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Which Depressive Symptoms are Associated with Help-Seeking Behavior?
ByungEun An,Soul Choi,SeongKweon Jeong,YunMi Shin 대한신경정신의학회 2007 PSYCHIATRY INVESTIGATION Vol.4 No.2
Objective-The purpose of this study is to understand the effect of perceived need and helpseeking behaviors on mental health problems in Korea and investigate which depressive symptoms are associated with help-seeking behavior. Methods-Participants were selected from a random sample of 365 people in 3 different Korean cities. A self-reported survey assessing the effect of perceived need and help-seeking behavior on mental health problems and the Beck Depression Inventory (BDI) were performed. Participants were divided into 3 groups, 1) those with perceived need and helpseeking behavior (PN with HS) 2) those with only perceived need (only PN) 3) those without perceived need (no PN). The intergroup differences in each specific symptom (affective, cognitive, neurovegetative) of the BDI were analyzed by analysis of variance (ANOVA) and Bonferroni’s post hoc test. Results-139 (40.9%) of the respondents exhibited perceived need, while only 40 (28.7%) demonstrated help-seeking behavior. The mean score of neurovegetative symptoms was significantly higher in the subjects with help-seeking behaviors (PN with HS) than in those without help-seeking behaviors (only PN, no PN). Conclusion-Only a small proportion (11.8%) of the sample ever sought help for mental problems, in spite of the high lifetime prevalence of depression. Lack of understanding of psychiatric problems is one of the major barriers to seeking help for mental health problems, indicating that widespread psychoeducation is needed to solve the disparity between the unmet needs and receipt of mental health services.
Park, Joon Ha,Cho, Jeong Hwi,Kim, In Hye,Ahn, Ji Hyeon,Lee, Jae-Chul,Chen, Bai Hui,Shin, Bich-Na,Tae, Hyun-Jin,Yoo, Ki-Yeon,Hong, SeongKweon,Kang, Il Jun,Won, Moo-Ho,Kim, Jong-Dai Medknow PublicationsMedia Pvt Ltd 2015 Chinese medical journal : CMJ Vol.128 No.21
<P><B>Background:</B></P><P>Water dropwort (<I>Oenanthe javanica</I>) as a popular traditional medicine in Asia shows various biological properties including antioxidant activity. In this study, we firstly examined the neuroprotective effect of <I>Oenanthe javanica</I> extract (OJE) in the hippocampal cornus ammonis 1 region (CA1 region) of the gerbil subjected to transient cerebral ischemia.</P><P><B>Methods:</B></P><P>Gerbils were established by the occlusion of common carotid arteries for 5 min. The neuroprotective effect of OJE was estimated by cresyl violet staining. In addition, 4 antioxidants (copper, zinc superoxide dismutase [SOD], manganese SOD, catalase, and glutathione peroxidase) immunoreactivities were investigated by immunohistochemistry.</P><P><B>Results:</B></P><P>Pyramidal neurons in the CA1 region showed neuronal death at 5 days postischemia; at this point in time, all antioxidants immunoreactivities disappeared in CA1 pyramidal neurons and showed in many nonpyramidal cells. Treatment with 200 mg/kg, not 100 mg/kg, OJE protected CA1 pyramidal neurons from ischemic damage. In addition, 200 mg/kg OJE treatment increased or maintained antioxidants immunoreactivities. Especially, among the antioxidants, glutathione peroxidase immunoreactivity was effectively increased in the CA1 pyramidal neurons of the OJE-treated sham-operated and ischemia-operated groups.</P><P><B>Conclusion:</B></P><P>Our present results indicate that treatment with OJE can protect neurons from transient ischemic damage and that the neuroprotective effect may be closely associated with increased or maintained intracellular antioxidant enzymes by OJE.</P>
Ahn, Ji Hyeon,Hong, Seongkweon,Park, Joon Ha,Kim, In Hye,Cho, Jeong Hwi,Lee, Tae-Kyeong,Lee, Jae-Chul,Chen, Bai Hui,Shin, Bich-Na,Bae, Eun Joo,Jeon, Yong Hwan,Kim, Young-Myeong,Won, Moo-Ho,Choi, Soo Y SPANDIDOS PUBLICATIONS 2017 MOLECULAR MEDICINE REPORTS Vol. No.
