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S Y Yoo

Publications and source records attributed to S Y Yoo.

At least 19 recordsLinked to original sources

Real-time compound ultrasonography: pictorial review of technology and the preliminary experience in clinical application of the abdomen.

The purposes of this essay are to illustrate the technology overview and theoretical benefits of real-time compound ultrasonography (US) and to present our preliminary clinical experience in the evaluation of normal and diseased abdomens. The application of compounding principles to real-time US and its recent reintroduction into mainstream commercial systems have offered new opportunities for its clinical application to the routine examination of the abdomen. In our early preliminary experience, this technique effectively suppressed many of the US artifacts, better depicted the margin or boundary of the lesion, and increased contrast resolution or lesion conspicuity. Therefore, we believe that real-time compound US is a promising technique that may enhance the diagnostic confidence of the examination in the evaluation of normal and diseased abdomens.

Abdomen↗

Is body mass index the prognostic factor in breast cancer?: a meta-analysis.

This study was performed to integrate the results of previous studies that investigated the relationship between body mass index (BMI) and prognosis in breast cancer. We reviewed the English literatures using the MEDLINE database from 1966 to 1999. The materials included 12 published articles with a total of 8,029 cases of breast cancer. The effect size was obtained from hazard ratio in each study. Homogeneity test was conducted before the integration of each effect size and the result demonstrated that the studies were heterogeneous. A random effect model was used to integrate the overall effect size. The integrated effect size was 1.56 (95% confidence interval, 1.22-2.00). In addition, publication bias should be accounted for because each published study was asymmetric in shape revealed by funnel plot. These results suggest that BMI have a prognostic significance in breast cancer. We believe that well-designed longitudinal studies, involving a large number of samples are required to resolve these issues.

Body Mass Index↗

Adaptive response is differently induced depending on the sensitivity to radiation-induced cell death in mouse epidermal cells.

We investigated the relationship between induction of radio-adaptive response and cell death in mouse normal and neoplastic epidermal cells. Mouse normal primary keratinocytes (PK), cancer-prone cells [v-rasHa-transfected mouse keratinocytes (ras-PK), and line 308 cells (mouse skin papilloma cells which have activated rasHa gene with A-to-T transversion at codon 61) were primed with a low dose of gamma-rays (0.01 Gy), and were challenged with a high dose (4 Gy) after a 4 or 7 h interval. The induction of cell death in PK was 2-10 times higher and was also more rapid in PK than in ras-PK or 308 cells. Low-dose pretreatment with a 4 h interval decreased cell death, and this adaptive response was prominent in PK, whereas it was less obvious in the cases of ras-PK and 308 cells. The response of each protein kinase C (PKC) isozymes to high-dose radiation, especially PKCalpha, PKCdelta, PKCepsilon, and PKCeta, were different between the normal and ras oncogene-activated neoplastic keratinocytes; translocation of these isozymes to membrane occurred more rapidly in normal than in neoplastic cells. Furthermore, low-dose pretreatment did not induce the translocation of PKCdelta in PK significantly more than in ras-PK and 308. Thus, the difference in the induction of radio-adaptive responses between mouse normal and neoplastic epidermal cells reflects difference in the rapidity of cell death, and responsiveness of PKC may affect this adaptive response.

Adaptation, Physiological↗

Inducible heat-shock protein 70 is involved in the radioadaptive response.

