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Biomedical subjects

W Maier

Publications and source records attributed to W Maier.

At least 253 records · Page 14Linked to original sources
PubMed1997

[Effects of high-strip density anti-scatter grid on image quality and radiation dose].

PURPOSE: Using a new type of a stationary high strip density grid (13/75) for plain films of the abdomen, the effect was evaluated with regard to quality and patient dose in comparison with an established moving radiographic grid (12/40). METHODS: The high strip density grid (13/75) was compared with a 12/40 grid using test objects and 100 patients per each grid type for plain films of the abdomen. The examinations were carried out via the screen-film system, speed class (SC) 400. Patients' weight, age and dose measurements were recorded. The image quality was evaluated via a multi-reader study using delineation of anatomical structures and a rating scale (score 1-5 or 1-3). RESULTS: Both measurements with test objects and patients abdominal plain films showed a decrease in radiation dose of 17% using the 13/75 grid, and 24%, respectively. The delineation of 4 out of 7 anatomical structures was slightly reduced with the new high strip density grid (maximum score reduction: 0.4), the image contrast, as well as the radiologists' subjective rating. CONCLUSION: Apart from an acceptable loss in image quality compared with the 12/40 grid, the new high strip density grid (13/ 75) enables a clear reduction in radiation dose.

Adult↗
PubMed1997

Functional promoter polymorphism of the human serotonin transporter: lack of association with panic disorder.

To probe the hypothesis of a role for a functionally relevant 44 bp insertion/deletion of the serotonin transporter promoter in the aetiopathogenesis of panic disorder, we determined the allele frequency of the variant in two samples (combined n = 158) of panic disorder patients (DSMIII-R) and compared it with its allele frequency in two ethnically matched control samples (combined n = 169). The fact that no difference could be observed (x 2 analysis) argues against a major role for this serotonin transporter promoter polymorphism in the aetiopathogenesis of panic disorder.

Alleles↗
PubMed1997

Middle ear pressure and dysfunction of the labyrinth: is there a relationship?

Relationships between middle ear pressure and non-infection-related cochleovestibular dysfunction have been suggested by several authors. According to some data, vertiginous attacks can be prevented by the insertion of a ventilation tube in patients suffering from Meniere's syndrome. The aim of our study was to investigate if the incidence of eustachian tube malfunction and pathologic middle ear pressure is frequent, and if routine implantation of ventilation tubes is reasonable in ears with dysfunctions of the labyrinth, including clinical Meniere's syndrome. So, we determined in our pressure chamber all active and passive parameters of eustachian tube function in 40 patients suffering from Meniere's syndrome, sudden sensory hearing impairment (SSHI), or vestibular neuronitis. Our results disclosed no nonrandom incidence of impaired tubal function among our patients compared to healthy control subjects. Pressure equalization was sufficient in most patients suffering from clinical Meniere's syndrome, and only one patient with vestibular neuronitis presented with a patulous tube. Our results show that impairment of vestibular or cochlear function is not regularly accompanied by eustachian tube dysfunction. Furthermore, no patient reported symptoms while pressure variation was performed. We conclude that variation of middle ear pressure does not usually play a role in the genesis of Meniere's syndrome, vestibular neuronitis, or SSHI. Thus, from our data, we cannot recommend routine implantation of tympanic ventilation tubes in patients suffering from Meniere's syndrome, vestibular neuronitis, or sudden hearing loss.

Compliance↗
PubMed1997

Model of complications of NIDDM. I. Model construction and assumptions.

OBJECTIVE: To develop a model of NIDDM for analyzing prevention strategies for NIDDM. RESEARCH DESIGN AND METHODS: A Markov type model with Monte Carlo techniques was used. Age, sex, and ethnicity of cohort was based on U.S. data. Incidence rates of complications were also based on community and population studies. RESULTS: Nonproliferative retinopathy, proliferative retinopathy, and macular edema are predicted in 79, 19, and 52%, respectively, of people with NIDDM; 19% are predicted to develop legal blindness. Microalbuminuria, gross proteinuria, and end-stage renal disease related to diabetes are predicted in 53, 40, and 17%, respectively. Symptomatic sensorimotor neuropathy and lower-extremity amputation are predicted in 31 and 17%, respectively. Cardiovascular disease is predicted in 39%. Higher rates of complications (1.1-3.0x) are predicted in minority populations. Predicted average life expectancy is 17 years after diagnosis. CONCLUSIONS: A probabilistic model of NIDDM predicts the vascular complications of NIDDM in a cohort representative of the incident cases of diabetes in the U.S. before age 75 years. Predictions of complications and mortality are consistent with the known epidemiology of NIDDM. The model is suitable for evaluating the effect of preventive interventions on the natural history of NIDDM.

