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Biomedical subjects

H Wehr

Publications and source records attributed to H Wehr.

At least 19 recordsLinked to original sources
PubMed2006

Differences in risk factors for dementia with neurodegenerative traits and for vascular dementia.

In 229 patients with dementia and in 144 control subjects, polymorphisms of apolipoprotein E (ApoE), low-density-lipoprotein (LDL)-receptor-related protein, alpha(2)-macroglobulin, interleukin (IL) 1beta, angiotensin-converting enzyme and of methylene tetrahydrofolate reductase genes were investigated. In plasma, antibodies against Chlamydia pneumoniae and lipids were determined. Dementia was classified as probable Alzheimer's disease (AD), probable dementia of vascular origin (VaD) and mixed dementia (MD). An association of the disease with ApoE and IL-1beta polymorphism and increased levels of LDL cholesterol were observed in AD and in MD but not in VaD.

Aged↗
PubMed2002

Dynamics of LDL oxidation in ischemic stroke patients.

OBJECTIVE: Oxidative modification of human low density lipoprotein (LDL) plays an important role in the development of atherosclerosis. The aim of this study was to evaluate the oxidative modification of LDL in the group of patients with ischemic stroke. MATERIAL AND METHODS: In the group of 43 patients 3 months after ischemic stroke and in the age and sex-matched control group, the kinetics of LDL oxidation and level of vitamin E were estimated. The susceptibility of LDL to oxidation was evaluated in isolated LDL exposed to in vitro oxidation. In 26 patients, after diet change, clinical and laboratory investigations were repeated 9 months later. RESULTS: In the patient group, susceptibility of LDL to oxidation was enhanced, lag phase was significantly shorter in comparison with the control group. After a change in diet, significant elongation of the lag phase was observed. CONCLUSION: Diet change improves LDL resistance to oxidation and may influence prognosis in stroke patients.

Aged↗
PubMed2001

Apolipoprotein E genotype, lipid levels and coronary heart disease in a Polish population group.

Genotype of apolipoprotein E has been identified in a group of randomly selected Polish subjects participating in a cross-sectional study performed within the POL-MONICA Program, the part of international study WHO-MONICA Project. The investigated group consisted of 170 persons, 92 males and 78 females aged 41-69 years (mean age 62.0+/-5.11). The observed frequency of apolipoprotein E alleles was: epsilon2 - 7.6%, epsilon3 - 81.8% and epsilon4 - 10.6%, which was similar to frequencies in the neighbouring European countries. Statistically significant lower means of total cholesterol (TC) and of low density lipoprotein cholesterol (LDL-C) levels in epsilon2 carriers and higher means of TC, of LDL-C and of triglycerides in epsilon4 carriers were observed as compared with noncarriers of respective alleles. Some nonlipid cardiovascular risk factors (hypertension (HT) and obesity) and coronary heart disease (CHD) showed a tendency to lower prevalence in the epsilon2 allele carriers as compared to noncarriers. In the epsilon4 allele carriers a tendency to higher prevalence of HT, but not of CHD was observed as compared to noncarriers of this allele.

Adult↗
PubMed2001

Familial defective apolipoprotein B-100 in a group of hypercholesterolaemic patients in Poland. Identification of a new mutation Thr3492Ile in the apolipoprotein B gene.

The prevalence of the familial defective apolipoprotein B-100 (FDB) Arg3500Gln mutation in 525 unrelated hypercholesterolaemic Polish subjects was evaluated. DNA samples were screened for FDB mutation using SSCP method. Presence of mutation was confirmed using a mismatch MspI PCR strategy. Plasma lipid levels and clinical characteristics of 13 patients identified as carriers of the mutation and of their 23 affected relatives were analysed and compared with non-affected ones. In the affected individuals a variable expression of lipid concentrations and of atherosclerosis symptoms were observed. The prevalence of FDB Arg3500Gln mutation in hypercholesterolaemic Polish subjects (3.7%) seems to be similar to the frequency reported in other Caucasian hypercholesterolaemic populations. The estimated prevalence of the mutation in general Polish population is relatively high being 1/250. The same haplotype at the apoB locus in the carriers of this mutation in Poland as in other populations from Western Europe suggests its common origin. In one hypercholesterolaemic subject a non-hitherto described mutation was identified. It consisted in C-->T transition in apoB codon 3492 leading to threonine to isoleucine substitution in 3492 position of apoB gene (Thr3492Ile).

