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Background Few studies have examined the relationship between the amounts of heavy metal and stroke incidence. The aim of this study was to explore the relationship between levels of heavy metals, including Pb, Hg, As, and Cd, in patients with acute ischemic stroke (AIS). Methods We selected patients with first-ever AIS onset within 1 week as our study group. Healthy controls were participants without a history of stroke or chronic disease, except hypertension. The serum levels of Pb, Hg, As, and Cd in participants in the experimental and control groups were determined. All participants received a 1-g infusion of edetate calcium disodium (EDTA). Urine specimens were collected for 24 h after EDTA infusion and measured for heavy metal levels. Results In total, 33 patients with AIS and 39 healthy controls were enrolled in this study. The major findings were as follows: (1) The stroke group had a significantly lower level of serum Hg (6.4 ± 4.3 μg/L vs. 9.8 ± 7.0 μg/L, P = 0.032, OR = 0.90, 95% CI = 0.81–0.99) and a lower level of urine Hg (0.7 ± 0.7 μg/L vs. 1.2 ± 0.6 μg/L, P = 0.006, OR = 0.27, 95% CI = 0.11–0.68) than the control group. (2) No significant difference in serum Pb (S-Pb), As (S-As), and Cd (S-Cd) levels and urine Pb (U-Pb), As (U-As) and Cd (U-Cd) levels was observed in either group. Conclusions Our study found low levels of serum and urine Hg in first-ever patients with AIS, providing new evidence of dysregulated heavy metals in patients with AIS. Electronic supplementary material The online version of this article (10.1186/s12929-018-0446-0) contains supplementary material, which is available to authorized users.

Autonomic dysfunctions including impaired baroreflex sensitivity (BRS) can develop after acute ischemic stroke (AIS) and may predispose patients to subsequent cardiovascular adverse events and serve as potential indicators of long-term mortality. This study aimed to determine the potential short-term prognostic significance of BRS after AIS. All patients admitted to Kaohsiung Veterans General Hospital within 72 h after onset of first-ever AIS between April 2008 and December 2012 were enrolled. Autonomic evaluation with continuous 10-minute monitoring of beat-to-beat hemodynamic and intracranial parameters was performed within 1 week after stroke by using the Task Force Monitor and transcranial Doppler. The 176 enrolled AIS patients were divided into high-BRS and low-BRS groups. All but two enrolled patients (who died within 3 months after stroke) attended scheduled follow-ups. The high-BRS group had significantly lower National Institutes of Health Stroke Scale (NIHSS) scores at 1 and 2 weeks after stroke and at discharge, lower modified Rankin scale (mRS) scores 1, 3, 6, and 12 months after stroke, and lower rates of complications and stroke recurrence compared to the low-BRS group. This study provides novel evidence of the utility of BRS to independently predict outcomes after AIS. Furthermore, modifying BRS may hold potential in future applications as a novel therapeutic strategy for acute stroke.

Aim To evaluate the association of cognitive impairment, depressive mood and sarcopenia among older men living in the veterans retirement community in southern Taiwan Methods This cross-sectional study recruited 353 men aged 65 years and older. In addition to demographic characteristics, all participants were measured for gait speed, handgrip strength and muscle mass by using bioelectrical impedance analysis (BIA). The diagnosis of sarcopenia was made according to the European Working Group on Sarcopenia in Older People criteria. Slow walking speed was defined as ≤0.8 meter/second. Low muscle strength was defined as the handgrip strength less than 22.5 kg which was adjusted according to Taiwanese norms. A height-adjusted muscle mass of 8.87 kg/m2 from a previous Taiwanese study was defined as low muscle mass. Cognitive function was evaluated by the Mini-Mental State Examination (MMSE), and the Geriatric Depression Scale-15 (GDS-15) was used for screening of depressive symptoms. Results Among the 353 participants (mean age 82.7 ± 5.3 years), 30.9% (109/353) were classified as sarcopenic. Multivariate logistic regression showed that sarcopenia was independently associated with cognitive impairment (adjusted OR 3.03, 95% CI 1.63–5.65, P

Background Asians have higher frequency of intracranial arterial stenosis. The present study aimed to compare the clinical features and outcomes of ischemic stroke patients with and without middle cerebral artery (MCA) stenosis, assessed by transcranial sonography (TCS), based on the Taiwan Stroke Registry (TSR). Methods Patients with acute ischemic stroke or transient ischemic attack registered in the TSR, and received both carotid duplex and TCS assessment were categorized into those with stenosis (≥50%) and without (

PurposeTo evaluate the postacute care (PAC) needs of elderly patients in a tertiary teaching hospital.MethodsAll elderly veterans admitted to a tertiary medical center were screened for their needs for PAC services from May 1 to October 31, 2009. Case managers evaluated the inclusion/non-inclusion criteria while visiting patients before their discharge. Comprehensive geriatric assessment (CGA) was performed before their transfer, if they agreed to receive the PAC service in addition to the complete medical history review.ResultsOverall, 409 elderly patients (96.8% male; mean age = 80.4 ± 5.4 years) meeting the inclusion/exclusion criteria were screened, and 103 (25.2%) had PAC service needs. All patients diagnosed with central nervous system and musculoskeletal conditions displayed a significant decrease (93.1 ± 10.8 to 43.6 ± 33.3, p

Nutritional status is important in stroke care, but little is known regarding to the prognostic role of nutritional status on long-term functional outcomes among stroke survivors. The main purpose of this study was to evaluate to the prognostic role of nutritional status on long-term functional outcomes among stroke survivors. Data of acute stroke registry in Kaohsiung Veterans General Hospital were retrieved for analysis. Overall, 483 patients (mean age = 70.7 ± 10.3 years) with first-ever stroke were found. Among them, 95 patients (19.7%) were malnourished at admission, 310 (mean age = 70.4 ± 10.1 years, 63.5% males) survived for 6 months, and 244 (78.7%) had good functional outcomes. Subjects with poor functional outcomes were older (74.7 ± 8.9 vs. 69.0 ± 10.1 years, p < 0.001), more likely to be malnourished (56.2% vs. 26.6%, p < 0.001), to develop pneumonia upon admission (23.3% vs. 12.7%, p = 0.027), had a longer hospital stay (23.5 ± 13.9 vs. 12.5 ± 8.2 days, p < 0.001), had a higher National Institutes of Health Stroke Scale (NIHSS) score (12.9 ± 9.3 vs. 4.9 ± 4.3, p < 0.001), poorer stroke recovery (NIHSS improvement: 6.9% vs. 27.4%, p = 0.005), and poorer functional improvement (Barthel index = BI improvement in the first month: 31.4% vs. 138%, p < 0.001). Older age (odds ratio = OR) = 1.07, 95% confidence interval (CI = 1.03-1.11, p

