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Biomedical subjects

W H Park

Publications and source records attributed to W H Park.

At least 19 recordsLinked to original sources
PubMed2006

Influence of bladder management on epididymo-orchitis in patients with spinal cord injury: clean intermittent catheterization is a risk factor for epididymo-orchitis.

STUDY DESIGN: Retrospective study, based on cases of spinal cord injury (SCI). OBJECTIVES: To establish hazard ratios for risk of epididymo-orchitis in SCI. SETTING: South Korea. METHODS: A total of 140 male patients injured before 1987 were eligible for this investigation and have been followed up on a yearly basis from January 1987 to December 2003. RESULTS: The average age at which the lesion occurred was 24.8 years old (range, 18-53). The average time since SCI was 16.9 years (range, 1-37). A total of 34 lesions (24.3%) were complete and 106 (75.7%) were incomplete. Over the 17 years, 39 patients (27.9%) were diagnosed with epididymo-orchitis. Epididymo-orchitis was more common for patients with a history of urethral stricture (66.7 versus 25.2%, P=0.014). We also found that epididymo-orchitis was more common for patients on clean intermittent catheterization (CIC) than with indwelling urethral catheterization (42.2% versus 8.3%, P=0.030). In multivariate analysis, patients on CIC had a 7.0-fold higher risk (odds ratio, 6.96; 95% confidence interval, 1.26-38.53; P=0.026); however, a history of urethral stricture lost statistical significance (P=0.074). For other variables, no positive association with epididymo-orchitis was observed. CONCLUSIONS: In this study, CIC was an independent risk factor for the development of epididymo-orchitis in patients with SCI. In addition, our findings suggest that urethral stricture may be a contributing factor for the development of epididymo-orchitis in these patients. Correct instructions about CIC are of utmost importance.

Adolescent↗
PubMed2001

Cystic rectal duplication: a rare cause of neonatal bladder-outlet obstruction and hydronephrosis.

A case of cystic rectal duplication (RD) is presented. A 7-day-old female was admitted with acute urinary retention, voiding difficulty, and abdominal distention since she was 4 days of age. Ultrasound and abdominal computed tomography (CT) demonstrated a huge, cystic mass in the pelvis and abdomen that resulted in acute urinary retention and bilateral hydronephrosis. CT-guided drainage of the lesion followed by transabdominal surgical excision resulted in a cure. Pathologic examination demonstrated a RD lined by respiratory epithelium.

Cysts↗
PubMed2001

Technical innovation for noninvasive and early diagnosis of biliary atresia: the ultrasonographic "triangular cord" sign.

In this article, we introduce our experience regarding a new and noninvasive diagnostic tool, using ultrasonography, for the early and definite diagnosis of biliary atresia. We have focussed on the ultrasonographic image of the cone-shaped periportal fibrous mass in infants with biliary atresia since 1992, and have finally identified a triangular or band-like periportal echogenicity ("triangular cord" sign), mainly cranial to the portal vein. Based on our experience and other reports from Japan and Singapore, the ultrasonographic triangular cord sign is a simple, time-saving, highly reliable, and definite tool in the diagnosis of biliary atresia from infantile intrahepatic cholestasis, representing a positive predictive value greater than 95%. We have proposed a new diagnostic strategy in the evaluation of infantile cholestasis, with emphasis on the ultrasonographic triangular cord sign.

Biliary Atresia↗
PubMed2001

Phenol block of peripheral nerve conduction: Titrating for optimum effect.

OBJECTIVES: To verify the dose-response relationship in phenol nerve block and to determine the concentration and volume of phenol injectate required for effective nerve conduction block. DESIGN: Before-after, experimental study. SETTING: A research institute laboratory. ANIMALS: Seventy-one New Zealand white rabbits. INTERVENTIONS: Group I (n = 48) received tibial nerve block by perineural injection (phenol, n = 40; saline, n = 8), group II (n = 21) by submerging the nerve in phenol solution. The 6 subgroups of group I each received different concentrations (3%, 4%, 5%) and volumes (0.1mL, 0.2mL, 0.3mL). The 2 subgroups of group II received 3% (n = 8) and 5% (n = 13) phenol. MAIN OUTCOME MEASURES: Compound muscle action potential (CMAP) and tension of triceps surae muscles by electric stimulation of the sciatic nerve were measured preintervention and at day 1, and weeks 1, 2, 4, and 8 postblock. Histologic studies were performed on 2 animals from group I. RESULTS: Two rabbits in group I died before results were obtained. In the remaining animals, CMAP amplitude reduced significantly (p <.05) as the volume of 5% phenol solution increased from 0.1mL, 0.2mL, to 0.3mL. A high concentration of phenol produced a more pronounced conduction block; however, no significant (p =.0589) difference existed among the 3 concentrations. Submerged tibial nerve had a greater degree of conduction block than perineurally injected nerve. Depth of the degeneration area in nerve fascicle varied with distance from the injection point. CONCLUSIONS: The nerve block effect of phenol can be titrated by adjusting the concentration and volume of phenol solution if the technique of application and localization of a block site are standardized.

