A fetal rhabdomyomatous nephroblastoma is considered to be a predominantly monophasic mesenchymal variant of Wilms' tumor, which acts less aggressively than a conventional Wilms' tumor despite its much larger size. Bilaterality of this tumor in a nine month-old girl, however, may negatively affect the overall prognosis. A radical nephrectomy for bulky masses in the left kidney and a partial nephrectomy for right kidney with five small tumor masses was performed at the same time. Two small tumor masses in the upper part of right kidney were left behind because of preserving minimal renal functional capacity. Pathological study revealed a mixed type of nephroblastoma which was composed predominantly of mesenchymal components with fetal rhabdomyomatous differentiation. After post-operative chemotherapy with vincristine, actinomycin D and adriamycin, and radiotherapy(2,130 rad), residual tumor masses became a single tumor 5 cm in diameter and well demarcated, which was resected at 15 months after first operation when the size and renal function of remained right kidney was appropriate to resect out the residual tumor. The tumor resected out at second operation was entirely composed of scattered differentiated fetal skeletal muscle cells in the fibrovascular tissue. Only a few entrapped epithelial components were seen but no blastemal cornponents were present. Follow up abdominal CT and ultrasonographic examinations revealed no evidence of tumor recurrence. The girl has developed normally without disease.

Complications after a median sternotomy incision, which is used currently in most open heart surgery, are serious, although it is infrequent. Reconstruction of the sternal defect resulting from dehiscence of median sternotomy is still big challenge to the most plastic surgeons. Since vascularized greater omentum was transposed to eliminate mediastinal wound problems, many vascularized regional muscle flaps became mainstay in reconstruction of median sternotomy wound. We treated 13 patients with median sternotomy dehiscence between October of 1993 and March of 1998. In two patients, the wound problems were so confined to superficial tissue that debrided and closed primarily. Eleven patients with deep wound infection were managed with vigorous debridement of all necrotic tissues and resultant defects were covered with regional muscle flaps: rectus myocutaneous flap(3) and bilateral pectoralis advancement flap(8). We used the pectoralis major advancement flaps without counter incision at humeral insertion site and the dissections were limited only medial to the anterior axillary line to preserve the axillary fold. In five patients with larger defects, we elevated muscle and cutaneous flaps separately to make these flaps more mobile. Large portion of two rectus abdominis flaps could not survive, whereas pectoralis advancement flaps had mo special wound problems. Only one patient developed fistula due to remained wire, regardless to flap surgery.
Debridement ; Fistula ; Humans ; Omentum ; Rectus Abdominis ; Sternotomy* ; Thoracic Surgery ; Wound Infection ; Wounds and Injuries

Clonorchiasis procucts diffuse dilatation of the small and medium sized intrahepatic bile ducts and its cholangiogram shows visualization of many bile ducts, especially, tertiary, quaternary, and more peripheral tributaries up to the 6th tributaries. In an attempt to clarify this cholangiographic sign quantitively, we counted the visualized smaller bile ducts in clonorchiasis and compared the number of visualized ducts in normal cholangiogram, recurrent pyogenic chlangitis and carcinoma of the extrahepatic ducts. In clonorchiasis the number of visualized smaller bile ducts was considerably geater than in normal subjects and recurrent pyogenic cholangitis, but there was no singnificant statistical differences in the number of visualized bile duct tributaries between clonorchiasis and carcinoma of the bile ducts. Thus it is considered that too many ducts sign is not a unique cholangiographic finding of clonorchiasis, but we believe that in the presence of this sign with other we l known cholangiographic findings, diagnosis of clonorchiasis is very easy.
Bile Ducts ; Bile Ducts, Intrahepatic ; Cholangitis ; Clonorchiasis* ; Diagnosis ; Dilatation

