PubMed HealthSearch

Biomedical subjects

V Neumann

Publications and source records attributed to V Neumann.

At least 19 recordsLinked to original sources

Mood disorders following traumatic brain injury: identifying the extent of the problem and the people at risk.

The extent of mood disorders following traumatic brain injury (TBI), and the possible risk factors, are investigated. New data are presented from a prospective study of consecutive hospital admissions. Six months post-TBI, 99 adults completed a standardized assessment of emotional state, the Wimbledon Self-Report Scale. Cognitive performance and the impact of the injury on everyday functioning were also assessed. The rate of clinically significant mood disorders (caseness) was 38%. Of the demographic or injury characteristics, only pre-injury occupational status predicted post-injury caseness. Those unoccupied pre-injury were more likely to report mood disturbance post-injury. In contrast, post-injury occupational status was not related to caseness either for the whole group or the subgroup of those previously occupied, despite the adverse effects on occupational functioning for a significant proportion of subjects. Associations were found between emotional state and cognitive and everyday functioning 6 months post-injury. Psychosocial disabilities appeared more strongly associated to mood disorders than did physical disabilities. A significant level of unmet need has been highlighted, and possible risk factors identified, which may inform the purchase and provision of TBI rehabilitation services. Follow-up data on these subjects are available and will be reported separately.

Activities of Daily Living

Immunization of pigs with a particle-mediated DNA vaccine to influenza A virus protects against challenge with homologous virus.

Particle-mediated delivery of a DNA expression vector encoding the hemagglutinin (HA) of an H1N1 influenza virus (A/Swine/Indiana/1726/88) to porcine epidermis elicits a humoral immune response and accelerates the clearance of virus in pigs following a homotypic challenge. Mucosal administration of the HA expression plasmid elicits an immune response that is qualitatively different than that elicited by the epidermal vaccination in terms of inhibition of the initial virus infection. In contrast, delivery of a plasmid encoding an influenza virus nucleoprotein from A/PR/8/34 (H1N1) to the epidermis elicits a strong humoral response but no detectable protection in terms of nasal virus shed. The efficacy of the HA DNA vaccine was compared with that of a commercially available inactivated whole-virus vaccine as well as with the level of immunity afforded by previous infection. The HA DNA and inactivated viral vaccines elicited similar protection in that initial infection was not prevented, but subsequent amplification of the infection is limited, resulting in early clearance of the virus. Convalescent animals which recovered from exposure to virulent swine influenza virus were completely resistant to infection when challenged. The porcine influenza A virus system is a relevant preclinical model for humans in terms of both disease and gene transfer to the epidermis and thus provides a basis for advancing the development of DNA-based vaccines.

Animals

Coadministration of DNA encoding interleukin-6 and hemagglutinin confers protection from influenza virus challenge in mice.

This study was conducted to investigate whether Accell gene gun coadministration of DNA encoding human interleukin-6 (IL-6) would enhance protective immune responses in mice to an equine influenza A virus hemagglutinin (HA) DNA vaccine. Mice that received HA DNA alone exhibited accelerated clearance of homologous challenge virus but were not protected from infection. In contrast, mice that received both HA and IL-6 DNA had no detectable virus in their lungs after challenge. These results strongly support the use of IL-6 as a cytokine adjuvant in DNA vaccination.

Animals

Response characteristics of cerebellar nuclear cells in the pigeon.

In birds, the output system of the cerebellum, the cerebellar nuclei, has not yet been studied electrophysiologically. Recordings from nuclear cells during electrical stimulation of the radial nerve revealed a uniform type of response consisting of an initial inhibition followed by a clear cut excitation. Responses with an initial excitation were rare. Response patterns and latencies suggest an input from Purkinje cells of the cerebellar cortex and a lack of collateral input from spinocerebellar pathways. This points to a fundamental difference from cerebellar nuclear cells in mammals, in which collateral input provides a prominent excitatory response under comparable experimental conditions.

Animals

Clozapine inhibits catalepsy induced by olanzapine and loxapine, but prolongs catalepsy induced by SCH 23390 in rats.

Loxapine (0.3 mg/kg s.c.), olanzapine (10 mg/kg s.c.) and SCH 23390 (R-(+)-chloro-2, 3, 4, 5-tetrahydro-3-methyl-5-phenyl-1-H-3-benzazepine; 1 mg/kg, s.c.), but not clozapine (10 mg/kg, s.c.), induced catalepsy in rats. Co-administration of clozapine (1, 3 and 10 mg/kg s.c.) dose-dependently inhibited loxapine-induced catalepsy. Clozapine (10 mg/kg s.c.) also prevented the induction of catalepsy by olanzapine. In addition, clozapine abolished the catalepsy induced by loxapine when it was administered after the response had fully developed. In contrast, the duration of SCH 23390-induced catalepsy was prolonged by clozapine, indicating that its anti-catalepsy effects against olanzapine and loxapine are unlikely to be caused by muscle relaxation, sedation or stimulation. Since SCH 23390-induced catalepsy is reported to be blocked by scopolamine, dizocilpine (MK-801) or 8-hydroxy-dipropylamino-tetralin, it is unlikely that muscarinic blockade, NMDA ion channel blockade and 5-HT1A receptor agonism, respectively, are involved in clozapine's action, but the mechanism by which clozapine exerts this anti-cataleptic effect remains unknown.

