Search PubMed⌕ Search

Biomedical subjects

M Vogt

Publications and source records attributed to M Vogt.

At least 217 records · Page 12Linked to original sources
PubMed1982

Analgesia, development of tolerance, and 5-hydroxytryptamine turnover in the rat after cerebral and systemic administration of morphine.

Morphine HCl (10 micrograms/0.5 microliter) was injected into the right striatum, the caudal aqueduct and the region of the nucleus raphe magnus of the rat. Turnover of 5-hydroxytryptamine (5-HT) in the brain was assessed by fluorimetric estimation of 5-hydroxyindol-3-ylacetic acid following the administration of probenecid. Injection into the right striatum (a region containing 5-HT terminals) increased 5-HT turnover in the right, but not in the left striatum or in the anterior medulla. The pain threshold was unaltered. Injection into the aqueduct accelerated 5-HT turnover in the anterior medulla, but the striata and spinal cord showed no such change. Analgesia was pronounced. Injection of morphine into the region of the nucleus raphe magnus analgesia and increased 5-HT turnover in the posterior medulla and the spinal cord. The action on the cord must have been the result of the stimulation of cells in the raphe. The effects of the local injections of morphine on 5-HT turnover were antagonized by systemic naloxone (1-2 mg/kg) in all the regions studied. When morphine was administered subcutaneously three times a day for five days, tolerance developed to the analgesic effect of morphine (7mg/kg). However, tolerance to its acceleration of 5-HT turnover was only seen in the spinal cord, not in striatum or anterior and posterior medulla. When morphine was withdrawn, its effects on analgesia and 5-HT turnover in the spinal cord recovered simultaneously. The results emphasize the likely part played by the descending serotoninergic pathway in the analgesic effect of morphine.

Animals↗
PubMed1982

Analysis of the env gene of a molecularly cloned and biologically active Moloney mink cell focus-forming proviral DNA.

A biologically active molecular clone of BALB/Moloney mink cell focus-forming (Mo-MCF) proviral DNA has been reconstructed in vitro. It contains the 5' half of BALB/Moloney murine leukemia virus (Mo-MuLV) DNA and the 3' half of BALB/Mo-MCF DNA. The complete nucleotide sequence of the env gene and the 3' long terminal repeat (LTR) of the cloned Mo-MCF DNA has been determined and compared with the sequence of the corresponding region of parental Mo-MuLV DNA. The substitution in the Mo-MCF DNA encompasses 1,159 base pairs, beginning in the carboxyl terminus of the pol gene and extending to the middle of the env gene. The Mo-MCF env gene product is predicted to be 29 amino acids shorter than the parental Mo-MuLV env gene product. The portion of the env gene encoding the p15E peptide is identical in both viral DNAs. There is an additional A residue in the Mo-MCF viral DNA in a region just preceding the 3' LTR. The nucleotide sequence of the 3' LTR of Mo-MCF DNA is similar to that of the 5' LTR of BALB/Mo-MuLV DNA with the exception of two single base substitutions. We conclude that the sequence substitution in the env gene is responsible for the dual-tropic properties of Mo-MCF viruses.

Animals↗
PubMed1981

[On the treatment of carcinoma of the thyroid (author's transl)].

Treatment of carcinoma of the thyroid includes, in addition to possible total surgical removal of thyroid and tumour tissue, obligatory radio-iodine treatment as well as administration of thyroid hormone in high dosage. Patients with anaplastic carcinoma as well as those with differentiated carcinoma which has broken into vessels or capsule or metastasized, are additionally given percutaneous radiation treatment. Cumulative survival rate for papillary thyroid carcinoma, treated according to this schema, was for women 95% after three years, 83% after five and 53% after ten years. Corresponding survival rates in men were 93%, 78% and 20% respectively. Rates for follicular thyroid carcinoma in women were 87% at three years, 75% at five and 50% at ten years. In men corresponding figures were 94, 77 and 50%. Dividing patients with differentiated thyroid carcinoma (210) into various risk groups, those with papillary and follicular carcinoma manifesting at an age under 45 years had a better prognosis than that after 45 years. Worst prognosis was with anaplastic thyroid carcinoma, when survival rates at one, three and five years were 41, 28 and 18%, respectively.

Adenocarcinoma↗
PubMed1981

Mapping, in the rat central nervous system, of morphine-induced changes in turnover of 5-hydroxytryptamine.

