Three types of flow reactors with different lengths (12-126 mm) and widths (0.4-2.0 mm) of channel were made on the silicon chip by microfabrication techniques for the chemiluminescent (CL) detection of epinephrine (EP) with lucigenin (Luc). The volume of each CL reactor was about 10 microL. A solution containing EP and Luc and a solution containing NaOH and periodate were injected successively into each inlet of the CL reactor in the range 20-100 microL/min with a pressure-driven flow system. The intensity of light emission was dependent on the geometry of the flow reactors. These results could be explained in terms of the differences in the diffusion length of the reactants in the flow reactors. The maximum light emission were linearly correlated, with the concentrations of EP over the range from the detection limit of 5.0 x 10(-8) mol/L up to 5.0 x 10(-6) mol/L on the use of the CL reactor with the most promising geometry.

Acridines↗

PubMedDate not supplied

Hepatosinusoidal leukaemia/lymphoma consisting of Epstein-Barr virus-containing natural killer cell leukaemia/lymphoma and T-cell lymphoma; mimicking malignant histiocytosis.

Previously diagnosed cases of hepatosinusoidal T-cell lymphoma and malignant histiocytosis (MH) may include lymphoid neoplasms of natural killer (NK) cell lineage associated with Epstein-Barr virus (EBV). Such hepatosinusoidal neoplasms were found to demonstrate hepatomegaly but not lymphadenopathy, and all were diagnosed by a liver biopsy. Sixteen adult patients diagnosed with hepatosinusoidal leukaemia/lymphoma (six NK-cell leukaemia/lymphomas [NKLLs], five instances of MH, three T-cell malignant lymphomas [T-MLs], and two adult T-cell leukaemia/lymphomas [ATLLs] were examined for EBV by in situ hybridization, then were studied immunohistochemically and subjected to a DNA analysis. Among our five patients with MH, neoplastic cells showed T-cells, but no histiocytic markers, and they were considered to have either a T-cell or NK-cell lineage. All NKLLs, MHs and T-MLs, except for ATLLs accompanied by reactive hemophagocytic histiocytes, varied in number in each case. In situ hybridization revealed the presence of EBV in the nuclei of atypical cells in all of the six lymphoid neoplasms of NK-cell lineage. Each case of MH and each T-ML which represented EBV demonstrated no definite T-cell or histiocytic markers. Patients with ATLL did not reveal EBV. In all patients with hemophagocytosis, EBV was present in the nuclei of the neoplastic lymphocytes, but not in the hemophagocytic cells. Finally, the 16 cases were reclassified into eight cases with EBV-containing NKLLs, six T-MLs, and two ATLLs. In addition, no true histiocytic neoplasms were observed. The mechanism of hemophagocytosis may be therefore the production of lymphokines (macrophage-activating factors) by neoplastic lymphocytes. EBV-associated hepatosinusoidal leukaemia/lymphoma may thus contain a lymphoid neoplasm of NK-cell lineage, which made it difficult to be distinguished from the previously designated malignant histiocytosis.

Adult↗

PubMedDate not supplied

A sequence-specific endonuclease, Endo.SceI, can efficiently induce gene conversion in yeast mitochondria lacking a major exonuclease.

Endo.SceI most likely initiates homologous recombination of yeast mitochondrial genome through sequence-specific double-strand scission of DNA. According to the double-strand break-repair model for the mechanism of homologous recombination, DNA ends created by sequence-specific endonucleases have to be processed by exonucleases. The major mitochondrial exonuclease (encoded by NUC1) has been shown to greatly affect the length of conversion tracts at the 21S rRNA locus when site-specific gene conversion is induced by omega endonuclease. In order to examine the role of the NUC1 nuclease in the Endo.SceI-induced recombination, recombination frequencies were measured after crossing of parental strains either in the presence or absence of NUC1 nuclease activity. The frequency of gene conversion in the oli2 locus induced by Endo.SceI was not reduced by disruption of the NUC1 gene. This result strongly implicates the presence of multiple exonucleases for the processing of the DNA ends created by sequence-specific endonucleases.

Base Sequence↗