Impact of exercise on bone mineral density, fall prevention, and vertebral fragility fractures in postmenopausal osteoporotic women.

Osteoporosis is the most prevalent bone disease worldwide and predisposes affected individuals to fragility fractures. Exercise has been shown to have multiple health benefits in post-menopausal osteoporotic women, but often recommendations regarding the benefits of specific exercise types are vague. Improving bone mineral density (BMD) is an essential component in any program to prevent osteoporotic vertebral fractures. The objective of this report is to briefly review the current understanding on the impact of exercise on BMD in postmenopausal women as it pertains to fragility fractures. Broad categories of exercises include aerobic, resistance, stretching, and balance. Tai Chi, Yoga, and Pilates are a heterogeneous group of specific exercise modalities that can span multiple categories. Current literature suggests that only resistance type exercises have a convincing impact on BMD. Core-strengthening exercises and attention to posture/balance can help mitigate falls. A number of barriers affect patient compliance and accessibility to exercise. In summary, exercise should be included in any multi-modality osteoporosis treatment plan with the goal of sustained exercise throughout life. If possible, osteoporotic women should be on a resistance-based regimen incorporating weight-bearing exercises, and also target posture and balance. Healthcare providers and educators should have resources readily available for patients.

Some capabilities for model-based and model-free linkage analysis using the program package S.A.G.E. (Statistical Analysis for Genetic Epidemiology).

For both model-free and model-based linkage analysis the S.A.G.E. (Statistical Analysis for Genetic Epidemiology) program package has some unique capabilities in analyzing both continuous traits and binary traits with variable age of onset. Here we highlight model-based linkage analysis of a quantitative trait (plasma dopamine ß hydroxylase) that is known to be largely determined by monogenic inheritance, using a prior segregation analysis to produce the best fitting model for the trait. For a binary trait with variable age of onset (schizophrenia), we illustrate how using age of onset information to obtain a quantitative susceptibility trait leads to more statistically significant linkage signals, suggesting better power.

Can phenotypic plasticity facilitate the geographic expansion of the tilapia Oreochromis mossambicus?

Climate influences the distribution of organisms because of the thermal sensitivity of biochemical processes. Animals may compensate for the effects of variable temperatures, and plastic responses may facilitate radiation into different climates. The tropical fish Oreochromis mossambicus has radiated into climates that were thought to be thermally unsuitable. Here, we test the hypothesis that thermal acclimation will extend the locomotory and metabolic performance range of O. mossambicus. Juvenile fish were acclimated to 14 degrees, 17 degrees, and 22 degrees C. We measured responses to acclimation at three levels of organization: whole-animal performance (sustained swimming and resting and recovery rates of oxygen consumption), mitochondrial oxygen consumption in caudal muscle, and metabolic enzyme activities in muscle and liver at 12 degrees, 14 degrees, 17 degrees, 22 degrees, and 26 degrees C. Thermal optima of sustained swimming performance (U(crit)) changed significantly with acclimation, but acclimation had no effect on either resting or recovery oxygen consumption. Fish compensated for cold temperatures by upregulating state 3 mitochondrial oxygen consumption and increasing activity of lactate dehydrogenase in the liver. The capacity for phenotypic plasticity in O. mossambicus means that the fish would not be limited by its locomotor performance or metabolic physiology to expand its range into cooler thermal environments from its current distribution.

Gender differences and temporal variation in the incidence of type 1 diabetes: results of 8012 cases in the nationwide Diabetes Incidence Study in Sweden 1983-2002.

OBJECTIVES: To establish the gender difference amongst newly diagnosed type 1 diabetic patients aged 15-34 years, considering age at diagnosis, temporal trend and seasonal variation at time of diagnosis. STUDY DESIGN: A population-based prospective study with a mean annual population at risk of 2.3 million. SETTING: All departments of medicine, endocrinology and paediatrics and primary health care units in Sweden. SUBJECTS: Incident cases of diabetes aged 15-34 years at diagnosis 1983-2002. MEASURE INSTRUMENT: Basic characteristics of patients at diagnosis were reported by the diagnosing doctor on a standardized form. Level of ascertainment was estimated at 80-90%. RESULTS: Amongst all incident cases (n = 8012), 74% was diagnosed with type 1 diabetes. The mean annual incidence rate of type 1 diabetes was 12.7/100,000, in men 16.4/100,000 and in women 8.9/100,000. The incidence of type 1 diabetes decreased slowly by increasing age but was in all age groups higher in men, yielding an overall male/female ratio of 1.8. In both genders the incidence of type 1 diabetes decreased in average of 1.0% per year. A seasonal pattern with significantly higher incidence during January-March and lower during May-July was seen in both genders. CONCLUSIONS: A clear male predominance of type 1 diabetes was seen in all ages. The temporal trend and the seasonal pattern was similar in men and women. Hence, internal factors related to the gender rather than differences in the exposure to environmental factors seem to explain the consistent male-female bias in the postpubertal risk of developing type 1 diabetes.

