In several pathologic conditions of the joints, it is rather frequent to find a swollen joint. The authors performed an analysis of the joint fluid proteins from 20 cases of rheumatoid arthrit is and 20 normal Kore an adults with the object of evaluating the significance of it s clinical application. The study was done with Beckman Model R System, Durrum type cell, and scanned with Model RB Analytrol. Scheicher and Schuell 2043-A paper was used with diethyl barbituric acid-sodium diethyl barbituratebuffer, pH 8.6, ionic strenght 0.075 and stianed with 0.1% bromphenol blue. The results obtained were as follows: 1) The amount of total protein was significantly increased with average of 4.80 + 1.249gm% in comparison with 2.34 + 0.553gm% in normal group. 2) Albumin fraction showed the average of 41.86 + 6.219% in comparison with 64.85 + 5.288% in normal group. 3) Alpha 2 globulin fraction disclosed the average of 10.19 + 3.379% in comparison with 4.24 + 1.158% in normal group, which was significantly increased one. 4) Gammaglobulin fraction was also significantly elevated with the average of 21.51 + 8.942% in comparison with 11.70 + 1.923% in normal group. 5) There was noted a decreased A/G ratio, the average of 0.74 + 0.196, in comparison with 1.911 + 0.430 in normal group.
Adult ; Arthritis, Rheumatoid ; Bromphenol Blue ; Humans ; Hydrogen-Ion Concentration ; Joints

No abstract available.
Buthionine Sulfoximine* ; Cell Line* ; Cisplatin* ; Humans* ; Lung Neoplasms* ; Lung* ; Stomach*

BACKGROUND: The objective responses of cisplatin and etoposide (PVP) combination chemotherapy as second-line therapy following CAV was high (40~50%) and, in several reports, PVP yields survival results that are at least as good as those obtained with cyclophosphamide or doxorubicin-based regimens and with less host-related toxicity in chemotherapy-naive patients. We conducted a phase II study to evaluate the effect of a combination of cisplatin and etoposide as a first-line therapy in patients with small cell lung cancer. METHODS: Sixty-one previously untreated small cell lung cancer patients with measurable lesion(s) received cisplatin(30 mg/m2 IV, day 1~3) and etoposide(100 mg/m2 IV, day 1~3). In patients with limited disease, after completion of 6 cycles of PVP chemotherapy, chest and prophylatic brain irradiation was performed in case of complete responder, chest irradiation only in partial responder. RESULTS: 1) Of 55 evaluable patients, 13(24%) had a complete response and 29(53%) had a partial response. 2) The median survival time was 55.8 weeks for all patients(N=55), 61.1 weeks for limited disease(N=31), 51.3 weeks for extensive disease(N=24). 3) The response duration was 29.1 weeks for responders(N=42). 4) There was no significant prognostic factors iufluencing response rates. 5) The toxicity was tolerable and there was no treatment-related deaths. CONCLUSION: The PVP combination chemotherapy as a first-line therapy was effective and well-tolerated in patients with small cell lung cancer.
Brain ; Cisplatin* ; Cyclophosphamide ; Drug Therapy ; Drug Therapy, Combination* ; Etoposide* ; Humans ; Small Cell Lung Carcinoma* ; Thorax

Recombinant human-interferon-gamma (rH-IFN-gamma) and verapamil (VRP), either alone or in combination, were evaluated in MTT assay for their modification effects on adriamycin-induced cytotoxicity against MKN-45, human stomach adenocarcinoma cells. VRP as a single agent did not inhibit the survival of MKN-45 at doses of up to 5.0 micrograms/ml. The survival of MKN-45 was inhibited by rH-IFN-gamma dose-dependently and further inhibited by the addition of VRP. However, the maximum growth inhibition of MKN-45 in any combination treatment with rH-IFN-gamma and VRP was less than 50% except in the highest concentration combinations (% survival: 47.9% at 10(4) U/ml of rH-IFN-gamma and 3.0 micrograms/ml of VRP). Adriamycin caused a concentration-dependent cytotoxicity and its cytotoxicity was significantly enhanced by the addition of rH-IFN-gamma and further enhanced by the combined use of rH-IFN-gamma and VRP. The modification effects of rH-IFN-gamma and VRP on adriamycin-induced cytotoxicity were evaluated in terms of modification index (MI), demonstrating that rH-IFN-gamma significantly increased in adriamycin-induced cytotoxicity and that the combined use of rH-IFN-gamma and VRP enhanced the adriamycin-induced cytotoxicity to a greater extent than did rH-IFN-gamma alone: MI values at 10(2) U/ml and 10(3) U/ml of rH-IFN-gamma were 1.7 and 3.1, respectively; those at 1.5 micrograms/ml and 3.0 micrograms/ml of VRP in the presence of 10(3) U/ml of rH-IFN-gamma were 4.4 and 6.0, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Adenocarcinoma/*drug therapy/pathology ; Antineoplastic Combined Chemotherapy Protocols/pharmacology ; Cell Survival/drug effects ; Doxorubicin/*pharmacology ; Drug Interactions ; Drug Resistance ; Drug Screening Assays, Antitumor ; Humans ; Interferon-gamma/*pharmacology ; Recombinant Proteins ; Stomach Neoplasms/*drug therapy/pathology ; Tumor Cells, Cultured ; Verapamil/*pharmacology

