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Biomedical subjects

S Rogde

Publications and source records attributed to S Rogde.

23 records · Page 2Linked to original sources

The C8A and C8B loci are closely linked on chromosome 1.

Close linkage was demonstrated between the loci governing the polymorphisms of complement component C8 alpha-gamma (C8A) and beta (C8B). Both C8 loci were linked to the chromosome 1 marker loci PGM1 and Rh. The distance between the two C8 loci and PGM1 appeared identical in males and females. A female/male ratio of 1.6 was observed between the two C8 loci and Rh. No evidence for linkage between the C8 loci and Fy was found. Preliminary results of this study were presented at the Eighth International Workshop on Human Gene Mapping, Helsinki, August 1985 (Rogde et al. 1985b).

Chromosomes, Human, Pair 1↗

Clivus epidural hematoma: a case report.

An acute traumatic epidural hematoma extending from the odontoid process to the dorsum sella is described. The mechanism for the formation of an extradural hematoma in this unusual location seems to be related to age and a severe hyperflexion injury.

Brain↗

Genetic polymorphism of complement component C8.

Extensive genetic polymorphism of complement component C8 was demonstrated by isoelectric focusing of serum or plasma samples followed by immunoblotting procedures. Using these methods, we could detect both alpha-gamma (C81) and beta (C82) chain polymorphisms in the same gel. Two-dimensional (2D) electrophoresis of C8 immunoprecipitates was used to obtain further information of the C8 patterns. Evidence was obtained that the C81 polymorphism resides in the structural gene of the C8 alpha chain. Both C8 systems show autosomal, chiefly codominant inheritance, and the distribution of phenotypes agrees with the Hardy-Weinberg equilibrium. Our findings suggest at least five different alleles in the C81 system; the gene frequencies of the two most common ones, C81*A and C81*B being 0.59 and 0.39, respectively. In C82 we found evidence for at least three codominant alleles, the gene frequencies for the two most common ones, C82*B and C82*A being 0.94 and 0.05, respectively. In addition, family studies disclosed the existence of a null allele, C82*Q0.

Alleles↗

Brain lesions in alcoholics. A neuropathological study with clinical correlations.

Among 8735 autopsies performed during a 5-year period at Ullevål Hospital in Oslo there were 70 cases of Wernicke's encephalopathy (0.8%) and 152 cases of alcoholic cerebellar atrophy (1.7%). Cerebellar atrophy was found in 26.8% of all examined alcoholics. Twenty-two of the cases with Wernicke's encephalopathy were active (acute and subacute) and 48 were inactive (chronic). Examination of the clinical records showed that stupor and coma were the dominating symptoms in active cases. A pure Korsakoff's psychosis with a selective memory defect was present in about one-third of the cases with inactive encephalopathy while the remaining had more or less pronounced global dementia ("alcoholic dementia"). It is suggested that inactive Wernicke's encephalopathy is the main underlying lesion both in Korsakoff's psychosis and "alcoholic dementia" but that additional lesions are present in the latter group. The brain weight in 545 male alcoholics was compared with that of 586 controls. Cases with non-alcoholic brain lesions were excluded from both groups. In alcoholics the brain weight was significantly lower than in controls in all age groups below 70 years. The mean weight difference was 31 g. The study thus confirmed the existence of a generalized alcoholic brain atrophy.

Aged↗