Park, S-H., Lee, S-J., Chung, H-Y., Kim, T-H., Cho, C-K., Yoo, S-Y. and Lee, Y-S. Inducible Heat-Shock Protein 70 Is Involved in the Radioadaptive Response. The thermoresistant (TR) clone of radiation-induced fibrosarcoma (RIF) cells showed an adaptive response, i.e. a reduced effect, after exposure to a higher challenging dose (4 Gy) when the priming dose (1 cGy) was given 4 or 7 h earlier, but RIF cells did not. Since inducible Hsp70 expression was different in cells of these two cell lines, the role of inducible Hsp70 in the adaptive response was examined. When inducible Hsp70 was transfected into RIF cells, the adaptive response was acquired. Transfection of inducible Hsp70 to NIH 3T3 mouse embryo cells also conferred radioresistance to the cells as assayed by clonogenic survival, [(3)H]thymidine incorporation, and an ELISA cell death detection kit. An increased tendency for the induction of an adaptive response was also observed. Interestingly, basal levels of Ca(2+)-dependent and independent Pkc activities were increased by transfection with inducible Hsp70 compared to those of control vector cells. Irradiation with gamma rays induced activation of Pkc within minutes in control vector cells, while transfection with inducible Hsp70 did not. Cellular redistribution to particulate fractions of Pkca, d and z after exposure gamma rays also was not detected. Furthermore, radioresistance by transfection with inducible Hsp70, as tested by clonogenic survival, disappeared after pretreatment with Pkc inhibitors, 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H7), prolonged treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA), and GF109203X. Taken together, these data suggest that radioresistance inducible by Hsp70 is associated with an elevated level of Pkc activity.

3T3 Cells↗

Hsp25-induced radioresistance is associated with reduction of death by apoptosis: involvement of Bcl2 and the cell cycle.

We previously demonstrated the protective effect of the small heat-shock protein against oxidative damage induced by tumor necrosis factor alpha. Here we have extended our studies of the possible role of Hsp25 in ionizing radiation-induced damage. For these studies, we transfected murine fibroblast L929 cells with the Hsp25 gene and selected three stably transfected clones. Hsp25 overexpression conferred radioresistance as detected by clonogenic survival and induction of apoptosis. Interestingly, the Hsp25-transfected cells showed an increase in the level of the anti-apoptosis molecule Bcl2. We also observed alterations of cell growth in the Hsp25-transfected cells. The cell cycle time of Hsp25-transfected cells was 3-4 h slower than that of vector-transfected control cells. Flow cytometry analysis of synchronized cells at late G(1) phase by mimosine treatment also showed the growth delay in Hsp25-overexpressing cells. In addition, reduced cyclin D1, cyclin A and Cdc2 levels and increased levels of Cdkn1a (also known as p21(Waf)) were observed in Hsp25-transfected cells, which probably caused the reduction in cell growth. In addition, synchronization by mimosine treatment only partially altered radioresistance in the Hsp25-transfected cells. Taken together, these data suggest that Hsp25-induced radioresistance is associated with growth delay as well as induction of Bcl2.

Animals↗

Influence of ionizing radiation on induction of apoptotic cell death and cellular redistribution of protein kinase C isozymes in mouse epidermal cells differing in carcinogenesis stages.

Although protein kinase C (PKC) plays an important role in cellular response to radiation, little is known about the specific role of each isoform in the radiation induced cellular response. In this study, the induction of apoptosis and subcellular distribution of PKC isoforms after gamma-ray irradiation were examined in three kinds of mouse epidermal cells with different stages of carcinogenesis (normal mouse keratinocytes, PK: v-rasHa transfected mouse keratinocytes, ras-PK; and neoplastic cells from mouse skin papilloma, 308 cells). The induction of apoptosis was different in normal and neoplastic cells; in normal cells after 16 Gy of radiation, apoptosis was 2-10 times higher than that in ras-PK or 308 cells, and was rapidly induced; other cells died more slowly, depending on the stage of carcinogenesis. The responses of each PKC, especially rapid translocation of PKCdelta and no response of PKCepsilon by radiation in normal cells may influence the induction of apoptosis by radiation.

Animals↗

Different induction of adaptive response to ionizing radiation in normal and neoplastic cells.

