Pressure necrosis secondary to negative pressure dressing.

Wound complications in patients with significant co-morbidities is common; however, in our patient the problem was compounded by the inappropriate placement of negative pressure dressing.

Influences of land use on water quality of a diverse New England watershed.

Analysis of variations in major ion chemistry in the Mill River watershed reveals the importance of anthropogenic activities in controlling streamwater chemistry. Average concentrations of NO3- and SO4(2-) show a positive correlation with percent catchment area altered by human land uses, and concentrations of Cl- increase with road density. Water removal from municipal reservoirs increases the downstream concentration of NO3- and SO4(2-) over that predicted by land use changes, showing that removal of high quality upstream water concentrates pollutants downstream. In salt-impacted streams, Cl- exceeds Na- by 10-15% due to cation exchange reactions that bind Na+ to soil. The net effect of nonpoint source pollution is to elevate ANC in the most developed areas, which impacts the natural acidity of a large swamp. The sum of base cations (C(B)) exceeds ANC for all samples. Plotting C(B) against ANC and subtracting Cl- quantifies the impact of road salt from the impact of the addition of strong acids.

Immunoglobulin concentration and Gm allotypes in a family with thirty-three cases of myotonic dystrophy.

Serum IgG, IgA, and IgM concentrations were measued in 120 members of a family with 33 cases of Dystrophia myotonica (Dm) and 27 members who were "possibly affected". The Dm individuals had significantly lower serum concentrations of IgG and IgA (P<0.01), while the "possibly affected" did not differ from the matched pair controls. IgG subclass concentrations were measured and GM and Am types determined. The lower concentration of IgA in the affected individuals was not associated with a particular Am type. The concentration of IgG3 was barely lower in the effected than in the controls (P=0.05), but there were no differences for IgG1. When IgG3 concentratin was compared according to Gm haplotype, only the two affected individuals who were Gm gg had a statistically significant lower concentration than the 12 controls (P<0.02). Thus, there is no evidence that a particular subclass of IgG is being hypercatabolized in our Dm patients. A rare Gm haplotype, Gm(-, n, b) had entered the family with two brothers; it is not known whether this codes for an IgG1-IgG3 hybrid molecule or a normal IgG1 molecule with an unknown Gm allele or a gamma 1 deleted Gm haplotype.

Additions to the myotonic dystrophy linkage group.

One hundred and thirty members of a family with 33 cases of Dystrophia myotonica (Dm) were tested for various genetic markers including Km, Jk, Lu and Se. All individuals tested were Lua negative, but many were heterozygous for the other markers. Except for two cases all patients with Dm were positive for Km3 and Jka and they were secretors. Assuming the genes are linked and that the order of the loci is Km, Jk, Lu, Se, Dm, then there were 22 meioses informative for Dm and in 10 of these a recombination must have occurred between two of the five loci. Looking at individual pairs of loci, there were no recombinations between Km and Jk in seven informative meioses, three recombinations out of 10 meioses informative for Jk/Se, no recombinations between Se and Dm in five informative meioses and three recombinations out of 12 meioses informative for Jk/Dm.

A search for association between IgD concentrations and immunoglobulin allotypes in 936 sera from a genetic isolate in Newfoundland.

Immunoglobulin allotype (Gm) data has been analysed agaonst immunoglobulin D (IgD) concentrations in a population study in Newfoundland. There was no significant difference between the distribution of IgD concentrations in people homozygous for the alleles G1m(f) and G3m(b) when compared with people homozygous for the alleles G1m(a) and G3m(g). These findings, involving 573 homozygous individuals as opposed to ninety-eight in an earlier study on a New York population, do not confirm the earlier findings. Thus a genetic influence on IgD concentration by Gm genes or genes closely linked to them is not universally demonstrable by typing for these four markers and by using the Mancini technique for mearusing IgD concentration.

The operation of immunological networks in Graves' disease.

