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Biomedical subjects

A Peters

Publications and source records attributed to A Peters.

At least 91 records · Page 5Linked to original sources
PubMed2000

Daily mortality and fine and ultrafine particles in Erfurt, Germany part I: role of particle number and particle mass.

Increases in morbidity and mortality have been observed consistently and coherently in association with ambient air pollution. A number of studies on short-term effects have identified ambient particles as a major pollutant in urban air. This study, conducted in Erfurt, Germany, investigated the association of mortality not only with ambient particles but also with gaseous pollutants and indicators of sources. Part I of this study concentrates on particles. Data were collected prospectively over a 3.5-year period from September 1995 to December 1998. Death certificates were obtained from the local authorities and aggregated to daily time series of total counts and counts for subgroups. In addition to standard data for particle mass with diameters < or = 2.5 microm (PM2.5)* or < or = 10 microm (PM10) from impactors, a mobile aerosol spectrometer (MAS) was used to obtain size-specific number and mass concentration data in six size classes between 0.01 microm and 2.5 microm. Particles smaller than 0.1 microm were labeled ultrafine particles (three size classes), and particles between 0.1 and 2.5 microm were termed fine particles (three size classes). Concentrations of the gases sulfur dioxide (SO2), nitrogen dioxide (NO2), and carbon monoxide (CO) were also measured. The daily average total number concentration was 18,000 particles/cm3 with 88% of particles below 0.1 pm and 58% below 0.03 microm in diameter. The average mass concentration (PM2.5) was 26 microg/m3; of this, 75% of particles were between 0.1 and 0.5 microm in diameter. Other average concentrations were 38 microg/m3 for PM10, 17 microg/m3 for SO2, 36 microg/m3 for NO2, and 600 microg/m3 for CO. Ambient air pollution demonstrated a strong seasonality with maximum concentrations in winter. Across the study period, fine particle mass decreased, whereas ultrafine particle number was unchanged. The proportion of ultrafine particles below 0.03 microm diameter increased compared with the proportion of other particles. During the study, concentrations of SO2 and CO also decreased, whereas the concentration of NO2 remained unchanged. The data were analyzed using Poisson regression techniques with generalized additive modeling (GAM) to allow nonparametric adjustment for the confounders. Both the best single-day lag and the overall association of multiple days fitted by a polynomial distributed lag model were used to assess the lag structure between air pollution and death. Mortality increased in association with level of ambient air pollution after adjustment for season, influenza epidemics, day of week, and weather. In the sensitivity analyses, the results proved stable against changes of the confounder model. We saw comparable associations for ultrafine and fine particles in a distributed lag model where the contribution of the previous 4 to 5 days was considered. Furthermore, the data suggest a somewhat more delayed association of ultrafine particles than of fine particles if single-day lags are considered. The associations tended to be stronger in winter than in summer and at ages below 70 years compared to ages above 70 years. Analysis of the prevalent diseases mentioned on death certificates revealed that the overall association for respiratory diseases was slightly stronger than for cardiovascular diseases. In two-pollutant models, associations of ultrafine and fine particles seemed to be largely independent of each other, and the risk was enhanced if both were considered at the same time. Furthermore, when the associations were summed for the six size classes between 0.01 and 2.5 microm, the overall association was clearly stronger than the associations of the individual size classes alone. Associations were observed for SO2, NO2, and CO with mortality despite low concentrations of these gases. These associations disappeared in two-pollutant models for NO2 and CO, but they remained stable for SO2. The persistence of the SO2 effect was interpreted as artifact, however, because the SO2 concentration was much below levels at which effects are usually expected. Furthermore, the results for SO2 were inconsistent with those from earlier studies conducted in Erfurt. We conclude that both fine particles (represented by particle mass) and ultrafine particles (represented by particle number) showed independent effects on mortality at ambient concentrations. Comparable associations for gaseous pollutants were interpreted as artifacts of collinearity with particles from the same sources.

Adolescent↗
PubMed1999

Increases in heart rate during an air pollution episode.

This paper assesses whether air pollution increases resting heart rates in 2,681 men and women aged 25-64 years who participated in the MONICA (monitoring of trends and determinants in cardiovascular disease) Augsburg cohort. Increases in heart rate were observed during the air pollution episode in January 1985 compared with non-episode days adjusted for cardiovascular risk factors and meteorologic parameters. Consistently, heart rates were also elevated at high concentrations of sulfur dioxide, total suspended particulates, or carbon monoxide. Acceleration in heart rates indicates an altered autonomic control of the heart in association with air pollution, which may contribute to the observed health effects in association with air pollution.