Lower levels of plasma 25-hydroxyvitamin D among young adults at diagnosis of autoimmune type 1 diabetes compared with control subjects: results from the nationwide Diabetes Incidence Study in Sweden (DISS).

AIMS/HYPOTHESIS: Low plasma vitamin D concentrations may promote the development of type 1 diabetes. To test this hypothesis, we measured plasma 25-hydroxyvitamin D (25OHD) in young adults with type 1 diabetes. METHODS: The nationwide Diabetes Incidence Study in Sweden (DISS) covers 15- to 34-year-old people with newly diagnosed diabetes. Blood samples at diagnosis were collected during the 2-year period 1987/1988. Patients with islet antibodies (islet cell antibodies, GAD antibodies or tyrosine phosphatase-like protein antibodies) were defined as having autoimmune type 1 diabetes. Plasma 25OHD was measured in samples taken from 459 patients at the time of diagnosis, and in 138 of these subjects 8 years later. The results were compared with age- and sex-matched control subjects (n=208). RESULTS: At diagnosis, plasma 25OHD levels were significantly lower in patients with type 1 diabetes than in control subjects (82.5+/-1.3 vs 96.7+/-2.0 nmol/l; p<0.0001). Eight years later, plasma 25OHD had decreased in patients (81.5+/-2.6 nmol/l; p=0.04). Plasma 25OHD levels were significantly lower in diabetic men than in diabetic women at diagnosis (77.9+/-1.4 vs 90.1+/-2.4 nmol/l; p<0.0001) and at follow-up (77.1+/-2.8 nmol/l vs 87.2+/-4.5 nmol/l; p=0.048). CONCLUSIONS/INTERPRETATION: The plasma 25OHD level was lower at diagnosis of autoimmune type 1 diabetes than in control subjects, and may have a role in the development of type 1 diabetes. Plasma 25OHD levels were lower in men than in women with type 1 diabetes. This difference may be relevant to the high incidence of type 1 diabetes among young adult men.

HLA-DQB1 genotypes, islet antibodies and beta cell function in the classification of recent-onset diabetes among young adults in the nationwide Diabetes Incidence Study in Sweden.

AIMS/HYPOTHESIS: The World Health Organization considers an aetiological classification of diabetes to be essential. The aim of this study was to evaluate whether HLA-DQB1 genotypes facilitate the classification of diabetes as compared with assessment of islet antibodies by investigating young adult diabetic patients. SUBJECTS AND METHODS: Blood samples were available at diagnosis for 1,872 (90%) of the 2,077 young adult patients (aged 15-34 years old) over a 5-year period in the nationwide Diabetes Incidence Study in Sweden. Islet antibodies were measured at diagnosis in 1,869 patients, fasting plasma C-peptide (fpC-peptide) after diagnosis in 1,522, while HLA-DQB1 genotypes were determined in 1,743. RESULTS: Islet antibodies were found in 83% of patients clinically considered to have type 1 diabetes, 23% with type 2 diabetes and 45% with unclassifiable diabetes. After diagnosis, median fpC-peptide concentrations were markedly lower in patients with islet antibodies than in those without (0.24 vs 0.69 nmol/l, p<0.0001). Irrespective of clinical classification, patients with islet antibodies showed increased frequencies of at least one of the risk-associated HLA-DQB1 genotypes compared with patients without. Antibody-negative patients with risk-associated HLA-DQB1 genotypes had significantly lower median fpC-peptide concentrations than those without risk-associated genotypes (0.51 vs 0.74 nmol/l, p=0.0003). CONCLUSIONS/INTERPRETATION: Assessment of islet antibodies is necessary for the aetiological classification of diabetic patients. HLA-DQB1 genotyping does not improve the classification in patients with islet antibodies. However, in patients without islet antibodies, HLA-DQB1 genotyping together with C-peptide measurement may be of value in differentiating between idiopathic type 1 diabetes and type 2 diabetes.

