1,353 research outputs found
The Humoral Theory of Transplantation: Epitope Analysis and the Pathogenicity of HLA Antibodies.
Central to the humoral theory of transplantation is production of antibodies by the recipient against mismatched HLA antigens in the donor organ. Not all mismatches result in antibody production, however, and not all antibodies are pathogenic. Serologic HLA matching has been the standard for solid organ allocation algorithms in current use. Antibodies do not recognize whole HLA molecules but rather polymorphic residues on the surface, called epitopes, which may be shared by multiple serologic HLA antigens. Data are accumulating that epitope analysis may be a better way to determine organ compatibility as well as the potential immunogenicity of given HLA mismatches. Determination of the pathogenicity of alloantibodies is evolving. Potential features include antibody strength (as assessed by antibody titer or, more commonly and inappropriately, mean fluorescence intensity) and ability to fix complement (in vitro by C1q or C3d assay or by IgG subclass analysis). Technical issues with the use of solid phase assays are also of prime importance, such as denaturation of HLA antigens and manufacturing and laboratory variability. Questions and controversies remain, and here we review new relevant data
Product Market Competition, Union Organizing Activity, and Employer Resistence
We develop and estimate a model of the union's optimal extent of organizing activity that accounts for the decision of employers regarding resistance to union organizing. The central exogenous variable in the analysis is the quantity of quasi-rents per worker available to be split between unions and employers. We measure available quasi-rents per worker as the difference per worker between total industry revenues net of raw materials costs and labor costs evaluated at the opportunity cost of the workers. Using two-digit industry level data for thirty-five U.S. industries for the period 1955 through 1986, we find that both organizing activity and employer resistance to unionization are positively related to available quasi-rents per worker. However, there is still a strong negative trend in union organizing activity and a strong positive trend in employer resistance after controlling for quasi-rents per worker. Thus, the explanation for the decline in union organizing activity and the increase in employer resistance to unionization since the mid 1970's lies elsewhere.
Bredon cohomology and robot motion planning
In this paper we study the topological invariant reflecting
the complexity of algorithms for autonomous robot motion. Here, stands for
the configuration space of a system and is, roughly, the
minimal number of continuous rules which are needed to construct a motion
planning algorithm in . We focus on the case when the space is
aspherical; then the number depends only on the fundamental group
and we denote it . We prove that
can be characterised as the smallest integer such that the canonical
-equivariant map of classifying spaces can be equivariantly deformed into the
-dimensional skeleton of . The symbol
denotes the classifying space for free actions and
denotes the classifying space for actions with
isotropy in a certain family of subgroups of . Using
this result we show how one can estimate in terms of the
equivariant Bredon cohomology theory. We prove that where denotes the cohomological dimension of with
respect to the family of subgroups . We also introduce a Bredon
cohomology refinement of the canonical class and prove its universality.
Finally we show that for a large class of principal groups (which includes all
torsion free hyperbolic groups as well as all torsion free nilpotent groups)
the essential cohomology classes in the sense of Farber and Mescher are exactly
the classes having Bredon cohomology extensions with respect to the family
.Comment: This revision contains a few additional comments, among them is
Corollary 3.5.
Mechanisms of cell injury by activated oxygen species.
Current evidence suggests that O2- and H2O2 injure cells as a result of the generation of a more potent oxidizing species. In addition to O2- and H2O2, the third essential component of the complex that mediates the lethal cell injury is a cellular source of ferric iron. The hypothesis most consistent with all the available data suggests that O2- reduces a cellular source of ferric to ferrous iron, and the latter then reacts with H2O2 to produce a more potent oxidizing species, like the .OH or an equivalently reactive species. In turn, .OH initiates the peroxidative decomposition of the phospholipids of cellular membranes. .OH also damages the inner mitochondrial membrane. Upon mitochondrial deenergization, a sequence of events is initiated that similarly leads to the loss of viability of the cell. DNA represents a third cellular target of .OH. Depending on the cell type, oxidative DNA damage can be coupled to cell killing through a mechanism related to the activation of poly (ADP-ribose) polymerase
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