What is in a cause? Exploring the relationship between genetic cause and felt stigma

PURPOSE: Concern over stigma as a consequence of genetic testing has grown in response to the recent increase in genetic research and testing resulting from the Human Genome Project. However, whether a genetic or hereditary basis necessarily confers a stigma to a condition remains unexamined. METHODS: We performed a qualitative interview study with 86 individuals with one of four conditions: deafness or hearing loss, breast cancer, sickle cell disease, and cystic fibrosis. The first two groups were divided approximately between people who ascribed their conditions to a genetic or hereditary cause and those who did not. RESULTS: Respondents interpreted genetic or hereditary causes and nongenetic causes in a variety of ways. Subjects with breast cancer reported the most consistently negative interpretation of genetic cause. This response concerned future ill health, not an enduring sense of stigma. Deaf and hard of hearing subjects provided the most consistently positive comments about a genetic or hereditary basis to their condition, casting familial hearing loss as a vital component of group and individual identity. Respondents with sickle cell disease and cystic fibrosis offered similar and positive interpretations of the genetic cause of their condition insofar as it meant their conditions were not contagious. CONCLUSIONS: Although some subjects report feeling stigmatized as a result of their condition, this stigmatization is not uniformly associated with the condition's cause, genetic or otherwise. Instead, stigma emerges from a variety of sources in the context of the lived experience of a particular condition.     

Potential problem with fluorescence polarization immunoassay cross-reactivity to vancomycin degradation product CDP-1: its detection in sera of renally impaired patients

During the development of a homogeneous immunoassay for the antibiotic vancomycin, we observed in certain patient samples a quantitation difference between the enzyme multiplied immunoassay technique (EMIT) method and the comparison method, fluorescence polarization immunoassay (FPIA). This prompted us to evaluate the integrity of vancomycin in samples from renally impaired patients. Since it has been reported in the scientific literature that vancomycin degrades into an antibiotically inactive crystalline degradation product (CDP-1) in vitro, we developed high-performance liquid chromatography (HPLC) and liquid chromatography/mass spectrometry (LC/MS) methods to determine whether CDP-1 is present in patient sera. HPLC and LC/MS analysis on samples from renally impaired patients positively identified CDP-1 in fresh samples. Next, we tested the cross-reactivity of three currently available vancomycin immunoassays, radioimmunoassay (RIA) FPIA, and EMIT, to CDP-1 prepared in our laboratory. Our data suggest that CDP-1 is recognized by FPIA and RIA, both polyclonal antibody-based methods, but not by EMIT, which uses a monoclonal antibody.     

Studies on the serum proteins of chimeras: III. Detection of donor-type C′5 in allogeneic and congenic post-irradiation chimeras

Allogeneic and congenic post-irradiation chimeras were produced by bone marrow transfer from C′5 active donor mice into C′5 defective recipients. During the first 4 weeks after transfer many of the chimeras contained haemolytic complement activity in their sera. B6AF₁→A chimeras developed higher levels of activity than did B10D2 (new line)→ B10D2 (old line).

Spleen tissue, but not liver tissue, taken from the chimeric animals during this time period incorporated [¹⁴C]amino acid into MuB1 as demonstrated by autoradiography of immunoelectrophoretic patterns, suggesting localization of the active donor cells in the spleen rather than in the liver. Formation of donor-type IgG remained demonstrable for a more extended period after induction of chimerism than formation of MuB1.

A transplantable hepatoma in C57L/J, a C′5 active mouse strain, also incorporated [¹⁴C]amino acid into MuB1.