Adult↗
PubMed1997

Model of complications of NIDDM. II. Analysis of the health benefits and cost-effectiveness of treating NIDDM with the goal of normoglycemia.

OBJECTIVE: To analyze the health benefits and economics of treating NIDDM with the goal of normoglycemia. RESEARCH DESIGN AND METHODS: Incidence-based simulation model of NIDDM was used. Hazard rates for complications were adjusted for glycemia using risk gradients from the Diabetes Control and Complications Trial. Treatment costs were estimated from national survey data and clinical trials. Incremental costs and benefits were expressed in present value dollars (3% discount rate). Life-years were adjusted for quality of life, yielding quality-adjusted life-years (QALYs). RESULTS: Comprehensive treatment of NIDDM that maintains an HbA1c value of 7.2% is predicted to reduce the cumulative incidence of blindness, end-stage renal disease, and lower-extremity amputation by 72, 87, and 67%, respectively. Cardiovascular disease risk increased by 3% (no effect of treating glycemia is assumed). Life expectancy increased 1.39 years. The cost of treating hyperglycemia increased by almost twofold, which is partially offset by reductions in the cost of complications. The estimated incremental cost/QALY gained is $16,002. Treatment is more cost-effective for those with longer glycemic exposure (earlier onset of diabetes), minorities, and those with higher HbA1c under standard care. CONCLUSIONS: The incremental effectiveness of treating NIDDM with the goal of normoglycemia is estimated to be approximately $16,000/QALY gained, which is in the range of interventions that are generally considered cost-effective.

Adult↗
PubMed1997

The nasopalatine duct and the nasal floor cartilages in catarrhine primates.

The nasal floor structures in catarrhine primates have been studied on the basis of histological serial sections of older fetuses of Presbytis, Hylobates, Gorilla, Pan, Pongo and Homo. For outgroup comparisons, sections of the strepsirhine Daubentonia and the platyrrhine Callimico are presented; in these taxa the nasal floor cartilages are intimately connected not only with the nasopalatine duct (STENO) but also with the persisting vomeronasal organ (JACOBSON). Whereas the vomeronasal organ has disappeared as a functioning sensory organ in catarrhines (occasional embryonic vestiges are reported), the nasopalatine duct is retained in cercopithecoids, hylobatids and in Gorilla; in Pan, Pongo and Homo at least remnants of the duct and of the associated cartilages are preserved. The systematic meanings of these findings have been discussed.

Animals↗
PubMed1996

Fragile-X carrier females: evidence for a distinct psychopathological phenotype?

The present study examined 35 mothers (29 premutation carriers) of children with fragile-X syndrome in measures of intelligence and psychiatric disorders by comparing them with two control groups: a) 30 mothers of children in the general population and b) 17 mothers of non-fra-X retarded children with autism. Premutation carriers had a higher frequency of affective disorders than mothers from the general population. Preliminary data indicate that normally intelligent premutation carriers of the fra-X genetic abnormality have a similar frequency of affective disorders (DSM-III-R criteria [APA, 1987]) than mothers of autistic children. Neither carriers of the premutation nor carriers of the full mutation in the fra-X group obtained a diagnosis of the schizophrenia-spectrum (schizophrenia, schizophreniform disorder, and schizoaffective disorder). Carriers of the fra-X full mutation had considerably lower IQ than carriers of the fra-X premutation. There was a negative correlation between length of CGG repeats and IQ which failed to reach significance in both groups of fra-X carriers. Psychiatric morbidity was not restricted to carriers of the fra-X full mutation only but was also present in normal intelligent premutation carriers. Furthermore the age of onset of psychiatric morbidity in both groups of mothers of fra-X children as well as the group of mothers with autistic children was much earlier than the age when mental retardation had been diagnosed in their children. Increased psychosocial burden of raising a developmentally retarded child and/or feelings of guilt of being a fra-X carrier can therefore not fully explain our findings (three-fold higher frequencies of affective disorders compared to mothers from the general population).

Adult↗
PubMed1996

Systematic screening for mutations in the 5'-regulatory region of the human dopamine D1 receptor (DRD1) gene in patients with schizophrenia and bipolar affective disorder.

