652 research outputs found

    Braking of the overhead cranes by pneumohydraulic buffers in the accidents

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    The majority of the numerous animal studies of the effects of estrogens on cerebral ischemia have reported neuroprotective results, but a few have shown increased damage. Differences in hormone administration methods, resulting in highly different 17 beta-estradiol levels, may explain the discrepancies in previously reported effects. The objective of the present study was to test the hypothesis that it is the delivered dose per se, and not the route and method of administration, that determines the effect, and that high doses are damaging while lower doses are protective. One hundred and twenty ovariectomized female Wistar rats (n = 40 per group) were randomized into three groups, subcutaneously administered different doses of 17 beta-estradiol and subjected to transient middle cerebral artery occlusion. The modified sticky tape test was performed after 24 h and the rats were subsequently sacrificed for infarct size measurements. In contrast to our hypothesis, a significant negative correlation between 17 beta-estradiol dose and infarct size was found (p = 0.018). Thus, no support was found for the hypothesis that 17 beta-estradiol can be both neuroprotective and neurotoxic merely depending on dose. In fact, on the contrary, the findings indicate that the higher the dose of 17 beta-estradiol, the smaller the infarct.Funding Agencies|County Council of Ostergotland, Sweden</p

    Different methods for administering 17β-estradiol to ovariectomized rats result in opposite effects on ischemic brain damage

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    <p>Abstract</p> <p>Background</p> <p>Numerous stroke studies have controversially shown estrogens to be either neuroprotective or neurodamaging. The discordant results observed in rat brain ischemia models may be a consequence of discrepancies in estrogen administration modes resulting in plasma concentration profiles far from those intended. To test this hypothesis we reproduced in detail and extended an earlier study from our lab using a different mode of 17β-estradiol administration; home-made silastic capsules instead of commercial slow-release 17β-estradiol pellets. Four groups of female rats (n = 12) were ovariectomized and administered 17β-estradiol or placebo via silastic capsules. All animals underwent MCAo fourteen days after ovariectomy and were sacrificed three days later.</p> <p>Results</p> <p>In contrast to our earlier results using the commercial pellets, the group receiving 17β-estradiol during the entire experiment had significantly smaller lesions than the group receiving placebo (mean ± SEM: 3.85 ± 0.70% versus 7.15 ± 0.27% of total slice area, respectively; p = 0.015). No significant neuroprotection was found when the 17β-estradiol was administered only during the two weeks before or the three days immediately after MCAo.</p> <p>Conclusions</p> <p>The results indicate that different estrogen treatment regimens result in diametrically different effects on cerebral ischemia. Thus the effects of estrogens on ischemic damage seem to be concentration-related, with a biphasic, or even more complex, dose-response relation. These findings have implications for the design of animal experiments and also have a bearing on the estrogen doses used for peri-menopausal hormone replacement therapy.</p

    Limited neuropeptide Y precursor processing in unfavourable metastatic neuroblastoma tumours

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    Neuropeptide Y (NPY) is found at high concentrations in neural crest-derived tumours and has been implicated as a regulatory peptide in tumour growth and differentiation. Neuroblastomas, ganglioneuromas and phaeochromocytomas with significant concentrations of NPY-like immunoreactivity were investigated for different molecular forms of NPY and for significance of proNPY processing. Gel-permeation chromatography identified intact NPY (1–36) in all tumours, whereas proNPY (69 amino acids) was detected only in control adrenal tissue and malignant neuroblastomas. Purification of NPY-like immunoreactivity in tumour extracts and structural characterization revealed that both NPY (1–36) and the truncated form NPY (3–36) was present. The degree of processing of proNPY to NPY in tumour tissue was lower in advanced neuroblastomas with regional or metastatic spread (stage 3 and 4) (n = 6), (41%, 12–100%, median, range), compared to the less aggressive stage 1, 2 and 4S tumours (n = 12), (93%; 69–100%), (P = 0.012). ProNPY processing of less than 50% was correlated with poor clinical outcome (P = 0.004). MYCN oncogene amplification was also correlated to a low degree of proNPY processing (P = 0.025). In summary, a low degree of proNPY processing was correlated to clinical advanced stage and poor outcome in neuroblastomas. ProNPY/NPY processing generated molecular forms of NPY with known differences in NPY-receptor selectivity, implicating a potential for in vivo modulation of NPY-like effects in tumour tissue. © 2000 Cancer Research Campaig

