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1.
Brain Behav Immun Health ; 29: 100615, 2023 May.
Article in English | MEDLINE | ID: mdl-37008742

ABSTRACT

Physical symptoms such as fatigue and muscle weakness, and psychiatric symptoms like depression and anxiety are considered as complications and sequelae of COVID-19. This epidemiological study investigated the actual status of psychiatric symptoms and disorders caused by COVID-19, from four major university hospitals and five general hospitals in Fukuoka Prefecture, Japan, having a population of 5 million. We conducted a survey of psychiatric disorders associated with COVID-19 using Diagnosis Procedure Combination (DPC) data and the psychiatric records of the hospitals. In the study period from January 2019 to September 2021, 2743 COVID-19 admissions were determined from DPC data across the nine sites. These subjects had significantly more anxiety, depression, and insomnia, and were receiving higher rates of various psychotropic medications than controls influenza and respiratory infections. A review of psychiatric records revealed that the frequency of organic mental illness with insomnia and confusion was proportional to the severity of COVID-19 infection and that anxiety symptoms appeared independent of infection severity. These results indicate that COVID-19 is more likely to produce psychiatric symptoms such as anxiety and insomnia than conventional infections.

2.
Article in English | MEDLINE | ID: mdl-35897455

ABSTRACT

Quarantine imposed due to COVID-19 infection can exacerbate psychological distress, and it is important for a public mental health agency to identify factors that are predictive of high psychological distress in such situation. The aim of this study was to investigate whether gender, age, and the presence or absence of infectious disease symptoms affected psychological distress among asymptomatic or mildly ill COVID-19 patients who were quarantined. Participants were 436 asymptomatic or mildly symptomatic COVID-19-infected patients who were quarantined in a treatment facility between 1 May 2020 and 30 September 2021. We used Quantification Theory I analysis to investigate the effects of gender, age, and the nature of infectious disease symptoms on psychological distress. The results of the analysis showed that the contribution rate was 0.06. Among gender, age, presence of symptoms, and the nature of symptoms, age had the greatest effect on psychological distress, and being in one's teens to thirties was considered to exacerbate psychological distress the most. According to the results, the psychological distress of asymptomatic and mildly symptomatic COVID-19 patients isolated was affected by gender, age, and symptomology, especially due to age differences. However, the impact of these items on psychological distress was not considered significant.


Subject(s)
COVID-19 , Communicable Diseases , Psychological Distress , Adolescent , COVID-19/epidemiology , Humans , Japan/epidemiology , Quarantine/psychology
4.
Article in English | MEDLINE | ID: mdl-17393774

ABSTRACT

A rapid and sensitive high-performance liquid chromatographic method was validated and described for determination of paroxetine in human saliva. Following liquid-liquid extraction of the drug and an internal standard (dibucaine), chromatographic separation was accomplished using a C18 analytical column with a mobile phase consisting of 0.05 mol/L sodium phosphate buffer, pH 5.0, and acetonitrile (A 30:70, v/v; B 60:40, v/v). Paroxetine and the internal standard were detected by ultraviolet absorbance at 205 nm. The average recoveries of the drug and internal standard were 92.5% and 89%, respectively. The lower limits of detection and quantification were 1 and 4 ng/ml, respectively, and the calibration curve was linear over a concentration range of 4 ng/ml. The saliva level of paroxetine in patients with depression taking 10 to 40 mg/day of the drug was significantly correlated with the plasma level of paroxetine in each patient (r = 0.617, P < 0.004, n = 19). These data indicate that the saliva level of paroxetine could be a useful marker to predict the plasma level of the drug.


Subject(s)
Antidepressive Agents, Second-Generation/analysis , Chromatography, High Pressure Liquid/methods , Drug Monitoring/methods , Paroxetine/analysis , Saliva/chemistry , Antidepressive Agents, Second-Generation/blood , Biomarkers/blood , Depression/drug therapy , Depression/metabolism , Humans , Paroxetine/blood , Patient Compliance
5.
Br J Pharmacol ; 135(6): 1547-55, 2002 Mar.
Article in English | MEDLINE | ID: mdl-11906969

ABSTRACT

1. Several neuroleptics inhibited the 3 microM gamma-aminobutyric acid induced-chloride current (GABA-current) on dissociated rat dorsal root ganglion neurons in whole-cell patch-clamp investigations. 2. The IC(50) for clozapine, zotepine, olanzapine, risperidone and chlorpromazine were 6.95, 18.26, 20.30, 106.01 and 114.56 microM, respectively. The values for the inhibitory effects of neuroleptics on the GABA (3 microM)-current, which were calculated by the fitting Hill's equations where the concentrations represent the mean therapeutic blood concentrations, were ranked clozapine>zotepine>chlorpromazine>olanzapine>risperidone. These inhibitory effects, weighted with the therapeutic concentrations of neuroleptics, were correlated with the clinical incidences of seizure during treatment with neuroleptics. 3. Clozapine reduced the picrotoxin-inhibiton, and may compete with a ligand of the t-butylbicyclophosphorothionate (TBPS) binding site. 4. Haloperidol and quetiapine did not affect the peak amplitude of the GABA (3 microM)-current. However, haloperidol reduced the clozapine-inhibition, and may antagonize ligand binding to TBPS binding site. 5. Neuroleptics including haloperidol and quetiapine enhanced the desensitization of the GABA (3 microM)-current. However, haloperidol and quetiapine at 100 microM inhibited the desensitization at the beginning of application. 6. Blonanserin (AD-5423) at 30 and 50 microM potentiated the GABA (3 microM)-current to 170.1+/-6.9 and 192.0+/-10.6% of the control current, respectively. Blonanserin shifted GABA concentration-response curve leftward. Blonanserin only partly negatively interacted with diazepam. The blonanserin-potentiation was not reversed by flumazenil. Blonanserin is not a benzodiazepine receptor agonist. 7. The various effects of neuroleptics on the GABA-current may be related to the clinical effects including modifying the seizure threshold.


Subject(s)
Antipsychotic Agents/pharmacology , Chloride Channels/physiology , Ganglia, Spinal/drug effects , gamma-Aminobutyric Acid/physiology , Animals , Cells, Cultured , Chloride Channel Agonists , Chloride Channels/antagonists & inhibitors , Clozapine/pharmacology , Dibenzothiazepines/pharmacology , Dose-Response Relationship, Drug , Drug Synergism , Ganglia, Spinal/physiology , Haloperidol/pharmacology , Incidence , Membrane Potentials/drug effects , Membrane Potentials/physiology , Piperazines/pharmacology , Piperidines/pharmacology , Quetiapine Fumarate , Rats , Rats, Wistar , Seizures/epidemiology , Seizures/metabolism , gamma-Aminobutyric Acid/pharmacology
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