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J Hager

Publications and source records attributed to J Hager.

At least 19 recordsLinked to original sources
PubMed2005

Non-fermi-liquid behavior in quasi-one-dimensional Li0.9Mo6O17.

We present temperature dependent scanning tunneling spectroscopy data of the quasi-one-dimensional conductor Li0.9Mo6O17. The differential tunneling current in our low-temperature spectra shows a power-law behavior around the Fermi energy, which is expected for a clean Luttinger liquid. The power-law exponent is found to be 0.6. Spectra for a temperature range of 5 to 55 K can be fitted fairly well with a model for tunneling into a Luttinger liquid at the appropriate temperature. A fit with a model based on a zero bias anomaly is significantly worse compared to the Luttinger liquid model. No signature of a phase transition at T = 24 K is observed in our temperature dependent data.

Journal Article↗
PubMed2005

Initial results for urban metal distributions in house dusts of Syracuse, New York, USA.

A program of house dust sample collection and analysis has begun in Syracuse, New York, USA, in order to determine the feasibility of a geography-based exposure assessment for urban metals. The sampling program, and the protocols it employs, is described for two different types of wipe media, Ghost Wipes and Whatman Filters. Preliminary results show that strong spatial patterns of floor dust loading (mg dust per square foot) can be observed for data aggregated at a spatial scale of about 1600 m (approximately 2.5 km2). Floor dust metal concentrations were similar to those found in other urban environments, with some regional variation. The median floor dust Pb concentration was approximately 108 mg x kg(-1) for this initial data set of approximately 264 sampled residential locations, and varied from 50 to 1100 mg Pb x kg(-1).

Air Pollution, Indoor↗
PubMed2005

Haplotypes in the gene encoding protein kinase c-beta (PRKCB1) on chromosome 16 are associated with autism.

Autism is a developmental disorder characterized by impairments in social interaction and communication associated with repetitive patterns of interest or behavior. Autism is highly influenced by genetic factors. Genome-wide linkage and candidate gene association approaches have been used to try and identify autism genes. A few loci have repeatedly been reported linked to autism. Several groups reported evidence for linkage to a region on chromosome 16p. We have applied a direct physical identity-by-descent (IBD) mapping approach to perform a high-density (0.85 megabases) genome-wide linkage scan in 116 families from the AGRE collection. Our results confirm linkage to a region on chromosome 16p with autism. High-resolution single-nucleotide polymorphism (SNP) genotyping and analysis of this region show that haplotypes in the protein kinase c-beta gene are strongly associated with autism. An independent replication of the association in a second set of 167 trio families with autism confirmed our initial findings. Overall, our data provide evidence that the PRKCB1 gene on chromosome 16p may be involved in the etiology of autism.

Autistic Disorder↗
PubMed2003

Analysis of a retrieved Isola spinal system fractured in service.

A 1/4-in.diameter two-column Isola spinal system implanted in a 13-year-old girl suffering from cerebral palsy and a severe neuromuscular scoliosis of 120 degrees, was replaced 22 months after primary implantation. The system was removed due to fracture of the lower left (concave) bar, between its two cross connectors (i.e., the distal bypass connector and a transverse cross link), as a result of a postoperative infection and a subsequently developed pseudarthrosis. The retrieved implants were analyzed with the use of a multitechnique characterization procedure involving macroscopic and microscopic examination, micro-multiple internal reflectance FTIR spectroscopy, X-ray fluorescence (XRF) spectrometry, roughness measurement, and mechanical testing of the constituent material and components. Findings suggest that the spinal system failed due to in vivo loosening of a two-set screw tandem connector and subsequent overloading of the contralateral bar.

Adolescent↗
PubMed2002

The seventh prototype of the mini-spindle-pump: does it fulfill the expectations of a short-term pump?

According to recent trends to develop implantable nonpulsatile blood pumps for different function modes and times, our intention was and still is to build a Mini-Spindle-Pump for a pumping duration of about 14 days. Initial conception for this plan was the premise that the device in a mock circuit should move 4 L of water/min at a speed of 12,000 to 15,000 rpm against a pressure difference of 90 mm Hg between pump inlet and outlet. Despite the development of 6 different prototypes, this project was not realized. Under the above-mentioned conditions, the main problem of this type of blood pump, the blood trauma, could not be reduced to an adequate level, i.e., the Mini-Spindle-Pump is not a high speed pump. Therefore, a revision of the conception was necessary. The device in a mock circuit should transport 5 L of water/min at a speed of about 9,000 rpm against a pressure difference of 90 mm Hg between its inlet and outlet. Considering the implantability of the blood pump, the following measurements for its components were arrived at. The U-shaped blockformed plexiglas housing was enlarged to 120 x 40 x 40 mm (length of blood chamber 86 mm, inner diameter 27 mm), and the rotor with 5 windings was redesigned at a length of 64 mm (outer diameter 25 mm, inner diameter 6.7 mm). In a mock circuit, this 7th prototype transported with a speed of 9,000 rpm about 10 L of water/min at an afterload of 80 mm Hg. In acute animal experiments with calves up to 15 h of pumping duration, the device showed the expected efficiency. Experiments with a longer pumping duration are necessary to confirm that this prototype will fulfill the criteria of a short-term pump according to Dr. Y. Nosé's advice.

