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Biomedical subjects

L Hansen

Publications and source records attributed to L Hansen.

At least 235 records · Page 13Linked to original sources
PubMed1977

Antiparkinsonian agents and long-term neuroleptic treatment. Effect of G 31.406, orphenadrine, and placebo on parkinsonism, schizophrenic symptoms, depression and anxiety.

The need for medication with anticholinergic antiparkinsonian drugs was examined in 118 schizophrenic patients under long-term neuroleptic treatment. It was found that 1) none of 18 patients under treatment with low mg potency neuroleptics (chlorprothixene, clozapine, and thioridazine) had any need for anticholinergics; 2) of 60 patients under treatment with short-acting high mg potency neuroleptics (perphenazine greater than 16 mg daily and haloperidol greater than 2 mg daily) nine patients (15%) required medication with anticholinergics, whereas 3) of 40 patients under treatment with long-acting (depot) neuroleptics, 17 (43%) had a need for anticholinergic medication; and 4) no patient factors predisposing to the need for continued antiparkinsonian treatment could be identified. In an additional double-blind cross-over study of 12 patients presenting persisting neuroleptic-induced parkinsonism, it was found that G 31.406 (a new potentially antiparkinsonian drug), compared with placebo, had an antiparkinsonian effect (P less than 0.01) as well as an antidepressant effect (P less than 0.05). G 31.406 resulted in an improvement in anxiety and schizophrenia-score in some patients. Compared with placebo, orphenadrine had a more questionable effect on parkinsonism (0.05 less than P less than 0.01) and no significant effect on mental symptoms. There were no significant differences between the effects of G 31.406 and orphenadrine.

Administration, Oral↗
PubMed1975

[The development of the dysplastic hip-joint following intertrochanteric rotating varus-osteotomy (author's transl)].

Evaluation of radiographs of 267 children with 465 intertrochanteric rotating varus osteotomies, carried out between the ages of 15 months and 14 1/2 years. The period of follow-up varied between 2 and 15 1/4 years. 1. The CCD angle on the last radiograph was normal in 77%, once more in values in 16.2%, coxa vara in 7%. 2. The AT angle was about normal only in 58.3% (0-20 degrees); it relapsed in 8.4% (over 35 degrees); in 8.8% a corrected angle did not return after retrorotation, particularly on the left. 3. The Ac angle was normal in 63.3%. 4. The CE angle corresponded to the norm in 59.1%. 5. Good late results (normal angles and shape of head) occur only in 20%. If one omits the AT condition, they rise to 40%. 6. The main causes of return of valgus appear to be: too early operation before the fifth year, mainly when disregarding the dysplastic acetabular roof, insufficient correction of the CCD angle of over 115 degrees, and technical faults. For physiologic weightbearing by the acetabular roof an AT angle of 10 appears necessary. 7. When dysplasia of the acetabular roof is present, the polyaxial correction of the proximal end of femur must be combined with acetabuloplasty or pelvic osteotomy.

Adolescent↗
PubMedDate not supplied

Glycogen synthase kinase 3 alteration in Alzheimer disease is related to neurofibrillary tangle formation.

Highly phosphorylated tau protein is the main component of paired helical filaments (PHF), which comprise the neurofibrillary tangles (NFT) in some neurons of patients with Alzheimer disease (AD). Glycogen synthase kinase 3 (GSK3) phosphorylates tau in vitro at several sites also found to be phosphorylated in PHF-tau; tau is phosphorylated at these sites in both AD and normal control (NC) brains, although the extent of phosphorylation is far greater in tau from AD. If GSK3 levels are increased in AD, then tau phosphorylation and perhaps PHF formation may occur. To quantify GSK3, blots of AD and NC brain supernatant and particulate fractions were probed with antibodies to GSK3. In particulate fractions of AD compared to NC, GSK3 alpha immunoreactivity did not increase, but in fact, decreased 40%, and GSK3 beta immunoreactivity decreased 30%. GSK3 alpha and GSK3 beta levels correlated well with each other. GSK3 levels correlated negatively with numbers of NFT.

Aged↗
PubMedDate not supplied

Abnormalities in central nervous system development in osteogenesis imperfecta type II.

Osteogenesis imperfecta (OI) type II is a perinatally lethal condition resulting from mutations in type I collagen genes. In addition to characteristic skeletal anomalies, OI type II has recently been shown to be associated with neuropathological alterations, specifically perivenous microcalcifications, and impaired neuroblast migration. In light of these findings, and because type I collagen promotes neuritic maturation both in vitro and in vivo, we sought to determine if additional central nervous system (CNS) developmental anomalies could be found in previously autopsied OI type II cases, and if specific abnormalities correlate with OI subtypes. We retrospectively studied brains of nine patients diagnosed with OI. Of these, seven were OI type II: five were OI type IIA, one was type IIB, and one was type IIC. One OI type I specimen and one OI type III brain were included for comparison, as well as five controls. The IIC brain showed hippocampal malrotation, agyria, abnormal neuronal lamination, diffuse hemorrhage, and periventricular leukomalacia (PVL). The IIB brain had white matter gliosis, PVL, and perivascular calcifications, but was normally developed. Of the five type IIA brains, two showed migrational defects with coexisting PVL and gliosis, two were normally developed with similar white matter injuries, and one was grossly normal. These findings support the contention that collagen mutations might negatively impact CNS development.

Adult↗
PubMedDate not supplied

Report on a conference on organic solvents and the nervous system.

At two scientific conferences in 1985, one in Copenhagen sponsored by the Nordic Council of Ministers and the World Health Organization (WHO), the other in Raleigh, NC, it was concluded that chronic toxic encephalopathy may develop following long-term occupational exposure to organic solvents (1,2). The terms organic affective syndrome, mild and severe chronic toxic encephalopathy were suggested for this condition describing increasing severity. In May 1990, a conference on organic solvents and the nervous system was held in Copenhagen sponsored by the Commission of the European Communities and the Danish Ministry of the Environment (3). Scientists and representatives from the governments, industries, and labour organisations from the EEC and US participated.

Animals↗