Background— Stroke is a leading cause of death around the world. Improving the quality of stroke care is a global priority, despite the diverse healthcare economies across nations. The American Heart Association/American Stroke Association Get With the Guidelines-Stroke program (GWTG-Stroke) has improved the quality of stroke care in 790 US academic and community hospitals, with broad implications for the rest of the country. The generalizability of GWTG-Stroke across national and economic boundaries remains to be tested. The Taiwan Stroke Registry, with 30 599 stroke admissions between 2006 and 2008, was used to assess the applicability of GWTG-Stroke in Taiwan, which spends ≈1/10 of what the United States does in medical costs per new or recurrent stroke. Methods and Results— Taiwan Stroke Registry, sponsored by the Taiwan Department of Health, engages 39 academic and community hospitals and covers the entire country with 4 steps of quality control to ensure the reliability of entered data. Five GWTG-Stroke performance measures and 1 safety indicator are applicable to assess Taiwan Stroke Registry quality of stroke care. Demographic and outcome figures are comparable between GWTG-Stroke and Taiwan Stroke Registry. Two indicators (early and discharge antithrombotics) are close to GWTG-Stroke standards, while 3 other indicators (intravenous tissue plasminogen activator, anticoagulation for atrial fibrillation, lipid-lowering medication) and 1 safety indicator fall behind. Preliminary analysis shows that compliance with selected GWTG-Stroke guidelines is associated with better outcomes. Conclusions— Results suggest that GWTG-Stroke performance measures, with modification for ethnic factors, can become global standards across national and economic boundaries for assessing and improving quality of stroke care and outcomes. GWTG-Stroke can be incorporated into ongoing stroke registries across nations.

The differences in the intracellular Ca2+ responses to hormones in platelets from systemic lupus erythematosus (SLE) patients compared to normal humans have not been explored. This study examined the Ca2+ signaling and density of platelets in normal, inactive and active SLE patients. The platelet number per µl in inactive and normal groups did not differ, whereas the number in active SLE patients was smaller than the other two groups by 60%. The intracellular free Ca2+ levels ([Ca2+]i) in response to stimulation of four endogenous Ca2+ mobilizing hormones, 100 µM arachidonic acid (AA), 10 µM ADP, 10 nM platelet activation factor (PAF) and 1 µM thrombin, were investigated using the Ca2+-sensitive fluorescent dye, fura-2. The AA-induced [Ca2+]i rises in normal and inactive groups were similar. In contrast, the AA-induced [Ca2+]i rises in the active SLE group were significantly smaller than in the normal and inactive groups. The defect in the AA-induced [Ca2+]i rises in active SLE groups appears to be caused by defective Ca2+ influx and Ca2+ releasing pathways because the AA-induced responses were not altered by removal of extracellular Ca2+, whereas the AA-induced responses in normal and inactive SLE groups were reduced by removal of extracellular Ca2+, and the AA-induced Ca2+ release was smaller in the active SLE group. PAF, ADP and thrombin all induced [Ca2+]i rises in the three groups, but no significant differences were found among the three groups. Together, the results indicate that cell density and Ca2+ signaling in platelets from active SLE patients are altered in response to particular stimulators. In these regards, platelets from inactive SLE patients appear to be similar to those from normal humans.

Posterior reversible encephalopathy syndrome (PRES) is a potentially devastating neurologic syndrome, but timely treatment may lead to complete reversal of the disease course. We reviewed 12 cases of PRES and describe the clinical history and imaging findings, including conventional magnetic resonance imaging (MRI), diffusion-weighted imaging (DWI), and calculated apparent diffusion coefficient (ADC) maps, used to establish the diagnosis of PRES. Three male and nine female patients aged between 11 and 70 years (mean, 37 years) with clinical and imaging findings consistent with PRES were enrolled in the study. All patients had undergone conventional MRI and 10 had undergone additional DWI studies. Ten patients had follow-up MRI studies. DWI was performed using a 1.5T system with a single-shot spin-echo echo-planar pulse sequence. Initial and follow-up neuroimaging and clinical history were reviewed. Lesions were almost always present over the posterior circulation, mainly the parieto-occipital region, affecting primarily the white matter. The anterior circulation region, brainstem, cerebellum, deep cerebral white matter, and thalamus were also involved in five cases. Conventional MRI revealed hyperintensity on T2- weighted and fluid-attenuated inversion recovery images. DWI showed isointensity and increased signal intensity on ADC values in all cases, indicating vasogenic edema. Clinical and MRI follow-up showed that the symptoms and radiologic abnormalities could be reversed after appropriate treatment of the causes of PRES in most patients (9 of 10). In one patient, the ADC value was lower on follow-up images, indicating cytotoxic edema with ischemic infarct. DWI was a useful complement to MRI in the diagnosis of PRES.

In human neuroblastoma IMR32 cells, the effect of the anti-depressant maprotiline on baseline intracellular Ca 2+ concentrations ([Ca 2+ ] i ) was explored by using the Ca 2+ -sensitive probe fura-2. Maprotiline at concentrations greater than 100 μM caused a rapid rise in [Ca 2+ ] i in a concentration-dependent manner (EC 50 = 200 μM). Maprotiline-induced [Ca 2+ ] i rise was reduced by 50% by removal of extracellular Ca 2+ . Maprotiline-induced [Ca 2+ ] i rises were inhibited by half by nifedipine, but was unaffected by verapamil or diiltiazem. In Ca 2+ -free medium, thapsigargin, an inhibitor of the endoplasmic reticulum Ca 2+ -ATPase, caused a monophasic [Ca 2+ ] i rise, after which the increasing effect of maprotiline on [Ca 2+ ] i was abolished. U73122, an inhibitor of phospholipase C, did not affect maprotiline-induced [Ca 2+ ] i rises. These findings suggest that in human neuroblastoma cells, maprotiline increases [Ca 2+ ] i by stimulating extracellular Ca 2+ influx and also by causing intracellular Ca 2+ release from the endoplasmic reticulum via a phospholiase C-independent manner.

Information concerning acute myocardial infarctions (AMI) after heroin injection is limited. Only one report has described the association between heroin injections and AMI in a young woman. AMI after heroin injection in a patient with a normal coronary angiogram has not been reported. We report a 38-year-old man who developed AMI after heroin injection. He is probably the first case of AMI with normal coronary artery angiograms associated with heroin abuse. The heroin-induced toxic effect and/or coronary spasm are highly suspected to be the causes of the infarction episode.