PURPOSE: To evaluate the prevalence of the opacification of paranasal sinuses and to correlate the prevalence and severity of the sinus opacification with presence of upper respiratory infection (URI) in infants and children using CT. MATERIALS & METHODS: We analyzed CT scans of 162 children aged under 16 who have no signs and symptoms of paranasal sinusitis. Both sides of maxillary and ethmoidal sinuses were evaluated. We scored from 0 to 3 according to the degree of soft tissue opacification of each sinus and then summed up the scores of each sinus. We divided the children into 5 groups according to their age. We paid particular attention to the following respects: 1) the prevalence of the opacification of the paranasal sinuses in each group; 2) the difference in the prevalence between the children with and without URI ;3) the correlation between the severity of the sinus opacification and the presence of URI. RESULTS: Of 162 children, one or more paranasal sinus opacification was noted in 76(47 %):31(65%) less than 1 year old;11(52%) between 1 and 2 years old;16(53%) between 2 and 6 years old ;15(28%) between 6 and 12 years old;and 3(33%) above 12 years old. In children less than 1 year old, no significant difference in the prevalence of the sinus opacification was found between URI-positive(71%) and URI-negative(58%) subgroups. In chilren between 1 and 12 years old, although the prevalence of the sinus opacification in URI-positive subgroups was much greater than that in URI-negative subgroup, statistically significant difference was noted only in children between 2 and 6 years old. As to the correlation between the severity of the sinus opacification and the presence of URI, these was a statistically significant difference in children between 2 and 6 years old and between 6 and 12 years old. CONCLUSION: Although the exact pathophysiology is not fully understood, the opacification of the paranasal sinuses is not an uncommon finding at CT in children without the signs and symptoms of sinusitis. We think that the clinical correlation is essential in determining the diagnosis and treatment plan in cases that the sinus radiographs or CT scans show the abnormal findings.
Child* ; Diagnosis ; Humans ; Infant* ; Paranasal Sinuses ; Prevalence* ; Sinusitis* ; Tomography, X-Ray Computed

No abstract available.
Computer Simulation* ; Orthognathic Surgery*

No abstract available.
Computer Simulation* ; Orthognathic Surgery*

Adiponectin, an adipokine predominantly secreted from adipose tissue, exhibits diverse biological responses, including metabolism of glucose and lipid, and apoptosis in cancer cells. Recently, adiponectin has been shown to modulate autophagy as well. While emerging evidence has demonstrated that autophagy plays a role in the modulation of proliferation and apoptosis of cancer cells, the role of autophagy in apoptosis of cancer cell caused by adiponectin has not been explored. In the present study, we demonstrated that globular adiponectin (gAcrp) induces both apoptosis and autophagy in human hepatoma cell line (HepG2 cells) and breast cancer cells (MCF-7), as evidenced by increase in caspase-3 activity, Bax, microtubule-associated protein light chain 3-II (LC3 II) protein levels, and autophagosome formation. Interestingly, gene silencing of LC3B, an autophagy marker, significantly enhanced gAcrp-induced apoptosis in both HepG2 and MCF-7 cell lines, whereas induction of autophagy by rapamycin, an mTOR inhibitor, significantly prevented gAcrp-induced apoptosis in hepatoma cells HepG2. Furthermore, modulation of autophagy produced similar effects on gAcrp-induced Bax expression in HepG2 cells. These results implicate that induction of autophagy plays a regulatory role in adiponectin-induced apoptosis of cancer cells, and thus inhibition of autophagy would be a novel promising target to enhance the efficiency of cancer cell apoptosis by adiponectin.
Adipokines ; Adiponectin ; Adipose Tissue ; Apoptosis* ; Autophagy* ; Breast Neoplasms ; Carcinoma, Hepatocellular ; Caspase 3 ; Cell Line ; Gene Silencing ; Glucose ; Hep G2 Cells ; Humans ; MCF-7 Cells ; Metabolism ; Sirolimus

