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The aim of this work was the determination of apolipoprotein(a) [Lp(a)] in the patients three months after the onset of ischaemic stroke. A group of 56 patients was investigated. Stroke was diagnosed as caused by atherosclerotic changes in main cerebral arteries in 32 patients and in 11 by changes in cervical arteries. In 13 persons a lacunar stroke was recognised. The mean Lp(a) level and the median value were significantly higher in the group of patients after stroke as compared with 45 controls. A more frequent occurrence of Lp(a) level over 30 mg/dl considered as pathological was observed more often in the patients. No correlation was seen between Lp(a) and the resistance of LDL to oxidation nor between Lp(a) and the amount of products of LDL oxidation in vitro.

The aim of this work was the evaluation of low density lipoprotein (LDL) susceptibility to oxidation in the survivors of ischaemic stroke. The investigations were performed in 65 individuals at least three months after the onset of acute symptoms. In 24 patients stroke was caused by alterations in main cerebral arteries, in 19 by considerable narrowing of carotid artery, in 15 by alterations in small cerebral arteries with often accompanying hypertension and/or diabetes (lacunar stroke) and in 7 by embolism of cardiac origin in individuals with cardiac arrhythmia and coronary artery disease. The control group comprised 25 age matched persons without pathological symptoms. Plasma lipids and apolipoprotein B levels were determined as well as two antioxidants: alpha-tocopherol level and superoxide dismutase activity. The evaluation of lipid peroxidation was performed by determining thiobarbituric acid reacting substances (TBARS) and lipid peroxides (LPO) increase after 5 hours oxidation of isolated LDL in vitro in the presence of copper ions. The level of IgG directed against modified LDL was also evaluated. In the patients decreased HDL cholesterol level was observed as well as increased apolipoprotein B. In the group of thrombotic strokes high triglycerides were observed. alpha-tocopherol level was decreased in the group of cerebral strokes. The amounts of oxidation products did not differ between the whole group of patients after stroke and the controls. A significant increase concerned only the group of lacunar strokes. The evaluation of LDL susceptibility to oxidation in patients after stroke by measuring absorption at 234 nm and determining the time period necessary to the onset of intensive LDL oxidation will be the subject of a separate publication.

Wilson's disease is an autosomal recessive disorder characterized by inability to excrete copper, and manifests by hepatic, neurologic or/and psychiatric symptoms. The therapy is available if diagnosis is made in time. The hepatic form of the disease is rarely recognized in Poland. The authors describe two patients with Wilson's disease who developed acute hepatic failure leading to death, in the first case within few months, in the second within few weeks. The diagnosis was established in the terminal stage of the disease and attempts of treatment were uneffective.

During the last 12 years 4258 amniocenteses were performed between the 12th and 20th week of gestation (including 323 early amniocenteses carried out before 15th week). In every case, cytogenetical examination was performed and concentration of AFP was determined. In cases with elevated AFP level electrophoresis of AchE izoenzymes was performed. The results of the tests enabled us to calculate laboratory standard values of AFP in the amniotic fluid for 12th to 20th weeks of gestation. In 22 of 44 pregnancies with Down's syndrome the value of AFP concentration was below the 25th percentile of the laboratory normal value. In 5 of 10 pregnancies with Edward's syndrome AFP level exceeded significantly the 75th percentile of the laboratory norm. In two cases it was due to coexisting spina bifida and in one case due to omphalocele. In 28 amniotic fluid samples AFP concentration exceeded normal level and electrophoresis of AchE revealed additional band. In 26 cases increased values of AFP were due to open neural tube defect in the fetus: 13 cases of anencephaly and 13 cases of spina bifida; in the remaining two other cases omphalocele was found.

Nine patients with newly diagnosed Wilson's disease were treated with zinc sulphate for 12 months. Polish preparation Zincteral was administered in doses of 200 mg 4 times daily. The neurological status has improved in five cases. No adverse reactions of zinc sulphate were observed. The results were compared with the therapeutic effect, obtained in the group of 10 patients who received d-penicillamine (Cuprenil-Polfa) 1.0-1.5 g daily from the very beginning. In three cases drug was discontinued due to adverse reactions. In remaining seven cases, in five evidence of the clinical improvement of the neurological status was observed, but in one case during 12 months of observation progressing deterioration was noticed. Neurological state of one patient remained unchanged.

GGT (gammaglutamyl-transpeptidase) activity and HDL (high density lipoprotein) cholesterol were assayed in the group of 67 alcohol addicts entering a detoxication treatment after a period of an intensive drinking. The same assays were repeated following 1-2 and 6-12 days of the abstinence. Both markers have shown high values in about 80% of patients immediately after the period of heavy drinking. HDL cholesterol concentration was decreasing more rapidly than GGT activity. Both markers may be of a practical value. However, it seems that GGT activity as the less dynamic test is better for detection of heavy drinkers whereas HDL cholesterol assay will be useful for abstinence monitoring in the course of alcohol withdrawal. It shows well short-term fluctuations reflecting abstinence and its relapses. Both assays are simple and inexpensive.

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)

In 27 patients with reliably diagnosed Wilson's disease treated previously with penicillamine (Cuprenil, Polfa) for from 10 months to 12 years penicillamine was withdrawn due to various adverse effects and replaced with zinc sulphate (Polish preparation Zincteral) in doses of 200 mg 4 times daily for 12 months. The neurological status was improved in 6 cases. No adverse effects of zinc sulphate were observed.