1. It is known that the full clinical effect of morphine is not seen if those neurones of the central nervous system which contain 5-hydroxytryptamine (5-HT) have been inactivated. Morphine increases 5-HT turnover in brain and cord, and the present work is an attempt at mapping the sites at which turnover is accelerated. 2. The degree of interaction at various sites of the C.N.S. was measured by the increment in the content of 5-hydroxyindol-3-yl acetic acid (5-HIAA) elicited by morphine in rats pre-treated with probenecid. The effect was produced by as little as 3.5 mg morphine hydrochloride/kg; for the sake of convenience this dose was doubled in most experiments. Pre-treatment with probenecid was not necessary for the effect, but a minimum interval of 90 min between injection of morphine and analysis of the brain was essential. 3. Morphine did not act indiscriminately on all 5-HT neurons, as seen by the fact that the increment in 5-HIAA formation was independent of the density of 5-HT neurones in the tissue. Nor was there any relation between basal 5-HT turnover of a region and the size of its response to morphine. 4. Highly reactive sites were found in dorsal cord, medulla, superior colliculi, substantia nigra, thalamus, hypothalamus, amygdala and striatum. Cortical areas were less responsive, but with large differences among themselves. Hippocampus, central grey, olfactory bulb, cerebellum and white matter had lower or negligible increases in 5-HT turnover. There was no increase in the turnover of the (non-neural) 5-HT of the pineal gland. 5. The relation of the reactive sites to their content in endogenous opioids and to the probable localization of the pharmacological actions of morphine is discussed.

Animals↗
PubMed1980

[Decompensated liver cirrhosis caused by galactosemia in a 52-year-old man].

A 52-year-old oligophrenic man hospitalized for esophageal hemorrhage had histologically proven liver cirrhosis and died from massive rehemorrhage. As a neonate he had survived severe jaundice, had had delayed psychomotor development and remained severely retarded. At age 15 years, bilateral cataracts had been excised and from 18 to 25 years he had had occasional grand mal seizures. The triad oligophrenia, liver cirrhosis and cataracts, prompted suspicion of galactosemia. Deficiency of galactose-1-phosphate uridyltransferase was demonstrated in blood and post mortem tissue. At autopsy, liver cirrhosis and esophageal varices were confirmed and unilateral chronic pyelonephritis, bilateral nephrolithiasis and testicular atrophy were found. There was not brain pathology. The patient appeared to be the oldest nondiagnosed galactosemic and the first male patient in whom hypogonadism was documented.

Galactosemias↗
PubMed1979

The influence of cerebral 5-hydroxytryptamine on catalepsy induced by brain-amine depleting neuroleptics or by cholinomimetics.

1 Catalepsy was produced in rats and mice by the subcutaneous injection of either tetrabenazine or the butyrophenone U-32,802A (4'-fluoro-4-{[4-(p-fluorophenyl)-3-cyclohexen-1-yl]amino} butyrophenone hydrochloride). Catalepsy was evaluated by the duration of total immobility on a vertical grid.2 Pretreatment with p-chlorophenylalanine (PCPA) reduced the intensity of catalepsy by 50% or more, whereas its time course remained the same.3 5-Hydroxytryptophan (5-HTP), 10 mg/kg, enhanced the catalepsy induced by U-32,802A or tetrabenazine, provided it was administered soon (45 min) after the neuroleptic; injections at 90 min had no effect. Otherwise untreated rats given this dose of 5-HTP behaved normally on the grid.4 The anticataleptic effect of PCPA was reversed by 5-HTP.5 Measurable changes in 5-hydroxytryptamine (5-HT) metabolism in the rat forebrain accompanied the modification of catalepsy by 5-HTP and PCPA.6 Methysergide (5 mg/kg) given 30 min before the neuroleptics to either mice or rats reduced the catalepsy, assessed 2.5 h after the methysergide. It also prevented the increase in neuroleptic-induced catalepsy following 5-HTP, 10 mg/kg.7 Tryptophan, like 5-HTP, increased the catalepsy seen in mice after U-32,802A and tetrabenazine, and increased the production of 5-hydroxyindol-3-ylacetic acid in the forebrain.8 In the rat, intracerebroventricular injection of physostigmine produced catalepsy which was not modified by methysergide or PCPA but was abolished by atropine. Similarly, in the mouse, catalepsy induced by the subcutaneous injection of pilocarpine was abolished by atropine but not affected by either methysergide or 5-HTP.9 Atropine greatly reduced the catalepsy induced by U-32,802A and tetrabenazine but lowered striatal homovanillic acid (HVA) only after U-32,802A. D,L-DOPA, 20 mg/kg, diminished the cataleptogenic effect of both neuroleptics and raised striatal HVA.10 The results support the view that there is a facilitating or permissive action of 5-HT-containing neurones on neuroleptic-induced catalepsy.