Association between Graves' disease and HLA--B8 has been previously documented, as have been associations between 1 gG heavy chain allotype markers (Gm). We found a significant increase in the phenotype fnb/fb (ie. positivity for fb) in patients with Graves' disease compared to controls, raising the possibility of allotypic restriction of thyroid stimulating antibodies thought to be causally related to the disease. The influence of fb on the susceptibility to Graves' disease was found to be independent of HLA--B8 status suggesting that the immunological network operated by the Histocompatibility-linked genes is independent of that centered around IgG allotypes. It is postulated that, whereas the former genes determine the level of helper T lymphocyte function in the production of thyroid stimulating antibodies in Graves' disease, a person who also happens to carry the Gm marker fb would be assured of the production of IgG antibodies with thyroid stimulatory activity.

Serum genetic markers in a Newfoundland isolate with a familial aggregate of Hodgkin's disease.

Inherited genetic markers on the immunoglobulins and three other serum proteins were investigated in members of an isolated Newfoundland community. The frequencies found were compared with those from Europe. Whilst the incidence of the commonest variant forms were typically 'European', the occurrence of rare phenotypes pointed towards specific admixture from American Indians and Scandinavia. A possible contribution of these rare alleles, and of others, to pathogenesis in a familial aggregate of Hodgkin's disease within this community is discussed.

Gm phenotypes in autoimmune thyroid disease.

The Gm phenotype Gm f,b or Gm f,n,b was found in all forty patients with Graves' disease studied, contrasted with thirty-five out of forty controls and twenty out of thirty-one patients with thyroiditis. The difference between the two groups with autoimmune thyroid disease was significant. These results suggest that thyroid stimulating antibodies may be allotypically restricted.

Reversible dysfunction of T-lymphocytes in common variable immunodeficiency.

A 30-year-old man with recurrent sinopulmonary infections, eventually fatal, was found to have common variable immunodeficiency. In addition to low serum immunoglobulin concentrations he also had lymphopenia and cell-mediated immunodeficiency as shown by cutaneous anergy and a poor lymphocyte response to phytohemagglutinin (PHA) in vitro. However, intradermal injection of PHA produced a vigorous cutaneous response, showing that some cell-mediated responsiveness remained. The responsiveness of his lymphocytes to PHA was restored towards normal (confirmed by chromosome studies) by the addition of a small number of normal leukocytes to cultures; thus a reversible functional defect in his T-lymphocytes was revealed. Experiments indicated that the defect was cellular and not due to serum factors and it was concluded that normal leukocytes restored a missing factor to the patient's T-lymphocytes. Although counts of macrophage precursor cells in the bloodstream were low, thus contributing to the immunodeficiency, this could not have caused the reduced PHA response. Several relatives of this patient had lymphoma; two cousins had common variable immunodeficiency.

An immunoglobulin in Newfoundland with the genetic marker Glm/z) without Glm(a) in five siblings: a possible hybrid molecule.

Inheritance of Glm(z) without Glm(a) was found in five members of a Newfoundland family. The investigations were suggestive for the transmission of a Gm haplotype (z;n-;g) coding for Glm(z) and nGlm(a) at the Fd and Fc parts, respectively, of the IgGl heavy chain.

Attempt to restore lymphocytes with defective T-cell function by mixing with normal cells in vitro.

Blood leukocytes from a patient with T-cell immunodeficiency failed to respond to stimulation with phytohemagglutinin (PHA) in vitro although ample lymphocytes were present. Leukocytes from this patient were mixed in various proportions with normal leukocytes, and the mixtures were stimulated with PHA and cultured for three days. There was no restoration of PHA responsiveness of the patient's cells in the presence of normal cells. This would indicate that the defect in the patient's cell population was not due to the absence of any facilitating factor or cooperative function that could be provided by normal T cells or other blood leukocytes. Since in thymic aplasia the patient's own cells are rapidly restored to normal PHA responsiveness by an unknown facilitating factor after thymic transplantation, we suggest that this mixed-cell culture method might differentiate between patients who need a bone marrow transplant and those who will respond to a thymus transplant.