Since the beneficial effects of low-dose radiation (0.01 Gy) are usually observed in normal cells, we investigated whether the adaptive response was induced by low-dose radiation in neoplastic cells of different origin as well as in normal cells. Cell lines used in this experiment were as follows: mouse lymphocytes (NL); L929 cells established from mouse connective tissue; primary mouse keratinocytes (PK); line 308 from mouse papilloma; X-ray sensitive lymphoma cells, L5178Y-S and EL-4 cells from mouse lymphoma. The adaptive response was determined by cell survival and apoptosis. The involvement of apoptosis in the adaptive response was examined by ELISA and TUNEL assay. Adaptive response was induced by pretreatment with low-dose radiation of 0.01 Gy in normal cells such as NL, L929, and PK, but not in L5178Y-S, EL-4, and line 308 cells. In addition, the reduction of apoptosis by pretreatment with low-dose radiation was observed in NL, L929, and PK, but not in L5178Y-S, EL-4, and line 308 cells. These results suggested that the adaptive response could be induced by pretreatment with low-dose radiation and the phenomena were observed in normal cells, not in neoplastic cells. In addition, pretreatment with low-dose radiation reduced apoptosis, suggesting that an anti-apoptotic pathway may be involved in the adaptive response.

Adaptation, Physiological↗

Increased induction of Ca2+-mediated differentiation by gamma ray is mediated by endogenous activation of the protein kinase C signaling pathways in mouse epidermal cells.

PURPOSE: The aim of this study was to determine whether gamma-rays can affect Ca2+-induced differentiation in normal and neoplastic mouse epidermal cells. METHODS AND MATERIALS: After gamma-ray irradiation, primary and v-rasHa transformed mouse keratinocytes were cultured for 48 h in 0.12 mM Ca2+-containing media, and cellular translocation from cytosolic to particulated fraction of each PKC isozyme and expressions of differentiation markers were examined. RESULTS: Morphological difference was seen at 48 h after irradiation in both Ca2+-shifted normal and v-rasHa transformed cells; v-rasHa cells were more resistant to the radiation than normal cells. Radiation potentiated granular cell-differentiation marker expressions (filaggrin, loricrin, and SPR-1) in both normal and v-rasHa transformed cells. In the case of spinous cell markers, the expression of keratins K1 and K10, which are usually blocked in v-rasHa cells was increased after irradiation. However, there was no change of K8 expression level, which can be seen only after v-rasHa transfection. Cellular fractionation and immunoblot analysis with antibodies against PKCalpha, delta, epsilon, eta, and xi revealed that PKCalpha was responsible for the differentiation marker expression. CONCLUSIONS: These findings suggest that PKCalpha is an important component of the signaling pathway regulating radiation-induced differentiation in both normal and neoplastic epidermal cells.

Animals↗

Increased expression of ornithine decarboxylase by gamma-ray in mouse epidermal cells: relationship with protein kinase C signaling pathway.

The correlation between ornithine decarboxylase (ODC) protein induction and specific protein kinase C (PKC) isozyme expression by gamma-ray in 12-O-tetradecanoylphorbol-13-acetate (TPA)-treated normal and v-rasHa transformed mouse keratinocytes was examined. TPA at 100 nM was treated in primary mouse keratinocytes immediately after 4 Gy, 8 Gy and 16 Gy gamma-ray irradiation. After 4 hrs, cells were harvested and the protein expression levels of PKC isozymes (PKC alpha, -delta, -epsilon, -eta and -zeta) and ODC were examined. For v-rasHa infection, primary keratinocytes were infected with a defected retrovirus containing the v-rasHa gene. After 3 hrs of irradiation, each PKC isozyme and ODC protein expression were tested. Gamma-ray increases ODC protein expression in both TPA-treated normal and v-rasHa transformed mouse keratinocytes and this phenomenon correlated to the increased induction of PKC alpha without altering other PKC isozymes. Tyrosine phosphorylation of epidermal growth factor receptor protein was also stimulated during gamma-ray induced cellular changes in TPA-treated normal mouse keratinocytes. These results indicate that PKC alpha as an important regulator of mouse epidermal changes by gamma-radiation, contributes to the ODC expression occurring during exposure to tumor promoter, such as TPA, and epidermal neoplasia induced by ras activation.

Animals↗

Enhancement of radiation-inducible hepatic glutathione-S-transferases Ya, Yb1, Yb2, Yc1, and Yc2 gene expression by oltipraz: possible role in radioprotection.