Equipment Design↗
PubMed2001

Light control of Arabidopsis development entails coordinated regulation of genome expression and cellular pathways.

An expressed sequence tag-based microarray was used to profile genome expression underlying light control of Arabidopsis development. Qualitatively similar gene expression profiles were observed among seedlings grown in different light qualities, including far-red, red, and blue light, which are mediated primarily by phytochrome A, phytochrome B, and the cryptochromes, respectively. Furthermore, light/dark transitions also triggered similar differential genome expression profiles. Most light treatments also resulted in distinct expression profiles in small fractions of the expressed sequence tags examined. The similarly regulated genes in all light conditions were estimated to account for approximately one-third of the genome, with three-fifths upregulated and two-fifths downregulated by light. Analysis of those light-regulated genes revealed more than 26 cellular pathways that are regulated coordinately by light. Thus, light controls Arabidopsis development through coordinately regulating metabolic and regulatory pathways.

Arabidopsis↗
PubMed2001

Rationale and design of the LURIC study--a resource for functional genomics, pharmacogenomics and long-term prognosis of cardiovascular disease.

BACKGROUND AND AIM: Coronary artery disease (CAD), arterial hypertension and Type 2 diabetes mellitus are common polygenetic disorders which have a major impact on public health. Disease prevalence and progression to cardiovascular complications, such as myocardial infarction (MI), stroke or heart failure, are the product of environment and gene interaction. The LUdwigshafen RIsk and Cardiovascular Health (LURIC) study aims to provide a well-defined resource for the study of environmental and genetic risk factors, and their interactions, and the study of functional relationships between gene variation and biochemical phenotype (functional genomics) or response to medication (pharmacogenomics). Long-term follow-up on clinical events will allow us to study the prognostic importance of common genetic variants (polymorphisms) and plasma biomarkers. SETTING: Cardiology unit in tertiary care medical centre in south-west Germany. STUDY DESIGN: Prospective cohort study of individuals with and without cardiovascular disease at baseline. PATIENTS AND METHODS: LURIC is an ongoing prospective study of currently > 3300 individuals in whom the cardiovascular and metabolic phenotypes CAD, MI, dyslipidaemia, hypertension, metabolic syndrome and diabetes mellitus have been defined or ruled out using standardised methodologies in all study participants. Inclusion criteria for LURIC were: German ancestry (limitation of genetic heterogeneity) clinical stability (except for acute coronary syndromes [ACSs]) availability of a coronary angiogram (this inclusion criterium was waived for family members provided that they met all other inclusion and exclusion criteria) Exclusion criteria were: any acute illness other than ACSs any chronic disease where non-cardiac disease predominated a history of malignancy within the past five years. Exclusion criteria were pre-specified in order to minimise the impact of concomitant non-cardiovascular disease on intermediate biochemical phenotypes or on clinical prognosis (limitation of clinical heterogeneity). A standardised personal and family history questionnaire and an extensive laboratory work-up (including glucose tolerance testing in non-diabetics and objective assessment of smoking exposure by determination of cotinine plasma levels) was obtained from all individuals after informed consent. A total of 115 ml of fasting venous blood was sampled for the determination of a pre-specified wide range of intermediate biochemical phenotypes in serum, plasma or whole blood, for leukocyte DNA extraction and immortalisation of B-lymphocytes. Biochemical phenotypes measured included markers of endothelial dysfunction, inflammation, oxidative status, coagulation, lipid metabolism and flow cytometric surface receptor expression of lympho-, mono- and thrombocytes. In addition, multiple aliquots of blood samples were stored for future analyses. RESULTS: A total of 3500 LURIC baseline measurements were performed in 3316 individuals between July 1997 and January 2000. The baseline examination was repeated within a median of 35 days in 5% of study participants (n = 166, including a third examination in 18 after a median of 69 days) for pharmacogenomic assessment of lipid-lowering therapy and for quality control purposes. A five-year follow-up on major clinical events (death, any cardiovascular event including MI, stroke and revascularisation, malignancy and any hospitalisation) is ongoing. The clinical phenotypes prevalent at baseline in the cohort of 2309 men (70%) with a mean age of 62 +/- 11 years and 1007 women (30%), mean age 65 +/- 10 years, were angiographically-documented CAD in 2567 (79%), MI in 1368 (41%), dyslipidaemia in 2050 (62%) with hypercholesterolaemia > or = 240 mg/dl (27%), hypertriglyceridaemia > or = 150 mg/dl (44%) and HDL-cholesterol < or = 35 mg/dl (38%) in individuals not treated with lipid-lowering agents, systemic hypertension in 1921 (58%), metabolic syndrome in 1591 (48%), Type 2 diabetes in 1063 (32%) and obesity defined by body mass index > or = 30 kg/m2 in 770 (23%). Control patients in whom CAD had been ruled out angiographically were five years younger than those with CAD (59 +/- 12 and 64 +/- 10 years, respectively; p < 0.001), twice as often females (48% compared to 25% females in the CAD group, p < 0.001) and had significantly less cardiovascular risk factors than individuals with CAD. The prevalence of specific cardiovascular risk subsets in LURIC, such as the elderly (> or = 75 years), was 375 (11%), while 213 (6%) were young adults (< 45 years) and 904 (27%) were postmenopausal women (90% of all females). A low risk status (< or = 1 out of the four traditional risk factors: dyslipidaemia, smoking, hypertension and diabetes mellitus) was identified in 314 (9%) individuals of the entire cohort (5% in CAD and 26% in controls, p < 0.001) and 97 (3%) carried none of the four risk factors (1% in CAD and 9% in controls, p < 0.001). (ABSTRACT TRUNCATED)