Cigarette smoking and the risk of goitre and thyroid nodules amongst parous women.

OBJECTIVES: To clarify the mechanisms by which smoking is associated to toxic and nontoxic goitre and thyroid nodules. DESIGN: Cohort study. SETTING: Sweden. SUBJECTS: A cohort of 874,507 parous women identified through the Medical Birth Registry, with smoking behaviour assessed through self-reported information at the first pre-natal visit, and follow-up between 1983 and 1997. MAIN OUTCOME MEASURES: Hospital diagnoses of toxic and nontoxic goitre and thyroid nodules, identified by record-linkage with the national Inpatient Registry. Cox regression was employed to estimate the hazard ratio (HR) of smokers compared with nonsmokers and the corresponding 95% confidence limits (CL). RESULTS: There was a significantly increased risk of goitre and nodules amongst smokers. The positive association was stronger for toxic (age adjusted HR = 1.94, CL = 1.74-2.16) than for nontoxic goitre and nodules (age-adjusted HR = 1.26; CL = 1.14-1.38). There was generally no clear risk trend with regard to amount smoked (below and above 10 cigarettes per day). Elevated body mass attenuated these associations, whilst being born in Swedish areas of endemic goitre enhanced the association with nontoxic goitre and nodules. CONCLUSIONS: Smoking enhances the risk of thyroid goitre and nodules requiring hospital admission. Iodine deficiency and body weight are likely to be important modifiers of the risk of thyroid hyperplastic diseases amongst smokers.

Peri-operative glucose control and development of surgical wound infections in patients undergoing coronary artery bypass graft.

Elevated blood glucose following coronary artery bypass graft (CABG) is associated with an increased risk of surgical wound infection (SWI). It is unclear whether hyperglycaemia, the diabetic state, the longstanding vascular effects of diabetes, or the systematic inflammatory response confers the increased vulnerability to SWI. This study was designed to examine the significance of postoperative blood glucose control as a risk factor for SWI after vein graft harvesting on the leg and sternotomy. Patients with and without diabetes had a CABG within 60 days to be eligible. The present study was part of a larger protocol investigating SWI following CABG in a total of 374 patients. Potential risk factors, duration of diabetes, pre-operative glycated haemoglobin (HbA(1c)) and presence of long-term complications were recorded. All patient records were reviewed retrospectively to record 10% glucose infusions during the operation, and blood glucose concentrations and insulin therapy on postoperative days 0, 1 and 2. Patients were contacted by telephone 30 and 60 days after surgery and interviewed in accordance with a questionnaire about symptoms and signs of wound infection. In the present study, it was not possible to separate the effect of diabetes as a risk factor for SWI from that of hyperglycaemia. However, in the subgroup of patients without a pre-operative diagnosis of diabetes, increased blood glucose concentrations during postoperative days 0, 1 and 2 was associated with an increased risk of mediastinitis.

Distribution of estrogens, 17beta-estradiol and estrone, in Canadian municipal wastewater treatment plants.

The distribution of female hormones, 17beta-estradiol and estrone, was determined in effluents of 18 selected municipal treatment plants across Canada. Replicate 24-h composite samples were collected from the influent and final effluent of each treatment plant, and the removal efficiency compared to the operational characteristics of the plants. In conventional activated sludge and lagoon treatment systems, the mean concentrations of 17beta-estradiol and estrone in influent were 15.6 ng/l (range 2.4-26 ng/l) and 49 ng/l (19-78 ng/l). In final effluents, the mean concentrations of both 17beta-estradiol and estrone were reduced to 1.8 ng/l (0.2-14.7 ng/l) and 17 ng/l (1-96 ng/l), respectively. 17beta-estradiol was removed effectively, >75% and as high as 98%, in most of the conventional mechanical treatment systems with secondary treatment. The removal of estrone was much more complex with removal varying from 98% to situations where the concentrations in the effluent were elevated above that detected in the influent. The estrogenicity, measured using a transfected estrogen receptor in yeast (YES) assay, was also variable, ranging from high removal to elevations of estrogenicity in final effluent. Although the apparent removals were not statistically correlated with either hydraulic (HRT) or solid (SRT) retention times, plants or lagoons with high SRT were very effective at reducing the levels of hormones. Well-operated plants that achieved nitrification also tended to have higher removal of hormones than those that did not nitrify. Laboratory aerobic reactor experiments confirmed the rapid removal of 17beta-estradiol, estrone, and estrogenicity when exposed to sewage slurries.

