Biomedical subjects
Publications and source records attributed to H J Lin.
A 64-year-old man developed diffuse gastrointestinal polyposis, protein-losing enteropathy, skin pigmentation, hair loss, and unique nail changes. He also exhibited pulmonary tuberculosis and impaired immunity with skin anergy, poor lymphocyte mitogens stimulation test, and low serum immunoglobulin. We discuss the relationship of infection, nutrition, immunity, and the Cronkhite-Canada syndrome.
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Regulatory sequences of the human fetal gamma-globin gene were studied by constructing composite gamma/beta globin promoters and comparing their function to that of intact beta promoters in human K562 cells. The beta-globin gene with either 1,600 or 127 basepairs of beta promoter sequence was not expressed after stable introduction into K562 cells, consistent with the known inactivity of the beta-globin gene in these cells. In contrast, a gamma/beta promoter composed of a gamma fragment spanning positions -408 to -137 joined to the 127-bp beta promoter was able to drive the beta-globin gene. The gene appeared to be inducible with hemin. A zeta-globin 5' flanking fragment also activated the beta promoter. The function of a series of composite gamma/beta promoters was then assessed by their ability to drive directly the neomycin resistance gene, again in stably transformed cells. The -408 to -137 gamma fragment activated the beta promoter in an orientation-specific manner in this assay. Deletion analysis showed that regulatory sequences were present between positions -259 and -137 of the fetal gamma-globin gene flanking region.
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Sera from 31 HBsAg-positive Chinese patients with inoperable hepatocellular carcinoma (HCC) were tested for hepatitis B virus DNA (HBV DNA) by means of dot hybridisation and Southern blot technique. HBV DNA probes were prepared from human plasma. Eighteen of the patients were HBeAb-positive, 12 were HBeAg-positive and one case had neither marker. Serial specimens were obtained from 16 cases over 5-42 weeks, while the patients were treated with recombinant leukocyte A interferon (rIFN-A) or adriamycin. Seven patients (2 HBeAg-positive, 5 HBeAb-positive) were positive for HBV DNA. In two patients HBV DNA and HBV DNA polymerase (DNAp) appeared in serum weeks after rIFN-A or adriamycin treatment was started. In two other cases, HBV DNA that was initially present disappeared during rIFN-A treatment. In a fifth patient HBV DNA persisting after adriamycin treatment diminished after change of treatment to rIFN-A. With one possible exception the HBV DNA detectable by Southern blot technique was composed chiefly of sequences 2.2-3.2 kb size indicating the presence of unintegrated DNA forms. DNAp activities were raised in the presence of HBV DNA in 4 patients. These findings show that HBV replication can be activated or suppressed in advanced HCC. Treatment with rIFN-A may have been effective in suppressing HBV DNA synthesis, but the number of cases studied was too small to arrive at a definite conclusion on this point.
We have used molecular hybridization techniques to show that hepatitis B virus (HBV) DNA from different individuals may have substantial differences in sequence homology. Seven specimens of HBV DNA were isolated from plasma of different blood donors. Samples were applied as dots to membranes and nick-translated to form probes. Densitometry of the radioautograms showed that hybridization was most extensive with probe prepared from the same specimen. The hybridization bias was statistically significant (P less than .02) and visible to the naked eye. Hybridization to probes that were digested with nuclease S1 before nick translation did not eliminate the bias. Nor was the bias related to the d/y subdeterminants; on the average, 15 other specimens hybridized equally well to probes prepared from HBV with the same or different subdeterminant. Many specimens among 37 other serum samples showed greater or lesser degrees of homology to different probes, as demonstrated by reprobing of samples fixed to nylon membranes.
A pilot cord blood TSH screening program for congenital hypothyroidism was commenced in Hong Kong in April 1982. By April 1984, 14 411 neonates born in two hospitals were screened for this disorder. Five cases of primary hypothyroidism and two cases of transient hypothyroidism were detected. The detection of cases of congenital hypothyroidism with only moderately elevated cord blood TSH values means that the recall rate will remain high.
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Hypoglycemia is frequently reported in hemodialysis patients on propranolol. The effects of beta-blockers on the glucose, alanine and free fatty acid responses to glucagon challenge (2 mg) in fourteen hemodialysis patients were studied. Patients on propranolol had impaired glycemic response while those on metoprolol had decreased response only before dialysis. There was a significant negative correlation between propranolol level (log-transformed) and glycemic responses, suggesting that propranolol has direct effect on the latter. Hemodialysis patients had fasting alanine levels comparable to those of normal subjects. After glucagon challenge, the decrements in alanine level had no consistent relationship to the impaired glycemic response. Thus suppression of gluconeogenesis is unlikely to be the prime cause of propranolol-induced hypoglycemia. The basal free fatty acid levels were significantly lower among hemodialysis patients on propranolol. This limited availability of free fatty acid as well as the inhibitory effect on hepatic glucagon-stimulated glucose output may contribute to the predisposition to hypoglycemia in dialysis patients given propranolol. The results suggest that metoprolol has less interference on energy substrate supply in hemodialysis patients under fasting conditions.
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