     

Electrocardiological profile and proarrhythmic effects of quinidine,verapamil and their combination: a mapping study

Quinidine and verapamil are widely used as antiarrhythmic agents and their combination is often used in the treatment of supraventricular tachycardia. This study was undertaken to clarify, whether these drugs exert proarrhythmic effects on the ventricles in therapeutic concentrations and whether possible arrhythmogenic effects might be enhanced by combination. Isolated rabbit hearts perfused according to the Langendorff technique were treated with increasing concentrations of quinidine (0.05 to 3.5 M) or verapamil (5 to 50 M) or of their combination (70:1 or 10:1; quinidine:verapamil) corresponding to common low, medium and high free therapeutic concentrations. The epicardial activation process was measured using a computer assisted mapping system for unipolar multichannel recording (256 channels simultaneously).Both substances prolonged the atrioventricular conduction time PQ. This effect was even more pronounced if the 70:1 combination was administered. The activation pattern was altered by both drugs and their combination to the same extent as became obvious from analysis of local activation vectors and of localisation of breakthroughpoints of epicardial activation for heart beats under control conditions and under drug treatment. The epicardial potential durations were prolonged by quinidine and to the same degree by the combinations, but not by verapamil alone. The total activation time was prolonged under the influence of quinidine and if the 70:1 combination was given. Both substances exerted a negative inotropic effect which was enhanced in an additive manner if both drugs were combined. In parallel the coronary flow was diminished.From these results it is concluded that (1) in this therapeutic concentration range quinidine possess a greater proarrhythmic risk than verapamil, (2) that both drugs' PQ prolonging effect can be enhanced by combination, (3) that combination does not enhance the proarrhythmic effects but the negative inotropic effects.     

Erythematodes and nervous system (author's transl)

Lupus erythematodes is related to the vegetative nervous system in Raynaud's disease, the butterfly distribution in the face, the involvement of the lateral part of the eyebrows (Hertoghe) and in cerebral attacks. Involvement of peripheral and central animal nervous systems is common and produces primary and secondary syndromes. Prominent are polymyositis or lupus-myopathy, in the brain mainly functional psychoses, epileptiform attacks, and a variety of focal, often very massive, signs. There are very clear differences from the neurologic signs of dermatomyositis, less so from arteritis nodosa and even less from progressive sclerodermia. Peripheral neurologic syndromes in lupus erythematosus are less common and more subtle than in arteritis nodosa. Bio-electric parameters of the petitmal-trias have been found. The relative absence of collagenoses from the spinal cord is also noticed in lupus erythematosus. Signs of involvement here appear to be limited and often subacute. Differential diagnosis has to consider many neurologic diseases, a special problem when MS is simulated just as in sclerodermia. Since cerbral attacks appear early in about 5%, the use of anticonvulsive drugs, particularly of the hydantoin group, provides special problems. Signs of myasthenia demand further attention. The neuropathologic changes are known in essential points and can obviously hardly be mistaken for inflammatory processes due to other causes. Certain basic facts appear to apply to other collagenoses. All 4 "grand" or "classic" collagen diseases are very similar and have much in common, but also show more or less definite differences. This is true for their clinical and anatomical appearance and last but not least to their neurologic aspects. The "roof-concept" of Collagenosis" is once more proved to be justified. As far as is known today the autonomic system plays a decisive and obligatory role only is sclerodermia. This syndrome is also the only one which contains the odd phenomenon of atrophy of which the best-known form is facial hemia-atrophy.     

Measurement Issues in Health Disparities Research

Background. Racial and ethnic disparities in health and health care have been documented; the elimination of such disparities is currently part of a national agenda. In order to meet this national objective, it is necessary that measures identify accurately the true prevalence of the construct of interest across diverse groups. Measurement error might lead to biased results, e.g., estimates of prevalence, magnitude of risks, and differences in mean scores. Addressing measurement issues in the assessment of health status may contribute to a better understanding of health issues in cross-cultural research.
Objective. To provide a brief overview of issues regarding measurement in diverse populations.
Findings. Approaches used to assess the magnitude and nature of bias in measures when applied to diverse groups include qualitative analyses, classic psychometric studies, as well as more modern psychometric methods. These approaches should be applied sequentially, and/or iteratively during the development of measures.
Conclusions. Investigators performing comparative studies face the challenge of addressing measurement equivalence, crucial for obtaining accurate results in cross-cultural comparisons.