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Biomedical subjects

S Hansen

Publications and source records attributed to S Hansen.

At least 289 records · Page 16Linked to original sources
PubMed1982

Parkinson's disease: a disorder due to nigral glutathione deficiency?

Amino acid analysis of autopsied human brain showed reduced glutathione (GSH) content significantly lower in the substantia nigra than in other brain regions. GSH was virtually absent in the nigra of patients with Parkinson's disease. Oxidative degradation of L-DOPA and dopamine in vivo may generate reactive oxygen species (hydrogen peroxide, superoxide, hydroxyl radical, or singlet oxygen) which can damage membranes and other cellular components. Since GSH is an important natural antioxidant, a deficiency of GSH in the substantia nigra could make this region vulnerable to oxidative injury. If confirmed, the hypothesis that loss of nigrostriatal dopaminergic neurons results from a regional GSH deficiency could have important therapeutic implications for the management and prevention of Parkinson's disease.

Adult↗
PubMed1982

Participation of the lateral midbrain tegmentum in the neuroendocrine control of sexual behavior and lactation in the rat.

Electrolytic lesions were placed in the ventrolateral midbrain and their effects on lactational performance and sexual behavior were assessed. The neuronal injury, situated just above the lateral tip of the substantia nigra in the lateral tegmentum, caused an immediate impairment in lactational performance as measured by the weight gain of the offspring, and interfered also with the hormonal induction of sexual receptivity and proceptivity. In similarly lesioned male rats, mounting behavior was virtually absent, but nociceptive thresholds and locomotor activity in the open-field remained unaltered. It seems likely that some, but not all, of these effects were due to disruption of a pathway carrying somatosensory information relevant for lactation and sexual behavior.

Animals↗
PubMed1982

On the role of the dorsal mesencephalic tegmentum in the control of masculine sexual behavior in the rat: effects of electrolytic lesions, ibotenic acid and DSP 4.

The work presented here concerns the way in which the dorsal midbrain tegmentum (DMT) participates in the control of sexual behavior. It was first established that electrolytic DMT lesions accelerate mating in the male rat, primarily by abbreviating the post-ejaculatory interval. Since the effective lesions were accompanied by decreases in the in vitro synaptosomal uptake of [3H]noradrenaline (NA) in hippocampus and hypothalamus, the behavioral effects of DSP4 (which elicits degeneration in NA nerve terminals derived primarily from the locus coeruleus) were examined. The long-term behavioral consequences of DSP4, however, were to decrease copulatory rate despite substantial NA denervation of brain and spinal cord. Ibotenic acid-induced neuronal degeneration in the DMT, on the other hand, accelerated copulatory behavior while leaving NA innervation of hippocampus and hypothalamus unaffected. The magnitude of the behavioral effect in ibotenic acid-treated rats was less than that induced by electrolytic DMT lesions. It is tentatively suggested on the basis of these-experiments that DMT cell bodies may form part of a system regulating sexual arousal mechanisms, whilst activity in a non-adrenergic fiber system running in the dorsal tegmental bundle may be required for active inhibition of sexual behavior after ejaculation. In additional experiments it was found that DSP4 treatment of female rats produced negligible effects on sexual behavior, estrous cyclicity and processes related to lactation.

Amines↗
PubMed1982

Effects of ibotenic acid-induced neuronal degeneration in the medial preoptic area and the lateral hypothalamic area on sexual behavior in the male rat.

It is well known that electrolytic lesions in the medial preoptic area (MPOA) and the lateral hypothalamic area (LHA) seriously impair masculine sexual behavior in the rat. We here report that bilateral infusions of the neurotoxin, ibotenic acid (IBO), in the MPOA were as effective as electrolytic lesions in eliminating copulation whereas no behavioral effects were detected following similar infusions in the LHA. Histological examination of MPOA and LHA following IBO exposure revealed extensive degeneration of neuronal cell bodies with little evidence of non-specific damage. Also, immunohistochemical studies suggested that the serotonergic innervation of the MPOA remained largely intact in spite of IBO treatment; similarly, the damage inflicted by IBO in LHA on tyrosine hydroxylase-immunoreactive fibers in the medial forebrain bundle was insignificant. These data suggest that: (i) the functional integrity of MPOA nerve cell bodies is necessary for the expression of sexual behavior, and (ii) disruption of mating produced by electrolytic LHA lesions is due to disruption of medial forebrain bundle fiber systems. Behavioral observations of non-copulating males suggested that the MPOA injury did not interfere with all aspects of their sexual interaction with the estrous female; rather, they appeared specifically unable to perform the reflexive pelvic thrust pattern normally associated with mounting. We here report, however, that the ability to perform mounts with pelvic thrusts was temporarily restored in the vast majority of MPOA-injured males by the i.p. administration of the ergot derivative, lisuride. About 50% of these MPOA-damaged males even ejaculated, often after a low number of intromissions and short ejaculation latencies. On the other hand, injections of naloxone (an opiate receptor antagonist) failed to activate mounting in MPOA-lesioned or castrated rats. On the basis of these findings the possible ways in which steroid hormone-sensitive brain areas might interact with monoamine-containing pathways are discussed.U

Animals↗
PubMed1982

Influence of phage T3 and T7 gene functions on a type III(EcoP1) DNA restriction-modification system in vivo.

