No abstract available.
Avidin*

No abstract available.

No abstract available.
Animals ; Asian Continental Ancestry Group* ; CHO Cells ; Cricetinae ; Cricetulus* ; Female ; Hepatitis B Surface Antigens* ; Hepatitis B Vaccines ; Humans ; Ovary*

Torsion of a mucocele of the vermiform appendix is an extremely rare condition and also a rare cause of an acute abdomen with a clinical presentation that is indistinguishable from acute appendicitis, and thus, the condition is diagnosed during operation. Here, the authors describe the case of a 78-year-old female, who presented with intermittent abdominal pain. The appendix had a pelvic position and the torsion was counterclockwise. In addition, the torsion was associated with mucocele of the appendix, which was considered a secondary factor of torsion. Appendectomy and drainage were performed.
Abdomen, Acute ; Abdominal Pain ; Aged ; Appendectomy ; Appendicitis ; Appendix ; Drainage ; Female ; Humans ; Mucocele ; Torsion Abnormality

Somatic mutations that lead to hyperactivation of epidermal growth factor receptor (EGFR) signaling are detected in approximately 50% of lung adenocarcinoma in people from the Far East population and tyrosine kinase inhibitors are now the standard first line treatment for advanced disease. They have led to a doubling of progression-free survival and an increase in overall survival by more than 2 years. However, emergence of resistant clones has become the primary cause for treatment failure, and has created a new challenge in the daily management of patients with EGFR mutations. Identification of mechanisms leading to inhibitor resistance has led to new therapeutic modalities, some of which have now been adapted for patients with unsuccessful tyrosine kinase inhibitor treatment. In this review, we describe mechanisms of tyrosine kinase inhibitor resistance and the available strategies to overcoming resistance.
Adenocarcinoma* ; Clone Cells ; Disease-Free Survival ; Drug Resistance ; Epidermal Growth Factor* ; Far East ; Genes, erbB-1 ; Humans ; Lung* ; Protein-Tyrosine Kinases ; Receptor, Epidermal Growth Factor* ; Treatment Failure

When ultrasound or computed tomographic (CT) scans demonstrate a focal mass within the pancreas, the radiologist or gastroenterologist assumes that it is carcinoma. Statistically this is the correct diagnosis. However, distinguishing pancreatitis from carcinoma by ultrasound and CT is occassionally impossible. Similarly, abnormalities seen on ERCP, such as simultaneous obstruction of both the common bile duct and adjacent pancreatic duct (double duct sign), has been shown to occur in pancreatitis as well as in the more commonly diagnosed pancreatic carcinoma. We experienced 3 cases af focal pancreatic masses that mistaken a carcinoma. And so, knowledge that such a mass can be benign in a clinical setting sbould result in an organiged approach to the correct diagnosis and avoidance of any unnecessary operations.
Cholangiopancreatography, Endoscopic Retrograde ; Common Bile Duct ; Diagnosis ; Inflammation* ; Pancreas ; Pancreatic Ducts ; Pancreatitis* ; Ultrasonography

To investigate the relationship between insulin response and morphometric changes of the mitochondria of pancreatic beta-cell, this study was performed using hyperglycemia and streptozotocin as oxidative stresses. Adult and neonatal rats were used. Intravenous glucose tolerance test (IVGTT) and morphologic examination of pancreas using immunohistochemical stain, in situ end-labeling method and electron microscopic study were performed. Various mitochondrial parameters were measured by image analyzer. Immunohistochemical stain revealed a markedly reduced islet size and decreased number of beta-cells and the increased number of non-beta-cell in adult and neonatoal streptozotocin group, and the appearance of insulin positive cells throughout the exocrine parenchyma in neonatal streptozotocin group. Three days after injection of streptozotocin in adult streptozotocin group, TUNEL stain showed increased apoptotic cells in islets. Ultrastructurally, beta-cells in adult streptozotocin group showed increase in number and size of mitochondria, and disruption of mitochondrial structures. Hyperglycemic group and neonatal streptozotocin group showed preserved mitochondrial ultrastructure. Ultrastructural morphometric study revealed increase in size and number of mitochondria and decrease in mitochondrial contour index in adult streptozotocin-treated rats, which suggested mitochondrial degeneration. Hyperglycemic group showed mild increase in size of mitochondria. Increased number of mitochondria was also observed in neonatal streptozotocin group. IVGTT revealed marked decrease in insulin response in adult streptozotocin group, and non-insulin-dependent diabetes mellitus pattern in glucose and insulin response in neonatal streptozotocin group. Hyperglycemic group showed a glucose and insulin response similar to control group. The above results suggest that a severe oxidative injury may cause degeneration and disruption of mitochondria of pancreatic beta-cell, and may be associated with substantial apoptotic cell death. The changes in the morphology and the number of mitochondria may result from streptozotocin treatment within neonatal period and hyperglycemia treatment, which may be associated with changes in insulin response.
Adult ; Animals ; Cell Death ; Diabetes Mellitus ; Diabetes Mellitus, Type 2 ; Glucose ; Glucose Tolerance Test ; Humans ; Hyperglycemia ; In Situ Nick-End Labeling ; Insulin* ; Mitochondria ; Oxidative Stress ; Pancreas ; Rats ; Streptozocin