BACKGROUND: Tissue inhibitor of metalloproteinase is a natural inhibitor that counteracts proteolytic enzymes essential to the invasion of cancer cell. Whether or not TIMP-2 gene transfer via adenovirus could inhibit the invasion of lung cancer cell in vitro was evaluated for the future purpose of gene therapy against lung cancer. METHODS: Recombinant adenvirus-TIMP-2(Ad-TIMP-2) was generated by homologeous recombination after pACCMV-TIMP-2 and pJM17 were cotransfected into 293 cell by standard calcium phosphate coprecipitate mathod. Calu-6, one of the most invasive lung cancer cells, was transduced with Ad-TIMP-2 or Ad-β-gal. An-chorage-independent growth and invasiveness were assessed by soft agar clonogenicity assay and invasion assay using two-chamber, well divided by matrigel. RESULTS: Ad-TIMP-2 transduced calu-6 cells produced bilolgically active TIMP-2 more than 50 times more than parental calu-6. TIMP-2 gene transfer did not suppress the in vitro tumorgenicity. However, two chamber well assay revealed that Ad-TIMP-2 transduction reduced the invasiveness of calu-6 efficiently (12% compared with parental cell) even at low 10moi. CONCLUSION: Even though TIMP-2 gene transfer did not inhibit in vitr tumorigenicity, it did inhibit invasion of lung cancer cell in vitro. The inhibition of invasion by Ad-TIMP-2 may be a useful strategy for the treatment of lung cancer.
Adenoviridae* ; Agar ; Calcium ; Genetic Therapy ; Humans ; Lung Neoplasms* ; Lung* ; Parents ; Peptide Hydrolases ; Recombination, Genetic ; Tissue Inhibitor of Metalloproteinase-2*

No abstract available.
Cell Line* ; Cisplatin* ; Humans* ; Interferon-gamma* ; Lung Neoplasms* ; Lung* ; Stomach* ; Tumor Necrosis Factor-alpha*

No abstract available.
Cell Line* ; Cisplatin* ; Humans* ; Interferon-gamma* ; Lung Neoplasms* ; Lung* ; Stomach* ; Tumor Necrosis Factor-alpha*

No abstract available.
Cell Line, Tumor* ; Doxorubicin* ; Epirubicin* ; Humans*

OBJECTIVES: Multiple lung cancers and/or precancerous lesions can be developed because many bronchi are exposed to carcinogens simultaneously according to the concept of 'Field Cancerization'. We had performed a careful bronchoscopic examination and analysed the patients of double bronchial lesions who received the separate pathologic evaluation. METHODS: We studied 21 patients of double bronchial lesions among 1855 patients of bronchoscopic examination from April 1990 to December 1993 in Korea Cancer Center Hospital. We classified the patients into three groups(double malignancies of different histology, double malignancies of same histology, and combination of malignant and benign lesions) and analysed the histologic type, location, radiologic findings, and clinical parameters. RESULTS: Among 21 patients, six patients had double malignancies of different histology, eight had double malignancies of same histology, and seven had combination of malignant and benign lesions. Out of 14 double malignant cases, 11 cases are considered as synchronous multiple primary lung cancers. Combination of squamous cell carcinomas was found in 5 cases, combination of small cell carcinoma and squamous cell carcinoma was found in 4 cases. Combination of adenocarcinoma and squamous cell carcinoma and combination of squamous cell carcinoma and poorly differentiated carcinoma were found in 1 case respectively. All patients of synchronous multiple primary lung cancers were male and had long smoking history(average 40 pack years). Among 21 cases of double bronchial lesions, only one lesion could be detected by prebronchoscopic radiologic examination including chest CT in 15 cases. CONCLUSIONS: The presence of double bronchial lesions including multiple primary lung cancers and the limitation of radiologic examination to detect early bronchial lesions encourage us to examine the whole bronchi carefully and to perform pathologic evaluations.
Adenocarcinoma ; Bronchi ; Bronchoscopy ; Carcinogens ; Carcinoma, Small Cell ; Carcinoma, Squamous Cell ; Humans ; Korea ; Lung Neoplasms ; Male ; Smoke ; Smoking ; Tomography, X-Ray Computed

No abstract available.
Carcinoma, Non-Small-Cell Lung* ; Genes, Retinoblastoma* ; Retinoblastoma*