Early infectious complications of liver-intestinal transplantation in children: preliminary analysis.
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Biomedical subjects
Publications and source records attributed to M Green.
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A total of 471 Israel Defense Forces (IDF) blood donors identified as hepatitis B virus (HBV) carriers were examined a few months after blood donation. When compared to the general population of IDF blood donors the HBV carriers were older, belonged to certain ethnic groups and were predominantly males. Physical examination revealed minimal findings: 1 (0.3%) had splenomegaly and 5 (1.6%) had hepatomegaly. Fifty-two individuals (11.1%) had elevated liver enzymes. E antigen was present in 3.2% of HBV carriers, 94% had anti-e antibodies and 1.9% had anti-delta antibodies. Of 258 carriers tested for HBV DNA, 29 (11.2%) were positive. Abnormal liver enzymes were significantly associated with the presence of e antigen as well as with the presence of HBV DNA.
Margaret Green and Karen Moss describe how they and the staff at one primary school together devised a month-long programme of health promotion events to encourage children to think positively and responsibly about their health and safety. The project involved colleagues from the health services as well as from other agencies and organisations, to demonstrate the breadth of issues involved in maintaining good health.
RNA molecules that can bind to the Rev protein of HIV-1 have been isolated from random sequence nucleic acid pools based on a minimal Rev-binding element (RBE) found within the Rev Responsive Element (RRE). While the selected sequences are related to the wild-type element, they also contain substitutions that allow them to bind Rev up to 10-fold better in vitro. A hypothesized homopurine pairing at G48:G71 is generally replaced by A48:A71; the occasional selection of C48:A71 suggests that R71 may be in a syn conformation. These data support the structural model for the RBE originally proposed by Bartel et al. (1). Additional interactions with the Rev protein are promoted by the sequence CUC ... UYGAG, found in one class of high-affinity aptamers, but absent from the wild-type element. Within each class of aptamers different residues and substructures covary with one another to generate optimal Rev-binding surfaces. The interdependencies of different nucleotide substitutions suggest structural models for both the wild-type RBE and the selected high-affinity aptamers.
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The TRG1/PDI1 gene of Saccharomyces cerevisiae is essential for growth and encodes a lumenal endoplasmic reticulum (ER) glycoprotein that is structurally related to thioredoxin and is involved in the secretory pathway. We have tested whether the yeast Trg1/Pdi1 protein can be replaced in vivo by three members of the mammalian thioredoxin-related protein family, protein disulfide isomerase (PDI), ERp72, and ERp61. Multicopy plasmids containing galactose-inducible rodent PDI and ERp72 genes support germination and growth of haploid trg1 null mutants in galactose-containing media, whereas the ERp61 gene is inactive. Strains expressing PDI or ERp72 instead of Trg1 are thermosensitive. An overproduced mutant Trg1 protein lacking the HDEL retention signal supports growth, whereas a truncated version of the protein containing only one thioredoxin-like domain is inactive. The mammalian proteins were localized to both the soluble and microsomal membrane fraction of yeast cells. Our observations indicate that the two unglycosylated mammalian proteins PDI and ERp72 are capable of replacing at least some of the critical functions of Trg1, in spite of the fact that the three proteins diverge considerably in sequences surrounding the thioredoxin-related domains.
The HIV-1 transactivator protein Tat is essential for viral gene expression and replication. Tat is taken up by cells and transactivates the HIV-LTR promoter in the cell nucleus. The present studies show that cells adhere to both synthetic and recombinant Tat, and, using synthetic peptides, we localize the binding site to a region spanning amino acid residues 49-57 (peptide Tat49-57). Tat49-57 also inhibited cell attachment to solid phase full-length Tat peptide and to recombinant Tat protein. Using Tat peptide affinity chromatography, we identified a 90-kDa cell surface protein that binds to Tat. The 90-kDa protein could be eluted from the Tat column using the Tat49-57 peptide. A 90-kDa cell surface Tat binding protein was also identified by coprecipitation with Tat after incubation with radiolabeled cell membrane preparations. Co-precipitation of the 90-kDa protein was inhibited by competition with a Tat49-65 peptide, but not with Tat55-86. Our findings suggest that cellular attachment to Tat is mediated through a 90-kDa cell surface protein that binds to a Tat domain between amino acids 49 and 57.
