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Biomedical subjects

J R Martin

Publications and source records attributed to J R Martin.

At least 181 records · Page 10Linked to original sources
PubMed1982

Effects of chlordiazepoxide and imipramine on maze patrolling within two different maze configurations by psychogenetically selected lines of rats.

Male rats of two lines of rats psychogenetically selected and bred for extremes in performance in shuttle box avoidance received an acute IP injection of chlordiazepoxide (CDP; 2.5, 5.0, 10.0 mg/kg), imipramine HCl (IMI: 0.33, 1.0, or 3.0 mg/kg), or vehicle. The rats were placed, 35 min after injection, in an enclosed maze with either a simple configuration with an unilluminated central arena or a complex configuration with a brightly illuminated central arena, and spontaneous maze patrolling was evaluated. Total locomotor activity during the 6-min maze test was significantly reduced by 5--10 mg/kg CDP for both RHA/Verh and RLA/Verh lines of rats in both the simple and the complex maze configurations. Treatment with 10 mg/kg CDP reduced the total explored area for both rat lines in both maze configurations. In addition, the maze area explored by RHA/Verh rats was also reduced by 5.0 mg/kg CDP for the simple configuration and by 2.5 and 5.0 mg/kg CDP for the complex configuration. Entry into the unilluminated central field of the simple maze was reduced by 5--10 mg/kg CDP only in RHA/Verh rats. In contrast, 2.5 mg/kg CDP significantly increased entry into the brightly illuminated central arena of the complex maze for the RLA/Verh rats. The doses of IMI used were without effect on the parameters of maze patrolling behavior evaluated, with the single exception that the locomotor activity of RHA/Verh rats tested in the simple maze configuration was decreased by 3.0 mg/kg IMI. The results indicate that, although the effects of CDP were generally similar for total activity and the area explored in the two psychogenetic lines investigated, there was a qualitative difference in its effect on entry into an illuminated arena.

Animals↗
PubMed1982

Primary demyelination in visna. An ultrastructural study of Icelandic sheep with clinical signs following experimental infection.

Two Icelandic sheep with clinical signs of visna appearing 6-7 years after intracerebral infection with visna virus were killed, fixed by perfusion and the central nervous system lesions examined by light and electron microscopy. Both sheep showed similar pathological changes. In the brain there was a severe periventricular inflammatory process with small foci of liquefaction necrosis and scattered small granulomas. In some areas of inflammation there was evidence of primary demyelination but it was not prominent. In the spinal cord there were focal plaques of primary demyelination. At the ultrastructural level the spinal cord lesions showed unambiguous primary demyelination with many naked axons; various stages of remyelination with peripheral type of myelin were also common. These observations indicate that the CNS lesions of visna, as seen in Icelandic sheep, fall into two categories: (a) an inflammatory process which often begins within weeks of infection and which occurs in the majority of infected animals in the absence of clinical paresis; and (b) focal demyelinating lesions of the spinal cord which are seen in sheep with clinical paresis but are uncommon in animals prior to onset of clinical signs. Both types of lesions may coexist.

Animals↗
PubMed1982

Cerebrospinal fluid immunoglobulins in sheep with visna, a slow virus infection of the central nervous system.

Icelandic sheep were injected intracerebrally with visna virus, which produces a persistent infection of the CNS accompanied by encephalomyelitis and focal demyelinating lesions. Studies were conducted on two groups of sheep, with short-term infections (25 sheep sampled 1-3 months after infection) and long-term infections (14 sheep sampled 5-6 years after infection). Quantitative determination of CSF immunoglobulin levels 5 years after infection indicated that IgM concentration was usually elevated, IgG2 was occasionally elevated and IgG1 was rarely elevated. CSF oligoclonal bands were seen in about half the sheep examined 5 years after infection. There was a correlation between high titers of CSF antiviral antibody and both elevated CSF IgM concentration and CSF oligoclonal bands. Serum/CSF IgG1 ratios indicated that the blood-brain barrier was apparently intact in long-term visna infection, consistent with intrathecal synthesis of IgM and of antiviral antibody. The alterations in CSF immunoglobulins in visna resemble those found in other persistent CNS virus infections and in multiple sclerosis.

