Despite current advances in multimodality therapies, such as surgery, radiotherapy, and chemotherapy, the outcome for patients with high-grade glioma remains fatal. Understanding how glioma cells resist various therapies may provide opportunities for developing new therapies. Accumulating evidence suggests that the main obstacle for successfully treating high-grade glioma is the existence of brain tumor stem cells (BTSCs), which share a number of cellular properties with adult stem cells, such as self-renewal and multipotent differentiation capabilities. Owing to their resistance to standard therapy coupled with their infiltrative nature, BTSCs are a primary cause of tumor recurrence post-therapy. Therefore, BTSCs are thought to be the main glioma cells representing a novel therapeutic target and should be eliminated to obtain successful treatment outcomes.
Adult Stem Cells ; Brain Neoplasms* ; Brain* ; Drug Therapy ; Glioma ; Humans ; Radiotherapy ; Recurrence ; Stem Cells*

Pseudomyxoma peritonei may result from implantation of benign or malignant tumor in peritoneal cavity and is filled with gelatinous material (termed "Jelly Belly") in abdominal cavity. Its origin is usually an appendiceal or ovarian mucinous adenoma or cystadenocarcinoma, but other primary origin such as uterus, intestine, pancreas and stomach umor have been reported. Generally, pseudomyxoma peritonei is slowly progressive and has low grade malignant potential. This report presents a unusual long term survival after evacuation of 15,000 cc of gelatinous material from abdominal cavity which was the low grade mucinous adenocarcinoma and a review of the current literature, management and new its concept. The origin of pseudomyxoma peritonei of this case was most likely from appendiceal mvcinous adenocarcinoma.
Abdominal Cavity ; Adenocarcinoma ; Adenocarcinoma, Mucinous ; Adenoma ; Cystadenocarcinoma ; Gelatin ; Intestines ; Mucins ; Pancreas ; Peritoneal Cavity ; Pseudomyxoma Peritonei* ; Stomach ; Uterus

Backgound: The placement of stents in coronary arteries has been shown to reduce acute closure and restenosis in comparison to balloon angioplasty. However, clinical use of intracoronary stents is impeded by the subacute stent thrombosis and hemorrhagic complications associated with the anticoagulant regimen. It's known that the complete stent deployment with high pressure inflation and new antiplatelet agents are effective in reduction of subacute thrombosis and hemorrhage. So we evaluated initial results (success and complication rate) after high pressure-stent deployment with new anticoagulation protocol. METHODS: One hundred and ninety one patients with 201 lesions were treated with 231 stents of various types. The high pressure balloon inflation and antiplatelets agents were used in all cases. Final high pressure balloon inflation guided by IVUS were performed in 23 consecutive cases with incomplete stent deployment according to angiographic findings. RESULTS: 1) The indications of stenting (n=210) were De novo in 124 (59%), bailout procedure in 57 (27%), suboptimal result after PTCA in 19 (8%), and restenosis after PTCA in 14 (6%). The location of lesions were LAD in 101, RCA in 67, circumflex in 28, ramus intermedius in 3, and LMT artery in 2 lesions. Angiographic morphologic characteristics were type A in 2, type B in 158 (B1: 57, B2: 101), and type C in 22 lesions. 2) The angiographic and clinical success rate was 96% (192/201) and 92% (186/201) respectively. 3) In angiographic analysis, the baseline average reference vessel dirmeter was 3.33+/-0.35 mm. Baseline minimum lumen diameter (MLD) was 0.58+/-0.29 mm, with baseline percent diameter stenosis of 82.86+/-8.64%. The final stent diameter was 3.37+/-0.29 mm, with mean final percent stenosis of 0.63+/-8.25. The mean MLD after stenting was significantly increased (p<0.001). The mean MLD within stent increased 14%, from 2.91+/-0.39 mm at the nominal balloon inflation (inflation pressure=7 atm) to 3.37+/-0.29 mm at high pressure balloon inflation (inflation pressure <0A65B>12atm) (p<0.001). The length of lesions in GR I (cook), GR II, and Micro II stents were significantly longer than ones in PS, Cordis, Wiktor, Nir (p<0.001). 4) In intravascular ultrasound analysis, the mean lumen CSA at the tightest point within stent increased 11%, from 8.4+/-2.4 mm2 at the intial intravascular ultrasound to 9.4+/-2.1 mm2 at the final intravascular ultrasound (p<0.001). 5) The procedural and postprocedural complications were 2 acute closures associated with AMI and emergent CABG, 1 subacute closure which was revascularized by bail out stenting, 5 major hemorrhage requiring transfusion associated with 1 CVA and 2 metabolic acidosis induced by acute renal failure, and 5 death. CONCLUSION: The high pressure stent deployment procedure and new anticoagulation protocol associating tidopidine and aspirin without coumadin or prolonged heparin infusion allow us to obtain an acceptably low subacute thrombosis or bleeding complication rate. These results are encouraging and allow a wide use of coronary stenting.
Acidosis ; Acute Kidney Injury ; Angioplasty, Balloon ; Arteries ; Aspirin ; Constriction, Pathologic ; Coronary Vessels* ; Hemorrhage ; Heparin ; Humans ; Inflation, Economic ; Platelet Aggregation Inhibitors* ; Stents* ; Thrombosis ; Ultrasonography ; Warfarin

