No abstract available.

Endocrine disruptors are known to cause harmful effects to human through various exposure routes. These chemicals mainly appear to interfere with the endocrine or hormone systems. As importantly, numerous studies have demonstrated that the accumulation of endocrine disruptors can induce fatal disorders including obesity and cancer. Using diverse biological tools, the potential molecular mechanisms related with these diseases by exposure of endocrine disruptors. Recently, pathway analysis, a bioinformatics tool, is being widely used to predict the potential mechanism or biological network of certain chemicals. In this review, we initially summarize the major molecular mechanisms involved in the induction of the above mentioned diseases by endocrine disruptors. Additionally, we provide the potential markers and signaling mechanisms discovered via pathway analysis under exposure to representative endocrine disruptors, bisphenol, diethylhexylphthalate, and nonylphenol. The review emphasizes the importance of pathway analysis using bioinformatics to finding the specific mechanisms of toxic chemicals, including endocrine disruptors.
Computational Biology ; Endocrine Disruptors ; Humans ; Obesity

Obstruction of the common bile duct (CBD) by direct extension of a tumor is occasionally found in patients with a hepatic neoplasm, but a bile duct tumor embolus caused by intrabiliary transplantation of a free floating tumor is a rare complication of a hepatocellular carcinoma. A patient of ours was recently observed with a fragment of tumor from a primary hepatocellular carcinoma (HCC) that obstructed the distal CBD. A-46-year-old man was admitted to our hospital with a distal CBD mass, measuring 1.2x1.5 cm, found by a biliary computed tomography (CT) scan. Four month prior to his admission, he had undergone a right hemihepatectomy for a HCC accompanied by direct intrahepatic bile duct invasion, without obstructive jaundice. On admission, there were no abnormal findings in the physical and laboratory examinations. An Endoscopic retrograde cholangiopancreatography and papillotomy had been performed, which showed an irregular shaped filling defect in the distal CBD. Endoscopic nasobiliary drainage (ENBD) was carried out for biliary decompression. Partially extracted soft tissue from the CBD by ERCP revealed a HCC. On performed a pylorus- preserving pancreaticoduodenectomy, a 1cm sized tumor remnant was found attached to the mucosa of the intrapancreatic portion of the bile duct, but without any invasive growth into the submucosa. The tumor may have been an intrabiliary transplantation from the HCC in the right lobe through the bile duct. When an obstructive mass is found in the distal CBD, tumor embolus should be considered, and a radical pancreaticoduodenectomy can be adopted as a safe and effective treatment modality.
Bile Ducts ; Bile Ducts, Intrahepatic ; Carcinoma, Hepatocellular* ; Cholangiopancreatography, Endoscopic Retrograde ; Common Bile Duct* ; Decompression ; Drainage ; Embolism* ; Humans ; Jaundice, Obstructive ; Liver Neoplasms ; Mucous Membrane ; Neoplastic Cells, Circulating ; Pancreaticoduodenectomy

PURPOSE: A pancreatic ductal adenocarcinoma is one of the most fatal cancers, as the majority of the patients present with locally advanced or metastatic tumors in the late stages of the disease. However, there is no simple, sensitive, noninvasive, and inexpensive test for the early detection of pancreatic ductal adenocarcinomas. In recent studies, S100A4 has emerged as an important protein in the tumorgenesis of pancreatic adenocarcinomas. METHODS: The possibility of the expression of S100A4 as a new tumor marker of pancreatic adenocarcinomas was confirmed using immunohistochemistry to 32-pancreatic ductal adenocarcinomas, 20 IPMN (intraductal papillary mucinous neoplasm), 8 serous cystadenomas, 5 chronic pancreatitis and 3 neuroendocrine tumors. RESULTS: Thirty-one (96.9%) ductal adenocarcinoma cases and 11 (55.5%) IPMN expressed S100A4, whereas all normal pancreatic tissues (47 cases), chronic pancreatitis and endocrine tumors did not. The expression of S100A4 was associated with the degree of dysplasia in IPMN, but not with the differentiation of ductal adenocarcinomas. CONCLUSION: The overexpression of S100A4 in adenocarcinomas and early emerging IPMN may suggest its potential as a diagnostic marker for the early detection of pancreatic ductal adenocarcinomas.
Adenocarcinoma* ; Carcinoma, Pancreatic Ductal ; Cystadenoma, Serous ; Humans ; Immunohistochemistry ; Mucins* ; Neuroendocrine Tumors ; Pancreas* ; Pancreatic Ducts ; Pancreatitis, Chronic ; Biomarkers, Tumor

We reported a case of a 55-year-old patient who presented with palpitation after swallowing. Initial surface electrocardiogram revealed ventricular preexcitation utilizing a left lateral bypass tract. The orthodromic atrioventricular reentrant tachycardia (AVRT) was induced during electrophysiologic studies. After successful ablation of the AVRT utilizing a left lateral free wall bypass tract, 2 different atrial tachycardias (ATs) were induced under isoproterenol infusion. When the patient swallowed saliva or drank water, 2 consecutive beats of atrial premature complexes (APCs) preceded another non-sustained AT repeatedly, which was coincident with the patient's symptom. The preceding APC couplet had the same activation sequence with one induced AT, and the subsequent non-sustained AT had the same activation sequence with the other induced AT, respectively. We first targeted the preceding 2 consecutive APCs at the left posterior interatrial septum. The following non-sustained AT was also eliminated following ablation of the APCs. After ablation, the patient remained free from the swallowing-induced atrial tachyarrhythmias during the one year follow-up.
Atrial Premature Complexes ; Catheter Ablation ; Deglutition ; Electrocardiography ; Follow-Up Studies ; Humans ; Isoproterenol ; Middle Aged ; Saliva ; Tachycardia* ; Water ; Wolff-Parkinson-White Syndrome*