Previous studies have shown that radiation in combination with oltipraz enhances hepatic microsomal epoxide hydrolase expression. The effects of gamma-ray radiation exposure in combination with oltipraz on the expression of hepatic glutathione-S-transferase (GST) subunits Ya, Yb1, Yb2, Yc1, and Yc2 were examined in the rat. Northern RNA blot analyses revealed that GST mRNA levels were altered in response to daily 3- or 0.5-Gy doses of radiation. The hepatic GST mRNA levels were transiently decreased at 3 and 8 hr after a single 3-Gy dose of radiation. The GST Ya, Yb1, Yb2, Yc1, and Yc2 mRNA levels were increased by 2-4-fold at 15 and 24 hr after irradiation with 3 Gy, followed by return to the levels of untreated rats at 48 hr after treatment. The treatment of animals with oltipraz alone resulted in dose-related increases in the GST Ya, Yb1, Yc1, and Yc2 mRNA levels, whereas Yb2 mRNA levels were, minimally increased. Although a single dose of oltipraz (30 mg/kg orally) caused a minimal 2-fold elevation in the hepatic GST Ya mRNA level, exposure of animals to both oltipraz and 3-Gy radiation resulted in a 4-fold relative increase in GST Ya mRNA level, indicating that the Ya mRNA expression was additively enhanced by the combination treatment. The Yb1/2 and Yc1/2 mRNA expressions were also enhanced by oltipraz in combination with radiation. Multiple exposure of rats to daily 0.5-Gy radiation caused time-related increases in GST gene expression. The greatest enhancement in GST expression was observed at 24 hr after a single 0.5-Gy dose of radiation in conjunction with oltipraz (e.g., a 9-fold relative increase in GST Ya), whereas the relative additive increases in GST mRNA were less pronounced at day 3 or 5 after treatment. These increases in the GST mRNA levels were consistent with those in the immunochemically detectable GST protein levels. Histopathological examinations revealed that exposure of rats to radiation (0.5 Gy/day for 3-5 days) caused mild-to-moderate hepatocyte degeneration with sinusoidal congestion, whereas oltipraz (30 mg/kg/day for 3 days) was effective in blocking the radiation-induced liver injury. The enhanced expression of these GST isoforms by oltipraz may be associated in part with its hepatoprotective effect against the injury caused by ionizing radiation.

Animals↗

Enhancement of radiation-induced hepatic microsomal epoxide hydrolase gene expression by oltipraz in rats.

The effects of radiation exposure in conjunction with oltipraz, a chemopreventive agent, on the expression of the gene encoding hepatic microsomal epoxide hydrolase (mEH) were examined in rats. Rats exposed to a single dose of 3 Gy gamma rays exhibited timerelated changes in the hepatic mEH mRNA level. Whereas the mEH mRNA level was transiently decreased at 3 and 8 h after irradiation, the mRNA levels were increased 3- to 4-fold at 15 to 48 h postirradiation, returning to the level in untreated animals at 72 h. Treatment of rats with oltipraz resulted in 1- to 19-fold increases in hepatic mEH mRNA levels 24 h post-treatment at doses of 5-200 mg/kg. Although treatment with oltipraz at a dose of 30 mg/kg affected the mEH mRNA level minimally (i.e. approximately 2-fold), 3 Gy whole-body irradiation along with oltipraz treatment resulted in a 9-fold increase in the mEH mRNA level at 24 h post-treatment. Treatment of animals with both oltipraz and 3 Gy gamma radiation for 3 consecutive days resulted in a 7-fold increase in mEH mRNA, showing that the increases in mEH mRNA were enhanced by the combination treatment. In rats irradiated with 3 Gy for 5 consecutive days, however, the mEH mRNA level failed to increase due to cell injury. Studies were further designed to assess the effects of 0.5 Gy ionizing radiation and concomitant oltipraz treatment. RNA blot analysis showed that mEH mRNA levels failed to be significantly altered at 3, 8, 15, 24 and 48 h after a single dose of 0.5 Gy. Nonetheless, exposure of animals to 0.5 Gy daily for 3 to 5 consecutive days caused a 3-fold elevation in the hepatic mEH mRNA level. Furthermore, treatment of animals with both oltipraz (30 mg/kg/day) and 0.5 Gy of gamma rays resulted in an enhanced elevation in the mEH mRNA level at 24 h post-treatment compared to the individual treatment, resulting in a 7-fold relative increase. The enhanced expression of hepatic mEH mRNA by 0.5 Gy gamma radiation and oltipraz was also observed after treatment for 3 to 5 days (8- to 6-fold relative increases). Western immunoblot analyses showed that hepatic microsomes produced from the rats treated with 0.5 Gy daily for 3 to 5 days resulted in a approximately 2-fold induction of hepatic mEH and that rats exposed to radiation in combination with oltipraz showed 3-fold increases in the liver mEH protein. Thus the relative increase in mEH mRNA levels was consistent with the expression of the protein. These results demonstrate that ionizing radiation causes alterations in hepatic mEH gene expression with the induction of the protein and that the mEH gene expression is enhanced by oltipraz treatment.