The effects of quercetin, a natural polyphenolic compound, on voltage-dependent L-type Ca 2 + current (I C a ,L) in rat pituitary GH 3 cells were investigated with the aid of the whole-cell voltage-camp technique. Quercetin (0.5-200 pM) stimulated I C a , l l. in a concentration-dependent manner. The current-voltage (/-V) relationship of I C a , L was slightly shifted to more negative potentials in the presence of quercetin. The EC 5 0 value of the quercetin-induced stimulation of I C a , L was about 7 μM. The presence of quercetin (5 μM) shifted the steady state inactivation curve of I C a , L to a more negative potential by approximately -10 mV. Although quercetin might increase intracellular cyclic AMP, sp-cAMPS did not affect I C a , L . In addition, neither flavone nor wortmannin had any effect on the amplitude of I C a , L , while epicatechin and genistein slightly suppressed it. Quercetin (50 μM) decreased the amplitude of tetrodotoxin-sensitive Na current in GH 3 cells. Under current-clamp configuration, quercetin could increase the firing frequency of actions potentials. Conversely, in NG108-15 neuronal cells, quercetin suppressed the amplitude of I C a , L . The quercetin-induced inhibition of ICa,L was abolished in NG108-15 cells preincubated with t-butyl hydroperoxide (1 mM). Quercetin-mediated stimulation of I C a , L in GH 3 cells was presumably not associated with the level of intracellular cyclic AMP, or with the activity of tyrosine or phosphoinositide 3-kinases. Therefore, the effects of quercetin on ion currents may, at least in part, contribute to the underlying mechanisms through which it affects neuronal or neuroendocrine function.

Chlorzoxazone, a centrally acting muscle relaxant, has been used as a marker for hepatic CYP2E1 activity. However, little is known about the mechanism of chlorzoxazone actions on ion currents in neurons or neuroendocrine cells. We thus investigated its effects on ion currents in GH(3) lactotrophs. Chlorzoxazone reversibly increased Ca(2+)-activated K(+) current (I(K(Ca))) in a concentration-dependent manner with an EC(50) value of 30 microM. The chlorzoxazone-stimulated I(K(Ca)) was inhibited by iberitoxin (200 nM) or clotrimazole (10 microM), but not by glibenclamide (10 microM) or apamin (200 nM). Chlorzoxazone (30 microM) suppressed voltage-dependent L-type Ca(2+) current. In the inside-out configuration, chlorzoxazone applied to the intracellular side of the patch did not modify single-channel conductance of large conductance Ca(2+)-activated K(+) (BK(Ca)) channels, but did increase channel activity by increasing mean open time and decreasing mean closed time. Chlorzoxazone also caused a left shift in the activation curve of BK(Ca) channels. However, Ca(2+)-sensitivity of these channels was unaffected by chlorzoxazone. 1-Ethyl-2-benzimidazolinone (30 microM), 2-amino-5-chlorobenzoxazole (30 microM) or chlormezanone (30 microM) enhanced BK(Ca) channel activity, while 6-hydroxychlorzoxazone (30 microM) slightly increased it; however, chlorphenesin carbamate (30 microM) had no effect on it. Under the current-clamp condition, chlorzoxazone (10 microM) reduced the firing rate of action potentials. In neuroblastoma IMR-32 cells, chlorzoxazone (30 microM) also stimulated BK(Ca) channel activity. The stimulatory effects of chlorzoxazone on these channels may be responsible for the underlying mechanism of chlorzoxazone actions on neurons and neuroendocrine cells.

Summary A small number of clustered visits by emergency department frequent users (EDFUs) may over-consume emergency care resources. We report the effectiveness of comprehensive geriatric assessment (CGA)-based multidisciplinary team (MDT) care for four EDFUs, in reducing ED visits. Case 1 had visited the ED twice/month due to chest discomfort. Her ED visits were significantly reduced to 0.2 visits/month following CGA-based MDT care. Case 2 had failed back surgery syndrome and bipolar disorder. His ED visit was reduced from 2.8 visits to 0.8 visits/month following CGA-based MDT intervention. Case 3 had chronic obstructive pulmonary disease, heart failure, and urinary incontinence, with a urinary catheter in place. He made 31 ED visits (5.1 visits/month) before his lung cancer and depression were discovered by CGA. He died 2 months later. Case 4 made 27 ED visits (2.7 visits/month) due to dizziness. His problems of early dementia and neglect were identified by CGA, and he visited the ED only once following MDT intervention. In conclusion, CGA-based MDT intervention successfully reduced ED visits among these EDFUs, but further investigation is needed to evaluate the effectiveness of geriatric services in the ED.

The effect of nordihydroguaiaretic acid (NDGA) on Ca(2+) signaling in C6 glioma cells has been investigated. NDGA (5-100 microM) increased [Ca(2+)]i concentration-dependently. The [Ca(2+)]i increase comprised an initial rise and an elevated phase over a time period of 4 min. Removal of extracellular Ca(2+) reduced NDGA-induced [Ca(2+)]i signals by 52+/-2%. After incubation of cells with NDGA in Ca(2+)-free medium for 4 min, addition of 3 mM CaCl2 induced a concentration-dependent increase in [Ca(2+)]i. NDGA (100 microM)-induced [Ca(2+)]i increases in Ca(2+)-containing medium was not changed by pretreatment with 10 microM nifedipine or verapamil. In Ca(2+)-free medium, pretreatment with the endoplasmic reticulum Ca(2+) pump inhibitor thapsigargin (1 microM) abolished 100 microM NDGA-induced [Ca(2+)]i increases. Inhibition of phospholipase C with 2 microM U73122 had little effect on 100 microM NDGA-induced Ca(2+) release. Several other lipoxygenase inhibitors had no effect on basal [Ca(2+)]i. Collectively, the results suggest that NDGA increased [Ca(2+)]i in glioma cells in a lipoxygenase-independent manner, by releasing Ca(2+) from the endoplasmic reticulum in a manner independent of phospholipase C activity and by causing Ca(2+) influx.

Background Discharge disposition planning is vital for poststroke patients. We investigated clinical factors associated with discharging patients to nursing homes, using the Taiwan Stroke Registry data collected from 39 major hospitals. Methods We randomly assigned 21,575 stroke inpatients registered from 2006 to 2008 into derivation and validation groups at a 3-to-1 ratio. We used the derivation group to develop a prediction model by measuring cumulative risk scores associated with potential predictors: age, sex, hypertension, diabetes mellitus, heart diseases, stroke history, snoring, main caregivers, stroke types, and National Institutes of Health Stroke Scale (NIHSS). Probability of nursing home care and odds ratio (OR) of nursing home care relative to home care by cumulative risk scores were measured for the prediction. The area under the receiver operating characteristic curve (AUROC) was used to assess the model discrimination against the validation group. Results Except for hypertension, all remaining potential predictors were significant independent predictors associated with stroke patient disposition to nursing home care after discharge from hospitals. The risk sharply increased with age and NIHSS. Patients with a cumulative risk score of 15 or more had an OR of 86.4 for the nursing home disposition. The AUROC plots showed similar areas under curves for the derivation group (.86, 95% confidence interval [CI], .85-.87) and for the validation group (.84, 95% CI, .83-.86). Conclusions The cumulative risk score is an easy-to-estimate tool for preparing stroke patients and their family for disposition on discharge.