Action Potentials↗
PubMed2001

Potential role of caspase-3 and -9 in arsenic trioxide-mediated apoptosis in PCI-1 head and neck cancer cells.

Arsenic trioxide (As2O3) has been shown to inhibit the proliferation of hematologic malignant cells. Previously, we reported that As2O3 had an antitumoral effect in head and neck cancer. Here, we investigated the induction of apoptosis and its mechanism in PCI-1 head and neck squamous carcinoma cells, after treatment with As2O3. Treatment with 2 microM of As2O3 caused apoptosis in PCI-1 cells following 3 days of exposure, which was detected by the annexin V-PI and DAPI staining methods. The cell death population was markedly increased, being 88% larger than the As2O3-untreated control cells. To address the mechanism of apoptosis, a Western blot assay was performed, showing that Bax was up-regulated without a change in Bcl-2. Activation of caspase-9 during As2O3-induced apoptosis was substantiated by monitoring the proteolysis of the caspase-9, which was associated with an increase of Apaf-1 and cytochrome c protein. PCI-1 cells rapidly changed the mitochondria membrane potential (DeltaPsim) after addition of As2O3. Furthermore, activation of caspase-3 was demonstrated by monitoring the proteolysis of the caspase-3 and by measuring caspase-3 activity with a fluorogenic substrate, which was associated with the cleavage of poly(ADP-ribose) polymerase. To examine the in vivo effect of As2O3, C3H mouse inoculated with syngenic SCC7 cells was treated by intratumoral injection of As2O3 (300 microg) every day, demonstrating that tumor mass was dramatically reduced on day 4, and revealed induction of apoptosis by TUNEL assay. These results suggest that apoptosis of PCI-1 cells by As2O3 is induced by activation of caspase-3 via cytochrome c, caspase-9 and Apaf-1 complex.

Animals↗
PubMed2000

Arsenic trioxide-mediated growth inhibition in MC/CAR myeloma cells via cell cycle arrest in association with induction of cyclin-dependent kinase inhibitor, p21, and apoptosis.

We investigated the in vitro effect of As2O3 on proliferation, cell cycle regulation, and apoptosis in human myeloma cell lines. As2O3 significantly inhibited the proliferation of all of eight myeloma cell lines examined in a dose-dependent manner with IC50 of approximately 1-2 microM. DNA flow cytometric analysis indicated that As2O3 (2 microM) induced a G1 and/or a G2-M phase arrest in these cell lines. To address the mechanism of the antiproliferative effect of As2O3, we examined the effect of As2O3 on cell cycle-related proteins in MC/CAR cells in which both G1 and G2-M phases were arrested. Western blot analysis demonstrated that treatment with As2O3 (2 microM) for 72 h did not change the steady-state levels of CDK2, CDK4, cyclin D1, cyclin E, and cyclin B1 but decreased the levels of CDK6, cdc2, and cyclin A. The mRNA and protein levels of CDKI, p21 were increased by treatment with As2O3, but those of p27 were not. In addition, As2O3 markedly enhanced the binding of p21 with CDK6, cdc2, cyclin E, and cyclin A compared with untreated control cells. Furthermore, the activity of CDK6-associated kinase was reduced in association with hypophosphorylation of Rb protein. The activity of cdc2-associated kinase was decreased, which was accompanied by the up-regulation of cdc2 phosphorylation (cdc2-Tyr15 phosphorylation) resulting from reduction of cdc25B and cdc25C phosphatases. As2O3 also induced apoptosis in MC/CAR cells as evidenced by flow cytometric detection of sub-G1 DNA content and annexin V binding assay. This apoptotic process was associated with down-regulation of Bcl-2, loss of mitochondrial transmembrane potential (delta psi(m)), and an increase of caspase-3 activity. These results suggest that As2O3 inhibits the proliferation of myeloma cells, especially MC/CAR cells, via cell cycle arrest in association with induction of p21 and apoptosis.

Apoptosis↗
PubMed2000

Cell cycle arrest induced by the vitamin D(3) analog EB1089 in NCI-H929 myeloma cells is associated with induction of the cyclin-dependent kinase inhibitor p27.