Cardiovascular Diseases↗
PubMed2000

Genetic variation in coronary heart disease and myocardial infarction: methodological overview and clinical evidence.

The precise molecular mechanisrms that lead to coronary artery disease (CAD) and myocardial infarction (MI) are not understood, despite a wealth of knowledge on predisposing risk factors and pathomechanisms. CAD and MI are complex genetic diseases; neither the environment alone nor a single gene cause disease, but a mix of environmental and genetic factors lead to atherosclerosis of the coronary arteries and subsequent manifestation of clinical disease. The biological complexity of atherosclerotic disease results from unknown or unpredictable interactions of many genetic and environmental factors which, by themselves, have only been partially identified. According to current knowledge, genetic variations in causative or susceptihility genes form the basis of molecular mechanisms that, together with environmental impact, lead to CAD/MI and determine its clinical course. Linkage analysis, which follows 'disease' alleles in families, or genetic association in a population of unrelated individuals are tools used in the search for chromosomal loci and candidate genes that are involved in these complex diseases. Progress in sequencing and mapping of the human genorne and efforts to identify all of the expected one million single nucleotide polymorphisms (SNPs) expected to be present in mankind will allow new approaches such as genome-wide association studies. The contribution of the current state of knowledge on genetic variation in man towards the dissection of CAD/MI as complex traits is sobering. Raised expectations with regard to the power of molecular genetic studies as compared to the traditional pathophysiological experimental approaches, lack of precise clinical phenotyping, lack of functional characterisation of gene variants, and the vast number of yet undetected genes may provide some explanation. Except for certain polymorphisms in lipid genes (i.e., apolipoprotein E [apo E]) or rare genetic variations (i.e., LDL receptor), which have a causal effect on both the intermediate (LDL-cholesterol level in plasma) and the clinical phenotypes (CAD/MI), the role of most gene polymorphisms is controversial or unknown. Despite the enormous progress in sequencing the human genome and in molecular genetic and bioinformatic techniques during the past decade, the progress in mapping and identifying genes responsible for complex traits such as CAD/MI has been modest and presents a formidable challenge to medical research in the 21st century.

Coronary Disease↗
PubMed1999

Comparison of clonidine 1 microgram kg-1 with morphine 30 micrograms kg-1 for post-operative caudal analgesia in children.