Adult↗
PubMed1999

Synthesis and sulfatase inhibitory activities of (E)- and (Z)-4-hydroxytamoxifen sulfamates.

We report the development of (E)- and (Z)-4-hydroxytamoxifen sulfamates as estrone sulfatase inhibitors, potential therapeutic agents for the treatment of breast cancer. Both compounds competitively inhibit estrone sulfatase isolated from rat liver with apparent Ki of 35.9 microM for (E)-4-hydroxytamoxifen sulfamate and an apparent Ki of > 500 microM for the (Z) isomer.

Animals↗
PubMed1999

Analytic approach to the design of transverse gradient coils with co-axial return paths.

Transverse gradient coils with co-axial return paths offer reduced acoustic noise compared with standard cylindrical gradient coils, due to local force balancing, and can also easily be made to have a length to diameter ratio that is less than one. Analytic expressions for the magnetic field and vector potential generated by this type of coil are described here, along with a formula for calculating the coil inductance. It is shown that these expressions allow the implementation of powerful analytic methods of coil design, as well as the incorporation of active magnetic screening. It is also demonstrated how the mathematics specifies the best parameters to use when designing coils with small numbers of elements. A head gradient coil for use at 3.0 T has been designed using the analytic approach described here. The process of coil design and construction is outlined and the performance of the coil in comparison with a similar standard cylindrical coil is described.

Brain↗
PubMed1999

[Arthrodesis of the talocalcaneal joint in adults. Indications, procedure, outcome].

Affections of the rear-foot-complex may occur because of various etiologies and show differing pathogenetic patterns. Besides posttraumatic changes, the rheumatoid arthritis, primary disorders and neurologic complications are registered. Biomechanically the hindfoot-complex is characterised by the joint play of ligamentous, bony and tendineal structures. Referring to diagnostics the clinical and radiologic examination are predominant. In the literature there is no uniform opinion concerning the therapeutic algorithm. The arthrodesis as a surgical procedure is commonly used, nevertheless important differences may be stated with regard to the choice of the osteosynthesis or the number of the joints to be fused. We present biomechanical models, diagnostic examinations and operative procedures in this context. Our own results of patients who underwent surgical interventions involving joints of the lower rear-foot using the Kitaoka hindfoot-score are demonstrated.

Adult↗
PubMed1999

Intravascular ("intimal") epithelioid angiosarcoma: clinicopathological and immunohistochemical analysis of three cases.

Angiosarcomas are rare malignant mesenchymal tumours, characterized morphologically by anastomosing vascular channels lined by atypical and proliferative active endothelial cells. An epithelioid cytomorphology of tumour cells is often seen focally in angiosarcoma, whereas purely epithelioid angiosarcomas are rare. Although angiosarcomas show a vascular differentiation they are almost never confined to pre-existing blood vessels. We describe three cases of intravascular epithelioid angiosarcoma arising in the carotid artery of a 60-year-old man, in the infrarenal part of the abdominal aorta and both renal arteries of a 69-year-old woman, and in the abdominal aorta of a 68-year-old man. In all cases malignant tumour tissue was found incidentally after disobliteration of thrombosed vessels. Histologically, purely epithelioid angiosarcoma composed of solid sheets of epithelioid tumour cells was seen; immunohistochemistry confirmed the endothelial differentiation of neoplastic cells. The reported cases show that angiosarcoma can occasionally arise within a pre-existing vessel.

Aged↗
PubMed1999

Serum leptin is associated with serum uric acid concentrations in humans.

This cross-sectional study aimed to evaluate the relationship between leptin and the cluster of abnormalities often referred to as the metabolic syndrome. The serum leptin concentration, body mass index (BMI), percent body fat, total fat mass (FM), waist and hip circumference, waist to hip ratio (WHR), prevalence of hypertension, and triglyceride (TG), lipoprotein, and uric acid concentration were determined in 86 type 2 diabetic (n = 59) and healthy (n = 27) subjects. Multiple regression analyses showed that the estimates of total body obesity (BMI, percent body fat, and total FM), sex, and serum uric acid concentration are independently associated with the serum leptin concentration. The finding of a positive correlation between serum leptin and uric acid levels suggests that leptin could be a pathogenic factor responsible for hyperuricemia in obesity.

