Tuberculosis cutis orificialis: an association with Evans' syndrome.
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Anemia, Hemolytic, Autoimmune↗
Biomedical subjects
S W Choi
Publications and source records attributed to S W Choi.
Allelic deletions of MCC/APC and p53 are frequent late events in human gastric carcinogenesis.
BACKGROUND/AIMS: Frequent allelic deletion affecting the mutated in colon cancer/adenomatous polyposis coli (MCC/APC) and p53 tumor suppressor gene loci has been reported in human cancers. However, simultaneous correlative analyses of these two abnormalities or their timing in gastric tumorigenesis have not been performed. METHODS: To ascertain the relation between and timing of allelic deletions of MCC/APC and p53 in gastric carcinogenesis, 52 matched sets of normal tissue, gastric carcinoma, and adjacent gastric dysplasia were evaluated. RESULTS: Allelic deletion was seen in 33% of informative cancers at MCC, in 34% at APC, and in 64% at p53. Losses involving MCC correlated exactly with those affecting APC. Limited mutational analysis failed to reveal point mutations in selected exons of MCC. The frequencies of allelic losses at the two loci did not differ significantly among histological types. There was no allelic loss in gastric dysplasia. Interestingly, allelic deletion at MCC/APC was never detected in tumors negative for allelic deletion of p53. CONCLUSIONS: These results suggest that allelic deletions involving p53 and MCC/APC are common late events in gastric cancer. They also imply that allelic deletions affecting MCC/APC may not occur independently of those involving p53 in gastric tumorigenesis.
Adenomatous Polyposis Coli↗
p53 protein overexpression and allele loss of p53 gene in gastric adenocarcinoma.
Gene alterations of p53 tumor suppressor gene such as point mutations, deletions or insertions occur in various human cancers. p53 protein overexpression was studied immunohistochemically in 80 gastric adenocarcinomas using an anti-human p53 antibody (Pab 1801) and the avidin-biotin-peroxidase technique. We have also analyzed allele loss of the human p53 gene in 54 cases of gastric adenocarcinoma using polymerase chain reaction and restriction fragment length polymorphism. p53 immunostaining was also demonstrated in 48 of 80 carcinomas (60%). Normal mucosa was always negative. No relation could be found between p53 immunostaining and the degree of differentiation. 21 of the 54 patients(39%) were informative for the p53 exon 4. In ten of these informative cases(47.6%), tumor DNAs showed allele loss when compared with nonmetastatic lymph node DNAs. Seven of the ten(70%) showed p53 immunoreactivity. These findings suggest that mutations of the p53 gene may play a role in the development of gastric adenocarcinoma and that allele loss of p53 frequently occurs in p53 immunoreactive gastric adenocarcinoma.
Adenocarcinoma↗
The expression of nuclear lamins in human liver: an immunohistochemical study.
The nuclear lamina is a meshwork of intermediate filaments adjacent to the inner nuclear membrane that in mammalian cells is predominantly composed of three proteins: lamin A, lamin B, and lamin C. Because lamin A and C (A-type lamins) expression has been shown to be lacking in several types of undifferentiated or rapidly proliferating cells, we investigated lamin expression in the human liver in conditions with hepatocellular regeneration (cirrhosis of various etiologies and macroregenerative nodules) and in hepatocellular carcinomas of various grades of differentiation. Immunohistochemical stains for A-type lamins and lamin B were performed on frozen tissue sections with the avidin-biotin complex method. Normal and regenerating hepatocytes, biliary epithelial cells (ductal and ductular cells), and hepatocellular carcinoma cells invariably expressed both A-type lamins and lamin B. These findings indicate that in hepatocellular regeneration and malignant transformation the production of both A-type lamins and lamin B is preserved.
Adult↗
The expression of p53 antigen in primary malignant epithelial tumors of the liver: an immunohistochemical study.
We examined the expression of mutant p53 gene products in primary malignant epithelial tumors of the liver. Fourteen of 68 hepatocellular carcinomas, one of seven hepatoblastomas and one of nine intrahepatic cholangiocarcinomas showed nuclear staining for p53 proteins. None of the surrounding non-tumorous tissues expressed nuclear staining. The detection of p53 proteins in tumor cells was significantly higher in hepatocellular carcinomas of Oriental patients (31.6%) compared to non-Orientals (6.7%, p < 0.015). No significant differences were seen in p53 antigen expression between hepatitis B and non-hepatitis B associated hepatocellular carcinomas in Oriental patients. These results suggest a role for other environmental factors, such as aflatoxin, in the etiology of p53 mutation in hepatocellular carcinoma in Oriental patients.