A possible dysregulation of dopaminergic neurotransmission has been implicated in a variety of neuropsychiatric diseases. In the present study we systematically searched for the presence of mutations in the 5'-flanking region of the dopamine D1 receptor (DRD1) gene. This region has previously been shown to contain a functional promoter [Minowa et al., 1992: Proc Natl Acad Sci 89:3045-3049; Minowa et al., 1993: J Biol Chem 268:23544-23551]. We investigated 119 unrelated individuals (including 36 schizophrenic patients, 38 bipolar affective patients, and 45 healthy controls) using single-strand conformation analysis (SSCA). Eleven overlapping PCR fragments covered 2,189 bp of DNA sequence. We identified six single base substitutions: -2218T/C, -2102C/A, -2030T/C, -1992G/A, -1251G/C, and -800T/C. None of the mutations was found to be located in regions which have important influence on the level of transcriptional activity. Allele frequencies were similar in patients and controls, indicating that genetic variation in the 5'-regulatory region of the DRD1 gene is unlikely to play a frequent, major role in the genetic predisposition to either schizophrenia or bipolar affective disorder.

Alleles↗
PubMed1996

Validity of the family history method in relatives of gerontopsychiatric patients.

It was the aim of the present study to evaluate the validity of the family history method in relatives of a sample of elderly subjects. A total of 201 relatives of patients and 89 relatives of control subjects were interviewed directly using the Composite International Diagnostic Interview and the Structured Interview for the Diagnosis of Dementia of the Alzheimer Type, Multi-infarct Dementia and Dementias of other Etiology. At least one relevant other could provide family history information on a respective subject. Family history information for psychiatric disorders including dementia (DSM-III-R) was neither accurate, nor sensitive (10 to 40%), but highly specific (> 95%). The sensitivity of the family history for dementia and depression increased in relation to the severity of the disorder. Relatives of patients were better informants than relatives of controls (at least for the presence of any psychiatric disorder). The use of several informants only slightly improved the sensitivity of the family history, without reducing the specificity to a significant extent. The combination of different sources of information may serve to reduce information biases. The evaluation of possible biases in future family studies is required to draw adequate conclusions from differences in familial loads.

Adult↗
PubMed1996

Systematic screening for mutations in the human serotonin 1F receptor gene in patients with bipolar affective disorder and schizophrenia.

Using single strand conformational analysis we screened the complete coding sequence of the serotonin 1F (5-HT1F) receptor gene for the presence of DNA sequence variation in a sample of 137 unrelated individuals including 45 schizophrenic patients, 46 bipolar patients, as well as 46 healthy controls. We detected only three rare sequence variants which are characterized by single base pair substitutions, namely a silent T-->A transversion in the third position of codon 261 (encoding isoleucine), a silent C-->T transition in the third position of codon 176 (encoding histidine), and an C-->T transition in position -78 upstream from the start codon. The lack of significant mutations in patients suffering from schizophrenia and bipolar affective disorder indicates that the 5-HT1F receptor is not commonly involved in the etiology of these diseases.

Base Sequence↗
PubMed1996

Human adenosine A2a receptor (A2aAR) gene: systematic mutation screening in patients with schizophrenia.

Several lines of evidence suggest an involvement of adenosine A2a receptor (A2aAR) mediated adenosinergic neuromodulation in the etiopathogenesis of schizophrenia. We therefore performed a systematic mutation scan of the complete coding region of the human A2aAR gene in a sample of 42 schizophrenic patients. We detected one rare naturally occurring receptor variant (Gly-340-Ser) and two silent mutations (405C/T and 1083C/T). To our knowledge the Gly-340-Ser substitution is the first naturally occurring molecular variant of the A2aAR identified. Determining the frequency of the three variants in 42 unrelated healthy controls, we observed a significant trend towards an overrepresentation of the 1083T variant in patients when compared to controls (p = 0.041). This trend was followed up in a large independent replication sample. However, we were not able to confirm the original trend in the second sample (p = 0.367). The Ser-340 variant was found in a single schizophrenic individual. Investigation of the patient's family revealed independent segregation between the Ser-340 variant and psychiatric illness. Our data suggest that genetically determined structural variation of the A2aAR does not play a major role in the development of schizophrenia.

Alleles↗
PubMed1996

Systematic screening for mutations in the human serotonin-2A (5-HT2A) receptor gene: identification of two naturally occurring receptor variants and association analysis in schizophrenia.

