There has been a rapid industrial progress in Korea since 1962 by the success of 5-year economic development plan, and the number of industrial work has also made a rapid increase. Consequently, the management of the occupational health for the purpose of promoting the health of industrial workers and improving the working environment is badly needed in these days. Health services on industrial noisy environment have been provided only for noise-induced hearing loss management until now. But gradually, modem diseases and death have come to be related to the stress and mental health, therefore noise-induced mental disorder, like a stress became very important. Thus, this study has been carried out to analyze the relationship between workers' stress symptoms and the perceived working environment and the perceived working conditions. This study included 786 industrial workers selected from II factories in Buchun. The results were as follows: 1. For demographic characteristics, most of the workers were males(75.7%), the 20~29 years old were 33.8% and those who graduated from high school were 56.1%. The workers whose monthly income ranged from 700,000 to 1,500,000 won were 37.9% and who has a religion were 49.0%. 2. For occupational characteristics, workers who had worked 5~10 years in the factories were 35.8%. Those who felt much for them workload were 42.7% and who worked more than 8 hours a day were 73.7%. Those who were dissatisfied with their pay and job were 51.1 % and 31.2%. The workers who responded ventilation condition of their worksites were bad were 50.4% and the dissatisfied with working environment of their worksites were 43.8%. 3. For the noise exposure level in worksite, workers who were exposed to 70∼90㏈ were 37.4%, 90∼100㏈ were 25.2% and 50∼70㏈ were 18.8%. 4. Workers∼ stress symptoms were significantly related to marital status and their monthly income(P〈0.05). Workers who were single and had lower monthly income showed higher PSI(Psychiatric Symptom Index) scores than those who were married and had higher monthly income. Higher PSI scores were also significantly related to the night-work, workload, dissatisfaction with their job, and bad relationship with their bosses or co-workers. 5. The higher noise exposure level in worksite from 80㏈ was, the more severe stress symptoms including PSI subparts were reported; Anxiety, Anger, Depression, and Cognitive disorder symptom(P〈0.001). 6. According to the results of stepwise multiple regression analysis, factors affecting workers' PSI scores were noise exposure level in worksite(R2=0.150), relationship with coworkers, amount of workload, monthly income and relationship with bosses orderly and the total R2 of this 6 factors was 29.7%.
Objectives: Recently, many studies have reported beneficial effects from the application of laser and light-emitting diode (LED) therapy for cerebral nervous disease. Transcranial laser therapy and LED therapy may be an effective method to treat diseases of the cerebral nervous system. This study aims to discuss the possibility of laser and LED therapy for cerebral nervous disease by reviewing literature about its effectiveness. Methods: We searched papers using PubMed, Science Direct, CINAHL, KTKP, Oasis and NDSL, using the keywords "Laser therapy, low-level", "Transcranial laser", "Transcranial light emitting diode" and "stroke", "traumatic brain injury", "dementia", "anxiety", "cognitive", "emotional effects", "psychiatric disorder", "multiple sclerosis", "Parkinson's disease". The search range included randomized controlled trials (RCTs) and clinical case series. Reviews and animal experiments were not included. Studies not matched with inclusion criteria were excluded. Results: A total 1,119 studies were found. 1,100 were excluded from scanning titles and abstracts and finally 9 articles were selected. Among the 9 articles, 5 were RCTs, one was a controlled study, and the other 3 were case reports. They reported that transcranial laser therapy and LED treatment had beneficial effects from photobiomodulation to the cerebral nervous system. Clinical evaluation factors showed favorable trends. Conclusions: Transcranial laser therapy and LED therapy seem to be effective to the cerebral nervous system and they may be a favorable choice for cerebral nervous disease.
The development of molecular biology has brought many changes in psychiatry. Molecular biology makes us possible to know the cause of mental disorders that provide the way to prevent the disorders, and to develop various accurate diagnostic and treatment methods for mental disorders. The author discusses the concept, cause, and treatment of mental disorders in the aspect of molecular biology. Importing the methods of molecular biology into psychiatry, we can anticipate to get a number of the goals of psychiatric genetics, including identification of specific susceptibility genes, clarification of the pathophysiological processes whereby these genes lead to symptoms, establishment of epigenetic factors that interact with these genes to produce disease, validation of nosological boundaries that more closely reflect the actions of these genes, and development of effective preventive and therapeutic interventions based on genetic counseling, gene therapy, and modification of permissive or protective environmental influences. In addition to their capacity to accelerate the discovery of new molecules participating in the nervous system's response to disease or to self-administered drugs, molecular biological strategies can also be used to determine how critical a particular gene product may be in mediating a cellular event with behavioral importance. Molecular biology probably enables us discover the environmental factors of mental disorders and allow rational drug design and gene therapies for mental disorders, by isolation of gene products that facilitate a basic understanding of the pathogenesis of these disorders. A specific genetic linkage may suggest a novel class of drugs that has not yet been tried. With respect to gene therapy, the hypothetical method would use a gene delivery system, most likely a modified virus, to insert a functional copy of a mutant gene into those brain cells that require the gene for normal function.
