No abstract available.

Recently the clinical estimation of gestational age has been of increasing concern particularly in premature babies because of its great aid in treament and expectation of future health. The clinical distinction between small-for-dates infants and premature babies offers great difficulty, but can be made readily if the gestational age is known. The author has investigated the clinical estimation of gestational age in 100 premature infants who were born at the Seoul National University Hospital, the Eul Ji Hospital and the So Wha Hospital from March to August in 1977, in order to evaluate the correlation between the gestationl age calculated from LMP and the clinically estimated gestaionl age using two charts designed by Brazie and Lubchenco, which were based on 16 physical criteria and 20 neurologic criteria with the following results. 1) The sex and age distribution of the 100 premature infants showed predominance in male and in the 34th336th weeks of gestional age. 2) The numbers of babies whose weight was appropriate, small and large for gestational age were 89, 9 and 2 respectively according to University of Colorado Medical Center Example, while they were 91, 4 and 5 according to the chart based on Rha's report in 1976 in Korea. 3) The correlation percentages between the gestational age determined by each of the 16 physical criteria and those calculated from LMP were as following; vernix (88%), skin and nail plates(88%), recoil-leg(75%), skin thickness appearance(73%), sole creases(68%), genitalia, testes and scrotum(67.5%) and so forth. 4) The correlation percentages between the gestational ages determined by each of the 20 neurologic criteria and those calculated from LMP were as following, pupillary reflex(94%), grasp reflex(90%), vertical positions(87%), head lag (83%), glabellar tap(81%), body extensors(80%), horizontal positions(80%), rooting reflex(80%), and so forth. 5) The correlation coefficiency between the clinically estimated gestational age using the above described two charts and that calculated from LMP was 0.98. And the regression formula for the latter (X) against the former (Y) was Y=0.786X+7.753. With the above results, the author could conclude that clinical estimation of the gestational age with the two charts of Brazie and Lubchenco was highly correlated and it deserves to be recommended for clinical purpose.
Age Distribution ; Colorado ; Genitalia ; Gestational Age* ; Hand Strength ; Head ; Humans ; Infant ; Infant, Newborn ; Infant, Premature* ; Korea ; Male ; Seoul ; Skin ; Testis

No abstract available.

No abstract available.
Tonsillectomy*

No abstract available.
Lithotripsy* ; Salivary Gland Calculi* ; Salivary Glands* ; Shock*

No abstract available.
Ceruloplasmin* ; Cholesterol, HDL* ; Copper* ; Humans ; Infant, Newborn* ; Iron* ; Zinc*

No abstract available.
Picibanil* ; Pleural Effusion, Malignant*

The intensive use of chemotherapeutic agents for the treatment of cancer has resulted in the cure or improved survival of many patients. But unfortunately, many cancers including human hepatocellular carcinoma (HCC) don't respond to chemotherapy. One of the major mechanisms for the drug resistance in the HCC is an elevated MDR1 RNA expression which makes cells become multidrug resistant. To overcome the multidrug resistance (MDR) phenotype, a high dose of verapamil is required both clinically and experimentally. Accordingly we have examined the MDR modulating effects with combinations of tamoxifen, cyclosporin A, and verapamil in vitro with the physiologically achievable concentrations of each agent, i.e., 2.0 microM/L for tamoxifen, 1.6 microM/L for cyclosporin A, and 2.5 microM/L for verapamil respectively in HCC lines. As expected, verapamil alone with the physiologically achievable concentration at which we tested didn't enhance the doxorubicin cytotoxicity in the HCC lines. Furthermore, any verapamil combination with cyclosporin A or tamoxifen was not effective in overcoming the doxorubicin resistance in the high MDR1 expressor (Hep-G2) line. However tamoxifen reduced the IC50 of doxorubicin by a factor of 1.9 in the low MDR1 expressor (SK-Hep1) and 1.1 in the high MDR1 expressor line (p< 10(-5) respectively). Of interest, combinations of tamoxifen and cyclosporin A showed a significant reduction in the IC50 of doxorubicin in both HCC lines. The IC50 of doxorubicin was reduced by a factor of 3.9 and 1.3, i.e., from 0.023943 micrograms/ml to 0.006157 micrograms/ml (p< 10(-5)) in the SK-Hep1 cell line, and 0.068819 micrograms/ml to 0.052442 micrograms/ml (p< 10(-5)) in Hep-G2 respectively when tamoxifen and cyclosporin A were administered together. Both the estrogen and progesterone receptors in the SK-Hep1 and Hep-G2 lines were less than 0.01 fmol/mg of cytosol protein, respectively. It is therefore suggested that the reversal of doxorubicin resistance is unrelated to their anti-estrogenic activity in the HCC lines. Three modulator combinations of tamoxifen, cyclosporin A, and verapamil were not more effective than the combination of tamoxifen and cyclosporin A on the sensitivity to doxorubicin. MDR modulators of tamoxifen, cyclosporin A, and verapamil didn't reduce the IC50 of cisplatin to the clinically achievable concentration range in HCC lines. In summary, the combination of tamoxifen and cyclosporin A at the concentrations normally seen after clinical administration of these modulators showed significant synergism on the sensitivity to doxorubicin in both low and high MDR1 expressor HCC lines. These data indicate the need for in vivo trials.
Antineoplastic Agents/*pharmacology ; Carcinoma, Hepatocellular/*physiopathology ; Cyclosporine/*pharmacology ; Drug Resistance ; Human ; Liver Neoplasms/*physiopathology ; Support, Non-U.S. Gov't ; Tamoxifen/*pharmacology ; Tumor Cells, Cultured/drug effects ; Verapamil/*pharmacology