<P>Calbindin-D28k (CB), calretinin (CR) and parvalbumin (PV), which regulate cytosolic free Ca<SUP>2+</SUP> concentrations in neurons, are chemically expressed in γ-aminobutyric acid (GABA)ergic neurons that regulate the degree of glutamatergic excitation and output of projection neurons. The present study investigated age-associated differences in CB, CR and PV immunoreactivities in the somatosensory cortex in three species (mice, rats and gerbils) of young (1 month), adult (6 months) and aged (24 months) rodents, using immunohistochemistry and western blotting. Abundant CB-immunoreactive neurons were distributed in layers II and III, and age-associated alterations in their number were different according to the species. CR-immunoreactive neurons were not abundant in all layers; however, the number of CR-immunoreactive neurons was the highest in all adult species. Many PV-immunoreactive neurons were identified in all layers, particularly in layers II and III, and they increased in all layers with age in all species. The present study demonstrated that the distribution pattern of CB-, CR- and PV-containing neurons in the somatosensory cortex were apparently altered in number with normal aging, and that CB and CR exhibited a tendency to decrease in aged rodents, whereas PV tended to increase with age. These results indicate that CB, CR and PV are markedly altered in the somatosensory cortex, and this change may be associated with normal aging. These findings may aid the elucidation of the mechanisms of aging and geriatric disease.</P>
Ahn, Ji Yun,Tae, Hyun-Jin,Cho, Jeong-Hwi,Kim, In Hye,Ahn, Ji Hyeon,Park, Joon Ha,Kim, Dong Won,Cho, Jun Hwi,Won, Moo-Ho,Hong, Seongkweon,Lee, Jae-Chul,Seo, Jeong Yeol Medknow PublicationsMedia Pvt Ltd 2015 Neural regeneration research Vol.10 No.8
<P>c-Fos is a good biological marker for detecting the pathogenesis of central nervous system disorders. Few studies are reported on the change in myocardial infarction-induced c-Fos expression in the paralimbic regions. Thus, in this study, we investigated the changes in c-Fos expression in the rat cingulate and piriform cortices after myocardial infarction. Neuronal degeneration in cingulate and piriform cortices after myocardial infarction was detected using cresyl violet staining, NeuN immunohistochemistry and Fluoro-Jade B histofluorescence staining. c-Fos-immunoreactive cells were observed in cingulate and piriform cortices at 3 days after myocardial infarction and peaked at 7 and 14 days after myocardial infarction. But they were hardly observed at 56 days after myocardial infarction. The chronological change of c-Fos expression determined by western blot analysis was basically the same as that of c-Fos immunoreactivity. These results indicate that myocardial infarction can cause the chronological change of immediate-early response gene c-Fos protein expression, which might be associated with the neural activity induced by myocardial infarction.</P>
Yoo, Ki-Yeon,Kim, In Hye,Cho, Jeong-Hwi,Ahn, Ji Hyeon,Park, Joon Ha,Lee, Jae-Chul,Tae, Hyun-Jin,Kim, Dae Won,Kim, Jong-Dai,Hong, Seongkweon,Won, Moo-Ho,Kang, Il Jun Medknow PublicationsMedia Pvt Ltd 2016 Neural regeneration research Vol.11 No.2
<P>In this study, we tried to verify the neuroprotective effect of <I>Chrysanthemum indicum</I> Linne (CIL) extract, which has been used as a botanical drug in East Asia, against ischemic damage and to explore the underlying mechanism involving the anti-inflammatory approach. A gerbil was given CIL extract for 7 consecutive days followed by bilateral carotid artery occlusion to make a cerebral ischemia/reperfusion model. Then, we found that CIL extracts protected pyramidal neurons in the hippocampal CA1 region (CA1) from ischemic damage using neuronal nucleus immunohistochemistry and Fluoro-Jade B histofluorescence. Accordingly, interleukin-13 immunoreactivities in the CA1 pyramidal neurons of CIL-pretreated animals were maintained or increased after cerebral ischemia/reperfusion. These findings indicate that the pre-treatment of CIL can attenuate neuronal damage/death in the brain after cerebral ischemia/reperfusion <I>via</I> an anti-inflammatory approach.</P>
Tae, Hyun-Jin,Park, Seung Min,Cho, Jeong Hwi,Kim, In Hye,Ahn, Ji Hyeon,Park, Joon Ha,Won, Moo-Ho,Chen, Bai Hui,Shin, Bich-Na,Shin, Myoung Cheol,Lee, Choong Hyun,Hong, Seongkweon,Lee, Jae-Chul,Cho, Jun D.A. Spandidos 2016 MOLECULAR MEDICINE REPORTS Vol. No.