A statistically significant association between a silent mutation (102T/C) in the serotonin-2A (5-HT2A) receptor gene and schizophrenia has recently been reported in a sample of Japanese patients and healthy controls. This finding suggests that genetic predisposition to schizophrenia may be affected by a functional 5-HT2A receptor variant that is in linkage disequilibrium with 102T/C. In the present study, we have sought to identify genetic variation in the 5-HT2A receptor gene by screening genomic DNA samples from 91 unrelated subjects comprising 45 patients with schizophrenia and 46 healthy controls by using single-strand conformation analysis. We have identified four nucleotide sequence variants. Two sequence changes would result in protein alterations: a substitution of threonine by asparagine at position 25 (Thr25Asn), and a substitution of histidine by tyrosine at position 452 (His452Tyr). In order to test for a possible contribution to the development of schizophrenia, we have determined allele frequencies in extended samples of unrelated patients and healthy controls. The two amino acid substitutions are found with similar frequencies in patients and controls, indicating that the presence of these variants is not causally related to the development of schizophrenia. However, the reported association of the non-coding polymorphism 102T/C with the disease has also been detected in our sample (P=0.041, odds ratio=1.28, 95% confidence interval 1.012-1.623).

Alleles↗
PubMed1996

Dopamine D3 receptor Gly9/Ser9 polymorphism and schizophrenia: no increased frequency of homozygosity in German familial cases.

Disturbances in the dopaminergic transmission have been implicated in the etiology of schizophrenia. Recently, an association of schizophrenia with increased homozygosity of a Gly9/Ser9 polymorphism in the dopamine D3 receptor gene (DRD3) has been reported (Crocq et al., 1992; Mant et al., 1994). This finding reflected a departure from the Hardy-Weinberg equilibrium in the genotype distribution observed in schizophrenic patients. The effect was found to be at its strongest in patients with a high familial loading. In the present study, we tried to replicate this finding in a sample of 146 German patients with a DSM-III-R diagnosis of schizophrenia. All patients had a positive family history of major psychiatric disorder including 70 patients with a family history of schizophrenia. Given our sample size, we have a power of 99.8% to detect 2. deviation from the Hardy-Weinberg equilibrium of the reported magnitude. However, we found no evidence of an excess of homozygosity in our schizophrenic patients. This seems to indicate that homozygosity for the Gly9/Ser9 polymorphism at the DRD3 locus is unlikely to confer susceptibility to schizophrenia in the German population. This held true whether the psychiatric diagnoses in the affected relatives of the patient samples was established by the family history or family interview method.

Adult↗
PubMed1996

Genetic relationship between dopamine transporter gene and schizophrenia: linkage and association.

This study explores the genetic relationship between schizophrenia and the dopamine transporter gene (DAT) by a variety of methods. In a sample of 48 families--each family containing at least one nuclear family with a pair of affected siblings--we performed linkage analysis using the maximum likelihood (LOD score) method as well as sibpair analysis (identity by descent). In addition, we investigated a sample of 108 nuclear families--index case affected with schizophrenia/chronic schizoaffective disorder--for association using the haplotype relative risk method. Linkage between schizophrenia and DAT using two- and three-point linkage analysis was excluded with all disease models employed. No evidence for association between haplotypes of the VNTR-probe of the DAT and schizophrenia has been detected. Thus, a contribution of the DAT gene to the genetic diathesis of schizophrenia is unlikely in the families studied.

Adult↗
PubMed1996

Confirmation of association between expanded CAG/CTG repeats and both schizophrenia and bipolar disorder.

Recent studies have suggested that expanded CAG/CTG repeats contribute to the genetic aetiology of schizophrenia and bipolar disorder. However, the nature of this contribution is uncertain and difficult to predict from other known trinucleotide repeat diseases that display much simpler patterns of inheritance. We have sought to replicate and extend earlier findings using Repeat Expansion Detection in an enlarged sample of 152 patients with schizophrenia, 143 patients with bipolar disorder, and 160 controls. We have also examined DNA from the parents of 62 probands with schizophrenia or bipolar disorder. Our results confirm our earlier, preliminary findings of an association between expanded trinucleotide repeats and both schizophrenia and bipolar disorder. However, our data do not support the hypothesis that trinucleotide repeat expansion can alone explain the complex patterns of inheritance of the functional psychoses neither can this mechanism fully explain apparent anticipation.

Adult↗