Adipose Tissue↗
PubMed1999

Elevated serum leptin concentrations in type 2 diabetic patients with microalbuminuria and macroalbuminuria.

Leptin levels are elevated in end-stage renal disease, suggesting an impairment of renal leptin degradation. The present study aimed to determine whether leptin levels are also elevated in patients with earlier stages of renal disease, ie, microalbuminuric and macroalbuminuric nephropathy. A total of 60 subjects were assigned to two study groups. Group A contained 10 type 2 diabetics with macroalbuminuria, 10 type 2 diabetics with normoalbuminuria, and 10 healthy control subjects. Group B contained 10 type 2 diabetics with microalbuminuria, 10 type 2 diabetics with normoalbuminuria, and 10 healthy controls. The subgroups of both study groups were matched for sex and body fatness. In group A, macroalbuminuric diabetic patients had higher serum leptin levels than the normoalbuminuric diabetics (11.90 +/- 2.98 v 4.13 +/- 0.92 ng/mL, P < .002) and control subjects (4.78 +/- 1.37 ng/mL, P < .006). In group B, microalbuminuric diabetics had higher serum leptin levels than the normoalbuminuric diabetics (21.16 +/- 5.80 v8.74 +/- 1.89 ng/mL, P < .04) and control subjects (10.06 + 3.00 ng/mL, P < .06). In both groups A and B, creatinine clearance was inversely correlated with the serum leptin level after adjusting for body fat. In conclusion, serum leptin levels are elevated in type 2 diabetic patients with microalbuminuria and macroalbuminuria, suggesting that renal leptin degradation is already impaired in the early stages of renal disease.

Adipose Tissue↗
PubMed1999

Changes of hemostasis, endogenous fibrinolysis, platelet activation and endothelins after percutaneous transluminal coronary angioplasty in patients with stable angina.

OBJECTIVES: This study investigated parameters of endogenous fibrinolysis, activation of coagulation and platelets, and endothelin levels before and after elective percutaneous transluminal coronary angioplasty (PTCA) in patients with stable coronary artery disease (CAD). BACKGROUND: Abrupt vessel closure is a serious short-term complication after PTCA and is often unforeseeable. Detailed insight into the effect of PTCA on hemostasis, platelets and the release of vasoconstrictive substances, which are among the mainly discussed mechanisms of abrupt vessel closure, is needed to enhance the safety of coronary intervention. METHODS: Plasma levels of markers of platelet activity, coagulation, endogenous fibrinolysis and endothelins were determined in 20 patients with stable CAD undergoing elective PTCA. The blood specimens were drawn before, immediately after, 1 h after intervention and on the next morning. RESULTS: All patients showed an initially uncomplicated PTCA. Regarding the efficacy of anticoagulation after receiving 15.000 IU heparin during PTCA, two groups were compared. In eight patients with ineffective anticoagulation production of thrombin and platelet activation directly after and 1 h after PTCA was significantly higher compared with 12 patients with effective anticoagulation. Despite the strong activation of coagulation, only a low fibrinolytic response could be observed. Endothelins rose significantly after PTCA in both groups but stayed longer on higher levels in patients with distinct thrombin generation. Three of the eight patients without sufficient heparin treatment suffered abrupt vessel closure. CONCLUSIONS: Initially uncomplicated dilation of coronary arteries leads to systemically measurable activation of coagulation and platelets in patients with ineffective doses of heparin and release of endothelins in all patients. Therefore, individual adjustment of anticoagulation and platelet inhibition in combination with effective antivasospastic substances are needed in every patient before, during and after initially uncomplicated PTCA to prevent this serious complication.

Aged↗
PubMed1999

The effect of aging on pars compacta of the substantia nigra in rhesus monkey.