Animals↗
PubMed1982

Spinal cord and optic nerve demyelination in experimental herpes simplex virus type 2 infection.

To produce a model of central nervous system (CNS) demyelination, three strains of herpes simplex virus type 2 (HSV-2) were injected intracerebrally into Swiss-Webster outbred mice. Animals developed pupillary abnormalities and leg weakness and, by light and electron microscopy, had focal lesions of primary demyelination in optic nerves and spinal cords. Oligodendrocytes and astrocytes in these lesions contained herpesvirus. Both mouse age and virus dose were important determinants of the rate and severity of the infectious process, as judged by mortality and clinical signs of disease. A low virus dose in older mice favored survival of neurologically abnormal mice beyond the acute stage of infection. When the MS, G, and 186 strains of HSV-2 were compared, no evidence of a major effect of virus strain on the clinical course or type of pathology was seen. This study demonstrates that HSV-2 can produce multifocal demyelination in the CNS in mice. The intracerebral route appears to be important in producing a model of more generalized demyelination unrelated to the site of injection than has been previously reported in other experimental herpesvirus infections. The possible relationship of this model to optic neuritis, neuromyelitis optica, and multiple sclerosis is discussed.

Animals↗
PubMed1982

Acetone and Butanol Production by Clostridium acetobutylicum in a Synthetic Medium.

The effect of the component concentrations of a synthetic medium on acetone and butanol fermentation by Clostridium acetobutylicum ATCC 824 was investigated. Cell growth was dependent on the presence of Mg, Fe, and K in the medium. Mg and Mn had deleterious effects when in excess. Ammonium acetate in excess caused acid fermentation. The metabolism was composed of two phases: an acid phase and a solvent one. Low concentrations of glucose allowed the first phase only. The theoretical ratio of the conversion of glucose to solvents, which was 28 to 33%, was obtained with the following medium: MgSO(4), 50 to 200 mg/liter; MnSO(4), 0 to 20 mg/liter; KCl, 0.015 to 8 g/liter (an equivalent concentration of K was supplied in the form of KH(2)PO(4) and K(2)HPO(4)); FeSO(4), 1 to 50 mg/liter; ammonium acetate, 1.1 to 2.2 g/liter; para-aminobenzoic acid, 1 mg/liter; biotin, 0.01 mg/liter; glucose, 20 to 60 g/liter.

Journal Article↗
PubMed1982

Diastereomeric fortimicin 1,2-epoxides. The preparation of the 1-deamino-2-deoxyfortimicins A and B and the 1,2-di-epi-fortimicins A and B.

The preparation of 1,2-anhydro-2',6'-di-N-benzyloxycarbonyl-1-deaminofortimicin B-4,5-carbamate (4) and its conversion to the two diastereomeric 2',6'-di-N-benzyloxycarbonyl-1-deamino-2-deoxy-1,2-epoxyfortimicin B-4,5-carbamates 7 and 13 are described. The olefin 4 was used for preparation of 1-deamino-2-deoxyfortimicin A (6d) while the beta-epoxide 13 was used for the preparation of 1,2-di-epi-fortimicin A (17b) and 2-amino-1-deamino-2-deoxy-1-hydroxyfortimicin A (19c). The in vitro antibacterial activities of 6d, 17b and 19c are reported.

Aminoglycosides↗
PubMed1982

Lethal encephalitis and non-lethal multifocal central nervous system demyelination in herpes simplex virus type 2 infections in mice.

Six-week-old Swiss-Webster mice were infected intracerebrally with a low dose of herpes simplex virus type 2 (HSV-2) and were studied by pathological, virological and immunological methods. One third of mice developed severe neurological disease and died during the first 31/2 weeks of infection, while the remaining two thirds survived this acute stage with relatively minor neurological signs. These survivors had multifocal demyelinative white-matter lesions in the CNS, and gray-matter lesions, if present, were few, small and usually minor. By contrast, groups of mice killed during the acute stage had a much greater proportion of gray-matter lesions, and these were frequently larger and more severe. Two subgroups could be identified in the acute stage. Mice with severe gray-matter disease, high virus titres, abundant viral antigen and later virus clearance had more severe neurological signs leading to death. By contrast, those destined to survive had pupillary signs alone, and pathologically had white-matter lesions of primary demyelination with minimal or no evidence of gray-matter involvement, low levels of detectable virus and earlier virus clearance. These results show that HSV-2 can produce non-lethal CNS disease in a high proportion of mice, even if infected by the intracerebral route, and that the lesions, which may be found throughout the CNS, are mainly in the white matter, and are demyelinative in type. Survivors of this infection may be useful in a search for evidence of herpes-virus persistence in the CNS, and for a role of this virus in chronic demyelinating disease.