Molecular karyotyping was applied to Pneumocystis carinii(Pc) from two strains of experimental rats, Sprague Dawley(SD) and Fisher(F), in Korea. Field inversion gel electrophoresis and contour clamped homogeneous electric field electrophoresis resolved 15 chromosomal bands from the Pc. The size of the bands was estimated 270kb to 684kb from SD rats, and 273kb to 713 kb from F rats. The bands of 283 kb from SD rats and of 273 kb from F rats stained more brightly suggesting duplicated bands. Total number of chromosomes was at least 16, and total genomic size was estimated 7 x 10(6) bp. All of the bands from F rats hybridized to the probe of repeated DNA sequences of Pc and the band of 448 kb size was proved to contain rDNA sequences, but Pc. chromosome bands from SD rats showed no reactions to the probes. The 2 different karyotypes of P. carinii from 2 strains of rats were maintained consistently for 2 years.
Electrophoresis- ; ; Korea- ; ; Nucleic-Acid-Hybridization ; Pneumocystis-carinii-isolation-and-purification ; Rats- ; *Karyotyping- ; ; *Pneumocystis-carinii-genetics ; *Rats,-Inbred-F344-microbiology ; *Rats,-Sprague-Dawley-microbiology

No abstract available.
Sepsis*

No abstract available.
Transplants

The plasminogen and plasmin system, which is mainly regulated by urokinase-type plasminogen activator (uPA), its receptor (uPAR) and its inhibitor (PAI-1), is generally believed to play a role in cancer invasion and metastasis. This study was conducted to investigate the role of uPA, uPAR and PAI-1 in the invasion and metastasis of gastric adenocarcinoma. The expression of mRNAs for uPA and PAI-1 was determined by Northern blot analysis in nine primary gastric cancer tissues, nine paired metastatic lymph nodes and normal gastric mucosa. The mRNA of uPA was not or faintly detected in normal mucosa, while the expression was increased in both primary gastric cancer tissues and metastatic lymph nodes to a similar degree. The mRNA expression for PAI-1 in the gastric cancer tissues was not different from that in the paired metastatic lymph nodes and normal mucosae. uPAR was determined by immunohistochemical staining, demonstrating that five (56%) and six (67%) out of nine primary gastric cancer tissues and nine paired metastatic lymph nodes were positive, respectively and the intensity was stronger in metastatic lymph nodes. The results support the concept that most gastric cancer cells may have an innately moderate level of uPA and uPAR, and that increase of uPAR expression can be considered to be closely associated with cancer invasion and metastasis.
Adenocarcinoma/*metabolism/pathology ; Gastric Mucosa/metabolism ; Gene Expression ; Human ; Immunoenzyme Techniques ; Lymph Nodes/metabolism/pathology ; Neoplasm Metastasis ; Plasminogen Activator Inhibitor 1/*biosynthesis/genetics ; Plasminogen Activators/*biosynthesis/genetics ; RNA, Messenger/biosynthesis ; Receptors, Cell Surface/*biosynthesis/genetics ; Stomach Neoplasms/*metabolism/pathology ; Support, Non-U.S. Gov't ; Urinary Plasminogen Activator/*biosynthesis/genetics

BACKGROUND AND OBJECTIVES: Inhalation injuries can produce a wide spectrum of negative clinical effects. Respiratory failure remains one of the leading causes of death in burned patients with inhalation injury. Despite advances in understanding of inhalation injury, few studies have focused on histopathologic findings of tracheal mucosa. The purpose of this study is to investigate histopathologic changes of tracheal mucosa in burned patients with inhalation injury. SUBJECTS AND METHOD: Tracheotomy was performed on 31 patients who was admitted to the Hospital center from May 2005 to March 2006. Thirty-one patients were divided into two groups : patients with inhalation injury (group I)(n=16), patients without inhalation injury (group II)(n=15). Tracheal mucosa were taken out during the tracheotomy. The tracheal mucosa were read blindly by one pathologist. RESULTS: Histopathologic examination showed the following finding in the tracheal mucosa of all patients in the group I : epithelial ulceration. Different findings were observed in the group I as time passed by after inhalation injury, such as interstitial edema, inflammatory cell infiltration, capillary dilatation, and increased fibrosis. No abnormal findings were observed in the tracheal mucosa in the group II. CONCLUSION: Inhalation injuries cause histopathologic damages to tracheal mucosa. The different histopathologic findings of tracheal mucosa that take place in time following inhalation injuries suggest to process an inflammatory reaction. The study in related to clinical features should be needed due to tracheal mucosa injury may produce respiratory complications.
Burns* ; Burns, Inhalation ; Capillaries ; Cause of Death ; Dilatation ; Edema ; Fibrosis ; Humans ; Inhalation* ; Mucous Membrane* ; Respiratory Insufficiency ; Trachea ; Tracheotomy ; Ulcer