Adult↗
PubMed2000

The level of serum lipids, vitamin E and low density lipoprotein oxidation in Wilson's disease patients.

UNLABELLED: The aim of this study was to estimate the level of lipids and of the main serum antioxidant, alpha-tocopherol (vitamin E), and to evaluate the susceptibility of low density lipoprotein (LDL) to oxidation in Wilson's disease patients. It was assumed that enhanced LDL peroxidation caused by high copper levels could contribute to the injury of liver and other tissues. The group investigated comprised 45 individuals with Wilson's disease treated with penicillamine or zinc salts and a control group of 36 healthy individuals. Lipids were determined by enzymatic methods, alpha-tocopherol by high performance liquid chromatography, the susceptibility of LDL to oxidation in vitro by absorption changes at 234 nm during 5 h and end-products of LDL lipid oxidation as thiobarbituric acid reacting substances. In Wilson's disease patients total cholesterol, LDL cholesterol and alpha-tocopherol levels were significantly lower compared with the control group. No difference in LDL oxidation in vitro between the patients and the controls was stated. CONCLUSION: enhanced susceptibility of isolated LDL for lipid peroxidation in vitro was not observed in Wilson's disease patients. One cannot exclude, however, that because of low alpha-tocopherol level lipid peroxidation in the tissues can play a role in the pathogenesis of tissue injury in this disease.

Adult↗
PubMed1995

Apolipoprotein E in alcoholics.

In 31 alcohol addicted patients entering detoxication treatment and in 14 social drinkers apolipoprotein E (Apo E) was assayed by radial immunodiffusion in the whole serum and after phosphotungstate Mg2+ precipitation. Serum Apo E level in the intoxicated individuals was increased compared with the controls. The Apo E increase was mostly due to the very low and low density (VLDL + LDL) fraction. The Apo E/cholesterol ratio in this fraction was increased. It is possible that increased Apo E concentration in VLDL contributes to their enhanced uptake by the liver.

Adult↗
PubMed1993

Acetaldehyde adducts and autoantibodies against VLDL and LDL in alcoholics.

Alcohol consumption markedly increases the hepatic output of very low density lipoprotein (VLDL), whereas it decreases the resulting low density lipoprotein (LDL) levels and apolipoprotein B. As ethylation of apoB-lysine renders LDL immunogenic and accelerates their clearance, and as alcoholics develop antibodies against acetaldehyde-protein adducts, we searched for antibodies against lipoproteins. We measured serum IgG, IgA, and IgM titers against VLDL, LDL and high density lipoprotein (HDL) in 10 non-alcoholics and 35 recently drinking alcoholics by ELISA assay. Alcoholics had higher IgG titers than non-alcoholics against VLDL and LDL; these were higher with VLDL than LDL or HDL. Using VLDL and LDL (but not HDL) from alcoholics gave the greatest response. There was no difference in IgA and IgM reactivity. To search for acetaldehyde adducts, we measured the reactivity of VLDL, LDL, HDL, and residual serum proteins against a rabbit anti P4502E1-acetaldehyde adduct IgG, which recognizes the adducts but not the unmodified proteins (except for P4502E1). ApoB-containing lipoproteins from alcoholics (and to a lesser extent non-lipoprotein proteins) reacted with anti-adduct IgG more strongly than those of non-alcoholics. The difference was striking for VLDL, less for LDL, and not detectable for HDL. This suggests that acetaldehyde reacts with apoB prior to its secretion from the liver and that the altered VLDL are partially removed prior to their conversion to LDL. In conclusion, alcoholics develop acetaldehyde adducts in apoB-containing lipoproteins, particularly VLDL. The immune response to these neoantigens could result in accelerated clearance of VLDL and LDL and decreased conversion of VLDL to LDL.

Acetaldehyde↗
PubMed1991

Serum beta-hexosaminidase and alpha-mannosidase activities as markers of alcohol abuse.