In a prospective randomized study in children, we compared caudal bupivacaine-clonidine with bupivacaine-morphine to evaluate whether clonidine can be used as an alternative to morphine in caudal anaesthesia. Caudal anaesthesia was administered in 36 children undergoing orchidopexy, hernia repair or circumcision, using 1.5 mL kg-1 bupivacaine 0.18% with either 1 microgram kg-1 clonidine (group 1) or 30 micrograms kg-1 morphine (group 2). Haemodynamic and respiratory parameters, anaesthetic requirements, recovery time and pain score were monitored for 24 h. Eleven children in group 1 and nine children in group 2 did not need any supplementary systemic analgesics throughout the 24-h observation period. Mean (+/- SD) duration of analgesia in the remaining patients was 6.3 h (+/- 3.3 h) in group 1 and 7.1 h (+/- 3.4 h) in group 2 (P = 0.43). Recovery time after anaesthesia was significantly longer in group 1 (16.6 +/- 8.8 min) than in group 2 (11.5 +/- 4.7 min) (P < 0.05). We conclude that analgesia provided by 1 microgram kg-1 clonidine added to caudal bupivacaine is comparable with that provided by 30 micrograms kg-1 caudal morphine with bupivacaine. Clonidine at this low dose did not cause respiratory depression.

Abdomen↗
PubMed1999

Isolated longitudinal rupture of the posterior tracheal wall following blunt neck trauma.

The authors report 3 female children (4, 5 and 12 years old) who suffered an isolated rupture of the posterior tracheal wall (membranous part) following a minimal blunt trauma of the neck. Such tracheal ruptures often cause a mediastinal and a cutaneous thoraco-cervical emphysema, and can also be combined with a pneumothorax. The following diagnostic steps are necessary: X-ray and CT of the chest, tracheo-bronchoscopy and esophagoscopy. The most important examination is the tracheo-bronchoscopy to visualize especially the posterior wall of the trachea. Proper treatment of an isolated rupture of the posterior tracheal wall requires knowledge about the injury mechanisms. The decision concerning conservative treatment or a surgical intervention is discussed. In our 3 patients we chose the conservative approach for the following reasons: 1) The lesions of the posterior tracheal wall were relatively small (1 cm, 1.5 cm, 3 cm) and showed a good adaptation of the wound margins. 2) No cases showed an associated injury of the esophageal wall. All of our patients had an uneventful recovery, the lesion healed within 10 to 14 days, and follow-up showed no late complications.

Child↗
PubMed1999

Theta-point behavior of diluted polymer solutions: can one observe the universal logarithmic corrections predicted by field theory?

In recent large-scale Monte Carlo simulations of various models of Theta-point polymers in three dimensions Grassberger and Hegger found logarithmic corrections to mean field theory with amplitudes much larger than the universal amplitudes of the leading logarithmic corrections calculated by Duplantier in the framework of tricritical O(n) field theory. To resolve this issue we calculate the universal subleading correction of field theory, which turns out to be of the same order of magnitude as the leading correction for all chain lengths available in present day simulations. Borel resummation of the renormalization group flow equations also shows the presence of such large corrections. This suggests that the published simulations did not reach the asymptotic regime. To further support this view, we present results of Monte Carlo simulations on a Domb-Joyce-like model of weakly interacting random walks. Again the results cannot be explained by keeping only the leading corrections, but are in fair accordance with our full theoretical result. The corrections found for the Domb-Joyce model are much smaller than those for other models, which clearly shows that the effective corrections of are not yet in the asymptotic regime. Altogether, our findings show that the existing simulations of Theta polymers are compatible with tricritical field theory, since the crossover to the asymptotic regime is very slow. Similar results were found earlier for self-avoiding walks at their upper critical dimension d(c)=4.

Journal Article↗
PubMed1999

Bactericidal activity of vancomycin in cerebrospinal fluid.

Intraventricular application of vancomycin is an effective therapeutic regimen for the treatment of shunt-associated staphylococcal ventriculitis. We examined the in vitro activity of vancomycin at high concentrations against Staphylococcus aureus ATCC 25923 and Staphylococcus epidermidis ATCC 12228 in human cerebrospinal fluid samples. Time-kill curves revealed equal efficacies for concentrations of 10, 100, and 300 microg/ml, and incubation times of 24 to 48 h were needed to achieve a 3 log(10) reduction of viable bacteria. A concentration of 5 microg/ml showed a slightly lower activity, but this difference was not significant. In an infant who was successfully treated for shunt-associated ventriculitis due to S. epidermidis by once-daily local administration of vancomycin (3 mg for 2 days and 5 mg for 4 days [0. 5 to 0.8 mg/kg of body weight]) the in vivo kill kinetics were similar to those for the in vitro results. These results support time-dose regimens that provide trough vancomycin levels of 5 to 10 microg/ml.

Adolescent↗
PubMed1999

Carotid occlusive disease: primary care of patients with or without symptoms.

