Biomedical subjects

Dong Goo Kim

Publications and source records attributed to Dong Goo Kim.

12 recordsLinked to original sources

PubMed2005

Preconditioning by extracorporeal liver support (MARS) of patients with cirrhosis and severe liver failure evaluated for living donor liver transplantation -- a pilot study.

PURPOSE: The aim of this prospective study was to evaluate the effectiveness of preconditioning molecular adsorbent recirculating system (MARS) treatment on patients with acute-on-chronic liver failure (AoCLF), who were awaiting living donor liver transplantation (LDLT). PATIENTS AND METHODS: Between January and December 2001, 10 consecutive AoCLF patients (with progressive hyperbilirubinemia (>20 mg/dl) and hepatic encephalopathy grade > or =2) were studied. MARS was used in eight of these patients who were evaluated for LDLT during 2001. Three AoCLF patients who received LDLT before clinical use of MARS were used as historical controls. RESULTS: Because of a shortage of donors, only five out of 10 patients considered for LDLT could receive transplants. Three patients were treated with MARS for 8 h the day before receiving LDLT, and all three survived. The remaining two patients who received transplants, and who were not pretreated with MARS, died from sepsis and multi-organ failure within 2 weeks. Four of the patients who did not receive transplants because of donor shortage died despite 1 or 3 MARS treatments, however bilirubin levels and grade of encephalopathy were significantly reduced in these patients. CONCLUSIONS: Results of this small pilot study suggest that MARS, by reducing the severity of jaundice and encephalopathy, might be effective as a bridging option in AoCLF patients awaiting LDLT.

Adult↗

PubMed2004

Isolated small bowel transplantation from a living-related donor at the Catholic University of Korea--a case report of rejection -free course-.

The bowel transplantation team at the Catholic Medical Center, Korea, on April 9 2004, accomplished a case of isolated small bowel transplantation (SBT) in a 57 year-old female with short bowel syndrome. The primary surgery was a jejunocolostomy due to mesenteric vein thrombosis, while maintaining 30 cm of the jejunum and colon distal to the splenic flexure. Her renal function was partially unbalanced. During more than 2 years of home TPN, the superior vena cava (VC) and subclavian veins had become occluded, but the inferior VC line remained. SBT was planned due to the repeated life-threatening infections of the last central line. One hundred and fifty centimeter of the distal ileum of the 27 year-old living-related donor, the patient's daughter, was harvested. The graft mesenteric artery and vein were anastomosed to the recipient's inferior mesenteric vessels. A proximal end-to-end jejuno-ileostomy and a distal end-to-side ileo-colostomy of the graft were made, creating a Bishop-Koop enterostomy for graft surveillance. A tube jejunostomy, via a gastrostomy, was established for early feeding and simultaneous gastric drainage. Induction with Daclizumab and immunosuppression consisted of tacrolimus and methylprednisolone, given intravenously, and then mycophenolate mofetil (MMF), enterally from day 3. The patient was discharged on day 42. A CMV infection on day 83 was successfully treated with 3 weeks of gancyclovir therapy. She has been nutritionally independent, with complete oral feeding, and free of rejection until day 170 after the transplantation.

Female↗

PubMed2004

Fasting-induced down-regulation of NADPH-diaphorase in the magnocellular PVN of rats.

In this study, we examined if glucocorticoids are required for the fasting-induced decrease of neuronal nitric oxide synthase (nNOS) in the magnocellular division of the paraventricular nucleus (PVN). Rats were adrenalectomized, subjected to 48 h of food deprivation with/without dexamethasone (5 mg/ kg, 4 subcutaneous injections with 12 h intervals), and the brain slices were processed for NADPH-diaphorase (NADPH- d) staining, a histochemical marker for nNOS in neuronal cells. In food deprived adrenalectomized rats, but not in free fed intact rats, dexamethasone significantly decreased NADPH-d staining in the magnocellular PVN. We previously reported that food deprivation decreases nNOS in the magnocellular PVN of intact rats. Thus, the present results together with our previous report suggest that although glucocorticoids are required for fasting-induced nNOS down-regulation in the magnocellular PVN, glucocorticoids may not be directly involved and some other molecular signals produced by food deprivation may play a pivotal role over glucocorticoid in the regulatory pathway for nNOS expression in this brain region.