This aim of this study was to re-evaluate the types of neurons present in pars compacta of the substantia nigra in the rhesus monkey, and then to determine the effects of aging on the morphology of both the neurons and neuroglial cells. The substantia nigra was therefore examined in Golgi impregnated material, in sections labeled with antibodies to tyrosine hydroxylase and to GABA, and in tissue embedded in plastic for light and electron microscopy. Three types of neurons were encountered: (1) large multipolar neurons with prominent Nissl bodies, (2) bipolar neurons that are medium sized and spindle-shaped, with Nissl bodies confined to the poles of the deeply indented nuclear envelopes, and (3) small multipolar cells with sparse Nissl substance. The large and medium neurons are believed to be dopaminergic and the small neurons GABA-ergic. With age, all of the neurons accumulate lipofuscin, especially the small multipolar neurons. In addition, Marinesco bodies appear within the nuclei of the large multipolar neurons. The dendrites are most severely affected by age; many of them lose organelles and their cytoplasm can become filled with vacuoles, membranous whorls, and dense bodies. In old monkeys many of the astrocytes have inclusions and in the neuropil there is a striking increase in the number of astrocytic processes. Also large spheroids appear. These appear to be derived from astrocytes and they have a core of dense granular material surrounded by a paler peripheral zone of cytoplasm from which processes can extend. Most of the oligodendrocytes have dense inclusions in their cytoplasm and many of the myelin sheaths break down. Microglial cells can become enormously swollen by phagocytosed material. Although both neurons and neuroglial cells are affected by age, no entities that could be construed to be dying neurons were encountered.

Aging↗
PubMed1999

Protective effect of insulin against hypoglycemia-associated counterregulatory failure.

Antecedent hypoglycemic episodes reduce the counterregulatory neuroendocrine response to hypoglycemia. The role of insulin in the mechanism responsible for the antecedent hypoglycemia causing subsequent counterregulatory failure has not been elucidated. We performed antecedent hypoglycemic clamps (56 mg/dL) lasting 2 h with differing degrees of hyperinsulinemia, which were followed by 6-h stepwise hypoglycemic clamps (76-66-56-46 mg/dL) on the next day. Experiments were carried out in 30 young, healthy men. Fifteen of these subjects were tested on 2 occasions. On 1 occasion the antecedent hypoglycemia was induced by insulin infusion at a rate of 1.5 mU/min x kg (low insulin-ante-hypo); on the other occasion the insulin infusion rate was 15.0 mU/min x kg (high insulin-ante-hypo). Both sessions were separated by at least 4 weeks, and their order was balanced across subjects. The remaining 15 subjects (control group) received the same stepwise hypoglycemic clamp as the other subjects, but without antecedent hypoglycemia. During the stepwise hypoglycemic clamp, the counterregulatory increases in ACTH, cortisol, and norepinephrine were significantly blunted after the low insulin-ante-hypo (P < 0.01, P < 0.05, and P < 0.05, respectively) but not after the high insulin-ante-hypo (P = 0.12, P = 0.92, and P = 0.19, respectively) compared to that in the control group. The cortisol, norepinephrine, and glucagon responses were greater after the high than after the low insulin-ante-hypo (all P < 0.05). In conclusion, the present study clearly demonstrates that even a single episode of mild hypoglycemia reduces neuroendocrine counterregulation 18-24 h later. Insulin has a moderate protective effect on subsequent counterregulation.

Adult↗
PubMed1999

Supraphysiological hyperinsulinemia acutely increases hypothalamic-pituitary-adrenal secretory activity in humans.

Hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis in association with hyperinsulinemia is frequently found in patients with type 1 and type 2 diabetes mellitus and in subjects with abdominal adiposity. We questioned whether insulin could cause HPA axis activation and, if so, whether this insulin action may arise at the adrenal level or at a central (i.e. hypothalamic-pituitary) level. Experiments lasting for 6 h each were done in 30 lean healthy men. In 15 men, insulin was infused at a rate of 1.5 mU min(-1) kg(-1). Plasma glucose concentration was held constant during an euglycemic clamp session and was decreased stepwise in a hypoglycemic clamp session. The sequence of the 2 clamp sessions was random, and a 4-weeks recovery period was allowed between the two sessions. The protocol was essentially the same in another 15 men, with the exception that insulin was infused at a rate of 15.0 mU min(-1) kg(-1). During the euglycemic clamp sessions, we found plasma ACTH levels to increase only in the high-, but not in the low-insulin group (group by time interaction, P < 0.01); serum cortisol levels were greater in the high than in the low-insulin group (P < 0.02). In the hypoglycemic clamp sessions, plasma ACTH levels increased in the same pattern in the 2 groups; serum cortisol was greater in the high than in the low-insulin group at the beginning of the clamp (plasma glucose approximately 4.1 mmol/L; P < 0.05). Our results demonstrate that insulin acutely stimulates the HPA secretory activity in humans. The pattern suggests an effect of insulin at both peripheral and central levels of the HPA axis.

Adrenal Glands↗
PubMed1998

[Pseudohyperthyroxinemia in endemic sprue--reversibility with a gluten-free diet].

