ABSTRACT
[3H]5-Hydroxytryptamine (5HT) platelet uptake was examined in a small group of hospitalised drug-free manic patients and in a larger group of drug-treated manic and schizophrenic patients compared to controls. 5HT platelet uptake was significantly higher in the manic group at the beginning of the illness episode than in either schizophrenics or controls. No difference was found in the uptake rates between the schizophrenics and controls. At discharge, manic patients had 5HT uptake values similar to control subjects. Manic patients with no previous history of either mania or depression had highly significant increases in 5HT platelet uptake compared to either schizophrenics, controls or manic patients with a previous history of manic-depression. No correlation was found between the initial increased 5HT uptake rate in the manic patient and the severity or duration of the illness episode, the length of hospitalisation or the gender of the patient.
Subject(s)
Bipolar Disorder/blood , Blood Platelets/metabolism , Serotonin/blood , Adult , Aged , Antipsychotic Agents/therapeutic use , Bipolar Disorder/drug therapy , Bipolar Disorder/genetics , Blood Platelets/drug effects , Depressive Disorder/blood , Drug Therapy, Combination , Female , Humans , Male , Middle Aged , Parasympatholytics/therapeutic use , Schizophrenia/bloodSubject(s)
Awareness , Bipolar Disorder/psychology , Cognition , Politics , Schizophrenic Psychology , Canada , HumansABSTRACT
An attenuated human poliovirus infection of cyclophosphamide (CY)-treated mice was developed as a model of persistent CNS enterovirus infections and as an investigation of the interaction of virus with motor neurons during persistence. Ten percent of mice inoculated intracerebrally with undiluted virus developed clinical disease by day 90, but of those treated with CY, 80% developed disease. At higher virus dilutions plus CY there was a marked increase in the incubation period. The latest onset of clinical disease occurred on day 146. Only paralyzed animals had pathologic changes in the spinal cord and virus antigen in anterior horn cells. Neutralizing antibodies were suppressed by CY, as were humoral and cellular immune responses to other antigens.
Subject(s)
Cyclophosphamide/toxicity , Enterovirus Infections/complications , Paralysis/etiology , Poliovirus/immunology , Animals , Antibodies, Viral/analysis , Antigens, Viral/analysis , Brain/microbiology , Brain/pathology , Dose-Response Relationship, Drug , Enterovirus Infections/immunology , Enterovirus Infections/pathology , Hemagglutination, Viral , Humans , Male , Mice , Mice, Inbred BALB C , Paralysis/immunology , Paralysis/pathology , Poliovirus/pathogenicity , Sindbis Virus , Spinal Cord/microbiology , Spinal Cord/pathology , Time Factors , Togaviridae Infections/complications , Togaviridae Infections/pathologyABSTRACT
An attenuated human poliovirus infection of cyclophosphamide (CY)-treated mice resulted in a persistent CNS infection. Persistence in asymptomatic animals occurred in 46% of CY-treated mice but in only 3% of untreated animals, and was confined primarily to the brain. Virus replication in the brain peaked by day 3 for all inoculum dilutions, but was lower with diluted virus. High virus titers in the spinal cord were found only in paralyzed animals and occurred late in the infection following inoculation of diluted virus. Thus, the level of virus replication in the brain was directly related to the amount of virus inoculated, and was correlated with the rapidity of virus transit to the spinal cord and the incubation time to paralysis.