The effect of oleamide, a sleep-inducing endogenous lipid in animal models, on intracellular free levels of Ca(2+) ([Ca(2+)](i)) in non-excitable and excitable cells was examined by using fura-2 as a fluorescent dye. [Ca(2+)](i) in pheochromocytoma cells, renal tubular cells, osteoblast-like cells, and bladder cancer cells were increased on stimulation of 50 microM oleamide. The response in human bladder cancer cells (T24) was the greatest and was further explored. Oleamide (10-100 microM) increased [Ca(2+)](i) in a concentration-dependent fashion with an EC(50) of 50 microM. The [Ca(2+)](i) signal comprised an initial rise and a sustained plateau and was reduced by removing extracellular Ca(2+) by 85 +/- 5%. After pre-treatment with 10-100 microM oleamide in Ca(2+)-free medium, addition of 3 mM Ca(2+) increased [Ca(2+)](i) in a manner dependent on the concentration of oleamide. The [Ca(2+)](i) increase induced by 50 microM oleamide was reduced by 100 microM La(3+) by 40%, but was not altered by 10 microM nifedipine, 10 microM verapamil, and 50 microM Ni(2+). In Ca(2+)-free medium, pre-treatment with thapsigargin (1 microM), an endoplasmic reticulum Ca(2+) pump inhibitor, abolished 50 microM oleamide-induced [Ca(2+)](i) increases; conversely, pretreatment with 50 microM oleamide reduced 1 microM thapsigargin-induced [Ca(2+)](i) increases by 50 +/- 3%. Suppression of the activity of phospholipase C with 2 microM U73122 failed to alter 50 microM oleamide-induced Ca(2+) release. Linoleamide (10-100 microM), another sleep-inducing lipid with a structure similar to that of oleamide, also induced an increase in [Ca(2+)](i). Together, it was shown that oleamide induced significant [Ca(2+)](i) increases in cells by a phospholipase C-independent release of Ca(2+) from thapsigargin-sensitive stores and by inducing Ca(2+) entry.

The effects of ceramide on ion currents in rat pituitary GH(3) cells were investigated. Hyperpolarization-elicited K(+) currents present in GH(3) cells were studied to determine the effect of ceramide and other related compounds on the inwardly rectifying K(+) current (I(K(IR))). Ceramide (C(2)-ceramide) suppressed the amplitude of I(K(IR)) in a concentration-dependent manner, with an IC(50) value of 5 microM. Ceramide caused a rightward shift in the midpoint for the activation curve of I(K(IR)). Pretreatment with PD-98059 (30 microM) or U-0126 (30 microM) did not prevent ceramide-mediated inhibition of I(K(IR)). However, the magnitude of ceramide-induced inhibition of I(K(IR)) was attenuated in GH(3) cells preincubated with dithiothreitol (10 microM). TNF alpha (100 ng/g) also suppressed I(K(IR)). In the inside-out configuration, application of ceramide (30 microM) to the bath slightly suppressed the activity of large conductance Ca(2+)-activated K(+) channels. Under the current clamp mode, ceramide (10 microM) increased the firing of action potentials. Cells that exhibited an irregular firing pattern were converted to those displaying a regular firing pattern after application of ceramide (10 microM). Ceramide also suppressed I(K(IR)) in neuroblastoma IMR-32 cells. Therefore, ceramide can produce a depressant effect on I(K(IR)). The blockade of this current by ceramide may affect cell function.

The effect of histamine on intracellular free Ca2+ levels ([Ca2+](i)) in MG63 human osteosarcoma cells was explored using fura-2 as a Ca2+ dye. Histamine increased ([Ca2+](i)) in a concentration-dependent fashion with an EC(50) value of 0.5 microM. Extracellular Ca2+ removal inhibited the ([Ca2+](i)) signals. Histamine failed to increase ([Ca2+](i)) in Ca2+-free medium after cells were pretreated with thapsigargin (an endoplasmic reticulum Ca2+ pump inhibitor). Addition of Ca2+ induced concentration-dependent ([Ca2+](i)) increases after preincubation with histamine in Ca2+-free medium. Histamine-induced intracellular Ca2+ release was abolished by inhibiting phospholipase C with 1-(6-((17beta-3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione (U73122). The ([Ca2+](i)) increase induced by histamine in Ca2+ medium was abolished by cimetidine, but was not altered by pyrilamine, nifedipine, verapamil, and La(3+). Together, this study shows that histamine increased in ([Ca2+](i)) in osteosarcoma cells by stimulating H2 histamine receptors. The Ca2+ signal was caused by Ca2+ release from the endoplasmic reticulum in a phospholipase C-dependent manner. The Ca2+ release was accompanied by Ca(2+) influx.

The effect of the antidepressant fluoxetine on Ca 2+ signaling in cultured cells was largely unknown. The effect of various concentrations of fluoxetine on [Ca 2+] i in populations of bladder female transitional cancer (BFTC) cells was evaluated by using fura-2 as a Ca 2+ probe. Fluoxetine increased [Ca 2+] i concentration dependently (20–100 μ M) with an EC 50 value of 30 μ M. The response was inhibited by 50–60% on extracellular Ca 2+ removal. In Ca 2+ -free medium, pretreatment with 1 μ M thapsigargin (an inhibitor of the endoplasmic reticulum Ca 2+ pump) abolished 50 μ M fluoxetine-induced Ca 2+ release; whereas pretreatment with fluoxetine did not alter the thapsigargin-induced Ca 2+ response. Addition of 3 mM Ca 2+ increased [Ca 2+] i after pretreatment with 50 μ M fluoxetine in Ca 2+ -free medium, suggestive of fluoxetine-induced capacitative Ca 2+ entry. Suppression of inositol 1,4,5-trisphosphate formation by 2 μ M U73122 (a phospholipase C inhibitor) did not affect 50 μ M fluoxetine-induced Ca 2+ release. Collectively, this study shows that fluoxetine increased [Ca 2+] i in bladder cancer cells in a concentration-dependent fashion, by releasing Ca 2+ from thapsigargin-sensitive Ca 2+ stores in an IP 3 -independent manner, and by inducing Ca 2+ influx from extracellular medium.

