[Detection of alpha-thalassemias in patients with microcytic hypochromic anemia or microcytosis by restriction endonuclease mapping].
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Biomedical subjects
Publications and source records attributed to C K Lin.
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The preceding paper presents evidence for the co-transcriptional expression of the ileS and lsp genes in Escherichia coli. To identify the promoter for the ileS-lsp operon, we have determined the nucleotide sequence of an 1.8-kilobase DNA fragment between the rpsT and IleS genes. The sequence data have revealed an open reading frame, designated gene X, which encodes a polypeptide with 312 amino acid residues. Both in vivo and in vitro expressions of the x gene result in the synthesis of a soluble protein with an apparent Mr of 35,000. The x gene is transcribed in the same direction as that of the ileS-lsp operon and opposite to that of the upstream adjacent rpsT gene. No transcription termination sequence can be discerned in the intercistronic region between the x and ileS genes. DNase I footprinting experiment revealed a RNA polymerase binding site at 170-151 base pairs upstream of the x gene.
We have isolated two spontaneous mutations that increase the expression of the Tn9-derived cat gene in Bacillus subtilis. These mutations, which appear to affect initiation of translation of chloramphenicol acetyltransferase (CAT; acetyl-CoA:chloramphenicol 3-O-acetyltransferase, EC 2.3.1.28) consist of a tandem duplication and triplication of a 55-base-pair sequence located at the 5' end of cat. Included in the repeated sequence are the Shine-Dalgarno site, initiation codon, and a region of dyad symmetry located within the structural portion of the cat gene. A striking feature of the mutated initiation sites is their potential to form stem-loop structures at the 5' end of the cat messenger RNA. Within the single-stranded loops of these structures are the ribosome binding site and initiation codon for the cat gene. It appears that the Gram-negative cat translation initiation site has mutated to permit efficient utilization in B. subtilis without directly affecting Shine-Dalgarno sequence homology. This report suggests that secondary structure in the vicinity of the Shine-Dalgarno site can exert a strong positive influence on the initiation of translation in B. subtilis.
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BACKGROUND: This study investigates the cell proliferation and the expression of p53 protein in Helicobacter pylori (H. pylori)-associated gastritis and assesses the effect of bacterial eradication on these epithelial factors. MATERIAL AND METHODS: Seventy-nine patients with H. pylori-associated gastritis were randomized into the control group (n = 38) and anti-H. pylori group (n = 41). Each patient received endoscopic examinations with gastric biopsy before and 8 weeks after the treatment. The specimens from gastric antrum were immunostained for monoclonal antibodies against the proliferating cell nuclear antigen (PCNA) and p53 protein. RESULTS: In the control group, the total labeling index (L.I.) of PCNA and the positive index (P.I.) of p53 in the whole foveolar epithelium were unchanged after treatment. In the anti-H. pylori group, 35 of 41 cases (85.3%) achieved eradication of H. pylori. Amongst the H. pylori-eradicated cases, the total L.I. of PCNA in the whole foveolar epithelium did not meaningfully alter after H. pylori elimination (p > 0.05). However, a significant reduction of L.I. was observed in the middle compartments of the gastric pits (before vs. after treatment: 14.0 vs. 7.3, p < 0.05). With regard to the p53 expression, the P.I.s were significantly decreased in the whole foveolar epithelium (before vs. after treatment: 0.57 vs. 0.17, p < 0.05) and in each compartment of the gastric pits (before vs. after treatment: [upper compartment]: 0.34 vs. 0.15, p < 0.05; [middle compartment]: 0.67 vs. 0.23, p < 0.05; [lower compartment]: 0.71 vs. 0.20, p < 0.05) after eradication of H. pylori. CONCLUSIONS: Bacterial eradication reverses the hyperproliferating status of the foveolar epithelium in patients with H. pylori gastritis and leads to a decrease in p53 accumulation in the epithelial cells.
Ninety patients with a strict diagnosis of aplastic anemia were observed during a 4-year period. The incidence of aplastic anemia is estimated to be much higher here than in western countries. A disproportionately large number of young males were noted among our patients. Two cases were congenital. One case presented a past history of paroxysmal nocturnal hemoglobinuria. The etiology of 8 cases (8.9%) could be attributed to drugs and/or chemicals. In the remaining 79 cases (87.8%), the causes of the disease were unknown. The carrier rate of the hepatitis B surface antigen in the patients with aplastic anemia was similar to that of the general population, and chronic hepatitis B infection was not considered a major etiological factor. Coexistence of abnormal liver functions at the initial presentation was noted in 21.9% of the patients. Exposure to unknown drugs by self-medication was possibly one of the major causes of the high incidence of aplastic anemia and the associated abnormal liver functions in our patients.