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  • 1
    Keywords: APOPTOSIS ; CELLS ; IN-VITRO ; BLOOD ; CELL ; Germany ; INHIBITION ; DISEASE ; HEART ; PATIENT ; MACROPHAGES ; SERA ; treatment ; ACID ; GLUTATHIONE ; PLASMA ; DECREASE ; cholesterol ; LDL ; LIPOPROTEIN ; PERIPHERAL-BLOOD ; OXIDATION ; cysteine ; arteriosclerosis,risk factors in hyperlipidemia,glutathione in atherosclerosis,redox status as a ris ; CORONARY-ARTERY DISEASE ; HEART-DISEASE ; N-ACETYL-CYSTEINE ; SERUM LEVELS
    Abstract: Treatment of hyperlipidemic patients with the thiol compound N-acetyleysteine (NAC) was previously shown to cause a significant dose-related increase in the high-density lipoprotein (HDL) -cholesterol serum level, suggesting the possibility that its disease-related decrease may result from a diminished thiol concentration and/or thiol/disulfide redox status (REDST) in the plasma. We therefore investigated plasma thiol levels and REDST in normo-/byperlipidemic subjects with and without coronary heart disease (CHD). The thiol level, REDST, and amino acid concentrations in the plasma and intracellular REDST of peripheral blood mononuclear cells (PBMC) have been determined in 62 normo- and hyperlipidemic subjects. Thirty-three of these subjects underwent coronary angiography, because of clinical symptoms of CHD. All groups of hyperlipidemic patients under test and those normolipidemic individuals with documented coronary stenoses showed a marked decrease in plasma thiol concentrations, plasma and intracellular REDST of PBMCs, and a marked increase in plasma taurine levels. Individual plasma thiol concentrations and plasma REDST were strongly negatively correlated with the serum LDL-cholesterol and positively correlated with the serum HDL-cholesterol level. Together with the earlier report about the effect of NAC on the HDL-cholesterol serum level, our findings suggest strongly that lower HDL-cholesterol serum levels may result from a decrease in plasma thiol level and/or REDST possibly through an excessive cysteine, catabolism into taurine. (C) 2003 Elsevier Inc
    Type of Publication: Journal article published
    PubMed ID: 14607527
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  • 2
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary A 60-year-old man is reported with idiopathic hemochromatosis and type III hyperlipoproteinemia. Regular phlebotomy therapy and fenofibrate treatment favorably influenced the disorder of iron metabolism and the lipid disease. Evidence is given that both errors of metabolism are independently inherited diseases, although the symptoms of the first (idiopathic hemochromatosis) may aggravate the expression of the second (type III hyperlipoproteinemia).
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Three probands heterozygous for a mutant of apolipoprotein AI (apo AIMarburg, Utermann et al. 1982a) were detected by screening of 2282 unrelated individuals resulting an a frequency estimate of about 1/750 in the German population. All three probands with apo AIMarburg had hypertriglyceridemia (triglyceride above 250 mg/dl) and subnormal HDL-cholesterol (below 30 mg/dl), but no other lipoprotein abnormalities. The kindreds of two probands with AIMarburg were studied. The family data are consistent with an autosomal codominant inheritance of the trait. A total of 16 heterozygous blood relatives with the mutant AIMarburg were detected in these kindreds. Analysis of the plasma lipid and lipoprotein levels in relation to the apo AI phenotype was complicated by the high prevalence of diabetes mellitus and thyroid disease in one kindred and of hyperlipidemia in both kindreds. No consistent relationship between plasma lipid and lipoprotein levels, and the mutant apo AI could be demonstrated. Instead the mutant apo AI and the dyslipoproteinemia seem to co-exist independently in these kindreds. Three sibs with the homozygous apo E-2/2 phenotype were detected in one kindred, and all three sibs had subnormal LDL-cholesterol and beta-VLDL, e.g., the lipoprotein abnormality characterizing primary dysbetalipoproteinemia. Genetic apo E phenotypes and the apo AI mutant segregated independently, indicating that the structural gene loci for apo E and apo AI are not closely linked.