Degradative transesterification of terephthalate polyesters to obtain DOTP plasticizer for flexible PVC

It has been found that dioctyl terephthalate (DOTP), a plasticizer for polyvinyl chloride (PVC), can be made from scrap terephthalate polyesters such as polyethylene terephthalate (PET) by a method known as degradative transesterification. It is recognized that this plasticizer is as good as plasticizer as commercial DOTP, and that it may potentially replace dioctyl phthalate (DOP). The production of DOTP from scrap PET is shown to be cost effective. The use of this technology may provide a solution to a part of our solid-waste problem.     

Understanding the relationship between relative and absolute risk

BACKGROUND: Relative risks are the most common statistics used to quantify the risk of mortal or morbid outcomes associated with different patient groups and therapeutic interventions. However, absolute risks are of greater value of both patient and physician in making clinical decisions. METHODS: The relationship between relative and absolute risks is explained using graphical aids. A program to estimate absolute risks from relative risks is available on the internet (see ftp://ftp.vanderbilt.edu/pub/biostat/absrisk+ ++.txt). This program uses a competing hazards model of morbidity and mortality to derive these estimates. RESULTS: When a patient's absolute risk is low, it can be approximated by multiplying her relative risk by the absolute risk in the reference population. This approximation fails for higher absolute risks. The relationship between relative and absolute risk can vary dramatically for different diseases. This is illustrated by breast cancer morbidity and cardiovascular mortality in American women. The accuracy of absolute risk estimates will be affected by the accuracy of relative risk estimates, by the appropriateness of the reference groups used to calculate relative risks, by the stability of cross-sectional, age-specific morbidity and mortality rates over time, by the influence of individual risk factors on multiple causes of mortality, and by the extent to which relative risks may vary over time. CONCLUSIONS: Valid absolute risk estimates are valuable when making treatment decisions. They can often be obtained over time intervals of 10 to 20 years when the corresponding relative risk estimates have been accurately determined.     

Single state elastoplastic friction models

For control applications involving small displacements and velocities, friction modeling and compensation can be very important. In particular, the modeling of presliding displacement (motion prior to fully developed slip) can play a pivotal role. In this paper, it is shown that existing single-state friction models exhibit a nonphysical drift phenomenon which results from modeling presliding as a combination of elastic and plastic displacement. A new class of single state models is defined in which presliding is elastoplastic: under loading, frictional displacement is first purely elastic and then transitions to plastic. The new model class is demonstrated to substantially reduce drift while preserving the favorable properties of existing models (e.g., dissipativity) and to provide a comparable match to experimental data     

Direct activity of human T lymphocytes and natural killer cells against Cryptococcus neoformans

Lymphocytes constitute a critical component of host defenses against cryptococcosis. Previously, we demonstrated that human lymphocytes cultured with interleukin-2 formed conjugates with, and directly inhibited the growth of, Cryptococcus neoformans. Here, we explore the anticryptococcal activity of freshly isolated, highly purified populations of human peripheral blood lymphocytes. Lymphocytes were incubated with encapsulated C. neoformans for 24 h, after which the lymphocytes were lysed, dilutions and spread plates were made, and CFU were counted. Fungistasis was determined by comparing growth in wells with and without lymphocytes. Nylon wool-nonadherent peripheral blood mononuclear cells (NWNA PBMC) were highly fungistatic, even if either T cells or natural killer (NK) cells were depleted by panning. A mixed population of T cells and NK cells, obtained by rosetting NWNA PBMC with sheep erythrocytes, completely inhibited cryptococcal growth, whereas the nonrosetting cells had little fungistatic activity. CD4+, CD8+, and CD16/56+ lymphocytes, isolated by positive immunoselection, had potent growth-inhibitory activity. In contrast, purified B cells had no activity. Fungistasis was seen even in the absence of opsonins. Antifungal activity was markedly diminished when surface receptors on NWNA PBMC were cleaved by treatment with trypsin or bromelain. Supernatants from stimulated lymphocytes or concentrated lymphocyte sonicates were not active. Lymphocyte-mediated fungistasis was seen with two different strains of C. neoformans. CD4+, CD8+, and CD16/56+ lymphocytes formed conjugates with C. neoformans, as observed under Nomarski differential interference contrast microscopy and videomicroscopy. These data demonstrate that freshly isolated peripheral blood T cells and NK cells have the capacity to bind and directly inhibit the growth of C. neoformans.     

Mid-infrared phase modulation via Stark effect on intersubbandtransitions in GaAs/GaAlAs quantum wells

Mid-infrared (~10 μm) electrorefractive effects of intersubband transitions in step GaAs/GaAlAs quantum wells are experimentally analyzed. A method for studying infrared electrorefraction of a two-dimensional structure via the Stark effect is used. The anomalous dispersion is measured over the entire spectral range of the transition and is found to be consistent with the Kramers-Kronig relations in the case of a Lorentzian absorption shape. A solution of Maxwell's equations in the multiquantum well structure is detailed and leads to a good agreement with experimental data. A standard interferometer and a lock-in technique allow a quasi-direct determination of phase and amplitude modulation with very good sensitivity. A theoretical approach based on a Lorentzian model and the solution of Maxwell's equations for a multiple QW (quantum well) structure agreed well with the data     

Genomic organization and allelic polymorphism of the human killer cell inhibitory receptor gene KIR103

Killer cell inhibitory receptors (KIR) belong to the immunoglobulin superfamily of molecules and are expressed on natural killer (NK) cells. The KIRs of the p58/p50 family have two immunoglobulin domains and are ligands for HLA-Cw antigens, whereas the p70/p70 delta family has three immunoglobulin domains and comprises ligands for HLA-B antigens and possibly some HLA-A antigens. Members of a third KIR family, KIR103, have two immunoglobulin domains but have highest nucleotide sequence homology to the p70 family. The ligands for KIR103 on target cells are currently unknown. We here report the complete genomic organization of KIR103. It spans about 12 kb of DNA and consists of eight exons of which exon 1 and exon 2 encode the leader sequence. Exon 3 encodes the first immunoglobulin domain (gamma 1), and exon 4 encodes the main part of the second immunoglobulin domain (gamma 3), which also contains sequences contributed by exon 5 and exon 6. Exon 6 encodes the transmembrane domain, whereas exons 7 and 8 encode most of the cytoplasmic domain. KIR103 is polymorphic, and two alleles, 103AS and 103LP, are defined in this study. Additional full-length cDNA clones for KIR103 have been isolated and are shown to be formed by alternative mRNA splicing with exon skipping. Some of these truncated KIR103 cDNA could encode shorter transmembrane molecules, whereas others lack the transmembrane domain and are candidate genes for secreted KIR products. KIR103 is localized to the KIR genetic region on chromosome 19q13.4.     

Increase in plasma propranolol caused by nicardipine is dependent on the delivery rate of propranolol

The influence of a single oral dose of nicardipine 30 mg on the pharmacokinetics and pharmacodynamics of propranolol 80 mg given as a conventional release formulation and as a slow release formulation was studied in two separate groups of 12 healthy volunteers. Nicardipine doubled the area under the curve (AUC) and Cmax of propranolol when given as a conventional formulation, but increased it only slightly when given as a slow release formulation. This pharmacokinetic interaction did not result in clinically relevant changes in pharmacodynamic responses. These results indicate that the enhancement of the bioavailability of propranolol by coadministration of nicardipine is dependent on the delivery rate of propranolol, suggesting that the interaction is mainly due to short-term haemodynamic effects of nicardipine leading to saturation of hepatic enzymes or functional shunting.