HISTORY: An increased concentration of free T3 (fT3) with normal TSH was repeatedly measured in a 58-year-old man with diarrhoea. Hyperthyroidism was diagnosed and he was treated with thyrostatic drugs. INVESTIGATIONS: Referred to our clinic, fT4 concentration, determined by routine ELISA, was found to be raised to 33.9 pmol/l, while fT3 and TSH levels were within normal limits. But the equilibrium-dialysis method gave a normal serum level also for fT4. Gastroscopy suggested coeliac disease, confirmed histologically. TREATMENT AND COURSE: The symptoms quickly improved on a gluten-free diet and the fT4 level returned to normal values even on routine measurement. CONCLUSION: The raised fT4 level with non-suppressed TSH was only revealed as a false finding by special non-routine laboratory methods. The reversibility and the close time relationship of the reported laboratory data with the clinical manifestations of the concomitant coeliac disease strongly suggested that changes in serum in the course of the latter disease played a role in these misleading laboratory results. An interference of coeliac disease with some laboratory tests has been previously described.

Celiac Disease↗
PubMed1998

Hepatocyte growth factor enables enhanced integrin-cytoskeleton linkage by affecting integrin expression in subconfluent epithelial cells.

Hepatocyte growth factor (HGF) exerts mitogenic and motogenic effects in different cell types. In the epithelial cell line mHepR1 we found that HGF induced pronounced alterations in cell morphology and promoted cell adhesion and spreading. To analyze the mechanisms how HGF affects these integrin mediated functions we studied the physical linkage of integrins with the cytoskeleton. First we found that HGF increased the expression of different integrin subunits in subconfluent cells and influenced the distribution of integrins on the cell surface. To address the physical association of integrins with the cytoskeleton we analyzed Triton X-100-extracted cell fractions using flow cytometry. Here we show that cultivation of the cells with HGF for 24 h prior to integrin cross-linking significantly enhanced the cytoskeletal anchorage of integrins. To further find out whether HGF directly induces an integrin-cytoskeleton link without subsequent cross-linking we added HGF to suspended cells but failed to detect cytoskeletally immobilized integrins in the detergent-insoluble cell fraction which could be related to the absence of a calcium response induced by HGF. Overall, the results indicate that HGF promotes the physical linkage of integrins to the cytoskeleton which requires additional stimulation of integrins.

Animals↗
PubMed1998

Mutation of BCL-6 gene in normal B cells by the process of somatic hypermutation of Ig genes.

Immunoglobulin (Ig) genes are hypermutated in B lymphocytes that are the precursors to memory B cells. The mutations are linked to transcription initiation, but non-Ig promoters are permissible for the mutation process; thus, other genes expressed in mutating B cells may also be subject to somatic hypermutation. Significant mutations were not observed in c-MYC, S14, or alpha-fetoprotein (AFP) genes, but BCL-6 was highly mutated in a large proportion of memory B cells of normal individuals. The mutation pattern was similar to that of Ig genes.

Adult↗
PubMed1998

Fetal hemoglobin in starvation ketosis of young women.

Ketones can reactivate the production of fetal hemoglobin (HbF) in vitro and in vivo. A reactivation of HbF by ketones, which are generated during starvation, remains largely speculative. Therefore, we investigated HbF in 31 women with anorexia nervosa or bulimia, using both of these as models of intermittent starvation ketosis. For comparison, we also studied 42 female control subjects matched for age. beta-Hydroxybutyrate levels were higher in patients than in controls (460 +/- 90 v 110 +/- 20 mumol/L; P < .0001). We correlated beta-hydroxybutyrate, metabolic, and hematologic parameters with HbF. HbF was measured with high pressure liquid chromatography. The data were analyzed with logistic regression analysis. An elevated HbF fraction (> 0.87%) was observed four times as often in patients than in controls (29% v 7%, P = .01). After adjustment for age, we found HbF elevations associated with beta-hydroxybutyrate levels (P = .005). No other correlations between the various metabolic/ hematologic parameters and HbF were significant. In conclusion, beta-hydroxybutyrate generated in starvation is associated with increased levels of HbF. Thus, unrestrained lipolysis can produce beta-hydroxybutyrate in sufficient quantities to induce a clinically measurable amount of HbF. These findings suggest that intermittent ketosis might also explain some increases of HbF in type 1 diabetes and pregnancy.

Adolescent↗