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Young-Jin Lim

Publications and source records attributed to Young-Jin Lim.

11 recordsLinked to original sources
PubMed2007

Korean panic disorder severity scale: construct validity by confirmatory factor analysis.

The Panic Disorder Severity Scale (PDSS) is a seven-item instrument used to rate the overall severity of panic disorder. This scale has previously evidenced excellent psychometric properties in a sample of patients with panic disorder, with or without agoraphobia. However, despite several factor-analytic PDSS studies, the number of factors has not been entirely consistent. Our objective in this study, then, was to evaluate the fit of two competing models to data collected with a sample of 176 patients with panic disorder. Patients (N = 176) who fulfilled DSM-IV criteria for panic disorder, with or without agoraphobia, underwent structured diagnostic assessments and PDSS interviews. Of the subjects, 102 were men and 74 were women. The mean age of the men was 41.2 (SD = 10.10) and of women, 41.0 (SD = 10.54). A model with two correlated factors was considered to be more appropriate in the description of the data with the following indices: Tucker-Lewis index = 0.94, comparative fit index = 0.96, root-mean-square error of approximation=0.08, and standardized root-mean-square residual = 0.04. These results were then cross-validated with subgroups of patients with panic disorder with agoraphobia (n = 128), without agoraphobia (n = 48), and with panic disorder after phamacotherapy (n = 62). Our results indicated that the correlated two-factor model developed and validated using Western samples could be appropriately generalized to Korean clinical samples. Furthermore, our results support the construct validity of the Korean version of the PDSS.

Adolescent↗
PubMed2007

Korean Anxiety Sensitivity Index-Revised: its factor structure, reliability, and validity in clinical and nonclinical samples.

The factor structure and convergent and discriminant validity of the Anxiety Sensitivity Index-Revised (ASI-R) were examined in a community sample, a student sample, and patients with panic disorder in Korea. Results from a confirmatory factor analysis (CFA) comparing our data to factor solutions commonly reported as representative of European American populations indicated a poor fit. A subsequent exploratory factor analysis (EFA) indicated that a four-factor solution provided the best fit. Correlations between the ASI-R and anxiety measures were moderately high, providing evidence of convergent validity. Implications for assessment with Koreans are discussed.

Adolescent↗
PubMed2006

Effects of intravenous anesthetics on the activity of glutamate transporter EAAT3 expressed in Xenopus oocytes: evidence for protein kinase C involvement.

We investigated the effects of the intravenous anesthetics, thiopental, etomidate and ketamine, on the activity of one type of glutamate transporters, EAAT3 (excitatory amino acid transporter type 3). Rat EAAT3 was expressed in Xenopus oocytes by injection of its mRNA. Using two-electrode voltage clamp, membrane currents were recorded after the application of L-glutamate (30 microM) in the presence or absence of various concentrations of the anesthetics. Thiopental (0.3-30 microM) and ketamine (3-1000 microM) did not affect EAAT3 activity. Etomidate decreased EAAT3 activity in a concentration-dependent manner (0.10-10 microM). Etomidate at 1 microM significantly decreased the Vmax, but not the Km of EAAT3 for glutamate. Chelerythrine, a protein kinase C (PKC) inhibitor, significantly decreased EAAT3 activity, however, there were no statistical differences among the chelerythrine, etomidate or chelerythrine plus etomidate groups. Likewise, the combination of staurosporine, another PKC inhibitor, and etomidate did not decrease the responses further compared with staurosporine or etomidate alone. Phorbol-12-myrisate-13-acetate, a PKC activator, abolished etomidate-induced decrease in EAAT3 activity. Since our results showed that thiopental and ketamine did not affect EAAT3 activity significantly, EAAT3 may not be a target for their anesthetic effects. Our results also suggest that etomidate, possibly via PKC, decreased EAAT3 activity at clinically relevant concentrations.

Alkaloids↗
PubMed2006

Immunostimulating factor isolated from actinobacillus actinomycetemcomitans stimulates monocytes and inflammatory macrophages.

Immunostimulating factor (ISTF) isolated from Actinobacillus actinomycetemcomitans which has been described previously, is distinct from lipopolysaccharide and induces proliferation of B cells. This study was undertaken to investigate whether ISTF might enhance the stimulation of other immune cells. Immunohistochemically, ISTF exhibited a profound stimulating effect on macrophages and dendritic cells as well as B cells in the spleen of BALB/c mice. ISTF was also recognized for its capacity to induce direct activation of mouse macrophages to produce IL-6, TNF-alpha, and NO and MHC class II expression. Therefore, it is postulated that ISTF stimulates macrophages and possibly other cells to produce a wide variety of proinflammatory mediators, which may be involved in the chronicity and tissue destruction of periodontal disease.