Segregation analyses of asthma and respiratory allergy: the Humboldt family study.

We performed segregation analyses of asthma and respiratory allergy based on data from 309 nuclear families comprising 1,053 individuals living in the town of Humboldt, Saskatchewan, in 1993, using the REGD program of the S.A.G.E. program package. For adults, information on asthma and history of respiratory allergy was provided by the subjects themselves, and for children by their parents. When asthma was considered as the trait in segregation analysis, models of no major effect, with or without familial effects, were rejected, but they were not rejected after adjusting for history of respiratory allergy. The major gene hypothesis was not rejected before adjusting for history of respiratory allergy. When respiratory allergy was analyzed as the trait, both major gene and multifactorial models fitted the data well, regardless of whether there was adjustment for asthma or not. Other covariates adjusted for in the segregation analyses were age, sex, number of household smokers, current smoking, number of household members, generation, and house type. The data suggest that a major gene related to respiratory allergy may explain the familial aggregation of asthma.

Objective threshold selection procedure (OTS) for segmentation of scanning laser confocal microscope images.

The determination of volumes and interface areas from confocal laser scanning microscopy (CLSM) images requires the identification of component objects by segmentation. An automated method for the determination of segmentation thresholds for CLSM imaging of biofilms was developed. The procedure, named objective threshold selection (OTS), is a three-dimensional development of the approach introduced by the popular robust automatic threshold selection (RATS) method. OTS is based on the statistical properties of local gray-values and gradients in the image. By characterizing the dependence between a volumetric feature and the intensity threshold used for image segmentation, the former can be determined with an arbitrary confidence level, with no need for user intervention. The identification of an objective segmentation procedure renders the possibility for the full automation of volume and interfacial area measurement. Images from two distinct biofilm systems, acquired using different experimental techniques and instrumental setups were segmented by OTS to determine biofilm volume and interfacial area. The reliability of measurements for each case was analyzed to identify optimal procedure for image acquisition. The automated OTS method was shown to reproduce values obtained manually by an experienced operator.

Optimal cell source for cardiovascular tissue engineering: venous vs. aortic human myofibroblasts.

Arterial vascular cells have been successfully utilized for tissue engineering in human cardiovascular structures, such as heart valves. The present study evaluates saphenous vein-derived myofibroblasts as an alternative, easy-to-access cell source for human cardiovascular tissue engineering. Biodegradable polyurethane scaffolds were seeded with human vascular myofibroblasts. Group A consisted of scaffolds seeded with cells from ascending aortic tissue; in group B, saphenous vein-derived cells were used. Analysis included histology, electron microscopy, mechanical testing, and biochemical assays for cell proliferation (DNA) and extracellular matrix (collagen). DNA content was comparable in both groups. Collagen and stress at maximum load was significantly higher in group B. Morphology showed viable, layered cellular tissue in all samples, with collagen fibrils most pronounced in group B. In conclusion, saphenous vein myofibroblasts cultured on biodegradable scaffolds showed excellent in vitro tissue generation. Collagen formation and mechanical properties were superior to aortic tissue derived constructs. Therefore, the easy-to-access vein cells represent a promising alternative cell source for cardiovascular tissue engineering.

Tissue engineering of small caliber vascular grafts.

OBJECTIVE: Previous tissue engineering approaches to create small caliber vascular grafts have been limited by the structural and mechanical immaturity of the constructs. This study uses a novel in vitro pulse duplicator system providing a 'biomimetic' environment during tissue formation to yield more mature, implantable vascular grafts. METHODS: Vascular grafts (I.D. 0.5 cm) were fabricated from novel bioabsorbable polymers (polyglycolic-acid/poly-4-hydroxybutyrate) and sequentially seeded with ovine vascular myofibroblasts and endothelial cells. After 4 days static culture, the grafts (n=24) were grown in vitro in a pulse duplicator system (bioreactor) for 4, 7, 14, 21, and 28 days. Controls (n=24) were grown in static culture conditions. Analysis of the neo-tissue included histology, scanning electron microscopy (SEM), and biochemical assays (DNA for cell content, 5-hydroxyproline for collagen). Mechanical testing was performed measuring the burst pressure and the suture retention strength. RESULTS: Histology showed viable, dense tissue in all samples. SEM demonstrated confluent smooth inner surfaces of the grafts exposed to pulsatile flow after 14 days. Biochemical analysis revealed a continuous increase of cell mass and collagen to 21 days compared to significantly lower values in the static controls. The mechanical properties of the pulsed vascular grafts comprised supra-physiological burst strength and suture retention strength appropriate for surgical implantation. CONCLUSIONS: This study demonstrates the feasibility of tissue engineering of viable, surgically implantable small caliber vascular grafts and the important effect of a 'biomimetic' in vitro environment on tissue maturation and extracellular matrix formation.

