild Alzheimer's disease. There were no statistically significant group differences for the ERP component (N2/P300) amplitudes or latencies. The P300 component latency was positively correlated with both the FVEP N2 and FVEP P2 component latencies in the patients with Alzheimer's disease but not in the control subjects or the depressed patients. A discriminant function, using two ERP and two FVEP component measures, gave an overall correct classification rate for dementia of 78%. In this study of very mildly impaired patients the FVEP latencies provided a more sensitive marker for the presence of cognitive dysfunction than P300 latency delay. CONCLUSIONS: The findings support the use of multimodal evoked potentials in the differential diagnosis of very mild Alzheimer's disease and normal aging.
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Patients with Alzheimer's disease (AD) have pathologic involvement of several important components of the primary auditory pathway, including the inferior colliculus, medial geniculate body, primary auditory cortex, and secondary auditory cortex. The main components of the brainstem auditory evoked response (BAER) and middle latency response (MLR) reflect the function of portions of the primary auditory pathway, including those affected pathologically in AD. The amplitude of the P1 component of the MLR reflects the degree of neuronal activity of midbrain portions of the ascending reticular activating system (ARAS) with cortical cholinergic projections. To determine whether there is dysfunction of the primary auditory pathway and ARAS in AD, we compared simultaneous BAER and MLR component latency and amplitude measurements in patients with mild-moderate AD (n = 35) and age-matched healthy elderly controls (n = 34). There were significant latency delays in brainstem transmission time (BAER I-V interpeak latency; p < 0.05) and in primary auditory cortex evoked potential generation (MLR Pa latency; p < 0.05) in the AD group compared with controls. In addition, there was a significant reduction in the P1 component amplitude of the MLR in the AD group (p < 0.01). These results indicate dysfunction of the primary auditory pathway and ARAS in patients with mild-moderate AD and support the hypothesis that impairment of auditory function and of arousal are intrinsic features of AD.
This article describes an approach to the evaluation of students' clinical performance. Specifically, the paper describes: (a) the history of the evaluation of clinical performance in nursing education; (b) the development of the Clinical Evaluation Tool (CET), an instrument designed to measure the clinical performance of nursing students across settings; and (c) the relationships between basic baccalaureate nursing students' scores on the CET and the following variables: age, college credits earned prior to entry to the program, grade point average at entry, college aptitude, and moral reasoning.
Auditory endogenous event-related potentials (ERPs) and flash visual evoked potentials (VEPs) were recorded in 26 elderly patients with idiopathic Parkinson's disease (PD), 14 with dementia and 12 non-demented, 16 elderly patients with Alzheimer dementia (AD) and 15 cognitively intact controls. ERP P3 and flash-VEP N2, P2 and delta (P2-P1) latency measures were significantly increased in the demented PD group compared with controls. The ERP P3 latency was also significantly delayed in the AD group compared with controls, but the differences in the flash-VEP measures from controls were not significant. No significant differences were noted between the PD groups, except for a significantly shorter flash-VEP N1 latency in the demented PD group; this was also the only significant evoked potential difference between the AD and PD dementia groups, which were otherwise electrophysiologically similar.
BACKGROUND: Myocardial stretch and increased ventricular filling can lead to increased rates of myocardial protein synthesis. In animal studies, left ventricular mass increases after pericardiectomy, suggesting relief of a biologically meaningful restraining role and a resultant stimulus for growth. The present study was designed to test the hypothesis that combined thoracotomy and pericardiotomy leads to left ventricular hypertrophy in patients with normal left ventricular ejection fraction undergoing elective bypass surgery. METHODS AND RESULTS: Twenty-five patients with normal left ventricular ejection fraction without active myocardial ischemia underwent Doppler and quantitative two-dimensional echocardiography 1 day before and 6 weeks and 7 months after elective coronary artery bypass surgery. The pericardium was left widely incised in all patients. Left ventricular end-systolic volume, end-diastolic volume, stroke volume, ejection fraction, end-systolic circumferential wall stress, and mass were measured. Left ventricular end-diastolic volume index increased from 51 +/- 11 mL/m2 to 62 +/- 14 mL/m2 (p < 0.05) at 6 weeks and to 66 +/- 14 mL/m2 (p < 0.05 versus baseline, p = NS versus 6 weeks) at 7 months. Left ventricular mass index increased from 109 +/- 23 g/m2 to 127 +/- 24 g/m2 (p < 0.05) at 6 weeks and to 131 +/- 23 g/m2 (p < 0.05 versus baseline, p = NS versus 6 weeks) at 7 months. There were no changes in systolic or diastolic blood pressures, end-systolic circumferential wall stress, or end-systolic volume. CONCLUSIONS: Patients with normal left ventricular ejection fraction develop increases in left ventricular end-diastolic volume and mass after coronary artery bypass surgery. These findings support the hypothesis that the increase in left ventricular end-diastolic volume associated with thoracotomy and pericardiotomy leads to myocardial growth and an increase in left ventricular mass.
The effects of the phorbol ester 4 beta-phorbol-12,13 dibutyrate (PDBu) and the protein kinase (PK) inhibitors H-7 and sphingosine were investigated on the short-term potentiation (STP) of the population excitatory postsynaptic potential (EPSP) induced by perfusion of N-methyl-D-aspartate (NMDA) in the stratum radiatum of CA1 of the rat hippocampal slice. Bath perfusion of 130 microM NMDA for 10 s caused an initial depression of the population EPSP followed by a STP, which averaged 46% and lasted 16 min. PDBu (100 nM) perfused for 2 h completely inhibited the NMDA induced STP, suggesting that the stimulation of PKC inhibited an NMDA receptor activated process which induced the STP. The protein kinase inhibitors H-7 and sphingosine did not alter the NMDA induced STP.
The effect of altered extracellular Ca concentration was studied on the N-methyl-D-aspartate (NMDA) induced short-term potentiation (STP) of the population excitatory post-synaptic potential recorded from the stratum radiatum of CA1 of the rat hippocampal slice. Perfusion of 130 microM of NMDA for 10 s in control media containing 2.0 mM extracellular Ca evoked an STP with a maximum amplitude of 46% and a duration of 16 min. Perfusion of media containing a reduced Ca concentration of 0.8 mM or 1.0 mM did not alter the amplitude or time course of the STP. However, raising the Ca concentration to 3.0 mM or 4.0 mM caused a significant reduction in the amplitude of the STP to 23% and 2% respectively. The abolition of the NMDA induced STP in 4 mM Ca could not have been produced by response saturation since an identical long-term potentiation (LTP) was produced in this high Ca media as in the control media. These studies show that the NMDA induced STP has a very different Ca dependency to LTP.