Genome analysis was performed on 69 adenovirus isolates from pharyngeal secretions of young children hospitalized with severe lower acute respiratory disease in Santiago, Chile, between 1984 and 1986. As expected, most isolated strains belonged to subgenus B (68.1%). Among the isolates of 1984, Ad7c was the dominant genotype (12 out of 23). The majority of isolates of 1986 were of the recently described genomic variant 3f. 相似文献
Sera from 79 patients with acute self-limiting hepatitis, 17 patients with acute hepatitis B evolving into chronic HBsAg carriership, and 43 chronic HBsAg carriers without a history of acute hepatitis were analyzed for presence of hepatitis B virus (HBV)-DNA by a molecular hybridization technique. In acute self-limiting hepatitis, HBV-DNA was cleared within a few weeks after the onset of clinical symptoms. The longest period of DNA positivity observed in this group was 42 days. In 29 of 52 patients HBV-DNA was cleared before HBeAg disappeared. Among 17 patients who became chronic HBsAg carriers, HBV-DNA was present for more than 6 months in all but one. Most of the HBsAg carriers eventually cleared HBV-DNA. The DNA clearance frequently preceeded the conversion of HBeAg to anti-HBe. Thus, in many patients there was a transitional period with HBeAg but without HBV-DNA. HBV-DNA was found to be a better index of impending chronicity than HBeAg since persistence of HBeAg for more than 42 days was noted in 10% of the patients who nevertheless cleared HBsAg within 6 months. By that time all those patients had turned negative for HBV-DNA. On the other hand, in 16 of the 17 patients who became chronic carriers of HBsAg, HBV-DNA as well as HBeAg persisted for more than 6 months. The present results also suggest that infectivity in acute hepatitis B is a feature mainly of the presymptomatic and early symptomatic period. 相似文献
Mutations in the human fibrillin 1 gene (FBN1) cause the Marfan syndrome (MFS), an autosomal dominant connective tissue disorder. Knowledge about FBN1 mutations is important for early diagnosis, management, and genetic counseling. However, mutation detection in FBN1 is a challenge because the gene is very large in size ( approximately 200 kb) and the approximately 350 mutations detected so far are scattered over 65 exons. Conventional methods for large-scale detection of mutations are expensive, technically demanding, or time consuming. Recently, a high-capacity low-cost mutation detection method was introduced based on denaturing high-performance liquid chromatography (DHPLC). To assess the sensitivity and specificity of this method, we blindly screened 64 DNA samples of known FBN1 genotype exon-by-exon using exon-specific DHPLC conditions. Analysis of 682 PCR amplicons correctly identified 62 out of 64 known sequence variants. In three MFS patients of unknown FBN1 genotype, we detected two mutations and eight polymorphisms. Overall, 20 mutations and two polymorphisms are described here for the first time. Our results demonstrate 1) that DHPLC is a highly sensitive (89-99%, P = 0.05) method for FBN1 mutation detection; but 2) that chromatograms with moderate and weak pattern abnormalities also show false positive signals (in all 45-59%, P = 0.05); 3) that the difference in the chromatograms of heterozygous and homozygous amplicons is mostly independent of the type of sequence change; and 4) that DHPLC column conditions, additional base changes, and the amounts of injected PCR products influence significantly the shape of chromatograms. A strategy for FBN1 mutation screening is discussed. 相似文献
The KIR2DL4 gene including a portion of exon 1 through exon 9 was sequenced from two families and eight cell lines from the International Histocompatibility Workshop (IHWS). Two known alleles and eight variants were detected. Overall, there were five synonymous and three non-synonymous changes when the variants were compared to the coding sequences of the most closely related known alleles plus a common frameshift change in five of the variant alleles. Alignment of the new variants with all known alleles showed that the regions encoding the extracellular region and the cytoplasmic tail were the most polymorphic. Two non-synonymous changes, P146H and L161V, occurred in an extracellular immunoglobulin-like domain. Five of the eight variants had a single adenine deletion in the exon encoding the transmembrane region, potentially resulting in a truncated protein lacking the cytoplasmic tail. The distribution of the deletion variant among many KIR2DL4 alleles may explain the high frequency of this variation in the population. Four of the eight consanguineous IHWS cell lines were found to be heterozygous for KIR2DL4 carrying two alleles that differed from one another by a few nucleotide substitutions. Analysis of intron sequences in the families revealed the nature and distribution of interspersed repeat elements which comprise 46% of the KIR2DL4 nucleotide sequence and consist of 12 elements including six SINEs (13.73% of the total length), one LINE (12.41%), and five LTR elements (19.51%). The results revealed the presence of extensive diversity in the KIR2DL4 gene. This is the first extensive report providing both exon and intron data in related individuals. 相似文献
Summary: Fluorinated bis(phenoxy‐imine)Ti complexes 1 – 3 combined with MgCl2/i‐BunAl(OR)3−n (MgCl2‐supported catalysts) were able to polymerize propylene in a living fashion at room temperature to provide slightly to highly syndiotactic poly(propylenes) (PPs) with extremely narrow distributions of molecular weight. These represent the first examples of MAO‐ and borate‐free group 4 metal‐based living catalysts. The supported complexes 2 and 3 formed PPs with higher syndiotacticity and Tm's than the corresponding homogeneous MAO‐activation systems (e.g., 3 : rr 97%, Tm 155 °C; MAO activation: rr 93%, Tm 152 °C). The measured Tm of 155 °C represents the highest known Tm for syndiotactic PPs synthesized at room temperature.
Polymerization of propylene to poly(propylene) with supported Ti‐based catalysts. 相似文献
Mimicking cell membrane and the biomolecular recognition associated with membranes represents a great technical challenge, yet it has opened doors to innovative diagnostic and therapeutic methods. Our work has focused on design and synthesis of a class of smart materials exploiting biological principals for use in biosensors: these materials are functional polymeric assemblies that mimic the cell membrane and conveniently report the presence of pathogens with a color change. Biologically active cell membrane components are incorporated into conjugated polymers with desirable optical properties and the binding of the target molecules onto the material triggers conformational and electronic shifts that are reflected in a chromatic change (a so-called biochromic shift) that is conveniently observed and recorded. Langmuir–Blodgett thin films and vesicle bilayers provide ideal configurations for precise delivery of the biological binding entity to the sensing interface, and for control of molecular orientation for effective biomolecular interaction. Polydiacetylenic membrane-mimicking materials containing cell surface receptor gangliosides and sialic acid residues, respectively were formulated into these architectures and used for colorimetric detection of bacterial toxins and influenza virus. One advantage of these biochromic conjugated polymer (BCP) sensors is that their molecular recognition and signal transduction functionalities are resident in a single functional unit, making them amenable to convenient microfabrication and use. 相似文献