Electrocardiographic prediction of abnormal genotype in congenital long QT syndrome: experience in 101 related family members.

INTRODUCTION: Previous studies showed that diagnosing congenital long QT syndrome (LQTS) is difficult due to variable penetrance and genetic heterogeneity, especially when subjects from multiple families with diverse mutations are combined. We hypothesized that a combination of clinical and ECG techniques could identify gene carriers within a single family with congenital LQTS. METHODS AND RESULTS: One hundred one genotyped members of a family with LQTS, including 26 carriers of a HERG mutation, underwent history and ECG analysis. Forty-eight family members also underwent exercise testing with QT and T wave alternans (TWA) analysis and 24-hour Holter monitoring with QT and heart rate variability analysis. A logistic regression model, which included age, gender, QTc, and QTc by age, provided the best prediction of gene carrier status, although there was substantial overlap (78%) of QTc among subjects with and without the mutation. QTc was not helpful as a discriminator in children < or = 13 years. TWA (observed infrequently) did not add significantly to the model's ability to predict abnormal genotype. CONCLUSION: Even in this homogeneous LQTS population, the phenotype was so variable that clinical and detailed ECG analyses did not permit an accurate diagnosis of gene carrier status, especially in children. Sustained microvolt TWA was a specific (100%) but insensitive (18%) marker for LQTS. Its ability to predict risk of arrhythmia in this population remains to be determined. Genetic testing serves an essential role in screening for carriers of LQTS.

Segregation analysis of asthma and respiratory allergy in population-based samples of families.

Class A regressive multiple logistic segregation models with a sibling covariate were used to investigate the underlying determinants of asthma and respiratory allergy (defined from specific IgE levels to inhaled allergens) in the randomly recruited Caucasian families from the Genetic Analysis Workshop 12 asthma data sets--Perth, Busselton, and Southampton. For asthma, both a purely multifactorial model and a major gene (dominant or recessive) model with multifactorial effects fitted the data. For respiratory allergy, a dominant, dominant with multifactorial effects and a purely multifactorial model all fitted the data. However, homogeneity of the three studies was rejected for both traits indicating that the three populations are significantly different and should be analyzed separately. This finding has implications for the meta-analysis of asthma linkage studies.

Evaluation of fluorescently labeled lectins for noninvasive localization of extracellular polymeric substances in Sphingomonas biofilms.

Three strains of Sphingomonas were grown as biofilms and tested for binding of five fluorescently labeled lectins (Con A-type IV-TRITC or -Cy5, Pha-E-TRITC, PNA-TRITC, UEA 1-TRITC, and WGA-Texas red). Only ConA and WGA were significantly bound by the biofilms. Binding of the five lectins to artificial biofilms made of the commercially available Sphingomonas extracellular polysaccharides was similar to binding to living biofilms. Staining of the living and artificial biofilms by ConA might be explained as binding of the lectin to the terminal mannosyl and terminal glucosyl residues in the polysaccharides secreted by Sphingomonas as well as to the terminal mannosyl residue in glycosphingolipids. Staining of the biofilms by WGA could only be explained as binding to the Sphingomonas glycosphingolipid membrane, binding to the cell wall, or nonspecific binding. Glycoconjugation of ConA and WGA with the target sugars glucose and N-acetylglucosamine, respectively, was used as a method for evaluation of the specificity of the lectins towards Sphingomonas biofilms and Sphingomonas polysaccharides. Our results show that the binding of lectins to biofilms does not necessarily prove the presence of specific target sugars in the extracellular polymeric substances (EPS) in biofilms. The lectins may bind to non-EPS targets or adhere nonspecifically to components of the biofilm matrix.

Genetic determinants of acute hypoxic ventilation: patterns of inheritance in mice.