Adrenalectomy↗

PubMed2004

RU486 blocks fasting-induced decrease of neuronal nitric oxide synthase in the rat paraventricular nucleus.

It has been reported that food deprivation decreases expression of neuronal nitric oxide synthase (nNOS) in the hypothalamic paraventricular nucleus (PVN). Food deprivation produces autonomic changes and the PVN nitric oxide has been suggested to be involved in regulation of autonomic functions. In order to understand the molecular mechanism by which food deprivation decreases nNOS expression in the PVN, we examined if plasma glucocorticoids, which reported to be elevated during food deprivation, mediates the fasting-induced down-regulation of the PVN-nNOS. Male Sprague-Dawley rats underwent 48 h of food deprivation, but not water deprivation, with/without subcutaneous RU486, glucocorticoid receptor antagonist, and the brain tissues were processed for immunohistochemistry with specific antibodies against nNOS. Immunoreactivity of phosphorylated cAMP response element-binding protein (pCREB) was also examined in the PVN sections, because nNOS promoter carries cAMP response element (CRE). Food deprivation significantly decreased both nNOS and pCREB immunoreactivity (-ir) in the medial parvocellular PVN, and RU486 blocked this reduction. In the posterior magnocellular PVN, nNOS-ir, but not pCREB-ir, was decreased by food deprivation, and RU486 exerted no effect. These results suggest that glucocorticoid receptor may mediate the fasting-induced down-regulation of nNOS in the parvocellular PVN, but not in the magnocellular PVN.

Animals↗

PubMed2004

Nitric oxide is involved in lithium-induced immediate early gene expressions in the adrenal medulla.

This study was conducted to determine if nitric oxide (NO) is involved in lithium-induced expression of c-Fos and inducible cAMP early repressor (ICER) in the adrenal gland. Rats received an intraperitoneal injection of isotonic lithium (76 mg/kg) with either an intracerebroventricle (i.c.v., 250 microg) or intraperitoneal (i.p., 30 mg/kg) N(omega)-nitro-L-arginine methyl ester (L-NAME) pretreatment. The adrenal expression of c-Fos and ICER was examined by in situ hybridization 1 h after the lithium injection. The cortical c-Fos/ICER expression induced by lithium was not modulated by L-NAME pretreatment. However, lithium-induced medullary expression of c-Fos was attenuated by central L-NAME, and ICER by systemic L-NAME. These results suggest that nitric oxide is, at least partly, involved in lithium-induced c-Fos/ICER expression in the adrenal medulla, and that central nitric oxide may play a different role from peripheral nitric oxide in lithium-induced activation of adrenal medulla.

Adrenal Medulla↗

PubMed2004

Adrenalectomy abolishes fasting-induced down-regulation of NADPH-diaphorase in the rat paraventricular nucleus.

This study was conducted to define the molecular mechanism of fasting-induced down-regulation of neuronal nitric oxide synthase (nNOS) expression in the hypothalamic paraventricular nucleus (PVN). Rats were adrenalectomized (ADX), and then either underwent food deprivation or received varying doses of dexamethasone for 48 h. The brain tissues were processed for NADPH-diaphorase (NADPH-d) staining, a histochemical marker of nNOS enzyme activity. Both the ADX and the sham operated rats showed a significant weight loss after 48 h of food deprivation. Food deprivation decreased the number of NADPH-d containing cells in the PVN of sham rats, however, not in the ADX rats. Dexamethasone dose- dependently decreased NADPH-d cells in the PVN of ADX rats. The effect of ADX or dexamethasone was limited to the parvocellular subdivision of PVN. These results suggest that the adrenal glucocorticoids may down-regulate nNOS expression in the PVN during food deprivation.