In 25-alcohol-dependent patients in whom detoxication treatment has been introduced serum total beta-hexosaminidase, thermostable beta-hexosaminidase, alpha-mannosidase and gamma glutamylotransferase (GGT) and serum high density lipoprotein (HDL) cholesterol were determined during alcohol withdrawal. The assays were also performed in a group of dependent individuals after a 1 month or longer period of abstinence. Marked increase in beta-hexosaminidase activity was observed in intoxicated patients. The activity decreased rapidly after the cessation of drinking, resembling the decrease in HDL cholesterol level in its dynamics. The alpha-mannosidase activity rise was less pronounced and its normalization was slow, similar to the GGT activity normalization rate. The rise of beta-hexosaminidase activity was mostly due to the thermostable component of the enzyme. Total beta-hexosaminidase or thermostable beta-hexosaminidase activity determinations appear to be simple and reliable markers of alcohol abuse.

Adult↗
PubMed1990

Abnormal low density lipoproteins composition in some chronic alcoholics: a possible mechanism.

Decreased plasma low density lipoproteins (LDL) cholesterol and apolipoprotein B (apo B) levels are observed in heavy alcohol drinkers. LDL composition was determined in 16 alcohol addicts immediately after a period of alcohol abuse. Cholesterol to apo B ratio in the LDL fraction was significantly higher in the alcoholic group when compared with controls. In half of them the ratio exceeded 1.75. LDL subfractionation showed that in all subjects with atypically high LDL cholesterol to apolipoprotein B ratio, most of the LDL was in the form of a light subfraction. Acetylation in vitro showed that the heavy LDL subfraction was modified to a greater extent than the light subfraction. This suggests that the low apo B levels often observed after heavy drinking may arise from enhanced removal of the heavy LDL subfraction from the bloodstream.

Acetaldehyde↗
PubMed1990

[Further steps in regional localization of the gene coding for human arylsulfatase B (ARSB): gene assignment to the section q11-qter of chromosome 5].

The structural gene coding for human arylsulfatase B (ARSB) has been assigned to chromosome 5 and then to 5p11-5qter by means of somatic cell hybridization. The somatic cell hybrids used in the present studies were derived from fusion experiments between Chinese hamster, a3 line (TK-) and human leukocytes from a patient carrying the reciprocal balanced translocation t (5;21) (q11;q22) according to the method described previously. About 90 independent hybrid clones were selected for further analysis. They were tested for the presence of human markers employing the methods routinely used. ARSB activity was checked upon as previously. Giemsa banding technique was used to identify human and hamster chromosomes in the hybrid cells. Human ARSB activity was detected in 12 hybrid clones; 6 of them appeared to be informative. Out of 78 clones negative for human ARSB, 3 containing the product of translocation, 5pter-5q11: 21q22-21qter were found. Human superoxide dismutase-1 (SOD1) activity, a marker for chromosome 21, was found in 27 clones. The informative hybrid clones both positive and negative for ARSB are presented in table I. Six informative clones retained the region 5q11-5qter as the only portion of chromosome 5 and they expressed the activity of human ARSB and hexosaminidase B (HEXB), a marker for 15q13. It seems worth-while to point out that human ARSB activity was found only in the hybrids which retained the product of the translocation carrying 5q11-5qter in high percentage of the cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Chondro-4-Sulfatase↗
PubMed1985

A case of Menkes disease cell culture examination and elastic cartilage electronmicroscopy.

A boy with clinical characteristics of Menkes disease was described. Extremely low serum copper concentration, low ceruloplasmin level and increased copper accumulation in cultured fibroblasts confirmed the diagnosis. Electronmicroscopy of elastic cartilage showed abnormalities of chondrocyte function and a derangement of extracellular substance polymerization.

Brain Diseases, Metabolic↗
PubMed1985

Low molecular weight copper binding proteins in Wilson disease.

Cultured fibroblasts deriving from Wilson disease patients were compared with the control ones in respect of copper accumulation and low molecular weight copper binding protein (metallothionein) properties. No evidence was obtained that metallothionein abnormality could be a primary cause of copper metabolism disturbances in Wilson disease. The determination of radioactivity, present in serum low molecular weight fraction 24 hours after intravenous injection of 64Cu, has been suggested as an additional tool in Wilson disease diagnosis in doubtful cases.

Copper↗