The ocr+ gene function (gp 0.3) of bacteriophages T3 and T7 not only counteracts type I (EcoB, EcoK) but also type III restriction endonucleases (EcoP1). Despite the presence of recognition sites, phage DNA as well as simultaneously introduced plasmid DNA are protected by ocr+ expression against both the endonucleolytic and the methylating activities of the EcoP1 enzyme. Nevertheless, the EcoP1 protein causes the exclusion of T3 and T7 in P1-lysogenic cells, apparently by exerting a repressor-like effect on phage gene expression. T3 which induces an S-adenosylmethionine hydrolase is less susceptible to the repressor effect of the SAM-stimulated EcoP1 enzyme. The abundance of EcoP1 recognition sites in the T7 genome is explained by their near identity with the T7 DNA primase recognition site.

DNA Replication↗
PubMed1982

Human CSF GABA concentrations: revised downward for controls, but not decreased in Huntington's chorea.

gamma-Aminobutyric acid (GABA) concentrations were measured in CSF specimens from two large groups of control subjects, one without neurological or psychiatric disease, and one with a variety of neurological disorders not known to involve altered GABAergic function in brain. CSF GABA was also measured in patients with Huntington's chorea and in patients with other choreiform disorders. GABA was measured in CSF by a modification of the ion exchange-fluorometric method that featured use of a relatively large cation exchange column, and a markedly decreased quantity of sulfosalicylic acid for deproteinization of CSF. Mean BABA concentrations in CSF were 87 and 77 nmol/liter for neurologically normal and abnormal control subjects, 82 nmol/liter for the Huntington's chorea patients, and 105 nmol/liter for patients with other forms of chorea. The mean concentration of homocarnosine was not reduced in CSF of Huntington's chorea patients as compared with controls. Mean CSF GABA concentrations found in control subjects were less than half the lowest control means previously reported. These low values are attributable in part to a reduction in on-column hydrolysis of conjugated forms of GABA in CSF, which can be produced by excessive sulfosalicylic acid, and in part to improved chromatographic resolution of GABA from other unknown o-phthalaldehyde-reactive compounds in CSF. Analysis of free GABA in CSF does not appear useful for diagnosis of suspected Huntington's chorea, nor as a possible predictive test for persons genetically at risk for Huntington's chorea.

Carbon Radioisotopes↗
PubMed1982

Concentrations of GABA and other amino acids in CSF from torsion dystonia patients.

Free amino acid concentrations were measured by conventional amino acid analysis, and gamma-aminobutyric acid (GABA) concentrations were determined, by an ion-exchange fluorometric technique, in CSF specimens from 16 patients with torsion dystonias and in CSF from a large number of control subjects. The mean CSF GABA concentration of the dystonia patients (97 +/- 11 nmol/L) did not differ significantly from the means for CSF GABA in two groups of adult control subjects. Mean concentrations of all commonly determined amino compounds were normal in the CSF of torsion dystonia patients, except for ornithine, which was modestly but significantly reduced.

Adolescent↗
PubMed1982

Anterior horn cell dysfunction in Alzheimer's disease.

Electrophysiological studies were undertaken on 29 patients with Alzheimer's Disease. A reduction in the number of functioning motor units was found in the extensor digitorum brevis muscle. The electrophysiological parameters of the motor unit potentials were increased compared to control values. Four of seven muscle biopsies showed abnormalities ranging from mild to severe. The results suggest dysfunction in the lower motor neurone in this disease.

Aged↗
PubMed1982

A double-blind clinical trial of isoniazid in Huntington disease.

Isoniazid (INH) was given to nine patients with Huntington disease (HD) in a double-blind, placebo-controlled crossover trial. In an earlier open trial, three of six patients had improved, and one of them remained improved after 7 years on INH. Only one patient benefited in the present trial. All patients excreted small amounts of hydrazine in their urine while taking INH, and it is this INH metabolic that elevates GABA content in brain. GABA concentrations were markedly increased in CSF during INH therapy. Lack of clinical improvement in most HD patients despite elevation of brain GABA content suggests that in the minority who are benefited, INH may be acting by some mechanism other than increase of GABAergic neuronal function.

Adult↗
PubMed1982

Histochemistry of the striated musculature in the opossum and human oesophagus.