Animals↗
PubMed1981

Herpes simplex virus types 1 and 2 and multiple sclerosis.

A hypothesis is proposed which states that multiple sclerosis (MS) is caused by herpes simplex virus type 2 (HSV-2) in persons lacking herpes simplex virus type 1(HSV-1) immunity. It is examined by comparing the epidemiology of these viruses with that of MS. The age at which HSV-2 infections are first detected, as well as the age of peak incidence are similar to those for MS. If age-specific HSV-1 immunity data from various places is compared, an inverse relationship of immunity levels with latitude is apparent, and may be related to the effects of ultraviolet irradiation on HSV-1 activation and transmission rates. Prior HSV-1 immunity, if related to subsequent risk of MS, would be protective. This hypothesis also appears to be consistent with the generalisations concerning effects of migration on subsequent rates of MS, and with certain other features of MS epidemiology.

Adult↗
PubMed1981

Effects of scopolamine, pilocarpine, and oxotremorine on the exploratory behavior of two psychogenetically selected lines of rats in a complex maze.

Rats of two psychogenetically selected lines received pretest IP injections of scopolamine hydrobromide (0.25, 1.0, or 4.0 mg/kg), pilocarpine hydrochloride (3.0, 6.0, or 12.0 mg/kg) or oxotremorine sesquifumarate (0.2, 0.4 or 0.8 mg/kg) and were subsequently placed in a complex enclosed maze of the Dashiell type that included a small, central, illuminated arena. Animals receiving pilocarpine or oxotremorine injections were pretreated with methscopolamine to counter the peripheral actions of these muscarinic cholinergic agonists. Following vehicle injections, Roman High-Avoidance rats (RHA/Verh) were significantly more active, explored more maze sectors, and required less time to activate the initial 24 different photocell units uniformly distributed throughout the maze than Roman Low-Avoidance rats (RLA/Verh). Scopolamine, pilocarpine, and oxotremorine depressed locomotor activity, reduced the explored area, and increased the time required to activate the initial 24 different photocell units within this complex maze for both RHA/Verh and RLA/Verh rats. Although the doses of scopolamine injected were approximately equally effective in both rat lines (except for total maze activity), the RHA/Verh rats exhibited significant alterations in several measures of maze patrolling after treatment with the lowest dose of pilocarpine, whereas the RLA/Verh rats did not. In contrast, most of the RLA/Verh rats exhibited very pronounced tremors following treatment with the highest dose of oxotremorine, but none of the RHA/Verh rats did. These results demonstrate that manipulation of the central cholinergic system with scopolamine, pilocarpine, or oxotremorine, despite their different pharmacological mechanisms, impair maze patrolling. Furthermore, the results suggest that the two psychogenetically bred lines of rats investigated are differentially sensitive to central cholinergic manipulation with the muscarinic receptor agonists pilocarpine and oxotremorine.

Animals↗
PubMed1981

Brain muscarinic cholinergic receptor binding in Roman high- and low-avoidance rats.

This experiment sought to determine whether the behavioral differences between the Roman high-(RHA/Verh) and low-avoidance (RLA/Verh) lines of rats could be related to differences in the number and/or affinity of brain muscarinic cholinergic receptors. The binding of the specific muscarinic antagonist 3H-quinuclidinyl benzilate to crude membrane preparations from the cerebral cortex, hippocampus and striatum was determined. There were no significant differences between the two rat lines for the number of muscarinic binding sites (Bmax) or the apparent dissociation constant (KD) as determined by Scatchard analysis of the saturation isotherms. These data indicate that the behavioral differences between RHA/Verh and RLA/Verh rats cannot be accounted for by differences in the number or affinity of brain muscarinic cholinergic receptors.

Animals↗