The effect of fendiline, an anti-anginal drug, on cytosolic free Ca(2+) levels ([Ca(2+)](i)) in MG63 human osteosarcoma cells was explored by using fura-2 as a Ca(2+) indicator. Fendiline at concentrations between 1 and 200 microM increased [Ca(2+)](i) in a concentration-dependent manner and the signal saturated at 100 microM. The Ca(2+) signal was inhibited by 65+/-5% by Ca(2+) removal and by 38+/-5% by 10 microM nifedipine, but was unchanged by 10 microM La(3+) or verapamil. In Ca(2+)-free medium, pre-treatment with 1 microM thapsigargin (an endoplasmic reticulum Ca(2+) pump inhibitor) to deplete the endoplasmic reticulum Ca(2+) store inhibited fendiline-induced intracellular Ca(2+) release. The Ca(2+) release induced by 50 microM fendiline appeared to be independent of IP(3) because the [Ca(2+)](i) increase was unaltered by inhibiting phospholipase C with 2 microM U73122. Collectively, the results suggest that in MG63 cells fendiline caused an increase in [Ca(2+)](i) by inducing Ca(2+) influx and Ca(2+) release in an IP(3)-independent manner.

The effect of oleamide, a sleep-inducing endogenous lipid in animal models, on intracellular free levels of Ca2+ ([Ca2+]i) in Madin-Darby renal tubular cells was examined using fura-2 as a fluorescent dye. Oleamide (5–50 μM) increased [Ca2+]i in a concentration-dependent fashion with an EC50 value of 20 μM. The [Ca2+]i signal comprised an initial rise and an elevated phase and was reduced by removing extracellular Ca2+ by 50%. After pretreatment with 5–50 μM oleamide in Ca2+-free medium, addition of 3 mM Ca2+ increased [Ca2+]i in a manner dependent on the concentration of oleamide. In Ca2+-free medium, pretreatment with thapsigargin (1 μM), an endoplasmic reticulum Ca2+ pump inhibitor, abolished [Ca2+]i increases induced by 20 μM oleamide; conversely, pretreatment with 20 μM oleamide reduced 1 μM thapsigargin-induced [Ca2+]i increases by 50%. Suppression of the activity of phospholipase C with 2 μM U73122 abolished 20 μM oleamide-induced Ca2+ release. Collectively, these data demonstrate that oleamide induced significant [Ca2+]i increases in renal tubular cells by a phospholipase C-dependent release of Ca2+ from thapsigargin-sensitive stores and by inducing Ca2+ entry via store-operated Ca2+ entry. Drug Dev. Res. 54:40–44, 2001. © 2001 Wiley-Liss, Inc.

We reviewed the medical records and imaging studies on the in-hospital patients to investigate the clinical and etiological patterns in hemorrhagic stroke in young patients. We evaluated 210 patients (131 males and 79 females) aged 15-45 years who had traumatic hemorrhagic stroke between April 1, 1986, and November 30, 1992. Nontraumatic intracerebral hemorrhage was diagnosed in 170 patients (80.9%). The main causes of nontraumatic intracerebral hemorrhage were hypertension, ruptured arteriovenous malformation, and blood dyscrasia. A cause was not found in 42 patients (24.7%). Subarachnoid hemorrhage was found in 40 patients (19.1%). The main causes were ruptured aneurysms and arteriovenous malformations. The overall in-hospital survival of young patients with hemorrhagic stroke was 64.7%. Young adults with nontraumatic intracerebral and subarachnoid hemorrhage are a heterogeneous group. Hypertension accounts for about one-third of intracerebral hemorrhage and is an important preventable cause of hemorrhagic stroke in young adults in Taiwan.

This study evaluated the safety and efficacy of levetiracetam as adjunctive therapy for partial seizures in everyday clinical practice in Asian populations. Patients aged ≥ 16 years ( N = 251) with inadequately controlled partial epilepsy were recruited from 29 centers across Asia. Levetiracetam was added to existing antiepileptic medication for 16 weeks at a starting dose of 500 or 1000 mg/day and titrated to a maximum of 3000 mg/day according to clinical response. The study completion rate was 86.9%. Adverse events were reported by 73.3% of patients and were generally mild, leading to treatment withdrawal in only 7.2%. The most common adverse events were somnolence (30.3%) and dizziness (14.7%). Compared with pretreatment baseline, 44.0% of patients had a ≥ 50% reduction in seizure frequency, with a median reduction of 46.4%, and 17.7% became seizure free during the treatment period. Levetiracetam was well tolerated and efficacious as adjunctive therapy for partial epilepsy in clinical practice among Asian populations.

Given the need for tools for early and accurate diagnosis, prediction of disease progression, and monitoring efficacy of therapeutic agents for AD, the study of cerebrospinal fluid (CSF) biomarkers has become a rapidly growing field of research. Several studies have reported conflicting data regarding the relationships between CSF biomarkers and dementia severity. In this study, we have focused on the identification of CSF biomarkers and their correlations with the impairment of different cognitive domains measured using the Cognitive Abilities Screening Instrument (CASI). Patients with AD (n=28), non-AD dementia (n=16), other neurological disorders (OND, n=14), and healthy controls (HC, n=21) were enrolled. Our results revealed significantly higher CSF total tau (t-tau) and lower amyloid-beta(42) levels in AD patients compared with those in HC and OND groups. Moreover, our data show that CSF t-tau levels, but not Abeta(42) levels, have an inverse correlation with the score of short-term memory in CASI for patients with AD (Spearman: r=-0.444; p=0.018). This data might indicate that the higher CSF t-tau level is associated with more NFT pathology and more severe impairment of short-term memory in AD patients.

Objective: To compare the effectiveness of the Minimum Data Set-based Depression Rating Scale (MDS-DRS) and Geriatric Depression Scale (GDS) in screening depression among older institutionalized Chinese men living in Taiwan. Method: MDS Nursing Home 2.1 Chinese version, Mini-Mental State Examination (MMSE), and short form Geriatric Depression Scale (GDS-15) were used among elderly residents in Banciao Veterans Home. Screening results of MDS-DRS and GDS-15, and relationship between 16 MDS Mood and Anxiety symptoms and depression were evaluated. Results: The prevalence of depression defined by MDS-DRS and GDS were 0.2% and 8.7%, respectively. Multiple logistic regression disclosed that E1a (OR: 12.9, 95% CI: 2.8-58.8, p = 0.001), E1k (OR: 15.6, 95% CI: 5.6-43.5, p < 0.001), and E1l (OR: 22.2, 95% CI: 6.1-83.3, p < 0.001) were all independent associative factors for GDS-defined depression but only explained 51.9% of all depressive subjects. Conclusions: The effectiveness of MDS-DRS is limited, and a new MDS-based depression screening instrument is needed.