Adenoma, Bile Duct↗
Loss of retinoblastoma gene and amplification of N-myc gene in retinoblastoma.
We have analyzed paired samples of genomic DNA from peripheral leukocyte and primary tumor tissue from nine patients with retinoblastoma (RB) and from two RB cell lines, WERI-Rb-1 and Y79, to detect the molecular alterations of the retinoblastoma susceptibility gene (RB-1) and N-myc gene. In Southern analysis, RB-1 deletions in tumor tissues were detected in five patients (56%), one of these revealed a total loss of RB-1. N-myc amplification was found only in one (11.1%) out of nine patients. We also observed a total loss of RB-1 in WERI-Rb-1, and a more than 100-fold amplification of N-myc in Y79. The analysis of the relationship between molecular events and clinical characteristics such as age, sex, tumor laterality did not reveal any specific correlation. These results suggest that genetic backgrounds of RB in Korean patients are quite similar to those of reported cases elsewhere. The high sensitivity of our method in detecting the RB-1 loss indicates that this method can be a useful tool for initially screening a large number of tumors.
Child↗
Involvement of cyclic GMP in the fusion of chick embryonic myoblasts in culture.
We found that a transient rise in cGMP levels, which was closely associated with the Ca2+ influx, occurred concomitant with the onset of myoblast fusion. The Ca2+ channel blocker D600 decreased both the cell fusion and the normal rise in cGMP levels. In contrast, the Ca2+ ionophore A23187 transiently increased cGMP levels and induced precocious fusion. In addition, the cGMP analog 8-Br-cGMP induced precocious fusion as A23187 did. The guanylate cyclase inhibitor, methylene blue delayed the fusion in a dose-dependent manner without significantly affecting cell alignment, proliferation, or muscle-specific protein expression. Furthermore, methylene blue delayed the normal rise in cGMP levels, and the fusion block imposed by methylene blue was significantly recovered by 8-Br-cGMP. On the basis of our present findings, we suggest that a Ca2+ influx-dependent rise in cGMP levels is an important step in myoblast fusion.
Animals↗
Effect of ursodeoxycholic acid on experimental hepatic porphyria induced by griseofulvin.
Griseofulvin(GF) has become the drug of choice as an antifungal agent for patients who suffer from many kinds of fungal infection. In order to clarify hepatic injury by griseofulvin(GF) overload and the effect of UDCA on GF-induced hepatic injury, the authors carried out biochemical, histologic, and ultrastructural studies of liver following treatment with griseofulvin and ursodeoxycholic acid(UDCA) in mice. Urine porphobilinogen excretion in the group treated with GF alone was significantly increased and reached the highest level in the 4th week and declined thereafter. Biochemical studies of the liver function showed no remarkable changes of serum bilirubin levels throughout the experimental period in all groups, except for SGPT and alkaline phosphatase activities which were significantly elevated and reached the highest level in the second week. Then they slightly decreased in GF treated groups(GF alone and GF plus UDCA) in comparison with the control group. Pathologic findings in the group treated with GF alone include focal liver cell necrosis(esp, zone 3), Mallory bodies in hepatocytes(esp, zone 1), Kupffer cell activation, and brown protoporphyrin pigments in the hepatocytes, bile canaliculi and interlobular bile ducts with a marked inflammatory cell infiltration in the portal tracts. Under the polarizing light microscope, bile ductular and canalicular thrombi showed a "Maltese cross" birefringence in mice treated with GF alone. There is no definite finding of fatty change in hepatocyte. Under the microscope, the liver appeared normal with an intact lobular architecture in the GF plus UDCA treated group. Electron microscopically, GF-induced changes include swelling of mitochondria, globular protoporphyrin crystals in the hepatocyte cytoplasm, markedly dilated bile cannaliculi and bile ducts and the formation of a Mallory hyaline bodies in the hepatocytes. There were no noticeable structural changes in the GF plus UDCA-treated group. Therefore the results suggest that GF causes hepatic injury, namely porphyria and cholestasis, and the treatment of UDCA may have cytoprotective and choleretic effects on GF-induced hepatic injuries.
