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K H Lin

Publications and source records attributed to K H Lin.

At least 181 records · Page 10Linked to original sources
PubMed1987

Reduced doses of hepatitis B immune globulin in the prevention of perinatal transmission of hepatitis B.

From October 1982 to May 1983, newborn infants of 79 hepatitis B surface antigen (HBsAg)-positive women were enrolled in a study of the efficacy of hepatitis B immune globulin (HBIG) in the prophylaxis of perinatal transmission of hepatitis B virus (HBV) infection. HBIG 0.5 ml or 0.25 ml was given to the newborn within 15 minutes of birth and at 3 and 6 months. The mother-infant pairs were followed-up every 3 months for at least 9 months. Similar observations of untreated infants were used for comparison. Among infants of hepatitis B e antigen (HBeAg)-positive carrier mothers, the HBsAg carrier rates at 3 months were similar in the 0.5-ml and 0.25-ml HBIG dose groups. At 12 months the difference--17.7% of 17, 40% of 15--did not reach statistical significance, but the differences between these rates and that of the untreated control-85.7% of 35--did. Among infants of HBeAg-negative carrier mothers, HBV infection rates in both dose groups were similar to those of untreated infants. In the treated groups at 12 months about 45% of infants of HBeAg-positive mothers and 90% of infants of HBeAg-negative mothers were still negative for HBsAg and anti-HBs. Vaccination to induce active antibody is necessary to prevent postnatal infection and chronic carriage of HBV. To reduce the cost of combined passive and active hepatitis B immunoprophylaxis in children born to HBeAg-positive carrier mothers, 0.25 ml of HBIG could be used instead of the usually recommended 0.5 ml.

Hepatitis B↗
PubMed1986

Characteristics and aldehyde dehydrogenase activity of four rat hepatoma cell lines produced by diethylnitrosamine-phenobarbital treatment.

Recent studies in our laboratory have shown that five established rat hepatoma cell lines provide a wide spectrum of tumor-associated aldehyde dehydrogenase (ALDH) activity representative of the range of activities of this enzyme seen in primary rat hepatocellular carcinomas. Four newly established rat hepatoma cell lines, RLT-2M, RLT-3C, RLT-9F, and RLT-5G, were derived from a primary hepatocellular carcinoma. The primary tumor was induced by a single injection of diethylnitrosamine (15 microM/g body weight) to a 1-d-old female S-D rat followed at weaning by chronic phenobarbital treatment. RLT-2M was established from outgrowths of minced tumor pieces. RLT-3C, RLT-9F, and RLT-5G were cloned from RLT-2M by the serial endpoint dilution. All four lines have been maintained in culture for over 100 passages. The ALDH phenotype in both the primary tumor and the four new cell lines was determined by total activity assay, gel electrophoresis, and histochemistry. By total activity assay, the primary tumor did not possess significant tumor-ALDH activity. In contrast, the four new cell lines expressed tumor-ALDH activity. However, they differed in their basal ALDH activities and in ALDH inducibility by 3-methylcholanthrene, benzo(a)pyrene, and phenobarbital. Additionally, significant decreases in tumor-ALDH activity occurred when cells from each line were passaged in vivo. The four lines have been characterized by light and electron microscopic morphology, tumorigenicity, chromosome number, doubling time, and colony formation efficiency in soft agar.

Aldehyde Dehydrogenase↗
PubMed1986

Marrow transplantation for thalassemia.