EB1089, a 1,25-dihydroxyvitamin D(3) analog, has been known to have potent antiproliferative properties in a variety of malignant cells in vitro and in vivo. In the present study, we analyzed the effect of EB1089 on human myeloma cell lines. EB1089 inhibited the proliferation of NCI-H929 cells and RPMI8226 cells in a dose-dependent manner among three myeloma cell lines tested. The antiproliferative effect of EB1089 on myeloma cells was related to the expression level of vitamin D receptor. To investigate the mechanism of the antiproliferative effect of EB1089, cell cycle analysis was attempted in EB1089-sensitive NCI-H929 cells. EB1089 (1 x 10(-8) M) efficiently induced G(1) arrest of the cell cycle. Analysis of G(1) regulatory proteins demonstrated that protein levels of CDK2, CDK4, cyclin D1, and cyclin A were decreased in a time-dependent manner, but not those of CDK6 and cyclin E, by EB1089. In addition, EB1089 (1 x 10(-8) M, 72 h) increased the protein level of the CDKI p27 and markedly enhanced the binding of p27 with CDK2 compared to EB1089-untreated cells. Furthermore, the activity of CDK2-associated cyclin kinase was decreased, which was accompanied by the reduction of cyclin-D1-, cyclin-E-, and cyclin-A-associated kinase activities, resulting in the hypophosphorylation of Rb protein. These results suggest that EB1089 can inhibit the proliferation of human myeloma cells, especially NCI-H929 cells, via a G(1) block in association with the induction of p27 and the reduction of CDK2 activity.

Antineoplastic Agents↗
PubMed2000

Induction of apoptosis by vitamin D3 analogue EB1089 in NCI-H929 myeloma cells via activation of caspase 3 and p38 MAP kinase.

EB1089, a novel 1,25-dihydroxyvitamin D3 analogue, has been known to have potent antiproliferative properties in a variety of malignant cells both in vitro and in vivo. In the present study, we analysed the effect of EB1089 on NCI-H929 human myeloma cells. EB1089 inhibited cell growth of NCI-H929 and efficiently induced the G1 phase arrest of the cell cycle in a dose-dependent manner. We could also detect apoptosis in NCI-H929 cells exposed to EB1089 (1 x 10-7 M for 72 h) using the sub-G1 group of the cell cycle by FACS and annexin V binding assays. Induction of apoptosis by EB1089 was associated with down-regulation of the Bcl-2 protein without change of the Bax protein. Regarding caspase activity, which plays a crucial role in apoptosis, EB1089-treated NCI-H929 cells revealed an increased activity of caspase 3 protease accompanied by degradation of the PARP protein in a dose- and time-dependent manner. In addition, EB1089 caused the down-regulation of p44 extracellular signal-related kinase (ERK) activity and up-regulation of the p38 kinase activity during apoptosis of NCI-H929 cells. These results suggest that EB1089 inhibits growth of NCI-H929 cells via G1 cell cycle arrest as well as apoptosis by activating p38 kinase and suppressing ERK activity.

Antineoplastic Agents↗
PubMed2000

Solitary sclerotic fibroma of the skin: degenerated sclerotic change of inflammatory conditions, especially folliculitis.

Two cases showing changes of sclerotic fibroma developed in association with an inflammatory process, especially folliculitis. The lesion in the first case showed a well-circumscribed, nonencapsulated nodule in the dermis, which consisted of a perifollicular fibrotic area and a peripheral sclerotic area. In addition to the usual findings of sclerotic fibroma, spindle cells were heavily infiltrated in a storiform and fascicular pattern around the degenerated hair follicle, suggestive of dermatofibroma. The lesion in the second case showed the typical findings of sclerotic fibroma in association with folliculitis and hair follicle remnants. Our observations suggest that solitary sclerotic fibroma of the skin may be a degenerated or sclerotic end stage of other fibrous conditions, such as dermatofibroma, and that it may be induced by inflammation, especially folliculitis.

Adult↗
PubMed2000

A case of linear scleroderma and myasthenia gravis.

We report a case of a 28-year-old woman with myasthenia gravis who developed linear scleroderma seven years later. Myasthenia gravis and scleroderma are rarely found in direct association with each other; there are only five such reported cases, all of which were systemic scleroderma patients. Although localized and systemic scleroderma are distinct entities, autoimmunity is believed to be involved in the pathogenesis of both. Myasthenia gravis and scleroderma may occur coincidentally, but an autoimmune predisposition seems to be the more likely underlying cause, as evidenced by an increased incidence of autoantibodies and autoimmune diseases.