Animals

Transmission of swine influenza virus to humans after exposure to experimentally infected pigs.

Two people developed symptoms of influenza 36 h after collecting nasal swabs from pigs experimentally infected with A/Sw/IN/1726/88 (Sw/IN). Pharyngeal swabs from these persons tested positive for influenza virus RNA 8 days after infection. Analysis of hemi-nested polymerase chain reaction (PCR) products indicated that the hemagglutinin (HA) segments of the isolates were genetically related to the HA of Sw/IN. Four influenza A virus isolates (A/WI/4754/94, A/WI/4756/94, A/WI/4758/94, A/WI/4760/94) were recovered from a 39-year-old man and 2 (A/WI/4755/94, A/WI/4757/94) from a 31-year-old woman. The HAs of the isolates were antigenically indistinguishable from the virus used to infect the pigs. Sequence analysis of the HA genes indicated they were 99.7% identical to the HA of the virus used in the experiment. Multisegment reverse transcription-PCR proved that all of the segments originated from Sw/IN, demonstrating that transmission of swine H1N1 viruses to humans occurs directly and readily, despite Animal Biosafety Level 3 containment practices used for these experiments.

Adult

Influence of nitric oxide on transepithelial transport in toad skin: effects of cholinergic agents and morphine.

The effects induced by L-arginine (L-Arg) on the short-circuit current and potential difference of Pleurodema thaul skin were investigated. L-Arg, but not D-Arg significantly increased the short-circuit current and potential difference when applied to the serosal surface. The effects of L-Arg were antagonized by amiloride, NG-nitro-methyl-L-arginine (L-NAME) and by methylene blue. Carbachol and acetylcholine induced significant increases of both electrical parameters of the toad skin. These effects of the muscarinic cholinergic drugs were potentiated by a low concentration of L-Arg and antagonized by L-NAME or methylene blue. Carbachol and acetylcholine induced significant increases of both electrical parameters of the toad skin. These effects of the muscarinic cholinergic drugs were potentiated by a low concentration of L-Arg and antagonized by L-NAME or methylene blue. Addition of dibutyryl cyclic guanosyl monophosphate (db cGMP) or dibutyryl cyclic adenosine monophosphate (db cAMP) increased short-circuit current and potential difference. The effects of db cGMP, but not those of db cAMP were antagonized by L-NAME. The consecutive application of db cGMP and db cAMP induced additive effects. These results suggest that L-Arg increases transport in toad skin presumably acting through the formation of nitric oxide, which then stimulates cytoplasmic guanylate cyclase and leads to increased Na+ and K+ transport. The effects of L-Arg and carbachol were antagonized by acute application of morphine; however, a rebound response was observed when carbachol or noradrenaline were given after prolonged exposure of the skin to morphine, which suggests an adaptive response of the skin involving both cGMP and cAMP. Responses to both nucleotides were unchanged by morphine.

Acetylcholine

Evidence for a 5-HT1D receptor-mediated hypothermic effect of the alpha 1-adrenoceptor agonist, SDZ NVI-085, in guinea-pigs.

The alpha 1-adrenoceptor agonist, SDZ NVI-085 ((-)-(4aR,10aR)-3,4,4a,5,10,10a-hexahydro-6-methoxy-4- methyl-9-(methylthio)-2H-naphth[2,3-b]-1,4-oxazine.HCl; 1 mg/kg i.p.), decreased body temperature of guinea-pigs. Two 5-HT1D receptor antagonists, GR127935 (N-[4-methoxy-3-(4-methyl-1-piperazinyl)phenyl]-2'-methyl-4'-(5-methyl- 1,2,4-oxadiazol-3yl)[1,1-biphenyl]-4-carboxamide) and PAPP (p-aminophenylethyl-m-trifluoromethylphenyl piperazine; both compounds at 1 mg/kg i.p., -30 min) blocked this response, whilst the alpha 1-adrenoceptor blocker prazosin (1 mg/kg i.p.) and the 5-HT1A receptor antagonist, SDZ 216-525 (methyl 4-(-[4-(1,1m3-trioxo-2H-1,2-benzoisothiazol-2-yl)butyl ]-1-piperazinyl)1H- indole-2-carboxylate; 1 mg/kg i.p.) were inactive. Another alpha 1-adrenoceptor agonist, St 587 (2-(2-chloro-5-trifluoromethylphenylimino)-imidazoline; 1 mg/kg i.p.) did not alter body temperature. SDZ NVI-085-induced hypothermia in guinea-pigs is probably mediated by 5-HT1D receptors.

Adrenergic alpha-1 Receptor Antagonists

Electrotherapy.

Explore the source record for details and available documents.