Animals↗

Present status of fast neutron therapy in Asian countries.

In Asian countries, fast neutron therapy was first introduced at the National Institute of Radiological Sciences (NIRS), and followed by the Institute of Medical Science (IMS), Tokyo University, and Korea Cancer Center Hospital (KCCH). At NIRS, 2,129 patients were treated with d(30 MeV)+Be neutrons between 1975 and 1994. There were 274 patients referred for the treatment with P(50.5 MeV)+Be neutrons at KCCH during the period of 1986 through 1992. Unfortunately, fast neutron therapy performed at IMS was discontinued in 1991, where 458 patients had been treated with d(14 MeV)+Be neutrons since 1976. At NIRS, a vertical beam with multileaf collimator system was used for treatment of patients referred. The results showed that local control rates were 79% (19/24), 53% (14/26), and 89.3% (50/56) for carcinoma of the salivary gland, osteogenic sarcoma and carcinoma of the prostate, while complications for those were found to be 8.8, 8.3 and 17.8%, respectively. In the treatment of carcinoma of the lung, results were better for patients with adenocarcinoma than those with squamous cell carcinoma. Of 32 patients suffering from Pancoast tumor, 14 achieved local control, whereas 2 of 32 patients developed complications. On the other hand, salvage surgery was required in the treatment of malignant melanoma. In the treatment of malignant glioma, dose localization has to be improved in the target area to confirm local control. Experiences performed at KCCH have shown that, of 53 patients suffering from unresectable primary or recurrent rectal carcinomas, 28 achieved local control. It was concluded from the experiences with fast neutrons in Asian countries that adenocarcinomas as well as slowly growing tumors are indications for fast neutrons and that dose localization has to be improved in order to advance high LET radiation therapy. Clinical trials with 70 MeV protons started at NIRS in 1979, where the aim of study has been focused on treatment of choroidal melanoma, whereas, at Tsukuba University, 250 MeV protons have been used in the treatment of tumors deeply seated. Based on experiences of fast neutrons and protons, clinical trials with heavy ions initiated at NIRS in October 1994. Clinical studies with high LET radiations will be performed by using heavy ions in order to pursue indications of particle radiation therapy.

Fast Neutrons↗

Pitfalls of nonoperative management of blunt abdominal trauma in children in Korea.

During the past decade, the nonoperative management of children with blunt abdominal trauma without operation has improved dramatically by virtue of the development of medical technology. However, missed injuries or complications after nonoperative management often are associated with serious morbidity. The authors evaluated 86 patients between 1990 and 1994 who had intraabdominal solid-organ injury (excluding retroperitoneal organs) owing to blunt trauma. The liver was injured in 43 cases, the spleen in 36, and the pancreas in 14. Initially, 68 patients (79%) were managed conservatively and 18 underwent surgery because of unstable vital signs or associated injuries. Three patients had delayed surgery more than 48 hours after trauma) because of initially missed injuries (complete infarction of the spleen, duodenal injury, major pancreatic injury). Eleven patients (17%) with nonoperative management had a total of 13 complications. The most common complications were pleural effusion and atelectasis. One patient had prolonged ileus owing to delayed absorption of an intraperitoneal hematoma, and the symptom was relieved by aspiration of the hematoma. A huge hepatic subcapsular hematoma developed in another patient and required percutaneous drainage with a pigtail catheter for 5 weeks. A pancreatic pseudocyst detected on the 16th hospital day also was drained with a pigtail catheter. A splenic abscess developed in another patient 24 days after a splenic injury, which was treated with ultrasound-guided aspiration. No patients died as a result of nonoperative management. In conclusion, even though patients with blunt abdominal trauma are stabilized and nonoperative management decided on, careful follow-up for a prolonged period is still necessary to prevent missed injuries or late complications.