Many investigators are trying to elucidate the pathogenesis of psychiatric disorders on the basis of neuroendocrine responses to stimulation or perturbation. Dexamethasone(DEX) suppression has been the most widely utilized as the prototypical challenge test. Dexamethasone suppression test(DST) has proven to be valuable in diagnosing the depressive spectrum disorder. Reported specificity of diagnosis of depression is relatively high, but sensitivity is limited. Some researchers used the combination of dexamethasone and corticotropin releasing hormone(CRH) in order to improve the sensitivity. They reported that combined DEX/CRH test is more sensitive than DST alone. In this study the authors modified the DEX/CRH test, i.e., we administered the insulin instead of CRH. Total subjects were 28(7 normal controls, 10 manic patients, 11 schizophrenic patients). Subjects were taken DEX(1.5mg p.o.) at 11 p.m., insulin 16 hours later(0.1 unit/kg i.v.). Five blood samples for the determination of cortisol and ACTH were serially drawn at 15 minute interval. The results are as followings : 1) The cortisol and ACTH levels of manic subjects increased following insulin administration. Manic subjects showed higher levels of cortisol and ACTH than schizophrenic and normal control subjects. The cortisol and ACTH levels of schizophrenic and normal control subjects did not show gross changes. 2) The sensitivity of the test was lower than that of reported DEX/CRH test.
Excess manganese (Mn) is neurotoxic. Increased manganese stores in the brain are associated with a number of behavioral problems, including motor dysfunction, memory loss and psychiatric disorders. We previously showed that the transport and neurotoxicity of manganese after intranasal instillation of the metal are altered in Hfe-deficient mice, a mouse model of the iron overload disorder hereditary hemochromatosis (HH). However, it is not fully understood whether loss of Hfe function modifies Mn neurotoxicity after ingestion. To investigate the role of Hfe in oral Mn toxicity, we exposed Hfe-knockout ($Hfe^{-/-}$) and their control wild-type ($Hfe^{+/+}$) mice to $MnCl_2$ in drinking water (5 mg/mL) for 5 weeks. Motor coordination and spatial memory capacity were determined by the rotarod test and the Barnes maze test, respectively. Brain and liver metal levels were analyzed by inductively coupled plasma mass spectrometry. Compared with the water-drinking group, mice drinking Mn significantly increased Mn concentrations in the liver and brain of both genotypes. Mn exposure decreased iron levels in the liver, but not in the brain. Neither Mn nor Hfe deficiency altered tissue concentrations of copper or zinc. The rotarod test showed that Mn exposure decreased motor skills in $Hfe^{+/+}$ mice, but not in $Hfe^{-/-}$ mice (p = 0.023). In the Barns maze test, latency to find the target hole was not altered in Mn-exposed $Hfe^{+/+}$ compared with water-drinking $Hfe^{+/+}$ mice. However, Mn-exposed $Hfe^{-/-}$ mice spent more time to find the target hole than Mn-drinking $Hfe^{+/+}$ mice (p = 0.028). These data indicate that loss of Hfe function impairs spatial memory upon Mn exposure in drinking water. Our results suggest that individuals with hemochromatosis could be more vulnerable to memory deficits induced by Mn ingestion from our environment. The pathophysiological role of HFE in manganese neurotoxicity should be carefully examined in patients with HFE-associated hemochromatosis and other iron overload disorders.
Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder characterized by motor, cognitive, and psychiatric symptoms, accompanied by marked cell death in the striatum and cortex. Stereotaxic injection of quinolinic acid (QA) into striatum results in a degeneration of GABAergic neurons and exhibits abnormal motor behaviors typical of the illness. The objective of this study was carried out to obtain basic information about whether parthenogenetic mouse embryonic stem (PmES) cells are suitable for cell replacement therapy of HD. To establish PmES cell lines, hybrid F1 (C57BL/6xCBA/N) mouse oocytes were treated with 7% ethanol for 5 min and cytochalasin-B for 4 hr to initiate spontaneous cleavage. Thus established PmES cells were induced to differentiate using bFGF (20ng/ml) followed by selection of neuronal precursor cells for 8 days in N2 medium. After selection, cells were expanded at the presence of bFGF (20 ng/ml) for another 6 days, then a final differentiation step in N2 medium for 7 days. To establish recipient animal models of HD, young adult mice (7 weeks age ICR mice) were lesioned unilaterally with a stereotaxic injection of QA (60 nM) into the striatum and the rotational behavior of the animals was tested using apomorphine (0.1mg/kg, IP) 7 days after the induction of lesion. Animals rotating more than 120 turns per hour were selected and the differentiated PmES cells (1$\times$10$^4$cells/ul) were implanted into striatum. Four weeks after the graft, immunohistochemical studies revealed the presence of cells reactive to anti-NeuN antibody. However, only a slight improvement of motor behavior was observed. By Nissl staining, cell mass resembling tumor was found at the graft site and near cortex which may explain the slight behavioral improvement. Detailed experiment on cell viability, differentiation and migration explanted in vivo is currently being studied.