Ten patients with homozygous beta thalassemia, aged from 1 year 7 months to 13 years, underwent bone marrow transplantation from siblings or parents. The first case received 12 mg/kg busulfan, 120 mg/kg cyclophosphamide, and 300 cGy total body irradiation before transplantation; he survives, with a graft, more than 680 days after transplantation. The other nine patients received 16 mg/kg busulfan and 200 mg/kg cyclophosphamide. Two died of transplantation-related complications on days 30 and 55. Seven survive 170 to 580 days after transplantation. Three of the seven surviving patients have durable engraftment (greater than 230 to greater than 550 days) while four patients have autologous hematopoietic recovery. Four of five patients who had less than 50 prior transfusions achieved engraftment. Only one of five patients who had more than 50 prior transfusions achieved engraftment (P less than 0.05). The six-month actuarial survival was 80%; six-month actuarial disease-free survival was 40%. These data demonstrate that bone marrow transplantation may cure thalassemia, but engraftment may be jeopardized among patients who have been heavily transfused or have received marrow from a donor who is not HLA-identical.

Actuarial Analysis↗
PubMed1984

Regulation of aldehyde dehydrogenase activity in five rat hepatoma cell lines.

Significant changes in aldehyde dehydrogenase (ALDH) activity occur during rat hepatocarcinogenesis in vivo. An NADP-dependent tumor ALDH isozyme has been studied extensively. To better understand the nature, origin, and importance of this tumor-associated phenotypic change, we have examined the ALDH activity of five well-established rat hepatoma cell lines, H4-II-EC3, HTC, McA-RH7777, JM1, and JM2. HTC, JM1, and JM2 express the tumor ALDH phenotype, as indicated by elevated NADP-dependent, benzaldehyde-oxidizing activity, the appearance of new isozymes by electrophoresis, and characteristic histochemical localization of ALDH activity in situ. The tumor ALDH phenotype is not detected in McA-RH7777 cells. H4-II-EC3 has intermediate tumor ALDH activity. Thus, the 5 cell lines provide a spectrum of tumor ALDH activities representative of the range of activities seen in vivo. Benzo(a)pyrene, 3-methylcholanthrene, and phenobarbital induce hepatic ALDH activity after treatment in vivo. The ability of these compounds to induce ALDH in vitro was assessed in H4-II-EC3, McA-RH7777, HTC, JM1, and JM2. Treatment of cell cultures for 72 hr with 3-methylcholanthrene (1.0 mM) increases the NADP-dependent ALDH activity in H4-II-EC3 and McA-RH7777 cell lines up to 34- and 11-fold, respectively. Treatment with benzo(a)pyrene (1.0 mM) also increases the NADP-dependent ALDH activity in both lines up to 17- and 48-fold, respectively. Treatment with 3-methylcholanthrene or benzo(a)pyrene increases ALDH activity 2-fold in HTC and JM2 but does not increase NADP-dependent ALDH activity in JM1. Only marginal increases in NADP-dependent ALDH are observed after phenobarbital treatment in 4 of 5 cell lines. The induction of ALDH is blocked by actinomycin D, alpha-amanitin, and cycloheximide. These studies support our hypothesis that changes in ALDH activity observed in vivo are due to mutational events occurring in initiated cells. It appears that rat hepatoma cell lines will provide an in vitro model for studying genetic regulation of the tumor ALDH.

Aldehyde Dehydrogenase↗
PubMed1983

[Association between hepatitis B surface antigenemia and HLA histocompatibility phenotypes].

To test whether HLA histocompatibility phenotypes might be associated with circulating hepatitis B surface antigen (HBsAg), we performed chi-square test with Yate's correction and Fisher's exact test on findings in 315 normal healthy hospital staffs with known HLA types and HBsAg status. A significant relation between locus A of HLA types and HBs antigenemia was demonstrated, with negative association suggested between A1, AW23, A26, A29, +AW30 +AW31 and AW32 types and HBs antigenemia. Another significant relation between locus B of HLA types and HBs antigenemia was shown, with negative association suggested between B7, B8, BW21, BW44 and BW49 and HBs antigenemia. There was no significant relation between locus C of HLA type and HBs antigenemia, but type CW4 was revealed to have a relative risk of 2.11. Therefore, previous suggestion that both susceptability and resistance to hepatitis B virus infection may be in part genetically determined and previous observation of population differences in HBsAg prevalences could be interpreted by these findings.

Adolescent↗