Alanine Transaminase↗
Abdominal Burkitt's lymphoma diagnosed by fine needle aspiration cytology--a case report.
A case of abdominal Burkitt's lymphoma diagnosed through aspiration cytology is described. This 9-year-old boy presented with abdominal pain and distention for three months accompanied by fever and night sweat during the last month. An abdominal sonography and CT scan showed hepatosplenomegaly and an intrahepatic mass with celiac lymph node enlargement, ascites, and pleural fluid. A peripheral blood smear showed a few blast cells. Aspiration of the abdominal mass revealed very cellular aspirates consisting of diffusely scattered small monotonous round cells. The cells had little cytoplasm, along with round nuclei that showed clear-cut nuclear membrane, coarse chromatin pattern, and multiple small prominent nucleoli. Differential diagnoses considered were small round cell sarcomas such as malignant lymphoma, neuroblastoma, Ewing's sarcoma, and rhabdomyosarcoma. Of these, malignant lymphoma of the small noncleaved cell type was most consistent with the results of several studies including immunohistochemical staining, peripheral blood smear, and bone marrow biopsy. The cells were positive for leukocyte common antigen (LCA) and showed finely vacuolated basophilic cytoplasm in both the peripheral blood smear and bone marrow biopsy, characteristic of Burkitt's lymphoma cells.
Biopsy, Needle↗
Pure signet ring cell type early gastric carcinoma with extensive lymph node metastases--a case report.
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Adenocarcinoma, Mucinous↗
Intelligent Li ion battery management based on a digital signal processor for a moving actuator total artificial heart.
An intelligent Li Ion battery management (ILBM) system was developed based on a digital signal processor (DSP). Instead of using relatively complicated hardware charging control, a DSP algorithm was used, and favorable characteristics in volume, mass, and temperature increase of the implantable battery were achieved. In vitro tests were performed to evaluate the DSP based algorithm for Li Ion charging control (24 V dc motor input power 16 W, 5 L/min, 100 mmHg afterload). In this article, the first improvement was volume reduction using a Li Ion battery (3.6 V/Cell, 900 mA, seven cells: 25.2 V, 22.7 W). Its volume and mass were decreased by 40% and 50% respectively (40*55*75 mm, 189 g), compared to previously reported results, with total energy capacity increased by 110% (more than 60 min vs 25 min run time in the other battery). The second improvement includes the ILBM, which can control the performance detection for each unit cell and has a low temperature rise. The ILBM's unit cell energy detection was important because the low performance of one cell dropped to 50% of the total performance along with a 20% increase in surface temperature. All electronics for a transcutaneous energy transmission (TET), battery, and telemetry were finalized for hybridization and used for total artificial heat (TAH) implantation.
Algorithms↗
A solar cell system for extension of battery run time in a moving actuator total artificial heart.
An implantable total artificial heart (TAH) system has strong dependence upon the external battery performance for operation. Even under sophisticated battery management control, the usable external battery performance continues to decrease, which limits TAH performance. One of the ways to overcome this energy problem is to use a solar system (SS). An SS can provide electrical power for the partial TAH drive or battery recharge. This article presents a new concept for use of the solar cell for obtaining double external battery performance. To achieve it, numeric simulations were carried out to obtain the proper magnitude of solar parameters. In the TAH used, the battery power for a cardiac output of 4-6 L/min is approximately 17 W/20 min. From simulated results, the optimal power and voltage of the SS were found to be 7 W, Voc = 27 V in the case of the 24 V motor. Each solar cell includes Voc = 0.5 V, Isc = 37 mA/cm2, FF (fill factor) = 0.77, and efficiency = 10%. Based on the simulation, the effect of solar power capacity on battery run time was studied. With use of 6.5 W SS (W 304 x H 245 x D 16 mm, 1.1 kg), battery performance decreased in vitro from 100% (fully charged) to > 55% vs 0% in the conventional battery system after 20 min operation. However, it dropped to below 20% when using W SS (W 192 x H 192 x D 16 cm, 0.6 kg). The results showed doubled battery run time could be obtained compared with a system without the SS. It was concluded that the proposed SS can be put to practical use as a future energy source for a TAH.
Biomedical Engineering↗