Abdominal Injuries↗

Protein biosynthesis in low dose ionizing radiation-adapted human melanoma cells.

Adaptive responses induced by low dose gamma-ray irradiation in human melanoma cells were examined using a clonogenic assay. Survival fractions were significantly increased in cells irradiated with low dose gamma-rays then 4 hrs later with high dose gamma-ray as compared to cells irradiated only with high dose gamma-rays. When low dose irradiation was given 20 hrs prior to high dose irradiation, however, no adaptive response was induced. Changes in protein biosynthesis in human melanoma cells were observed under the same conditions. Significant changes in protein biosynthesis occurred in the nuclear and membrane proteins of cells first irradiated with a low dose then a high dose of gamma-rays after 4 hrs. No such changes were found in cells irradiated with low dose gamma-rays 20 hrs prior to high dose irradiation, consistent with the results of the clonogenic assay. Our findings suggest that prior treatment with low dose gamma-rays induces an adaptive response that has a significant effect on the induction of the nuclear and membrane protein biosynthesis caused by high dose gamma-ray irradiation of human melanoma cells.

Adaptation, Physiological↗

Acute renal failure caused by fungal bezoar: a late complication of Candida sepsis associated with central catheterization.

The authors report a case of acute renal failure caused by fungal bezoar in the renal pelvis. The patient was successfully treated with bilateral percutaneous nephrostomy drainage. He had been admitted because of necrotizing enterocolitis, at the age of 26 days. Eventually, his bowel was reduced to 40 cm of small intestine, including 5 cm of terminal ileum. Candida sepsis developed during central total parenteral nutrition, at the age of 76 days. Five weeks after the diagnosis of systemic candidiasis, sudden anuria developed, and ultrasonography showed echogenic material in both renal pelvises. Bilateral percutaneous nephrostomy catheters were placed in the renal pelvises, and local irrigation with amphotericin B was performed for 3 weeks. The renal function of the baby was completely recovered, without systemic antifungal treatment.

Acute Kidney Injury↗

How important is the role of the internal anal sphincter in fecal continence? An experimental study in dogs.

It is a generalized concept that the internal anal sphincter (IAS) plays a significant role in fecal continence by generating high pressure in the anal canal at rest and relaxation during rectal distention. Agreement also exists on the importance of internal sphincter-saving anoplasty on anorectal malformations in establishing anal continence. Twelve dogs were divided into four groups. Group 1, a control group, was subjected to a perirectal dissection only. Group 2 underwent the same perirectal dissection plus a 2-cm resection of the anal canal. Group 3 underwent the perirectal dissection plus a 4-cm resection of the anal canal, and group 4 underwent perirectal dissection and transposition of the anus to the posterolateral portion of the voluntary muscle mass. Clinical continence was evaluated, and manometric results were compared with preoperative measurements. All dogs in groups 1, 2, and 3 were clinically continent without soiling except one in group 3, and also manometric results showed minimal change between preoperative and postoperative anal pressure profiles. The transposed anus of group 4 showed continuous fecal soiling. The anal resting pressure (ARP) was also decreased but still existed in this group. This experimental study showed that the IAS contributes to the anal resting tone. However, resection of the IAS did not completely interfere with fecal continence. The smooth muscle of pulled-through rectum seemed to partly take over the function of the IAS.

Anal Canal↗

Trends in radiation therapy facilities-1986 to 1991.

The Korean Society of Therapeutic Radiology has periodically conducted a national survey on the status of radiation therapy facilities in Korea. This paper summarized survey data on the status of radiation therapy facilities, manpower, megavoltage equipments, patient load, types of procedures performed and characteristics of the patients treated.

Data Collection↗