STRL33, A novel chemokine receptor-like protein, functions as a fusion cofactor for both macrophage-tropic and T cell line-tropic HIV-1

The chemokine receptors CXCR4, CCR2B, CCR3, and CCR5 have recently been shown to serve along with CD4 as coreceptors for HIV-1. The tropisms of HIV-1 strains for subgroups of CD4(+) cells can be explained, at least partly, by the selective use of G protein-coupled receptors (GPCRs). We have identified a novel human gene, STRL33, located on chromosome 3 that encodes a GPCR with sequence similarity to chemokine receptors and to chemokine receptor-like orphan receptors. STRL33 is expressed in lymphoid tissues and activated T cells, and is induced in activated peripheral blood lymphocytes. When transfected into nonhuman NIH 3T3 cells expressing human CD4, the STRL33 cDNA rendered these cells competent to fuse with cells expressing HIV-1 envelope glycoproteins (Envs). Of greatest interest, STRL33, in contrast with CXCR4 or CCR5, was able to function as a cofactor for fusion mediated by Envs from both T cell line-tropic and macrophage-tropic HIV-1 strains. STRL33-transfected Jurkat cell lines also supported enhanced productive infection with HIV-1 compared with control Jurkat cells. Despite the sequence similarities between STRL33 and chemokine receptors, STRL33-transfected cell lines did not respond to any in a panel of chemokines. Based on the pattern of tissue expression of the STRL33 mRNA, and given the ability of STRL33 to function with Envs of differing tropisms, STRL33 may play a role in the establishment and/or progression of HIV-1 infection.     

Reactivity of antibodies against conserved regions of pilins of Haemophilus influenzae type b

To identify epitopes on pilins of Haemophilus influenzae type b (Hib) that may also be immunologically available on assembled pili, antisera were developed against eight synthetic peptides that represent conserved and hydrophilic regions of Hib pilin. Seven of the eight peptides were immunogenic. Binding of the anti-peptide antibodies to purified pili of Hib strain Eagan was weak. However, when the purified pili were denatured by heating, binding of the anti-peptide antibodies improved considerably, suggesting that the epitopes defined by the peptides were more available for anti-peptide antibody binding on the denatured pilins than on purified pili. On Western blot analysis, strain variation was seen in the binding of some of the anti-peptide antibodies, notably those directed against peptides in the N-terminal half of the pilin. Thus, when pilins are assembled into pili, the epitopes defined by the seven immunogenic peptides appear to be altered so that binding of the anti-peptide antibodies is greatly reduced.     

Study of the beta -delayed neutron decay of 18N

The shortage of suitable liver donors for children has motivated the use of ABO-incompatible (ABO-I) grafts for transplantation in urgent situations. However, survival after ABO-I liver grafts has been reported at about 30% as compared with 80% in cases of ABO-identical or -compatible liver grafts. This difference has been attributed to antibody-mediated, hyperacute or chronic liver rejection, due to preformed ABO antibodies (alloantibodies). In this study, we report our results with ABO-I livers in children without alloantibodies at the time of transplantation. From January 1988 to June 1993, 143 OLT were performed in 122 children. Eight children received 8 ABO-I liver grafts. Of these, 7 patients were included in the study. All 7 were alloantibody free before OLT. Five children were spontaneously alloantibody free, while in 2 children, the plasma alloantibodies were eliminated before and after transplantation using intravenous infusion of specific blood group antigens of the donor blood group (soluble antigens). Immunosuppression consisted of a triple-drug treatment combining CsA, AZA, and steroids. The follow-up period was between 10 and 48 months. One child died from a surgical complication. Six children survived, but 1 died 10 months later from intestinal obstruction. There were no graft losses and no episodes of hyperacute or chronic rejection. The graft and patient survival rate was 71%. There was a 28% incidence of rejection, but all were mild (requiring steroid boluses only). Our results suggest that the absence of ABO alloantibodies at the time of and after transplantation can protect ABO-I liver grafts against antibody-mediated rejection, whether hyperacute or chronic, and that soluble antigens are effective in eliminating alloantibodies in children.     

Effects of solid retention time on the performance of submerged anoxic/oxic membrane bioreactor.

In this study, four similar bench-scale submerged Anoxic/Oxic Membrane Bioreactors (MBR) were used simultaneously to investigate the effects of solids retention time (SRT) on organic and nitrogen removal in MBR for treating domestic wastewater. COD removal efficiencies in all reactors were consistently above 94% under steady state conditions. Complete conversion of NH(4+)-N to NO(3-)-N was readily achieved over a feed NH(4+)-N concentration range of 30 to 50 mg/L. It was also observed that SRT did not significantly affect the nitrification in the MBR systems investigated. The average denitrification efficiencies for the 3, 5, 10 and 20 days SRT operations were 43.9, 32.6, 47.5 and 66.5%, respectively. In general, the average effluent nitrogen concentrations, which were mainly nitrate, were about 22.2, 27.6, 21.7 and 13.9 mg/L for the 3, 5, 10 and 20 days SRT systems, respectively. The rate of membrane fouling at 3 days SRT operation was more rapid than that observed at 5 days SRT. No fouling was noted in the 10 days and 20 days SRT systems during the entire period of study.     

A Stronger Complexity Result for the Single Machine Multi-Operation Jobs Scheduling Problem to Minimize the Number of Tardy Jobs

We consider the single machine multi-operation jobs scheduling problem to minimize the number of tardy jobs. Each job consists of several operations that belong to different families. In a schedule, each family of job operations may be processed in batches with each batch incurring a setup time. A job completes when all of its operations have been processed. The objective is to minimize the number of tardy jobs. In the literature, this problem has been proved to be strongly NP-hard for arbitrary due-dates. We show in this paper that the problem remains strongly NP-hard even when the due-dates are common and all jobs have the same processing time.     

Physicochemical Properties of Bread Baked from Flour Blended with Immature Wheat Meal Rich in Fructooligosaccharides

ABSTRACT: Grain of the soft white wheat cultivar Harus was harvested weekly from anthesis to maturity and fructooligosaccharides (FOS) contents were determined by reversed-phase high-performance liquid chromatography. Tests were carried out to determine the effect of adding immature wheat meal to a base flour of cultivar Russ (hard red spring) on the quality characteristics of bread. FOS content was also analyzed in baked bread, and the effect of transglutaminase in improving bread quality was examined. Marked decreases in FOS contents, such as 1-kestose and nystose, were observed with grain maturation. The overall quality of bread appeared to be acceptable, and the added FOS were retained after baking.     

NMR structure and mutagenesis of the FADD (Mort1) death-effector domain

When activated, membrane-bound receptors for Fas and tumour-necrosis factor initiate programmed cell death by recruiting the death domain of the adaptor protein FADD to the membrane. FADD then activates caspase 8 (also known as FLICE or MACH) through an interaction between the death-effector domains of FADD and caspase 8. This ultimately leads to the apoptotic response. Death-effector domains and homologous protein modules known as caspase-recruitment domains have been found in several proteins and are important regulators of caspase (FLICE) activity and of apoptosis. Here we describe the solution structure of a soluble, biologically active mutant of the FADD death-effector domain. The structure consists of six antiparallel, amphipathic alpha-helices and resembles the overall fold of the death domains of Fas and p75. Despite this structural similarity, mutations that inhibit protein-protein interactions involving the Fas death domain have no effect when introduced into the FADD death-effector domain. Instead, a hydrophobic region of the FADD death-effector domain that is not present in the death domains is vital for binding to FLICE and for apoptotic activity.