Of the half-million strokes that occur each year in the United States, 20 to 30% can be directly linked to carotid occlusive disease. The degree of stenosis involving the carotid bifurcation is an important predictor of stroke risk. Asymptomatic disease may be diagnosed on routine physical exam or screening of the carotid bifurcation in patients with risk factors for ischemic strokes. Symptomatic disease includes transient ischemic attacks, stroke in evolution, and complete stroke. Duplex ultrasound scanning is the standard test for the initial evaluation of carotid artery disease. Patients undergoing surgery should also have magnetic resonance angiography or an angiogram of the carotid vessels. Stroke prevention includes lifestyle modification such as cessation of smoking, strict dietary and medical management of hyperlipidemia, diabetes, and hypertension. Antiplatelet, anticoagulant, and thrombolytic therapy can be used where indicated.

Aged↗
PubMed1998

A genome-wide scan for human obesity genes reveals a major susceptibility locus on chromosome 10.

Obesity, a common multifactorial disorder, is a major risk factor for type 2 diabetes, hypertension and coronary heart disease (CHD). According to the definition of the World Health Organization (WHO), approximately 6-10% of the population in Westernized countries are considered obese. Epidemiological studies have shown that 30-70% of the variation in body weight may be attributable to genetic factors. To date, two genome-wide scans using different obesity-related quantitative traits have provided candidate regions for obesity. We have undertaken a genome-wide scan in affected sibpairs to identify chromosomal regions linked to obesity in a collection of French families. Model-free multipoint linkage analyses revealed evidence for linkage to a region on chromosome 10p (MLS=4.85). Two further loci on chromosomes 5cen-q and 2p showed suggestive evidence for linkage of serum leptin levels in a genome-wide context. The peak on chromosome 2 coincided with the region containing the gene (POMC) encoding pro-opiomelanocortin, a locus previously linked to leptin levels and fat mass in a Mexican-American population and shown to be mutated in obese humans. Our results suggest that there is a major gene on chromosome 10p implicated in the development of human obesity, and the existence of two further loci influencing leptin levels.

Alleles↗
PubMed1998

A polymorphism in the 5' untranslated region of the human ob gene is associated with low leptin levels.

OBJECTIVE: To search the human ob gene for mutations and evaluate their role in massive obesity. DESIGN: Direct mutation screening of the gene and case-control association study. Multivariate analyses for evaluation of differences in clinical parameters. SUBJECTS: Primary mutation screening: 24 morbidly obese subjects (body mass index (BMI) > 40 kg/m2). Association study: 395 unrelated morbidly obese subjects (BMI > 40 kg/m2), 121 lean, non-diabetic control individuals, 72 women of a random sample with an average BMI 32.5 kg/m2. RESULTS: We report the finding of a DNA variant in exon 1 of the human ob gene (A --> G substitution, base + 19). This variant showed a prevalence of 62% in our study population. Association analyses under different genetic models (dominant, co-dominant, recessive) showed no significant evidence for an association of this variant with BMI. However, obese individuals homozygous for the G-allele showed significantly lower leptin concentrations compared to obese patients either heterozygous or homozygous for the A-allele after correction for BMI. CONCLUSION: Recent linkage studies have shown evidence for linkage of the hsob locus with obesity. Our study provides further evidence that a defect in the ob gene in linkage disequilibrium with the G-allele of exon 1 might be involved in obesity by affecting leptin concentrations.

Adult↗
PubMed1998

The production of the Alzheimer amyloid precursor protein (APP) in extraneuronal tissue does not increase in old age.

Alzheimer's disease (AD) is characterized by the cerebral deposition of beta-amyloid (A beta). A beta plaques also occur in the brains of healthy aged individuals, and A beta concentrations are increased in the cerebrospinal fluid (CSF) in old age. Based on results from an in vitro senescence model on human fibroblasts, it was proposed that the production of the beta-amyloid precursor protein (APP) was increased during aging. No information was available as to whether APP production was also augmented in aged humans. It was therefore the aim of the present study to analyze APP in connective tissue, skeletal muscle, peripheral blood mononuclear cells, and serum samples from young and aged healthy individuals. APP production was assessed by Northern and Western blotting. The expression of the different APP isoforms was studied by reverse transcription-polymerase chain reaction (RT-PCR) technique. The results demonstrate that APP messenger ribonucleic acid (mRNA) and protein concentrations were identical in blood and tissue samples from young and aged individuals and that there were no age-dependent changes in the APP isoform production pattern. Thus, our data strongly argue against the possibility of an altered production of APP during healthy aging and underline the point that in vitro aging models may not accurately reflect the in vivo situation.

Adult↗