Churg-Strauss syndrome or allergic granulomatosis and angiitis is an uncommon systemic vasculitis chracteristized by asthma, hypereosinophilia, mono or polyneuropathy, non-fixed pulmonary infiltrates, paranasal sinus abnormality and extravascular eosinophil infiltration. Gastrointestinal manifestations occur in about 42% of patients. However, ulcer formation in gastrointestinal tract mucosa is a rare manifestation, usually discovered upon laparotomy or autopsy. We experienced a case of 40-year-old woman with Churg-Strauss syndrome, who presented multiple colonic ulcers on colonoscopy. She also had bronchial asthma, polyneuritis, peripheral blood eosinophilia and hemorrhagic bullous skin lesions with extravascular eosinophil infiltration. She improved with high dose corticosteroid and cyclophosphamide. We report this case with a review of the literature.
Adult ; Asthma ; Autopsy ; Churg-Strauss Syndrome ; Colon* ; Colonoscopy ; Cyclophosphamide ; Eosinophilia ; Eosinophils ; Female ; Gastrointestinal Tract ; Humans ; Laparotomy ; Mucous Membrane ; Neuritis ; Polyneuropathies ; Skin ; Systemic Vasculitis ; Ulcer* ; Vasculitis

PURPOSE: To overcome the limitations of cancer gene therapy using replication-incom- petent adenovirus, we generated E1B 55 kD-deleted adenovirus (YKL-1) by polymerase chain reaction (PCR) and homologous recombination. We then investigated tumor-specific virus replication and cytotoxicity of YKL-1 in vitro and in vivo. MATERIALS AND METHODS: YKL-1 was constructed by reintroducting E1A and E1B 19 kD into pTG-CMV El/E3-deficient adenoviral vector and inducing homologous recombination in E. coli. The recombinant vector pYKL-1 was transfected into 293 cells to generate YKL-1. The properties of newly constructed YKL-1 was defined by PCR and immuno- blotting analysis. Virus replication was examined by infecting human normal and cancer cells on 6-wells at multiplicity of infection (MOI) of 10 for 3 days. Virus was then recovered and titered. Cytopathic effect was analyzed by infecting human normal and cancer cells on 24-wells at MOIs of 10, 1 or 0.1 for 7 to 10 days and staining them with crystal violet solution. Inhibition of tumor growth was examined in human cancer cell xenografts in nu/nu mice by intratumoral injection of YKL-l. RESULTS: PCR and immunoblotting analysis confirmed that YKL-1 contained E1A and E1B 19 kD but not E1B 55 kD. In human normal cells, virus replication and subsequent cytopathic effect of E1B 55 kD-deleted adenovirus YKL-1 was markedly attenuated by larger than 2 to 3 log in magnitude, compared to that of wild-type ad-XJ. In contrast, YKL-1 was capable of replicating and inducing cytotoxicity i.n most human cancer cells. C33A and Hep3B containing p53 mutation were much more sensitive, whereas HeLa and H460 with wild type p53 were relatively resistant to YKL-1. Finally, the tumor growth was dramatically retarded by intratumoral injection of YKL-1 in C33A cervical cancer xenograft and the histology showed significant necrosis by intratumoral injection of YKL-1. CONCLUSION: The results here demonstrated the ability of preferential virus replication and cytotoxicity of ElB 55 kD-deleted adenovirus YKL-1 in human cancer cells. Therefore, these indicated a promising potential of YKL-1 as an antitumoral virus agent and a selective replication-competent virus vector.
Adenoviridae* ; Animals ; Genes, Neoplasm ; Genetic Therapy ; Gentian Violet ; Heterografts ; Homologous Recombination ; Humans ; Immunoblotting ; Mice ; Necrosis ; Polymerase Chain Reaction ; Uterine Cervical Neoplasms ; Virus Replication*