<P>Proto-oncogene c-Fos (c-Fos) is frequently used to detect a pathogenesis in central nervous system disorders. The present study examined changes in the immunoreactivity of c-Fos in the paraventricular nucleus of the hypothalamus (PVNH) and paraventricular nucleus of the thalamus (PVNT) following myocardial infarction (MI) in rats. Infarction in the left ventricle was examined by Masson's trichrome staining. Neuronal degeneration was monitored for 56 days after MI using crystal violet and Fluoro-Jade B histofluorescence staining. Changes in the immunoreactivity of c-Fos were determined using immunohistochemistry for c-Fos. The average infarct size of the left ventricle circumference was ~44% subsequent to MI. Neuronal degeneration was not detected in PVNH and PVNT following MI. c-Fos immunoreactive (<SUP>+</SUP>) cells were infrequently observed in the nuclei of the sham-group. However, the number of c-Fos<SUP>+</SUP> cells was increased in the nuclei following MI and peaked in the PVNH and PVNT at 3 and 14 days, respectively. The number of c-Fos<SUP>+</SUP> cells were comparable with the sham group at 56 days after MI. Therefore, MI may induce c-Fos immunoreactivity in PVNH and PVNT, this increase of c-Fos expression levels may be associated with the stress that occurs in the brain following MI.</P>
Kim, In Hye,Jeon, Yong Hwan,Lee, Tae-Kyeong,Cho, Jeong Hwi,Lee, Jae-Chul,Park, Joon Ha,Ahn, Ji Hyeon,Shin, Bich-Na,Kim, Yang Hee,Hong, Seongkweon,Yan, Bing Chun,Won, Moo-Ho,Lee, Yun Lyul Medknow PublicationsMedia Pvt Ltd 2017 Neural regeneration research Vol.12 No.6
<P>Ischemic preconditioning elicited by a non-fatal brief occlusion of blood flow has been applied for an experimental therapeutic strategy against a subsequent fatal ischemic insult. In this study, we investigated the neuroprotective effects of ischemic preconditioning (2-minute transient cerebral ischemia) on calbindin D28k immunoreactivity in the gerbil hippocampal CA1 area following a subsequent fatal transient ischemic insult (5-minute transient cerebral ischemia). A large number of pyramidal neurons in the hippocampal CA1 area died 4 days after 5-minute transient cerebral ischemia. Ischemic preconditioning reduced the death of pyramidal neurons in the hippocampal CA1 area. Calbindin D28k immunoreactivity was greatly attenuated at 2 days after 5-minute transient cerebral ischemia and it was hardly detected at 5 days post-ischemia. Ischemic preconditioning maintained calbindin D28k immunoreactivity after transient cerebral ischemia. These findings suggest that ischemic preconditioning can attenuate transient cerebral ischemia-caused damage to the pyramidal neurons in the hippocampal CA1 area through maintaining calbindin D28k immunoreactivity.</P>
Ahn, Ji Hyeon,Chen, Bai Hui,Yan, Bing Chun,Park, Joon Ha,Kang, Il Jun,Lee, Tae-Kyeong,Cho, Jeong Hwi,Shin, Bich-Na,Lee, Jae-Chul,Jeon, Yong Hwan,Hong, Seongkweon,Lee, Young Joo,Choi, Soo Young,Won, Mo SPANDIDOS PUBLICATIONS 2018 MOLECULAR MEDICINE REPORTS Vol.17 No.1
<P>GABAergic projections terminate on numerous hippocampal interneurons containing calcium binding proteins (CBPs), including calbindin D-28k (CB), calretinin (CR) and parvalbumin (PV). Memory deficits and expression levels of CB, CR, and PV were examined in the hippocampal subregions following systemic scopolamine (Scop; 1 mg/kg) treatment for 4 weeks in mice. Scop treatment induced significant memory deficits from 1 week after Scop treatment. CB, CR and PV immunoreactivities distributions were in hippocampal subregions [CA1 and CA3 regions, and the dentate gyrus (DG)]. CB immunoreactivity (CB<SUP>+</SUP>) was gradually decreased in all subregions until 2 weeks after Scop treatment, and CB<SUP>+</SUP> was decreased to the lowest level in all subregions at 3 and 4 weeks. CR<SUP>+</SUP> in the CA1 region was gradually decreased until 2 weeks and hardly observed at 3 and 4 weeks; in the CA3 region, CR<SUP>+</SUP> was not altered in all subregions at any time. In the DG, CR+ was gradually decreased until 2 weeks and lowest at 3 and 4 weeks. PV<SUP>+</SUP> in the CA1 region was not altered at 1 week, and gradually decreased from 2 weeks. In the CA3 region, PV<SUP>+</SUP> did not change in any subregions at any time. In the DG, PV<SUP>+</SUP> was not altered at 1 week, decreased at 2 weeks, and lowest at 3 and 4 weeks. In brief, Scop significantly decreased CBPs expressions in the hippocampus ≥3 weeks after the treatment although memory deficits had developed at 1 week. Therefore, it is suggested that Scop (1 mg/kg) must be systemically treated for ≥3 weeks to investigate changes in expression levels of CBPs in the hippocampus.</P>