Adjuvants, Immunologic↗
PubMed2004

Overexpression of redox factor-1 negatively regulates NO synthesis and apoptosis in LPS-stimulated RAW 264.7 macrophages.

Redox factor-1 (Ref-1) is a ubiquitously expressed protein with proven roles as a modulator of redox-sensitive transcription, and as an endonuclease in the base excision repair pathway of oxidatively damaged DNA. Although Ref-1 is induced by a variety of oxidative stress and protects cells against oxidative stress, the function of Ref-1 in regulating nitric oxide (NO) synthesis has not been elucidated to date. We investigated the role of Ref-1 in regulating NO synthesis and NO-mediated apoptosis employing adenoviral-mediated overexpression of Ref-1 in lipopolysaccharide (LPS)-stimulated macrophage RAW 264.7 cells. LPS treatment produced NO synthesis and NO-mediated apoptosis. Forced overexpression of Ref-1 suppressed LPS-stimulated NO synthesis. In parallel with this, Ref-1 also mitigated alteration of inducible NO synthase expression and NO-mediated apoptosis. Our findings suggest that Ref-1 is implicated in protection against cell death resulting from oxidative stimuli containing NO.

Adenoviridae↗
PubMed2004

Sphingosine may have cytotoxic effects via apoptosis on the growth of keloid fibroblasts.

Keloids are often resistant to treatment, causing much suffering to the patient. Our previous work found that ceramide (Cer) inhibits growth of fibroblasts via apoptosis. However, when compared to normal fibroblasts (NFs), which are quiescent, keloid fibroblasts (KFs) rapidly proliferate and are reported to be resistant to apoptosis via Cer. Sphingosine (Sph) is a metabolite product of ceramide that has some different biochemical properties. Thereofore, we investigated the cytotoxic effects of Sph on cultured fibroblasts from keloid lesions and normal skin in order to evaluate the possibility of using Sph in the treatment of keloid. We used the lactic dehydrogenase (LDH) method, MTT method, and propidium iodide (PI) method. Sph had cytotoxic effects via apoptosis on both the KFs and NFs. Our results indicate that Sph may be applicable to the future treatment of keloid.

Apoptosis↗
PubMed2003

Continuous mixed venous oxygen saturation, not mean blood pressure, is associated with early bupivacaine cardiotoxicity in dogs.

PURPOSE: To investigate changes of continuous mixed venous oxygen saturation (cSvO(2)) and mean arterial blood pressure (MBP) in dogs with bupivacaine-induced cardiac depression. METHODS: Bupivacaine was infused into pentobarbital-anesthetized mongrel dogs (n = 8) at a rate of 0.5 mg.kg(-1).min(-1) until the MBP was 40 mmHg or less (end of bupivacaine infusion; BIE). The infusion time was divided into the early period, first 30 min of bupivacaine infusion and the late period, which was from 30 min of bupivacaine infusion until BIE. cSvO(2) was monitored using a fibreoptic pulmonary artery catheter, and MBP and cardiac output (CO) were measured every ten minutes after the initiation of bupivacaine infusion. Arterial blood gas, serum electrolyte and bupivacaine concentration were measured simultaneously. The relationships between CO and cSvO(2), and of CO vs MBP were compared by regression analysis in the early and late periods. RESULTS: The Pearson's correlation coefficients between CO and cSvO(2) were 0.782 (P = 2.1 x 10(-7)) in the early period and 0.824 (P = 1.3 x 10(-6)) in the late period. The correlation coefficients between CO and MBP were 0.019 (P = 0.921) in the early period and 0.799 (P = 4.8 x 10(-6)) in the late period. CONCLUSIONS: cSvO(2), but not MBP, is associated with CO changes in bupivacaine-induced cardiac depression during the early period of bupivacaine intoxication. Decrease of MBP with low cSvO(2) observed during the late period might imply severe cardiac depression induced by bupivacaine infusion.

Anesthetics, Local↗
PubMed2003

Effects of ethanol on the rat glutamate excitatory amino acid transporter type 3 expressed in Xenopus oocytes: role of protein kinase C and phosphatidylinositol 3-kinase.