Insulinoma is a rare tumor, occurring more often in women and in the older age range. Eighty percent of patients have a single benign tumor, usually 2cm in diameter, located with about equal frequency in body, head or tail of pancreas and amenable to surgical cure. About 10% have multiple tumors. The remaining 10% of patients have metastatic malignant insulinoma. The symptom of insulinoma is characterized by the periodic attack of hypoglycemia of blood sugar level below 50mg%, by fasting or exertion, and rapid relief of symptom by oral or intravenous administration of glucose. Symptom often lead to misdiagnosis as a neurologic or psychiatric disorder. A case described by authors was 44-year old female with the chief complaints of the loss of consciousness, epileptic seizure although she has been treated by anticonvulsants. Serum blood sugar and insulin level during fasting sugested insulinoma but abdominal computed tomography shows no definitive mass in pancreas. Celiac angiography revealed insulinoma. She transfered to the defartment of General Surgery and was performed enucleation. Microscopic findings shows the islet cell tumor of pancreas. A brief review of the literature was made.
Journal of the Korean Academy of Child and Adolescent Psychiatry
/
v.8
no.2
/
pp.217-231
/
1997
This paper first reviewed the current neurological theories concerning the etiology of ADHD and secondly, examined results of studies that applied neuropsychological assessment methods in the examination of ADHD children both here in Korea and abroad. ADHD children were found to exhibit characteristic responses indicating deficits in vigilance, sustained attention, distractibility, allocation and regulation of attention in many assessments of attention, in addition to deficits in executive functioning, working and associative memory. Such neuropsychological assessment results suggest that in addition to dysfunction in the frontal lobe and the reticular activation system, dysfunction may exist in other neural pathways involving many areas of the brain. However, because a substantial number of neuropsychological assessment tools being employed in Korea for ADHD children had been developed abroad, a Korean standardization project involving ADHD and normal control children, in addition to other child psychiatric population pools must be conducted in order to obtain appropriate age norms and test validity, and in order to make possible a more accurate and precise comparison and interpretation in the assessment of ADHD children.
Journal of the Korean Academy of Child and Adolescent Psychiatry
/
v.11
no.1
/
pp.144-149
/
2000
A psychogenic seizure is a disorder which is occasionally met by neurologists and psychiatrists. The most important thing that clinicians should do is differential diagnosis with true epileptic seizures. Especially psychiatrists are expected to be able to diagnose psychogenic seizures through a thorough history taking and an observation of clinical features to some degree before the confirmatory diagnoses. We experienced a case of 11-year-old girl with psychogenic seizure which was characterized by obvious psychological and environmental stress, clinical features, and good outcome by prompt a loboratoy examination and psychiatric intervention. To diagnose and treat childhood psychogenic seizures, we suggest that it is very important to examine the familial background and take a thorough history, and perform psychoeducational intervention in addition to electroencephalogram.
Objectives Adrenergic alpha 1 and 2 receptors work as pathways to control the serotonergic neuron moderation and mirtazapine acts as antagonist of these receptors. The adrenoreceptor alpha 1a (ADRA1A) gene, which encodes adrenergic alpha 1 receptor, has Arg-347Cys genetic polymorphism and the polymorphism has strong relationship with many neuro-psychiatric diseases. In this study, we explored the relationship between ADRA1A R347C polymorphism and mirtazapine treatment response in Koreans with major depression. Methods 352 patients enrolled in this study, and the symptoms were evaluated by 17-item Hamilton Depression Rating (HAMD-17) scale. After 1, 2, 4, 8, and 12 weeks of mirtazapine treatment, the association between ADRA1A R347C polymorphism and remission/response outcomes was evaluated. Results Treatment response to mirtazapine was significantly better in T allele carriers than C allele homozygotes after 12 weeks of mirtazapine monotherapy. The percentile decline of HAMD-17 score in T allele carriers was larger than that of C allele homozygotes. ADRA1A R347C genotypes were not significantly associated with remission. Conclusions The result showed that treatment response to mirtazapine was significantly associated with ADRA1A R347C genetic polymorphism. T allele carriers showed better treatment response than C allele homozygotes. It can be supposed that T allele carriers have a trend of better treatment response to mirtazapine monotherapy.
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