Adult↗
PubMed2000

A case of primary cutaneous actinomycosis.

Primary cutaneous actinomycosis is very uncommon because of the exclusively endogenous habitat of the organism. We report a case of primary cutaneous actinomycosis characterized by histopathological "sulfur granules". The patient had a well-defined subcutaneous nodule on the left thigh without any other lesion and was treated with surgical excision and subsequent oral ampicillin for six weeks. There has been no recurrence during a 1-year period of follow-up.

Actinomycosis↗
PubMed2000

A case of acinic cell adenocarcinoma on the left hemifacial area.

Acinic cell adenocarcinoma is a rare salivary gland tumor which predominantly occurs in the parotid gland. A 46-year-old man presented with a left preauricular mass of one month duration; the pathologic report showed acinic cell adenocarcinoma. He was transferred to the oral and maxillofacial surgery department, and a total parotidectomy was performed. We present this interesting case of acinic cell adenocarcinoma from the parotid gland with cutaneous involvement.

Biopsy, Needle↗
PubMed2000

Effect of a novel vitamin D3 analog, EB1089, on G1 cell cycle regulatory proteins in HL-60 cells.

Progression of cell cycle in eukaryotes is regulated by a series of the cyclin-dependent kinases (CDKs) and cyclin-dependent kinase inhibitors (CDKIs). It has been shown that 1,25(OH)2D3 is able to arrest cell cycle at G1 phase in malignant cells including HL-60 cells. EB1089 is a novel 1,25(OH)2D3 analog that has more potent antileukemic properties with reduced hypercalcemic effect in vitro and in vivo than 1,25(OH)2D3. In the present study, we examined the effect of EB1089 on HL-60 cells at the protein levels of several G1 regulatory proteins. Exposure of HL-60 cells to EB1089 (1x10-8 M) for 3 days showed the G1 block by FACS analysis. The level of p21 was markedly induced in HL-60 cells treated with EB1089 at 24 h, and p27 were progressively increased in a time-dependent manner. The expressions of CDK2 and CDK6 were down-regulated during G1 block of HL-60 cells, and CDK4 is progressively elevated. In addition, level of cyclin D1 was increased in a time-dependent manner, however, no change of cyclin E was noted through the G1 to S traverse. Immunoprecipitation study demonstrated that p27 did not bind to CDK2, CDK4 and CDK6 in EB1089-treated HL-60 cell extracts. In contrast, complexes immunoprecipitated from EB1089-treated HL-60 cells with antibodies CDK2 and CDK6 contained higher amounts of immunodetectable p21 protein compared to untreated HL-60 cells, whereas no detectable change was noted with anti-CDK4 antibody. Furthermore, the kinase activities of CDK2 and CDK6 were decreased while little change was observed in CDK4 activity. These data indicated that p21 protein is a strong candidate for the control of G1 progression in EB1089-treated HL-60 cells, and its major target molecules are CDK2 and CDK6.

Antineoplastic Agents↗
PubMed1999

Effect of arsenic trioxide on cell cycle arrest in head and neck cancer cell line PCI-1.

Arsenic trioxide (As(2)O(3)) has been shown to inhibit the proliferation of hematologic malignant cells. However, little is known about the effect of As(2)O(3) on solid tumor. In this study, we investigated the antitumoral effect of As(2)O(3) on head and neck cancer cell lines in vitro. Treatment of As(2)O(3) inhibited the proliferation of all of 4 cell lines examined in a dose-dependent manner. To address the mechanism of antitumoral effect of As(2)O(3), cell cycle analysis was attempted in As(2)O(3)-most sensitive PCI-1 cells. Treatment of As(2)O(3) (2 microM) induced efficiently G2/M arrest in PCI-1 cells following 3 days of exposure. During the G2/M arrest, cyclin-dependent kinase inhibitor, p21, was increased in a time-dependent manner. Analysis of cell cycle regulatory proteins demonstrated that As(2)O(3) (2 microM) did not change the steady-state levels of CDK2, CDK4, CDK6, cyclin D1, cyclin E and cyclin A, but decreased the protein levels of cdc2 and cyclin B1. Furthermore, treatment of As(2)O(3) markedly enhanced the binding of p21 with cdc2, and the activity of cdc2 kinase was decreased in a time-dependent manner. These results suggest that As(2)O(3) inhibits the proliferation of head and neck cancer cells via G2/M arrest in association with the induction of p21 and the reduction of cdc2 kinase activity.

Antineoplastic Agents↗