Background/Purpose MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes) syndrome is often associated with A3243G point mutation of mitochondrial DNA (mtDNA). We previously described a MELAS family characterized by harboring an additional ∼260 bp tandem duplication in the D-loop and a novel C3093G point mutation in the 16S rRNA gene of mtDNA in the proband. We studied the clinical progression and fluctuation of mtDNA mutations in this Taiwanese MELAS family. Methods We followed up the clinical course in all members of this family (1 proband, her mother and 3 sons) for 12 years. Mutations of mtDNA in serial muscle biopsies of the proband and blood samples and hair follicles taken at different time points from the members of this family were analyzed. Results The proband developed repeated stroke-like episodes, chronic intestinal pseudo-obstruction, polyneuropathy, progressive renal failure and dilated cardiomyopathy with heart failure. During the follow-up period, the mother and one of the siblings of the proband developed stroke-like episodes at age 62 and 12, respectively. There was no significant difference in the proportions of mtDNA with A3243G mutation among five serial muscle biopsies of the proband. In one carrier (I-2), the proportion of A3243G mutated mtDNA in blood cells was slightly increased with disease progression. Conclusion This study underlines the importance of early detection of extraneuromuscular symptoms in the members of a family with MELAS syndrome by adequate follow-up. The age of onset of stroke-like episode in MELAS syndrome may be as late as 62 years. We suggest that the manifestations of MELAS syndrome in this family might be associated with the additional ∼260 bp tandem duplication in the D-loop region and the coexistence of C3093G mutation in the 16S rRNA gene with the A3243G mutation of mtDNA.

A 69-year-old woman developed deep coma and brain stem areflexia after subarachnoid hemorrhage. Due to unstable vital signs, she was not a candidate for an apnea test. Computed tomographic angiography revealed absence of intracranial circulation, and brain death was diagnosed.

1. The effect of maprotiline, an antidepressant, on human prostate cells is unclear. In the present study, the effect of maprotiline on [Ca 2 + ] i and growth in PC3 human prostate cancer cells was measured using the fluorescent dyes fura-2 and tetrazolium, respectively. 2. Maprotiline caused a rapid, concentration-dependent increase in [Ca 2 + ] i (EC 5 0 = 200 μmol/L). The maprotiline-induced [Ca 2 + ] i increase was reduced by removal of extracellular Ca 2 + or pretreatment with nicardipine. 3. The maprotiline-induced Mn 2 + influx-associated fura-2 fluorescence quench directly suggests that maprotiline caused Ca 2 + influx. 4. In Ca 2 + -free medium, thapsigargin, an inhibitor of the endoplasmic reticulum Ca 2 + -ATPase, caused a monophasic [Ca 2 + ] i increase, after which the effects of maprotiline of increasing [Ca 2 + ] i were abolished. In addition, pretreatment with maprotiline reduced a major portion of the thapsigargin-induced increase in [Ca 2 + ] i . 5. U73122, an inhibitor of phospholipase C, abolished the ATP (but not maprotiline)-induced increase in [Ca 2 + ] i . 6. Overnight incubation with 1-10 μmol/L maprotiline did not alter cell proliferation, although incubation with 30-50 μmol/L maprotiline decreased cell proliferation. 7, These findings suggest that maprotiline rapidly increases [Ca 2 + ] i in human prostate cancer cells by stimulating both extracellular Ca 2 + influx and intracellular Ca 2 + release and that it may modulate cell proliferation in a concentration-dependent manner.

In Madin-Darby canine kidney (MDCK) cells, the effect of maprotiline, an antidepressant, on intracellular Ca(2+) concentration ([Ca(2+)](i)) was measured using fura-2. Maprotiline (2.5 microM) caused a rapid rise of [Ca(2+)](i) in a concentration-dependent manner (EC(50) 200 microM). Maprotiline-induced [Ca(2+)](i) rise was reduced by removal of extracellular Ca(2+) or by addition of La(3+), but was not altered by voltage-gated Ca(2+)-channel blockers. Maprotiline-induced Mn(2+) influx-associated fura-2 fluorescence quench directly suggests that maprotiline caused Ca(2+) influx. In Ca(2+)-free medium, thapsigargin, an inhibitor of the endoplasmic reticulum Ca(2+)-ATPase, caused a monophasic [Ca(2+)](i) rise, after which the increasing effect of maprotiline on [Ca(2+)](i) was nearly abolished; also, pretreatment with maprotiline reduced a portion of thapsigargin-induced [Ca(2+)](i) rise. U73122, an inhibitor of phospholipase C, abolished [Ca(2+)](i) rise induced by ATP (but not by maprotiline). Overnight incubation with 1-10 microM maprotiline enhanced cell viability, but 20-50 microM maprotiline decreased it. These findings suggest that maprotiline rapidly increases [Ca(2+)](i) in renal tubular cells by stimulating both extracellular Ca(2+) influx and intracellular Ca(2+) release, and may modulate cell proliferation in a concentration-dependent manner.

The effects of arvanil (N-arachidonoyl-vanillyl-amine), a structural hybrid between capsaicin and anandamide, on ion currents in a mouse neuroblastoma and rat glioma hybrid cell line, NG108-15, were examined with the aid of the whole-cell voltage-clamp technique. Arvanil (0.2-50 microM) caused an inhibition of voltage-dependent L-type Ca(2+) current (I(Ca,L)) in a concentration-dependent manner. Arvanil produced no change in the overall shape of the current-voltage relationship of I(Ca,L). The IC(50) value of arvanil-induced inhibition of I(Ca,L) was 2 microM. Arvanil (5 microM) could shift the steady-state inactivation curve of I(Ca,L) to a more negative potential by approximately -15mV. No effect of arvanil (20 microM) on delayed rectifier K(+) current (I(K(DR))) was observed; however, capsaicin (20 microM), glyceryl nonivamide (20 microM) and capsinolol (20 microM) suppressed it significantly. Arvanil (20 microM) caused a slight reduction in the amplitude of erg (ether-a-go-go-related)-mediated K(+) current (I(K(erg))) without modifying the activation curve of this current, while capsaicin and glyceryl nonivamide were more effective in suppressing I(K(erg)). Under current-clamp configuration, arvanil decreased the firing frequency of action potentials. Arvanil-mediated inhibition of I(Ca,L) appeared to be independent of its binding to either vanilloid or cannabinoid receptors. The channel-blocking properties of arvanil may, at least in part, contribute to the underlying mechanisms by which it affects neuronal or neuroendocrine function.