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract— The effects of maximal electroshock (MES) and phenytoin on metabolites and cyclic nucleotides in layers of frozen-dried cerebellum have been investigated. The four layers (molecular, Purkinje-cell rich, granular and white matter) had remarkably homogeneous distributions of P-creatine, ATP, glucose, glycogen, lactate, GABA and the cyclic nucleotides. MES caused dramatic decreases in P-creatine, ATP, and glucose at 10 s after treatment, followed by a decrease in glycogen at 30 s. Lactate levels were elevated, and GABA was unchanged. Cyclic AMP concentrations were increased at 10s and cyclic GMP at 30 s. Phenytoin modified most of the MES induced changes in all the layers, although white matter was less affected by MES and/or phenytoin. Lactate concentrations were increased by MES and these effects were not altered when phenytoin was administered. The most dramatic effects of phenytoin were on the changes in cyclic nucleotides. Cyclic AMP concentrations were elevated after MES but the values returned to normal more rapidly when phenytoin was present. The drug almost obliterated the MES induced changes in cyclic GMP. The possible relationship of cyclic nucleotide concentrations and the modulation of seizure activity is discussed.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract— Levels of glucose, lactate, GABA and cyclic nucleotides were examined in discrete layers of the cerebellum and cerebral cortex of mice following treatment with the anticonvulsant, sodium valproate, and/or the convulsant, isoniazid. The concentrations of the metabolites were essentially uniform among the layers of each region, whether from control or from drug-treated mice. Metabolite concentrations in the isoniazid-treated mice were determined either 30 min after administration (preconvulsive state), or immediatley after the onset of seizures. Glucose and lactate, two markers of energy status in the brain, were only minimally affected by drug treatment. However, the levels of GABA and cyclic nucleotides were markedly different from control values in the drug-treated animals. In the preconvulsive state, GABA levels in cerebellar layers were depressed and the cyclic nucleotides were elevated in most layers of both regions. At the onset of seizures, the reduction of GABA and the elevation of cyclic AMP in both regions was more pronounced than during the preconvulsive state. While the concentration of cyclic GMP remained elevated in the cerebellar layers at the onset of seizures, the level in the cerebral cortex returned to control values. Valproate elevated GABA in all the layers of both regions and decreased the cyclic GMP in the cerebellar layers. Generally, when valproate was administered in combination with isoniazid, it dampened the isoniazid induced changes in the metabolites. The events leading up to a seizure as well as those that sustain it may be reflected by the disparate responses of the metabolites in the cerebellum and cerebral cortex.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Journal of Organometallic Chemistry 187 (1980), S. 321-329 
    ISSN: 0022-328X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-1440
    Keywords: Apolipoprotein E ; Autoimmune hyperlipidemia ; Hepatic triglyceride lipase ; Immunoglobulin A ; Multiple myeloma ; Type III hyperlipoproteinemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We studied a 58-year-old woman with severe therapy-refractory hyperlipidemia, xanthomatosis, and multiple myeloma (immunoglobulin A, lambda light chain). The lipid disorder became evident about half a year prior to the expression of myelomatosis. Clinical symptoms were similar to those found in classical type III hyperlipoproteinemia but the underlying metabolic defect was different from the one described in this primary dyslipoproteinemia. The patient has the heterozygous apolipoprotein E3/2 phenotype and her VLDL-cholesterol/serum-triglyceride ratio is unusually low at 0.05. Evidence is given that the hyperlipoproteinemia is due to an impaired catabolism of intermediate density lipoproteins probably because of a reduced hepatic triglyceride lipase activity.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-1440
    Keywords: Acute phase reaction ; Allograft rejection ; Liver transplantation ; Serum amyloid A protein