Leptin, an adipose tissue-derived hormone, has exhibited the potent hepatotoxic effects. However, the underlying molecular mechanisms are not fully understood. In this study, we have elucidated the mechanisms by which leptin exerts cytotoxic effects in hepatocytes, particularly focusing on the role of interleukin-1β (IL-1β) signaling. Leptin significantly induced maturation and secretion of IL-1β in cultured rat hepatocytes. Interestingly, inhibition of IL-1β signaling by pretreatment with an IL-1 receptor antagonist (IL-1Ra) or gene silencing of type I IL-1 receptor (IL-1R1) markedly abrogated leptin-induced cell cycle arrest. The critical role of IL-1β signaling in leptin-induced cell cycle arrest is mediated via upregulation of p16, which acts as an inhibitor of cyclin-dependent kinase. In addition, leptin-induced apoptotic cell death was relieved by inhibition of IL-1β signaling, as determined by annexin V/7-AAD binding assay. Mechanistically, IL-1β signaling contributes to apoptotic cell death and cell cycle arrest by suppressing AKT and activation of p38 mitogen-activated protein kinase (p38MAPK) signaling pathways. Involvement of IL-1β signaling in cytotoxic effect of leptin was further confirmed in vivo using hepatocyte specific IL-1R1 knock out (IL-1R1 KO) mice. Essentially similar results were obtained in vivo, where leptin administration caused the upregulation of apoptotic markers, dephosphorylation of AKT, and p38MAPK activation were observed in wild type mice liver without significant effects in the livers of IL-1R1 KO mice. Taken together, these results demonstrate that IL-1β signaling critically contributes to leptin-induced cell cycle arrest and apoptosis, at least in part, by modulating p38MAPK and AKT signaling pathways.

Leptin, an adipokine predominantly produced from adipose tissue, is well known to induce tumor growth. However, underlying molecular mechanisms are not established yet. While p53 has long been well recognized as a potent tumor suppressor gene, accumulating evidence has also indicated its potential role in growth and survival of cancer cells depending on experimental environments. In the present study, we examined if p53 signaling is implicated in leptin-induced growth of cancer cells. Herein, we demonstrated that leptin treatment significantly increased p53 protein expression in both hepatic (HepG2) and breast (MCF-7) cancer cells without significant effect on mRNA expression. Enhanced p53 expression by leptin was mediated via modulation of ubiquitination, in particular ubiquitin specific protease 2 (USP2)-dependent manner. Furthermore, gene silencing of p53 by small interfering RNA (siRNA) suppressed leptin-induced growth of hepatic and breast cancer cells, indicating the role of p53 signaling in tumor growth by leptin. In addition, we also showed that knockdown of p53 restored suppression of caspase-3 activity by leptin through modulating Bax expression and prevented leptin-induced cell cycle progression, implying the involvement of p53 signaling in the regulation of both apoptosis and cell cycle progression in cancer cells treated with leptin. Taken together, the results in the present study demonstrated the potential role of p53 signaling in leptin-induced tumor growth.
Adipokines ; Adipose Tissue ; Apoptosis ; Breast Neoplasms* ; Breast* ; Caspase 3 ; Cell Cycle ; Gene Silencing ; Genes, Tumor Suppressor ; Leptin ; RNA, Messenger ; RNA, Small Interfering ; Ubiquitin ; Ubiquitination

Leptin, an adipose tissue-derived hormone, has exhibited the potent hepatotoxic effects. However, the underlying molecular mechanisms are not fully understood. In this study, we have elucidated the mechanisms by which leptin exerts cytotoxic effects in hepatocytes, particularly focusing on the role of interleukin-1β (IL-1β) signaling. Leptin significantly induced maturation and secretion of IL-1β in cultured rat hepatocytes. Interestingly, inhibition of IL-1β signaling by pretreatment with an IL-1 receptor antagonist (IL-1Ra) or gene silencing of type I IL-1 receptor (IL-1R1) markedly abrogated leptin-induced cell cycle arrest. The critical role of IL-1β signaling in leptin-induced cell cycle arrest is mediated via upregulation of p16, which acts as an inhibitor of cyclin-dependent kinase. In addition, leptin-induced apoptotic cell death was relieved by inhibition of IL-1β signaling, as determined by annexin V/7-AAD binding assay. Mechanistically, IL-1β signaling contributes to apoptotic cell death and cell cycle arrest by suppressing AKT and activation of p38 mitogen-activated protein kinase (p38MAPK) signaling pathways. Involvement of IL-1β signaling in cytotoxic effect of leptin was further confirmed in vivo using hepatocyte specific IL-1R1 knock out (IL-1R1 KO) mice. Essentially similar results were obtained in vivo, where leptin administration caused the upregulation of apoptotic markers, dephosphorylation of AKT, and p38MAPK activation were observed in wild type mice liver without significant effects in the livers of IL-1R1 KO mice. Taken together, these results demonstrate that IL-1β signaling critically contributes to leptin-induced cell cycle arrest and apoptosis, at least in part, by modulating p38MAPK and AKT signaling pathways.