The effects of timosaponin A-III (TA-III), from Rhizoma Anemarrhenae, on Ca(2+) mobilization in vascular endothelial cells and smooth muscle cells and on vascular tension have been explored. TA-III increased intracellular Ca(2+) concentrations ([Ca(2+)](i)) in endothelials cells at a concentration larger than 5 microM with an EC(50) of 15 microM, and increased [Ca(2+)](i) in smooth muscle cells at a concentration larger than 1 microM with an EC(50) of 8 microM. Within 5 min, the [Ca(2+)](i) signal was composed of a gradual rise, and the speed of rising depended on the concentration of TA-III. The [Ca(2+)](i) signal was abolished by removing extracellular Ca(2+) and was recovered after reintroduction of Ca(2+). The TA-III-induced [Ca(2+)](i) increases in smooth muscle cells were partly inhibited by 10 microM nifedipine or 50 microM La(3+), but was insensitive to 10 microM verapamil and diltiazem. TA-III (10-100 microM) inhibited 0.3 microM phenylephrine-induced vascular contraction, which was abolished by pretreatment with 100 microM N(omega)-nitro-L-arginine (L-NNA) or by denuding the aorta. TA-III also increased [Ca(2+)](i) in renal tubular cells with an EC(50) of 8 microM. Collectively, the results show for the first time that TA-III causes [Ca(2+)](i) increases in the vascular system. TA-III acted by causing Ca(2+) influx without releasing intracellular Ca(2+). TA-III induced relaxation of phenylephrine-induced vascular contraction via inducing release of nitric oxide from endothelial cells.

Nordihydroguaiaretic acid (NDGA) is widely used as a pharmacological tool to inhibit lipoxygenases; however, recent evidence suggests that it increases renal intracellular [Ca2+]i via novel mechanisms. Here the effect of NDGA on Ca2+ signaling in MG63 osteoblastic cells was explored using fura-2 as a Ca2+ indicator. NDGA (2-50 microM) increased [Ca2+]i in a concentration-dependent manner. The signal comprised an initial rise and an elevated phase over a time period of 4 min. Removing extracellular Ca2+ reduced 2-50 microM NDGA-induced signals by 62+/-2%. After incubation with 50 microM NDGA in Ca2+-free medium for several minutes, addition of 3 mM CaCl2 induced an increase in [Ca2+]i. NDGA (50 microM)-induced [Ca2+]i increases were not changed by pretreatment with 10 microM of verapamil, diltiazem, nifedipine, nimodipine and nicardipine. In Ca2+-free medium, pretreatment with the endoplasmic reticulum Ca2+ pump inhibitor thapsigargin (1 microM) inhibited 50 microM NDGA-induced [Ca2+]i increases by 69+/-3%. Inhibition of phospholipase C with 2 microM U73122 had little effect on 50 microM NDGA-induced Ca2+ release. Several other lipoxygenase inhibitors had no effect on basal [Ca2+]i. At a concentration that did not increase basal [Ca2+]i, NDGA (1 microM) did not alter 10 microM ATP- or 1 microM thapsigargin-induced [Ca2+]i increases. Alteration of protein kinase C activity with 1 nM phorbol 12-myristate 13-acetate or 2 microM GF 109203X did not affect 50 microM NDGA-induced [Ca2+]i increases. Together, the results show that NDGA increased [Ca2+]i in osteoblasts in a lipoxygenase-independent manner, by releasing stored Ca2+ in a fashion independent of phospholipase C activity, and by causing Ca2+ influx.

The effect of histamine on intracellular free Ca2+ levels ([Ca2+]i) in PC3 human prostate cancer cells and the underlying mechanism were evaluated using fura-2 as a Ca2+ dye. Histamine at concentrations between 0.1 and 50 microM increased [Ca2+]i in a concentration-dependent manner with an EC50 value of 1 microM. The [Ca2+]i response comprised an initial rise and a slow decay, which returned to baseline within 3 min. Extracellular Ca2+ removal inhibited 50% of the [Ca2+]i signal. In the absence of extracellular Ca2+, after cells were treated with 1 microM thapsigargin (an endoplasmic reticulum Ca2+ pump inhibitor), 10 microM histamine did not increase [Ca2+]i. After pretreatment with 10 microM histamine in a Ca2+-free medium for several minutes, addition of 3 mM Ca2+ induced [Ca2+]i increases. Histamine (10 microM)-induced intracellular Ca2+ release was abolished by inhibiting phospholipase C with 2 microM 1-(6-((17 beta-3- methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione (U73122), and by 10 microM pyrilamine but was not altered by 50 microM cimetidine. Collectively, the present study shows that histamine induced [Ca2+]i transients in PC3 human prostate cancer cells by stimulating H1 histamine receptors leading to Ca2+ release from the endoplasmic reticulum in an inositol 1,4,5-trisphosphate-dependent manner, and by inducing Ca2+ entry.

The response of the L-type Ca2+ current (ICa,L) in pituitary GH3 cells to variations in the action potential (AP) waveform was examined using the whole-cell configuration of the patch-clamp technique. ICa,L evoked during an AP waveform exhibited an early and a late component. The early component occurred on the rising phase of the AP; the late component coincided with the falling phase. Prolonging the falling phase of the AP increased the Ca2+ charge carried by ICa,L, although the amplitude of the late ICa,L was reduced. Prolonging the peak voltage of the AP waveform, however, increased the amplitude of the late component. ICa,L inactivated during a train of AP waveforms. When Ba2+ was used as the charge carrier, current inactivation during a train of APs decreased. Likewise, ICa,L evoked by the AP templates with irregular bursting pattern was inactivated. When the repetitive firing of APs with depolarizing potentials was replayed to cells, Ca2+ entry was not only spread over the entire AP, but also occurred during the interspike voltage trajectory. After application of thyrotropin releasing hormone (TRH; 10 microM), ICa,L in response to rectangular pulses was increased and the current/voltage relation shifted slightly to more negative values. TRH (10 microM), thapsigargin (10 microM) or cyclopiazonic acid (30 microM) enhanced the late component of the AP-evoked ICa,L. TRH also attenuated the inactivation of ICa,L during a train of APs. These results indicate that in pituitary GH3 cells, the time course and kinetics of ICa,L during the AP waveforms is distinct from that evoked by rectangular voltage clamp. Changes in the shape and firing pattern of APs in GH3 cells can modulate Ca2+ influx through L-type Ca2+ channels. Ca2+ release from internal stores may affect the magnitude of AP-evoked ICa,L in these cells.