BACKGROUND: Glutamate is a major excitatory neurotransmitter in the central nervous system. Glutamate transporters play a critical role in maintaining extracellular glutamate concentrations. We investigated the effects of ethanol on a neuronal glutamate transporter, excitatory amino acid transporter type 3 (EAAT3), and the role of protein kinase C (PKC) and phosphatidylinositol 3-kinase (PI3 K) in mediating these effects. METHODS: EAAT3 was expressed in Xenopus oocytes by injection of EAAT3 messenger RNA. By using a two-electrode voltage clamp, membrane currents were recorded after the application of l-glutamate. Responses were quantified by integration of the current trace and reported as microcoulombs. Data are mean +/- SEM. RESULTS: Ethanol enhanced EAAT3 activity in a concentration-dependent manner. At 25, 50, 100, and 200 mM of ethanol, the responses were significantly increased compared with control values. Kinetic study demonstrated that ethanol (50 mM) significantly increased Vmax (3.48 +/- 0.2 microC for control versus 4.16 +/- 0.24 microC for ethanol; n = 19; p < 0.05) without a significant change in the Km (65.6 +/- 11.1 microM for control versus 55.8 +/- 9.6 microM for ethanol; n = 19; p > 0.05) of EAAT3 for glutamate. Preincubation of the oocytes with phorbol-12-myristate-13-acetate (PMA) significantly increased EAAT3 activity (0.98 +/- 0.08 muC for control versus 1.28 +/- 0.09 microC for ethanol; n = 19; p < 0.05). However, there was no statistical difference among the responses of EAAT3 to PMA, ethanol, or PMA plus ethanol. Although the PKC inhibitors chelerythrine and staurosporine did not decrease the basal EAAT3 activity, they abolished the enhancement of EAAT3 activity by ethanol. Pretreatment with wortmannin, a PI3 K inhibitor, also abolished the ethanol-enhanced EAAT3 activity. CONCLUSIONS: These results suggest that acute ethanol exposure increases EAAT3 activity at clinically relevant concentrations and that PKC and PI3 K may be involved in mediating these ethanol effects.

Amino Acid Transport System X-AG↗
PubMed2003

The neurotoxicity of epidural hyaluronic acid in rabbits: a light and electron microscopic examination.

UNLABELLED: Because hyaluronic acid (HA) has an antiinflammatory effect and prevents and/or reduces tissue adhesion, we believed it possible that epidurally-administered HA during epidural adhesiolysis procedures could alleviate pain in patients with chronic lower back pain. Therefore, we performed this pre-clinical trial evaluation of epidurally-administered HA neurotoxicity by light microscopy (LM) and electron microscopy (EM) in rabbits. Twenty rabbits were randomly divided into two groups, a normal saline (NS) group (n = 10) and a HA group (n = 10). Saline (0.2 mL/kg of 0.9% solution) and the same volume of HA were injected into the epidural space. No rabbits showed any sensory-motor or behavior change during the 3-wk period, except for one rabbit in the NS group that showed decreased appetite, activity, and weight loss. By LM, two rabbits in the NS group showed abnormal findings considered to be the result of trauma and infection associated with epidural catheterization. EM findings showed no significant neurotoxic findings in either group. In conclusion, epidurally-administered HA did not cause neurotoxicity in rabbits. IMPLICATIONS: We performed a pre-clinical trial evaluation on the neurotoxicity of hyaluronic acid administered epidurally by light microscopy and electron microscopy in rabbits. Epidurally-administered hyaluronic acid did not produce any sign of neurotoxicity in rabbits.

Animals↗
PubMed2002

Expression of inducible nitric oxide synthase in skin lesions of acute herpes zoster.

Histopathologically, the skin lesions of acute herpes zoster (AHZ) are characterized by epidermal necrotic vesicles with inflammation. Nitric oxide (NO) is generated from L-arginine by nitric oxide synthase (NOS), and immune inflammation involves the activation of NOS in both effector cells and target cells. NO can cause apoptosis and necrosis of target cells such as keratinocytes. We proposed that a large burst of NO in AHZ may cause the epidermal necrosis. Skin biopsies were taken from 13 patients with AHZ. The expression of inducible-type NOS (iNOS) was examined by immunoperoxidase staining and reverse transcription-polymerase chain reaction (RT-PCR). In the skin specimen of AHZ, moderate-to-strong staining for iNOS was observed in inflammatory cells and necrotic keratinocytes, while weak staining was observed in non-necrotic peripheral keratinocytes. RT-PCR using skin specimen of AHZ corroborated the immunoperoxidase findings, yielding bright bands for iNOS. Normal control skin showed minimal or negative expression both by immunoperoxidase stains and RT-PCR. Increased expression of iNOS is consistent with the hypothesis that high level of NO induced by iNOS may be associated with the epidermal necrosis with inflammation seen in the skin lesions of AHZ.

Adult↗