Electric Stimulation Therapy

Sulphasalazine in the management of psoriatic arthritis.

There are few 'second-line' drugs available for the treatment of PSA and their use is often limited by toxicity. Thirty-nine patients with active PSA recruited from two rheumatology units were randomly allocated to either enteric-coated sulphasalazine (SASP) or placebo and followed for 24 wk. Six patients in the SASP group and 11 on placebo discontinued therapy before 24 wk. Evaluation of effect of treatment revealed significant improvements in articular index in both groups at 12 wk. By 24 wk the articular index in placebo group was still showing benefit. In addition to articular index the SASP group improved significantly in terms of visual analogue scale, duration of morning stiffness and ESR. SASP is effective in PSA but the partial clinical response to placebo indicates the importance of placebo-controlled studies in this variable disease.

Adolescent

The effect of non-steroidal anti-inflammatory drugs on faecal flora and bacterial antibody levels in rheumatoid arthritis.

The faecal flora and bacterial antibody levels of 22 patients with active rheumatoid arthritis (RA) were compared with those of 26 patients with osteoarthritis (OA) undergoing comparable treatment with non-steroidal anti-inflammatory drugs (NSAIDs), and a further 22 patients with OA who were not receiving NSAIDs. Faecal counts of Clostridium perfringens were significantly higher in the RA patient group and in those OA patients receiving NSAIDs, compared with those OA patients not taking NSAIDs (P = 0.032, P = 0.0004 respectively). Total aerobic and anaerobic counts were, however, identical in all three groups. Levels of serum IgA antibody to the alpha toxin of Cl. perfringens were higher in the RA group and in the OA group taking NSAIDs than in OA patients not taking NSAIDs (P = 0.011, P = 0.055). Serum IgG antibody to alpha toxin was higher in the RA group than in OA patients both on and off NSAIDs (P = 0.019, P = 0.0072) and also a group of normal controls (P = 0.032). These results suggest that the increased faecal counts of Cl. perfringens together with the associated increased antibody levels seen in this and previous studies are more likely to result from NSAID therapy used to treat the disease than from a disease specific change in bowel flora.

Adult

Effect of progesterone on norepinephrine release from mouse adrenergic terminals in vitro.

1. The in vitro effect of progesterone on norepinephrine (NE) release and contractile activity was analyzed in uterine horns from estrogen-primed and progesterone-primed mice. 2. Progesterone (6-10 nmol/ml) evoked the release of [3H]NE above basal levels from uterine horns in both experimental conditions, the effect of progesterone on estrogen-primed being more important than on progesterone-primed mice uterus. 3. Progesterone also increased electrically evoked [3H]NE release in estrogen-primed uterine tissue, nevertheless no effect was observed in progesterone-primed ones. 4. Progesterone (0.6-10 nmol/ml) inhibited uterine horn isometric contractions only in estradiol-primed mice. This effect was partially blocked in uterine horns from reserpine-treated mice and when propanolol (1 microM) was added to the preparation of estradiol-primed mice uterus.

Adrenergic Fibers

The action of progesterone on sodium transport of isolated toad skin. Further evidences of a metabolic action.

To understand the mechanism of progesterone inhibition of the sodium influx in the toad skin, the effects of the hormone on the active sodium transport and oxidative metabolism of the transporting cells were examined. A direct relationship was observed between the initial value of the short circuit current and the sensitivity of a given skin toad preparation to progesterone. Progesterone had a higher effect on the sodium potential than on any other parameter of an equivalent electrical circuit of toad skin. Direct measurement of oxygen consumption indicated that progesterone can act as a blocking agent of the respiratory chain of the sodium transporting cells of toad skin.

Animals

Supersensitivity of atherosclerotic rabbit aorta to ergometrine is mediated by 5-HT2 receptors.

The concentration response curve of ergometrine in aortae from rabbits fed a high cholesterol diet for 12 weeks is biphasic. The first phase of the biphasic curve is antagonized by ketanserin, spiperone and cyproheptadine, but not by prazosin. pKB values are compatible with a 5-HT2 receptor mediated effect. The second phase is shifted to the right by prazosin, ketanserin and spiperone but not by cyproheptadine. In this case the pKB values are compatible with an alpha 1-adrenoceptor mediated effect. The concentration response curves for ergometrine and phenylephrine in aortae from control rabbits are monophasic and pKB values again indicate an alpha 1-adrenoceptor mediated response. Thus, ergometrine contracts the aortae of normal and cholesterol-fed rabbits via activation of alpha 1-adrenoceptors. The supersensitivity observed in atherosclerotic strips seems to reflect the appearance of a high affinity component mediated by 5-HT2 receptors.

Animals

[Etiologic and pathogenetic aspects of the demyelinating process in multiple sclerosis].

In our opinion there is no specific germ for multiple sclerosis. The pathogenic process is developed after a clinically "silent" period and results in a demyelinization process. Partially genetical aspects have to take into account for certain disease processes. Up to now both, the theory of infection as well as the neuroallergetic theory are of importance.

Adult