Animals↗
PubMed1979

Genome organization of retroviruses. VI. Heteroduplex analysis of ecotropic and xenotropic sequences of moloney mink cell focus-inducing viral RNA obtained from either a cloned isolate or a thymoma cell line.

The genome of a recombinant murine leukemia virus capable of inducing focal areas of morphological alteration in mink lung fibroblasts was studied by heteroduplex analysis. The dual-tropic recombinant virus was isolated from a thymoma cell line (Th16.3) and is referred to as BALB/Moloney mink cell focus-inducing virus (BALB/Mo-MCF virus). The nucleic acid sequences of RNA from virions obtained from either a thymoma cell line (Th16.3) or a clonal isolate (BALB/Mo-MCF81) were compared with the genomes of ecotropic and xenotropic viruses. The following inferences were drawn (i) A single nonhomologous region (substitution loop alpha) of about 0.7 kilobase was observed in a heteroduplex formed between Moloney murine leukemia virus complementary DNA (cDNA) and BALB/MoMCF81 RNA. This nonhomology region was mapped between 1.71 and 2.40 kilobases from the 3' end of the genome. (ii) The predominant class of heteroduplexes formed between virion RNA obtained from the thymoma cell line (Th16.3) and Moloney murine leukemia virus cDNA showed a substitution loop similar to that observed with the RNA obtained from a cloned isolate, BALB/Mo-MCF81. However, there were other molecules with additional regions of nonhomology. (iii) Heteroduplexes formed between NZB xenotropic RNA and ecotropic Moloney murine leukemia virus cDNA exhibited four major nonhomology regions extending 0.75 to 1.46, 2.0 to 2.8, 3.6 to 4.3, and 7.4 to 7.9 kilobases from the 3' end of the genome. (iv) The MCF-specific substitution loop alpha (1.71 to 2.40 kilobases) appeared as a duplex region when NZB xenotropic RNA was hybridized to cDNA transcripts synthesized by virions obtained from thymoma cell line Th16.3. The position of the other substitution loops observed in a heteroduplex formed between NZB xenotropic RNA and Moloney murine leukemia virus cDNA was not affected. (v) Heteroduplexes formed between xenotropic BALB virus 2 cDNA and NZB xenotropic RNA demonstrated a large degree of nucleic acid sequence homology. Of the 29 heteroduplexes examined, 24 appeared to be homoduplexes, and in the remaining 5 heteroduplexes only one region of nonhomology located between 3.2 and 3.8 kilobases from the 3' end of the genome could be identified. Hybridization of BALB virus 2 xenotropic RNA to NZB xenotropic cDNA followed by digestion with single-strand-specific nuclease S1 showed an 80% sequence homology.

Animals↗
PubMed1979

Production of catalepsy and depletion of brain monoamines by a butyrophenone derivative.

1 The cataleptic and monoamine-depleting effects of a butyrophenone derivative (4'-fluoro-4-[[4-(p-fluorophenyl)-3-cyclohexen-1-yl]-amino]-butyrophenone hydrochloride, U-32, 802A) were studied in rats and mice and compared with those of tetrabenazine. 2 Catalepsy was evaluated by means of a modified grid test which allowed the repetition of the test in the same animal several times without affecting the results. Both drugs produced a dose-related cataleptic state of similar time course. 3 Like tetrabenazine, U-32, 802A induced a large reduction in the content of 5-hydroxytryptamine, dopamine and noradrenaline in different parts of the brain, with a concomitant elevation in the metabolites 5-hydroxyindol-3-yl acetic acid and homovanillic acid. The time courses of the catalepsy and the reduction in brain monoamines were very similar. 4 The activity of U-32, 802A suggested that the drug, although chemically a butyrophenone, might act primarily at the presynaptic organelle for storage of monoamines in a way similar to tetrabenazine.

Animals↗