Adrenalectomy↗

PubMed2004

N(omega)-nitro-L-arginine methyl ester attenuates lithium-induced c-Fos, but not conditioned taste aversion, in rats.

Lithium chloride (LiCl) at doses sufficient to induce conditioned taste aversion (CTA) causes c-Fos expression in the relevant brain regions and activates the hypothalamic-pituitary-adrenal (HPA) axis. It has been suggested that nitric oxide (NO) in the central nervous system may play a role not only in the activation of HPA axis but also in CTA learning, and that LiCl may activate the brain NO system. To determine the role of NO in lithium-induced CTA, we examined the lithium-induced CTA, brain c-Fos expression, and plasma corticosterone level with Nomega-nitro-L-arginine methyl ester (L-NAME) pretreatment. Intraperitoneal L-NAME (30 mg/kg) given 30 min prior to LiCl significantly decreased lithium-induced c-Fos expression in the brain regions implicated in CTA learning, such as the hypothalamic paraventricular nucleus (PVN), central nucleus of amygdala (CeA), and nucleus tractus of solitarius. However, either the lithium-induced CTA acquisition or the increase in plasma corticosterone was not attenuated by l-NAME pretreatment. These results suggest that NO may be involved in lithium-induced neuronal activation of the brain regions, but not in the CTA acquisition or the HPA axis activation.

Amygdala↗

PubMed2003

Central Nomega-nitro-L-arginine methyl ester does not influence lithium-induced c-Fos and conditioned taste aversion.

LiCl at doses sufficient to induce conditioned taste aversion (CTA) causes c-Fos expression in the brain regions implicated in CTA formation. It has been reported that nitric oxide (NO) may play a role in CTA learning and LiCl increases both the synthesis and activity of NO synthase (NOS) in the brain. In this study, we examined the effect of central Nomega-nitro-L- arginine methyl ester (L-NAME) on the brain c-Fos expression and CTA learning induced by lithium in rats. In the results, intracerebroventricular L-NAME given prior to lithium did not change either the lithium-induced CTA or c-Fos in the relevant brain regions. This suggests that the brain NO system may not be involved in the neuronal activation during lithium-induced CTA formation.

Animals↗

PubMed2003

Systemic 5-hydroxy-L-tryptophan down-regulates the arcuate CART mRNA level in rats.

This study was conducted to determine if serotonin (5-hydroxytryptamine; 5-HT) system correlates with the hypothalamic expression of cocaine-amphetamine-regulated transcript (CART) gene. Rats received intraperitoneal 5-hydroxy-L-tryptophan (5-HTP; a single or three daily injections at a dose of 100 mg/kg/10 ml), and CART mRNA level in the hypothalamus was examined by in situ hybridization at different time points. The 5-HT contents of the hypothalamus as well as the brainstem was increased persistently by 5-HTP injections, and food intake and body weight gain reduced. CART mRNA level decreased significantly in the hypothalamic arcuate nucleus by three daily 5-HTP, but not by a single injection. The pair-fed group of the chronic 5-HTP did not show a decrease in the arcuate CART mRNA level. The plasma leptin level markedly decreased in the chronic 5-HTP group, compared to the saline group, however, still higher than the pair-fed group with a statistical significance. These results suggest that 5-HT may suppress CART mRNA expression in the arcuate nucleus, not only by leptin signaling via its anorectic effect on the control of food intake, but also by some non-leptin mediated pathway.

5-Hydroxytryptophan↗

PubMed2003

Dexamethasone blocks the refeeding-induced phosphorylation of cAMP response element-binding protein in the rat hypothalamus.