Acutely lowering ambient O(2) tension increases ventilation in many mammalian species, including humans and mice. Inheritance patterns among kinships and between mouse strains suggest that a robust genetic influence determines individual hypoxic ventilatory responses (HVR). Here, we tested specific genetic hypotheses to describe the inheritance patterns of HVR phenotypes among two inbred mouse strains and their segregant and nonsegregant progeny. Using whole body plethysmography, we assessed the magnitude and pattern of ventilation in C3H/HeJ (C3) and C57BL/6J (B6) progenitor strains at baseline and during acute (3-5 min) hypoxic [mild hypercapnic hypoxia, inspired O(2) fraction (FI(O(2))) = 0.10] and normoxic (mild hypercapnic normoxia, FI(O(2)) = 0.21) inspirate challenges in mild hypercapnia (inspired CO(2) fraction = 0.03). First- and second-filial generations and two backcross progeny were also studied to assess response distributions of HVR phenotypes relative to the parental strains. Although the minute ventilation (VE) during hypoxia was comparable between the parental strains, breathing frequency (f) and tidal volume were significantly different; C3 mice demonstrated a slow, deep HVR relative to a rapid, shallow phenotype of B6 mice. The HVR profile in B6C3F(1)/J mice suggested that this offspring class represented a third phenotype, distinguishable from the parental strains. The distribution of HVR among backcross and intercross offspring suggested that the inheritance patterns for f and VE during mild hypercapnic hypoxia are consistent with models that incorporate two genetic determinants. These results further suggest that the quantitative genetic expression of alleles derived from C3 and B6 parental strains interact to significantly attenuate individual HVR in the first- and second-filial generations. In conclusion, the genetic control of HVR in this model was shown to exhibit a relatively simple genetic basis in terms of respiratory timing characteristics.

Major gene segregation of actinic prurigo among North American Indians in Saskatchewan.

Actinic prurigo is an idiopathic, familial photodermatosis seen especially in American Indians. Segregation analysis was performed on 12 Saskatchewan pedigrees with American Indian ancestry, comprising a total of 1,148 individuals, ascertained via probands diagnosed with actinic prurigo. Although a high degree of familial aggregation has been noted in the past and dominant inheritance has been suggested, no formal segregation analysis has been attempted. Actinic prurigo has a variable age of onset and, therefore, age at the time of censoring must be taken into account in the analysis. However, as these ages of 57% of the unaffected individuals were missing, an algorithm was devised to impute the missing ages from known birth years in the family based on the age differences among relatives and spouses. Using these imputed ages, simple dominant inheritance with incomplete penetrance and a single age of onset distribution was found. The method for imputing the ages at examination was evaluated, as was the correction for ascertainment, by using alternative methods and comparing the results. Regardless of the method used, a dominant mode of inheritance without any multifactorial component remained the best hypothesis.

Microembolic signals and clinical outcome in patients with acute stroke--a prospective study.

The occurrence of microembolic signals (MES) in patients with transient ischemic attack (TIA) or stroke has already been described; the influence of the time interval between onset of symptoms and transcranial Doppler monitoring (TCD) on the MES rate or MES prevalence and the possible prognostic value of the early detected MES rate on the outcome of TIA or stroke symptoms in a 3 month interval are discussed. In a prospective study we evaluated 61 patients consecutively admitted to our stroke unit after their first ischemic neurological deficit involving the vascular territory of MCA and/or ACA. All of the patients underwent a 30-minute bilateral transcranial Doppler monitoring of their MCAs for the identification of MES. Monitoring was performed within 12.3 + -9.3 (average mean + -SD) hours of stroke onset for the first time, the second time 48 hours after first TCD monitoring. Prognosis for the recovery of neurological deficits was evaluated by using the Barthel index (BI) and Scandinavian Stroke Scale (SSS) at the time of admission of the patient to the stroke unit, and with Barthel indices after one month and after 3 months. As a result, 56% of all patients showed MES in at least one of the two registrations. MES were recorded not only on the symptomatic side. The MES prevalence between both TCD monitorings was significantly different (total MES prevalence: 1st TCD: 26 patients: 2nd TCD: 13 patients; p < 0.04; ipsilateral MES prevalence: 1st TCD: 19 patients; 2nd TCD: 9 patients; p < 0.01). The regression analysis showed a significant influence of the total MES rate on both neurological scores at admission (SSS: 0.03; Barthel index: 0.04), but not for the Barthel scores after one and three months. In conclusion, we found an influence of the time interval between onset of neurological symptoms of TIA or stroke on the MES rate and the prevalence of MES. The prevalence of MES or the MES rate, found after a short time interval to the onset of symptoms, did not have a prognostic value on the outcome of neurological deficits up to a three month follow-up.