The glucose nonfermenting gram-negative bacilli encountered about 10% of all gram-negative bacilli isolated from clinical material. Therefore, a rapid and correct identification of glucose nonfermenting gram-negative bacilli is impotent for a better management of infectious disease. There are many conventional systems for the identification of glucose nonfermenting gram-negative bacilli but most of them have problems and difficulties. Commercial Kit Systems exist and they are too expensive for daily use in Korea because of high cost. Based on 12 selected tests we propose a new code system, MCRCODE-N for rapid and inexpensive identification of glucose nonfermenting gram-negative bacilli. The selective 12 tests are oxidase, glucose oxidation motihty, urease, DNase arginine dehydrolase, nitrate reduction, gelatin Liquefaction, esculin hydrolysis, mannitol oxidation, maltose oxidation, Lactose oxidation. The 12 tests are divided 4 group and then each group has 3 tests. The result of each group is expressed by the number as below. The positive test is given by specific number (1st test=1, 2nd test=2, 3rd test=4), while any negative result is 0. Each 3 numbers of one group are added and make number of 1 digit. Four digit number is referred to the code book of MCRCODE-N system or MCRCODE system using computer (Apple-II model) created by authors. This MCRCODE-N system is suitable ones for out use in Korea. We propose the MCRCODE-N system for clinical use.
Arginine ; Clinical Coding* ; Communicable Diseases ; Deoxyribonucleases ; Esculin ; Gelatin ; Glucose Oxidase ; Glucose* ; Hydrolysis ; Korea ; Lactose ; Maltose ; Mannitol ; Urease

No abstract available.

No abstract available.
Animals ; Carcinogenesis* ; Rats*

No abstract available.
Animals ; Rats*

No abstract available.
Humans* ; Keratinocytes* ; RNA, Messenger*

No abstract available.
Cell Line* ; Genes, Tumor Suppressor* ; Humans* ; Lung Neoplasms* ; Lung*

Serum levels of alpha-1-Antitrypsin(AAT) were determined in 42 patients with hepatocellular carcinoma(HCC), 5 patients with metastatic liver cancer from stomach adenocarcinoma, 10 patients with liver cirrhosis, 10 patients with chronic hepatitis, and 66 controls by rocket immunoelectrophoresis using rabbit antiserum. The mean level of serum AAT was 225.5 +/- 73.0 mg/dl in 66 controls. The serum AAT in patients with HCC was 428.7 +/- 123.3 mg/dl, which was significantly higher than those in the controls and in patients with liver cirrhosis or chronic hepatitis(p less than 0.02). The level of AAT in metastatic liver cancer was similar to that in HCC. The positive cut-off value for elevation of serum AAT in this study was determined as above 445 mg/dl, the mean plus 3 standard deviations in the controls. Elevations of serum AAT were observed in 54.8%, 60.0%, and 10.0% of patients with HCC, metastatic liver cancer, and liver cirrhosis, respectively, while none of the patients with chronic hepatitis or the controls was positive. The serum AAT levels in 42 patients with HCC were analyzed with regard to sex, age, serum albumin, HBsAg, alpha-fetoprotein(AFP), and diameter of HCC, with no significant differences being observed between these factors and the serum AAT levels except for the diameter of the HCC. The positive rate in the HCC with a diameter of 10 cm or more was 74.1%, which was a significantly higher rate compared with 20.0% in the HCC with diameters less than 10cm. The positive rate of AFP for HCC was 61.9%, when 500 ng/ml of AFP was used as the cut-off value.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult ; Aged ; Carcinoma, Hepatocellular/blood/*diagnosis ; False Negative Reactions ; False Positive Reactions ; Female ; Humans ; Liver Neoplasms/blood/*diagnosis ; Male ; Middle Aged ; Tumor Markers, Biological/*blood ; alpha 1-Antitrypsin/*analysis

PURPOSE: The replacement of functional genes into cells that lack genes or mutant genes is the basis of gene therapy. In cancer, where cells often have multiple genetic defects, the replacement of critical genes may suffice to suppress cell growth or induce cell death. In malignant brain tumors, p53 mutation are among the most frequently observed genetic findings and inactivation p53 suggests that p53 plays a critical role in carcinogenesis and tumor progression. Therefore, we study the successful transfer of the wild-type p53 gene using a replicative deficient adenovirus vector into human glioma and medulloblastoma c~ell lines. Meterials and Methods: The human glioma cell line T-98G, U-87MG, U-373MG were used. To determine the efficiency of the adenovirus vector, cell lines were transfected with the Ad-p gal and analysed with X-Gal staining. Cell viability was determined by trypan blue exclusion every day after infection and Westem blot analysis was used to conform the expression of the exogenous p53 protein. RESULTS: Cell growth of the Ad-CMV-p53 infected U-373MG, and U-87MG was significantly suppressed. It appeared that exogenous p53 protein expression had an earlier ad more profound suppressive effect on U-373MG having a mutated p53 gene than on U-87MG having a wild-type p53. The expression of the exogenous p53 was more than 10 times higher than the expression of the endogenous p53. To examine the decreased viability, U-373MG was stained with Hochest 33258 and detected nuclear condensation and apoptic body. Staining results suggest that cells undergo apoptosis. CONCLUSION: The replicative deficient adenoviral vector can transfer and express p53 in human glioma cell lines in vitro, restoring wild-type p53 tumor suppressor functions. The restoration of normal p53-encoded protein in the mutant ceil lines induced cell death. The high expression of the newly transduced protein had different effects on the growth rate of the infected cell lines depending on the p53 status of the cells.
Adenoviridae* ; Apoptosis ; Brain Neoplasms ; Carcinogenesis ; Cell Death ; Cell Line* ; Cell Survival ; Genes, p53 ; Genetic Therapy ; Glioma* ; Humans ; Medulloblastoma ; Trypan Blue

No abstract available.

Body fluid Lactate dehydrogenase and its isoenzyme Measurement was performed in 132 patients: 8 cases with peritonitis, 21 cases with malignant ascites, 43 cases with liver cirrhosis, 48 cases with tuberculous pleuritis, 12 cases with malignant pleural effusion respectively. Body fluid protein and glucose contents, red blood cell counts, white blood cell counts, cytologic examination were also performed as a comparative study. The results were as follows: 1. Measurement of total LD and protein amount could differentiate between transudate and exudates in the ascitic fluids. 2. In the malignant exudate of ascites and pleural fluid, the activity of LD2 isoenzyme was statistically increased compared with that of inflammatory exudates and the activity of LD4 isoenzyme was also incereased compared with that of serum (P<0.05). 3. The inflammatory exudates of pleural fluid and ascites demonstrated the increase of LD5 isoenzyme activity statistically compared with that of serum and malignant exudates (P<0.05). 4. A difference of total LD activity between malignant ascites and inflammatory ascites was significant statistically, while this was not observed in the pleural exudate. 5. Total LD and LD5 isoenzyme activity didn't correlated with the number of white blood cells in the exudate.
Ascites ; Ascitic Fluid ; Body Fluids* ; Erythrocyte Count ; Exudates and Transudates ; Glucose ; Humans ; L-Lactate Dehydrogenase ; Lactic Acid* ; Leukocyte Count ; Leukocytes ; Liver Cirrhosis ; Peritonitis ; Pleural Effusion, Malignant ; Pleurisy