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Serum amyloid A protein (SAA) concentrations were monitored in 12 consecutive liver transplant recipients until the 70th postoperative day. Fourteen rejection episodes were identified histologically in 42 liver biopsies of the grafts. Of 12 rejections 8 (66.7%) were characterized by pronounced simultaneous increases in SAA concentrations in plasma, the mean peak value being 16.94 ± 8.82 mg/dl (range 4.58–28.55 mg/dl) compared with a mean normal value of 0.98 ±0.42 mg/dl in healthy controls. Of 42 biopsies 28 did not show histological evidence of graft rejection. Of 25 negative biopsies 24 (96.0%) were not accompanied by a parallel SAA increase in plasma. These findings demonstrate that measurements of SAA concentrations may provide a valuable non-invasive aid in identifying acute liver allograft rejection in humans.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-1440
    Keywords: Apolipoprotein E ; Bezafibrate therapy ; Chronic hemodialysis ; Familial dysbetalipoproteinemia ; Type III hyperlipoproteinemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Two patients with severe hyperlipidemia receiving long-term hemodialysis were classified as type III hyperlipoproteinemic subjects. They are homozygous for apolipoprotein E2 and have an elevated VLDL-cholesterol/plasma-triglyceride ratio. The dyslipoproteinemia was severely aggravated by the renal failure, but careful treatment with bezafibrate was able to effectively lower elevated serum lipids. Accurate diagnosis of lipid abnormalities in patients with chronic renal failure seems to be necessary to plan appropriate therapeutic interventions and to lower the risk for accelerated atherosclerosis.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1432-1440
    Keywords: Apolipoprotein E ; Familial dysbetalipoproteinemia ; Gemfibrozil ; Simvastatin ; Type III hyperlipoproteinemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Nineteen adult patients with type III hyperlipoproteinemia (HLP) and homozygosity for apolipoprotein (apo) E2 were treated with the 3-hydroxy-3-methyl glutaryl coenzyme A (HMG CoA) reductase inhibitor simvastatin (20 or 40 mg per day) alone or in combination with the fibrate derivative gemfibrozil (450 mg per day) during a 30-week outpatient study. With the 20-mg dose (n = 19) the mean plasma cholesterol level decreased from 13.24±8.04 8.04 at baseline to 8.04±4.19 mmol/l (mean reduction 39.3%; P〈0.05), and the mean plasma triglyceride level decreased from 13.47±19.22 to 7.84±7.71 mmol/l (−41.8%; NS); this was due to a decrease in very low density lipoprotein (VLDL) cholesterol from 8.95±8.64 to 4.94±4.24mmo1/l (−44.8%; NS), a decrease in low density lipoprotein (LDL) cholesterol from 3.54±0.93to 2.25 ± 0.59 mmol/l (−36.5%; P〈0.01), and an increase in high density lipoprotein (HDL) cholesterol from 0.72±0.28 to 0.85±0.34 (+18.1%; NS). Thirteen patients were treated with 40 mg simvastatin per day. Under this regimen there was a further significant decrease in LDL cholesterol from 2.33±0.62 to 1.81±0.49 mmol/l (−22.3%; P〈0.01). In six patients who remained hyperlipidemic on monotherapy combination drug therapy with simvastatin (40 mg per day) and gemfibrozil (450 mg per day) was given. Compared to simvastatin alone the addition of gemfibrozil further lowered plasma concentrations of total cholesterol by 14.9%, VLDL cholesterol by 23.5%, and triglycerides by 17.1%, although this was not statistically significant. No patient was discontinued from single or combination drug therapy, and no severe clinical or biochemical side effects were observed. The results of this study demonstrate the usefulness of simvastatin in the therapy of type III HLP and indicate that in individual patients who remain hyperlipidemic on monotherapy combination drug therapy with both of these drugs is effective in further reducing plasma concentrations of total cholesterol, VLDL cholesterol, and triglycerides. Although no patient in this investigation developed myopathy or rhabdomyolysis, combined fibrate-HMG CoA reductase inhibitor treatment should be considered only for severe forms of hyperlipidemia and for patients who do not respond sufficiently to mon-therapy of any of these drugs.
    Type of Medium: Electronic Resource
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