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Q-wave anterior myocardial infarctions due to occlusion of the left anterior descending artery (LAD) are generally associated with the most extensive left ventricular damage. The presence of abnormal Q waves on the electrocardiogram (ECG) provides important information to localize the site of left ventricular infarction. However, the relationship between abnormalities of the QRS morphology in the precordial leads and angiographic information such as ejection fraction and the site of LAD occlusion (before or after the first septal perforator) has not been studied extensively. Seventy-three patients with single-vessel disease with complete LAD occlusion, abnormal QRS morphology in leads V1-V4 on ECG, and abnormal wall motion with contrast ventriculography were studied retrospectively. LAD occlusions were proximal to the first septal perforator in 33 patients and distal in 40 patients. Q waves were present in 59 patients, and the other 14 patients had either minimal R waves (< 0.25 mm), poor R-wave progression, or R-wave regression. A significantly higher ejection fraction was associated with the presence of R wave in V2 (0.52 +/- 0.18 vs. 0.39 +/- 0.15 in the absence of R wave, p < 0.003). LAD occlusion after and before the first septal perforator was associated with R wave in V2 in 67 and 36% of patients, respectively. Sensitivity and specificity of predicting occlusion after the first septal perforator based on R wave in V2 was 0.68 and 0.64, respectively. In patients with anterior myocardial infarctions, occluded LAD artery, and abnormal QRS morphology in the precordial leads, the presence of R wave in V2 is a useful predictor of higher ejection fraction.(ABSTRACT TRUNCATED AT 250 WORDS)
We have recently shown that constitutively expressed members of the rel/NF-kappa B family of transcription factors bind the HRAS1 minisatellite, VTRHRAS1. We now report that, like other NF-kappa B binding sites, VTRHRAS1 displays pleiotropic transcriptional regulatory activity that is promoter- and cell-type-specific. Both enhancement and suppression are restricted to the human bladder carcinoma cell line EJ, in which we have previously defined a unique form of NF-kappa B p50. We also observe allelic variation in functional activity: the rare a2.1 allele, one member of a class of HRAS1 alleles overrepresented in the genomes of cancer patients, possesses twofold greater enhancer activity than the low-risk alleles, a0.1, a1, and a2. Finally, VTRHRAS1 enhancer activity is upregulated by the adenovirus E1A 13S gene product, demonstrating the potential of the minisatellite for influencing gene expression through several distinct interactions with the transcriptional apparatus.
Cutaneous reactions to vitamin K1 injections are reported infrequently. Most previously reported cases have been associated with liver disease, primarily alcoholic cirrhosis and viral hepatitis. Four new cases are reported. One patient had polycythemia vera and the Budd-Chiari syndrome, the second such report in the literature. The other three patients had no known hepatic disease. The reactions consisted of erythematous plaques at the injection site without progression to sclerodermatous plaques. Histopathologic examination in three cases showed spongiotic changes and mononuclear infiltrates typical of cutaneous reactions to vitamin K1. In one instance a neutrophilic infiltrate was associated with the reaction site. Our findings support the observation that liver disease is not a necessary condition for the occurrence of vitamin K1 hypersensitivity.
OBJECTIVES: The purpose of this study was to define the influence of dominant chamber morphology on ventricular performance after the Fontan procedure in patients with double-inlet ventricle. BACKGROUND: Previous studies have reported the impact of ventricular morphology on preoperative ventricular performance and surgical outcome. However, the influence on postoperative ventricular performance has not been addressed. METHODS: Twenty-six clinically asymptomatic patients > 1 year after repair (mean age at procedure 6.1 +/- 3.7 years) were evaluated with ventricular cineangiography and radionuclide blood pool studies (18 with a dominant left ventricular morphology [LV group], 8 with a dominant right ventricular morphology [RV group]) and compared with normal control subjects. RESULTS: Ventricular volume, mass and systolic variables were similar between patient groups. In the LV group, however, the mass/volume ratio was significantly elevated compared with values in control subjects (1.11 +/- 0.28, 0.97 +/- 0.19, p < 0.05), whereas this ratio in the RV group (0.90 +/- 0.11) was within the normal range and significantly lower than that in the LV group (p < 0.05). Mean right atrial and pulmonary artery pressures in the RV group were significantly higher than those in the LV group (p < 0.05). Peak filling rates (2.87 +/- 0.70, 2.41 +/- 1.15 and 3.84 +/- 0.51 end-diastolic volume/s [LV and RV groups and control subjects, respectively]) were significantly lower in both groups than in control subjects (p < 0.001), without intergroup difference. CONCLUSIONS: Ventricular filling abnormalities after atrial to pulmonary anastomosis are common regardless of the type of dominant ventricular morphology, and these abnormalities in patients with dominant right ventricular morphology do not coexist with ventricular hypertrophy. Such diastolic abnormalities may be related to either intrinsic myocardial or acquired factors, not to excessive hypertrophy alone. Those differences may become clinically more apparent with longer follow-up and may raise concerns over the long-term course.