The striated muscle component of the opossum oesophagus has been studied for fibre type as revealed by histochemical stains for succinic acid dehydrogenase, adenosine triphosphatase, nicotinamide adenine dinucleotide dehydrogenase and after staining with the periodic acid-Schiff reagent. The reactions were compared to those obtained in a single human oesophagus. In both species, the striated muscle consisted of Type II fibres throughout, but at the pharyngeal end, some Type I fibres passed into the muscularis externa from the lower pharyngeal constrictor and extended for a short distance along the oesophagus. Differences in the reactions to these histochemical stains indicated that the Type II fibres of the opossum oesophageal musculature are subtype A, while those of the human are subtype B.

Adenosine Triphosphatases↗
PubMed1982

Interaction of bacteriophage T7 with Hind-endonuclease-producing Haemophilus influenzae Rd cells.

In order to test the influence of the restriction endonucleases of Haemophilus species on in vivo DNA restriction of phage T7 and its close relative T3 as well as to determine whether the anti-DNA restriction effect of the T7 and T3 ocr+ gene is also expressed in Haemophilus cells, we studied the interaction of T7 and T3 with Haemophilus influenzae serotypes Rd and Rc and Haemophilus parainfluenzae. The results show that T7 and T3 are unable to infect these bacterial species because they do not absorb to the cells.

Adsorption↗
PubMed1982

A quantitative assessment of reinnervation in the polyneuropathies.

The severity of denervation and the extent of compensatory reinnervation in a number of neuromyopathies was investigated using our computer-assisted motor unit counting and subtraction techniques. Patients with the chronic neuropathies of diabetes mellitus, renal failure and alcoholism, the acute neuropathy of the Guillain-Barré syndrome, and the neuronopathies of motor neuron disease and Alzheimer's disease were studied. Reinnervation in the uremic and alcoholic neuropathies was poor, and considerably less than that found in diabetic neuropathy. In general, the neuronopathies showed better reinnervation than the chronic neuropathies. In the acute neuropathy of the Guillain-Barré syndrome, reinnervation continued over periods of up to 7 years from the onset of the illness. Within this group some patients showed poor reinnervation, whereas in others we found that all of the electrophysiological parameters studied returned to normal, with concomitant remodeling of previously large motor units to normal size as reinnervation progressed.

Alzheimer Disease↗
PubMed1982

A prospective randomized controlled trial of cefoxitin versus clindamycin-aminoglycoside in mixed anaerobic-aerobic infections.

Ninety patients infected with presumed penicillin resistant anaerobes were randomized to cefoxitin or clindamycin-aminoglycoside. Cefoxitin was comparable to clindamycin-aminoglycoside in cures of intestinal associated, 16 of 26 versus 11 of 21, and pelvic infections, 20 of 20 versus 22 of 23. Cefoxitin-resistant facultative-aerobic gram-negative rods were found in 16 of 45 patients with intestine associated infection. Probable antibiotic associated nephrotoxicity was less frequent in the patients in the cefoxitin group, zero of 46 versus seven of 44, p less than 0.05, although a false creatinine elevation was noted more frequent, seven of 46 versus one of 44, p less than 0.05. Infections causing failure in patients in the cefoxitin group more frequently contained cefoxitin resistant gram-negative rods at the time of failure than did infections causing failure in those in the clindamycin-aminoglycoside group that contained gentamicin-resistant gram-negative rods, eight of eight versus zero of eight, p less than 0.001. Cefoxitin may be adequate therapy for many patients with mixed anaerobic/aerobic infections; however, the addition of an aminoglycoside may be prudent in those with known, or suspected, cefoxitin resistant gram-negative rods.

Adolescent↗
PubMed1981

Cystinylglycine in plasma: diagnostic relevance for pyroglutamic acidemia, homocystinuria, and phenylketonuria.

Cystinylglycine, recently identified as a normal small peptide in human plasma, has diagnostic importance for several genetically determined disorders. We found cystinylglycine absent from the plasma of a patient with pyroglutamic acidemia, and the peptide was either absent or greatly reduced in plasma from patients with homosyctinuria. In the latter disorder, a different small peptide replaced cystinylglycine. It was identified as the mixed disulfide of homocysteine and cysteinylglycine. The mean plasma concentration of cystinylglycine was 13.6 +/- 3.6 mumol/l in adult control subjects, and concentrations of the mixed disulfide of homocysteine and cysteinylglycine varied between 2 and 10 mumol/l in the plasma of homocystinuric patients. Failure to separate cystinylglycine from phenylalanine with many rapid amino acid analyzer systems can lead to a misclassification of persons as heterozygotes for the phenylketonuria gene when heterozygosity testing is based on the phenylalanine/tyrosine molar ratio in fasting plasma.

Autoanalysis↗