We previously reported that dexamethasone pretreatment abolishes the refeeding-induced neuronal nitric oxide synthase (nNOS) expression in the rat paraventricular nucleus (PVN). It was reported that nNOS upstream carries cAMP response element (CRE) and nNOS expression is mediated by a CRE-binding protein (CREB)-dependent mechanism. In this study, CREB phosphorylation was co-localized in the nNOS neurons of the rat PVN regardless of feeding conditions. The relative amount of phosphorylated CREB in the hypothalamic tissue lysates increased by 1 h of refeeding following 48 h of food deprivation, and interestingly, this increase was blocked by dexamethasone administration before the food onset. These results suggest that glucocorticoids exert an inhibitory role in CREB phosphorylation directed by nutritional stimuli in the rat hypothalamus, and this inhibition may be related to nNOS gene expression in this brain region.

Animals↗

PubMed2003

[A clinical analysis on liver transplantation for hepatocellular carcinomas].

BACKGROUND/AIMS: Currently, the role of liver transplantation in the treatment of hepatocellular carcinoma (HCC) with cirrhosis is controversial. What remain to be determined are the best treatment protocol and who are likely to have a good outcome after liver transplantation. METHODS: Twenty-five patients with hepatocellular carcinoma underwent liver transplantation between 1993 and 2001 at the Department of Surgery, Catholic University of Korea. The follow-up period was from one month to 51 months. The pathologic findings, the recurrence, and survival of the 25 cases were analyzed. RESULTS: Two patients had a tumor larger than 5 cm in diameter and three patient had above 3 nodules in number. Five patients had bilobar tumors. Vascular invasion was present in 11 patients (45.8%). Among the 25 patients, postsurgical TNM staging was stage III in 3 patients, stage IVA in 5 patients, and stage IVB in 1 patient. Number of high risk patients were 16 (64%). During follow-up, 23 of the 25 patients (92%) were alive and the number of disease-free survivals was 21 among the 23 patients (91.3%). CONCLUSIONS: According to our small experience, HCC can be a good indication of liver transplantation, especially in low risk patients and even in the recurrent cases. A long-term survival can be achieved by aggressive treatment. However, the best protocol remains to be determined, especially for the case with large tumors.

Adult↗

PubMed2002

[Expression patterns of E-cadherin and beta-catenin according to clinicopathological characteristics of hepatocellular carcinoma].

BACKGROUND/AIMS: E-cadherin is involved in intercellular binding and cellular polarity formation. beta-catenin plays a fundamental role in regulation of the E-cadherin cell adhesion complex. The abnormalities of the components of the complex may disrupt this adhesive function. We investigated the expression patterns of E-cadherin and beta-catenin to determine the clinical significance of these proteins in hepatocellular carcinoma. MATERIALS/METHODS: Thirty-six hepaticellular carcinoma tissues and adjacent non-tumor specimens were analyzed. Subcellular distribution of E-cadherin and beta-catenin was examined by immunohistochemistry staining. We evaluated the patterns of the expression, and investigated the relationship with the cause of HCC; level of AFP; TNM stage; tumor size; growth types; metastasis; differentiation grade of HCC; and presence of portal vein thrombosis. RESULTS: Immunohistochemistry showed that all non-tumor tissues had membranous type staining of E-cadherin. All non-tumor tissues showed cytoplasmic type staining of beta-catenin, but no beta-catenin accumulation in nuclei was found. 58% (21/36) of HCC showed positive expression of E-cadherin in cytoplasmic membrane. The cytoplasmic expression of beta-catenin in HCC was 83% (30/36); nuclear expression in 14% (5/36); and no staining in 3% (1/36). Nuclear beta-catenin expression was observed in none (0/4) of the well-differentiated HCC; 17%(3/9) of moderate-differentiated HCC; and 17%(2/6) of poorly-differentiated HCC. There were no relationships between E-cadherin and beta-catenin expression with other clinicopathologic factors. CONCLUSIONS: Loss of cytoplasmic staining of E-cadherin and nuclear accumulation of beta-catenin were observed in HCC. Nuclear accumulation of beta-catenin was not found in well differentiated HCC but was found in poorly differentiated HCC.

Adult↗