Mutation of the p53 tumor-suppressor gene in exons 4 through 9 was examined in 34 cases of primary advanced gastric cancer using PCR-SSCP (polymerase chain reaction-single strand conformation polymorphism) and the results were compared with p53 protein expression as determined by immunohistochemistry (IHC) using a monoclonal antibody(DO-1). p53 protein detected by IHC was observed in 14 cases (41.2%) and genotypic mutation detected by PCR-SSCP in exons 4-9 was observed in 13 cases (38.2%) One case showed an aberrant band on PCR-SSCP both in Exon 7 and Exon 8/9. p53 alteration detected by either IHC or PCR-SSCP was observed in 19 cases (55.9%), but only 8 cases (23.5%) showed both p53 mutation and protein expression. We also tried to obtain the correlation between relative intensity of the shifted bands on PCR-SSCP and percentage of positive cells by IHC, but a significant correlation was not seen between relative intensity of shifted bands on PCR-SSCP and positve cell ratio. A discrepancy between p53 protein expression and p53 mutation is observed in primary gastric carcinomas. The reason for this discrepancy are not apparent. However, examination of gastric carcinomas for mutations in other exons may identify a better correlation with protein overexpression. The results obtained in this study suggest that the negative reaction for p53 immunohistochemistry may not necessarily mean no genetic alteration of the p53 locus.
Exons ; Immunohistochemistry* ; Stomach Neoplasms

It is well established that mast cell proliferation and maturation are regulated by two principle cytokines, IL-3 and the c-kit ligand stem cell factor (SCF). Previous reports have demonstrated that bone marrow-derived IL-3-dependent mast cells exhibit the characteristic apoptosis on removal of IL-3. To know how the number of mast cells is controlled, we observed the effects of nitric oxide (NO) on the murine bone marrow-derived cultured mast cells (BMCMC). Apoptosis was measured by the analysis of flow cytometric data and electrophoretic evidence of DNA fragmentation. Our data showed that sodiurn nitroprusside (SNP)-a NO releasing substance- induced apoptosis in BMCMC. Cell cycle analysis showed that the number of the G,/G, and S phase decreased markedly, while the percentage of cell in G,/M phase was increased. Also, SNP alone induced cell death, whereas SNP in combination with SCF markedly decreased cell death of BMCMC. SNP-induced apoptosis was partially inhibited by the treatment of BMCMC with SCF. Our results suggest that NO might have sorne role in the regulation of the number of mast cells.
Apoptosis ; Bone Marrow* ; Cell Cycle ; Cell Death ; Cytokines ; DNA Fragmentation ; Interleukin-3 ; Mast Cells* ; Nitric Oxide* ; Nitroprusside ; S Phase ; Stem Cell Factor

The epidermal growth factor receptor (EGFR) is a transmembrane glycoprotein whose expression is a possible cause of increased tumor cell proliferation and has recently been proposed as a prognostic parameter in some tumors. Expression of EGFR was studied immunohistochemically in 62 cases of human renal cell carcinomas to evaluate their possible prognostic roles. We also examined the correlation between EGFR expression and cell proliferation by immunohistochemical staining for proliferating cell nuclear antigen (PCNA). Fifty-six cases (90.3%) expressed EGFR, with staining largely confined to the cell membrane and cytoplasm. Staining intensity of EGFR was directly correlated with nuclear grade (p=0.000) and TNM stage (p=0.015). PCNA index was significantly higher in EGFR-positive tumors than in EGFR- negative tumors. There was a statistically significant positive correlation between PCNA index and increasing staining intensity of EGFR (p=0.000). In univariate survival analysis, EGFR expression was significantly associated with shortened survival. However, EGFR expression was not an independent prognostic factor by multivariate analysis. These findings suggest that EGFR expression may be an important cause of tumor cell proliferation in renal cell carcinoma and further studies are needed to evaluate whether EGFR expression analysis provides independent prognostic information.
Carcinoma, Renal Cell* ; Cell Membrane ; Cell Proliferation* ; Cytoplasm ; Epidermal Growth Factor* ; Glycoproteins ; Humans ; Multivariate Analysis ; Proliferating Cell Nuclear Antigen ; Receptor, Epidermal Growth Factor*