OBJECTIVE: Obturator neuropathy is a rare condition. Many neurosurgeons are unfamiliar with the obturator nerve anatomy. The purpose of this study was to define obturator nerve landmarks around the obturator foramen. METHODS: Fourteen cadavers were studied bilaterally to measure the distances from the nerve root to relevant anatomical landmarks near the obturator nerve, including the anterior superior iliac spine (ASIS), the pubic tubercle, the inguinal ligament, the femoral artery, and the adductor longus. RESULTS: The obturator nerve exits the obturator foramen and travels infero-medially between the adductors longus and brevis. The median distances from the obturator nerve exit zone (ONEZ) to the ASIS and pubic tubercle were 114 mm and 30 mm, respectively. The median horizontal and vertical distances between the pubic tubercle and the ONEZ were 17 mm and 27 mm, respectively. The shortest median distance from the ONEZ to the inguinal ligament was 19 mm. The median inguinal ligament lengths from the ASIS and the median pubic tubercle to the shortest point were 103 mm and 24 mm, respectively. The median obturator nerve lengths between the ONEZ and the adductor longus and femoral artery were 41 mm and 28 mm, respectively. CONCLUSION: The obturator nerve exits the foramen 17 mm and 27 mm on the horizontal and sagittal planes, respectively, from the pubic tubercle below the pectineus muscle. The shallowest area is approximately one-fifth medially from the inguinal ligament. This study will help improve the accuracy of obturator nerve surgeries to better establish therapeutic plans and decrease complications.
Cadaver ; Femoral Artery ; Ligaments ; Obturator Nerve* ; Spine

No abstract available.
Anisakiasis*

No abstract available.
Lung Neoplasms* ; Lung*

Ischemia-reperfusion injury is related with oxygen free radicals; a reason which has been suggested for this is the conversion of xanthine dehydrogenase (XDH) into xanthine oxidase (XO). In the present study, metabolic control of the enzymic conversion by modulating the cellular redox potential was attempted. An amino acid, aspartate, was tested as a possible candidate on the assumption that as a participant in the malate/aspartate shuttle, it might modify the cellular NADH/NAD+ balance. Its effect was studied by measuring the level of lipid peroxidation as a thiobarbituric acid-reactive substance (TEARS) and the conversion ratio of XDH to XO in the perfused-rat livers. The experimental animals, male Sprague Dawley rats were divided into three groups: control, ischemia and ischemia/reoxygenation. To each group, aspartate was infused at 2 mM level. ischemia alone did not affect the level of TEARS or the conversion ratio of the enzyme, regardless of aspartate infusion. In contrast, reoxygenation of previously ischemia liver significantly elevated the level of TEARS and decreased the ratio of XDH to XO; both this level and this ratio were ameliorated by aspartate. The protective role of aspartate against oxidative stress induced by ischemia/reoxygenation can be explained by the fact that aspartate may correct the increased NADH/NAD ratio by facilitating NAD regeneration from NADH through the coupled aspartate aminotransferase/malate dehydrogenase reaction and the malate-aspartate shuttle. Aspartate application may thus contribute to the development of a preventive strategy against ischemia/reperfusion-induced oxidative damages.
Animals ; Aspartic Acid* ; Free Radicals ; Humans ; Ischemia ; Lipid Peroxidation ; Liver* ; Male ; NAD ; Oxidation-Reduction ; Oxidative Stress* ; Oxidoreductases ; Oxygen ; Rats* ; Rats, Sprague-Dawley ; Regeneration ; Reperfusion Injury ; Xanthine Dehydrogenase ; Xanthine Oxidase