This study examined the effect of tamoxifen, an anti-breast cancer drug, on Ca2+ handling in bladder female transitional cancer cells. Changes in cytosolic free Ca2+ levels were recorded by using the Ca2+-sensitive dye fura-2. In a dose-dependent manner, tamoxifen induced intracellular free Ca2+ concentrations ([Ca2+]i) increases between 5 and 20 microM with an EC50 of 10 microM. External Ca2+ removal reduced the response by 60+/-6%. Addition of 3 mM Ca2+ caused a [Ca2+]i increase after pretreatment with 10 microM tamoxifen in Ca2+-free medium. In Ca2+-free medium, pretreatment with 10 microM tamoxifen abolished the [Ca2+]i increase induced by 1 microM thapsigargin, an endoplasmic reticulum Ca2+ pump inhibitor. Conversely, pretreatment with 1 microM thapsigargin prevented tamoxifen from releasing more Ca2+. Inhibition of phospholipase C-dependent inositol 1,4,5-tris-phosphate formation with 2 microM U73122 did not alter 10 microM tamoxifen-induced Ca2+ release. The [Ca2+]i increase induced by 5 microM tamoxifen was not altered by 10 microM La3+, nifedipine, verapamil, and diltiazem. Collectively, it was found that tamoxifen increased [Ca2+]i in bladder cancer cells by releasing Ca2+ from the endoplasmic reticulum Ca2+ stores in a manner independent of phospholipase C activity, and by inducing Ca2+ entry from external medium.

The assessment of brachial-artery FMD is a reliable, reproducible and noninvasive tool for evaluating endothelial dysfunction, which, together with endothelial inflammation, causes carotid atherosclerosis. Atorvastatin therapy can reverse endothelial dysfunction after 4 months, and may have significant anti-inflammatory effects if continued for more than 4 months. Importantly, statin therapy can be used to treat carotid atherosclerosis.

The rate of decline in the age-adjusted death rate from cerebrovascular disease (CVD) in Taiwan is not as rapid as in the United States and Japan, and the trends of CVD mortalities have not decreased steadily during the period 1972-1983. A low record of hypertension regulation (5.0%-12.7%), a high proportion (47.1%) of stroke due to cerebral hemorrhage (by clinical assessment), and a high fatality rate (40.1%) for cerebral hemorrhage may account partially for the slower declining rate. A geographic difference in the downward trend of CVD death rate was observed in this period. Districts remote from the major cities have had the lowest decline in CVD death rate.

Background Although the clinical effectiveness of community hospital-based postacute care (PAC) services has been shown, little was known regarding the impact of depression on the clinical outcomes of older patients receiving PAC services in Taiwan. Methods From January 2009 to August 2010, patients aged 65 years and older referred from tertiary medical centers or acute wards of community hospitals to PAC units were invited for study. All patients received the 4-week Comprehensive Geriatric Assessment-based intervention program in the PAC units. The functional assessment was composed of Geriatric Depression Scale–Short Form (GDS), Mini-Mental Status Examination, Barthel Index, Instrumental Activities of Daily Living, and Braden Score. Results Among the 401 participants (mean age, 82.0 years; 95.5% males), 66 (16.5%) patients were depressed at PAC unit admission. Depressed patients had significantly lower Barthel Index (38.1 ± 2.4 vs. 47.6 ± 1.2, p = 0.002) and Braden Score (17.7 ± 0.3 vs. 18.8 ± 0.2, p = 0.004) than nondepressed patients. Improvement was noted on all measures of functional outcome among patients receiving PAC services. Furthermore, GDS was significantly improved in depressed patients (from 6.4 ± 0.2 to 2.8 ± 0.2 in depressed patients vs. from 1.6 ± 0.1 to 0.9 ± 0.1 in nondepressed patients, p Conclusion Depression was common when patients were newly admitted to PAC services, which was highly associated with poorer physical function. Improvement in physical function and depressive symptoms among all patients after PAC service was found, and the presence of depressive symptoms at PAC admission did not predict any adverse outcome of PAC services.

A total of 72 ocular bruits in 50 patients with symptoms of atherothrombotic ischemic cerebrovascular disease were studied with continuous-wave Doppler ultrasonography with spectrum analysis (Dopscan). Fourteen patients also had conventional angiography, and 14 had digital subtraction angiography. Ocular bruits by augmentation flow due to occlusion (seven bruits, 9.7%) or tight stenosis (17 bruits, 23.6%) of the contralateral internal carotid artery accounted for only 24 ocular bruits (33.3%). In contrast, siphon stenosis ipsilateral to the ocular bruit was a very common finding. All 14 patients studied with conventional angiography had variable degrees of siphon stenosis ipsilateral to the ocular bruits; there was one angiography failure. We conclude that siphon stenosis can cause ocular bruit alone or can act in combination with augmentation flow by contralateral carotid occlusion or tight stenosis. The difference in their relative occurrence in our patients compared with previous reports probably reflects racial differences in the distribution of stenotic or occluded lesions of the carotid artery between our patients and Caucasian patients. The ocular bruit was the only auscultatory finding in more than a quarter of our patients (14 of 50, 28%).

We investigated the prevalence of stroke in Taiwan in an epidemiologic study of stroke, diabetes, and cardiovascular disease that used a two-phase survey design. The study population was drawn by cluster sampling and consisted of both urban and rural communities from four regions of Taiwan. There were 8,705 people 36 years of age or older interviewed during the period of October 1 to December 31, 1986, and 143 cases of completed stroke were later identified by a neurologist. The point prevalence rate for people aged 36 or older in our study was 1,642/100,000 population (95% confidence interval 1,389-1,942/100,000). Prevalence rates differed significantly among the four study regions and between urban and rural communities; prevalence was greater in northern Taiwan and in urban communities. Percentages of the major types of stroke in 143 stroke survivors were as follows: cerebral infarction 67.1% (96 cases), cerebral hemorrhage 14.0% (20 cases), subarachnoid hemorrhage 4.2% (six cases), and unclassified 14.7% (21 cases). Of the stroke survivors, 67.1% were independent in activities of daily living, and 75.5% were independent in ambulation. Hypertension, heart disease, diabetes mellitus, and a family history of stroke were significantly more common in stroke survivors than in strokefree individuals.

A 43-year-old woman suffered from low back pain and bilateral footdrop. A cisternal myelogram unexpected revealed multiple filling defects in the spinal canal extending from the lower cervical region to the caudal equina. Diagnostic exploration revealed numerous cystic organisms adhering to the spinal cord and nerve roots. Histopathological examination showed these organisms to be proliferative sparganum cestode larvae. Although these cestode larval infections have been reported a dozen times in humans from various parts of the world, this is probably the first reported case of spinal cord infection.

We report a case of right tentorium subdural hematoma (SDH) in a 72-year-old man a few days after he visited a sanitas per aqua (SPA) facility. He had directed high-pressure water onto his head and neck. The patient was admitted to the emergency room during his 3 rd day of severe throbbing and generalized headache. Cerebral computed tomography revealed a high-density SDH over the right tentorium. This is the first reported case of SPA-related SDH. Neurologists might consider the possibility that SPA use may be a factor in SDH or unexplained neurologic events in otherwise healthy persons.