    Risk of myocardial infarction at specific troponin T levels using the parameter predictive value among lookalikes (PAL)

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    AbstractBackgroundMyocardial infarction is more likely if the heart damage biomarker cardiac troponin T (cTnT) is elevated in a blood sample, indicating that cardiac damage has occurred. No method allows the clinician to estimate the risk of myocardial infarction at a specific cTnT level in a given patient.MethodsPredictive value among lookalikes (PAL) uses pre-test prevalence, sensitivity and specificity at adjacent cTnT limits based on percentiles. PAL is the pre-test prevalence-adjusted probability of disease between two adjacent cTnT limits. If a chest pain patient's cTnT level is between these limits, the risk of myocardial infarction can be estimated.ResultsThe PAL based on percentiles had an acceptable sampling error when using 100 bootstrapped data of 18 different biomarkers from 38,945 authentic lab measurements. A PAL analysis of an emergency room cohort (n=11,020) revealed that the diagnostic precision of a high-sensitive cTnT assay was similar among chest pain patients at different ages. The higher incidence of false positive results due to non-specific increases in cTnT in the high-age group was counterbalanced by a higher pre-test prevalence of myocardial infarction among older patients, a finding that was missed when using a conventional ROC plot analysis.ConclusionsThe PAL was able to calculate the risk of myocardial infarction at specific cTnT levels and could complement decision limits

    Автоматизированное рабочее место мастера участка тяговых подстанций КУП «Горэлектротранспорт»

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    Background: The elevated body swing test (EBST) is a behavioral test used to evaluate experimental stroke in rodents. The basic idea is that when the animal is suspended vertically by the tail, it will swing its head laterally to the left or right depending on lesion side. In a previous study from our lab using the EBST after middle cerebral artery occlusion (MCAo), rats swung contralateral to the infarct day 1 post-MCAo, but ipsilateral day 3 post-MCAo. This shift was unexpected and prompted us to perform the present study. First, the literature was systematically reviewed to elucidate whether a similar shift had been noticed before, and if consensus existed regarding swing direction. Secondly, an experiment was conducted to systematically investigate the suggested behavior. Eighty-three adult male and female Sprague-Dawley rats were subjected to MCAo or sham surgery and the EBST was performed up to 7 days after the lesion. Results: Both experimentally and through systematic literature review, the present study shows that the direction of biased swing activity in the EBST for rodents after cerebral ischemia can differ and even shift over time in some situations. The EBST curve for females was significantly different from that of males after the same occlusion time (p = 0.023). Conclusions: This study highlights the importance of adequate reporting of behavioral tests for lateralization and it is concluded that the EBST cannot be recommended as a test for motor asymmetry after MCAo in rats.Funding Agencies|Region Ostergotland/Linkoping University, Sweden</p

    Association Between Childhood Visual Acuity and Late Adolescent Psychotic Experiences: A Prospective Birth Cohort Study

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    A cross-sectional association between visual impairment and psychosis exists, but longitudinal evidence from children and young people is limited. We investigated whether childhood visual acuity was associated with subsequent psychotic experiences. Our sample was 6686 individuals from the Avon Longitudinal Study of Parents and Children (ALSPAC). We investigated whether our primary exposures, best corrected visual acuity at ages 7 and 11, were associated with psychotic experiences at ages 17 and 24. We also tested whether the following exposures at ages 7 and 11 were associated with subsequent psychotic experiences: requiring glasses, presence of any visual impairment, and between-eye visual acuity difference; and at age 7: strabismus, measures of binocular vision, history of eye patch, near vision impairment, and abnormal saccadic or pursuit eye movements. Analyses used multilevel models before and after adjusting for confounders. Odds of psychotic experiences increased with each 0.1-point deterioration in visual acuity score at age 11 (adjusted odds ratio [AOR] 1.23; 95% confidence interval [CI] 1.06–1.42), and at age 7 (AOR 1.18; 95% CI 1.00–1.40). Wearing glasses and visual impairment at age 11 were associated with psychotic experiences (AOR 1.63; 95% CI 1.21–2.19; AOR 1.64; 95% CI 1.23–2.19, respectively). There was no evidence of an association with other visual exposures. Visual acuity impairment in childhood is associated with psychotic experiences in late adolescence. Future research should aim to elucidate the nature of this association
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