The end-stage dilated cardiomyopathy is usually treated with cardiac transplantation although some limited success have also been obtained in selected patients using dynamic cardiomyoplasty or medical assist devices. Recently, a new surgical alternatives, called partial left ventriculectomy (PLV) was introduced by Randas J. V Batista in 1995. A 40-year-old man who had end-stage dilated cardiomyopathy refractory to optimal doses of medicines underwent partial left ventriculectomy (Batista's operation), which reduces ventricular volume to improve left ventricular function. The left ventricular ejection fraction increased from 20 % to 58 % at 4 month after operation.
Adult ; Cardiomyopathy, Dilated* ; Cardiomyoplasty ; Heart Transplantation ; Humans ; Stroke Volume ; Ventricular Function, Left

Russell body gastritis was first defined in 1998, but not many cases have been reported since then. The exact causes and process of this condition are unknown yet; however, considering the reported cases, it has been highly suggested to have correlation with Helicobacter pylori infection. Russell body gastritis has a non-specific clinical presentation of gastritis such as gastric mucosal edema in the macroscopic view. It can be mistaken as xanthoma, signet ring cell carcinoma, or a malignant lymphoma including mucosa-associated lymphoid tissue lymphoma and plasmocytoma. Russell body gastritis features polyclonal immunoglobulin and is differentiated from Mott cancer, of which immune globulin has monoclonal aspect. Authors report here two cases of Russell body gastritis with examined endoscopic findings as well as a review of related literature on the association of all reported cases of Russell body gastritis with H. pylori infection.
Carcinoma, Signet Ring Cell ; Edema ; Gastritis ; Helicobacter ; Helicobacter pylori ; Immunoglobulins ; Lymphoma ; Lymphoma, B-Cell, Marginal Zone ; Plasmacytoma ; Xanthomatosis

Intestinal epithelial cells (IECs) have been known to produce galactose-alpha1,4-galactose-beta1,4-glucose ceramide (Gb3) that play an important role in the mucosal immune response. The regulation of Gb3 is important to prevent tissue damage causing shiga like toxin. Epigallocatechin-3-gallate (EGCG) has been studied as anti-carcinogenic, anti-oxidant, anti-angiogenic, and anti-viral activities, and anti-diabetic. However, little is known between the expressions of Gb3 on IECs. The aim of this study was to examine the inhibitory effect of EGCG, a major ingredient of green tea, on Gb3 production via mitogen-activated protein kinases (MAPKs) and nuclear factor-kappa B (NF-kappa B) in the TNF-alpha stimulated human colon epithelial cells, HT29. To investigate how Gb3 is regulated, ceramide glucosyltransferase (CGT), lactosylceramide synthase (GalT2), and Gb3 synthase (GalT6) were analyzed by RT-PCR in HT 29 cells exposed to TNF-alpha in the presence or absence of EGCG. EGCG dose-dependently manner, inhibits TNF-alpha induced Gb3 expression by blocking in both the MAPKs and NF-kappaB pathways in HT29 cells. TNF-alpha enhanced CGT, GalT2 and GalT6 mRNA levels and EGCG suppressed the level of these enzymes enhanced by TNF-alpha treatment.
Apoptosis/drug effects ; Blotting, Western ; Catechin/*analogs & derivatives/pharmacology ; Cell Nucleus/drug effects/metabolism ; Cell Proliferation/drug effects ; Dose-Response Relationship, Drug ; Epithelial Cells/drug effects/metabolism/pathology ; Flow Cytometry ; Galactosyltransferases/genetics ; Gene Expression Regulation, Enzymologic/drug effects ; Glucosyltransferases/genetics ; HT29 Cells ; Humans ; Intestinal Mucosa/drug effects/metabolism/pathology ; Mitogen-Activated Protein Kinases/antagonists & inhibitors/*metabolism ; NF-kappa B/antagonists & inhibitors/*metabolism ; Phosphorylation/drug effects ; Protein Transport/drug effects ; RNA, Messenger/genetics/metabolism ; Research Support, Non-U.S. Gov't ; Reverse Transcriptase Polymerase Chain Reaction ; Trihexosylceramides/*biosynthesis ; Tumor Necrosis Factor-alpha/*pharmacology