Biomedical subjects
Publications and source records attributed to J Ring.
Serum concentrations of immunoglobulins were quantified in 110 patients with vitiligo, and the association with atopy was studied. Patients with vitiligo and simultaneous atopy presented lower IgE and higher IgA values compared to a reference group of patients with atopy alone.
The plasma concentrations of arginine vasopressin, oxytocin, angiotensin I and II were studied in patients with hymenoptera venom anaphylaxis (n = 50) and healthy volunteers (n = 25). There was no difference in arginine vasopressin: 5.52 +/- 0.45 fmol/ml vs. 3.99 +/- 0.41 fmol/ml or oxytocin: 28.10 +/- 1.13 fmol/ml vs. 26.24 +/- 1.80 fmol/ml between patients and controls. No correlation between the severity of clinical symptoms and the plasma levels of arginine vasopressin and oxytocin was found in patients. However, patients with a history of hymenoptera venom anaphylaxis showed significantly reduced angiotensin I and angiotensin II plasma levels as compared to controls (ANG I: 9.51 +/- 0.61 fmol/ml vs. 22.91 +/- 1.73 fmol/ml; ANG II: 2.84 +/- 0.16 fmol/ml vs. 6.95 +/- 0.33 fmol/ml). A significant inverse correlation between the severity of clinical symptoms and the plasma levels of angiotensin I and angiotensin II was observed; the lower the concentrations the more severe the clinical symptoms. Oxytocin immunoreactivity eluted from the HPLC column as a single peak with the same retention time as synthetic oxytocin. The vasopressin immunoreactive material could be characterized on HPLC as arginine-vasopressin and two other peptides of unknown nature which crossreacted with the vasopressin antibody. These findings suggest a possible role of angiotensin I and angiotensin II in hymenoptera venom anaphylaxis while arginine vasopressin and oxytocin are most likely not involved.
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A radioactive waste management program was developed for a large university and medical research complex to contain costs and to reduce the impact of the Low-Level Radioactive Waste Policy Act. The program takes advantage of decay-in-storage, incineration, special packaging techniques, and increased training and awareness. A series of metrics are presented to evaluate the effectiveness of the radioactive waste management program. Through the use of this program the amount of waste disposed of at commercial burial sites decreased from 98% to 1.61% of the waste generated. At the same time the volume of waste generated per laboratory declined by almost 45%, from 0.35 m3 (12.31 ft3) to 0.19 m3 (6.80 ft3).
Components of the renin angiotensin system, namely renin, angiotensinogen, angiotensin I and II and aldosterone were measured in plasma of patients with hymenoptera venom anaphylaxis (n = 50) and healthy non-allergic controls (n = 25). Patients with a history of anaphylactic reactions to hymenoptera venom who did not undergo immunotherapy showed significantly reduced renin, angiotensinogen, angiotensin I and angiotensin II in plasma as compared with controls (P < 0.05). There was no difference in the aldosterone concentration between patients and controls. Angiotensin I, angiotensin II, renin and angiotensinogen levels were the same in male and female patients. There was also no difference in the angiotensin I, II, renin or angiotensinogen levels between young and older patients. A significant inverse correlation between the severity of clinical symptoms and the plasma levels of renin (r = -0.382, P < 0.001), angiotensinogen (r = -0.567, P < 0.0001), angiotensin I (r = -0.656, P < 0.0001) and angiotensin II (r = 0.0762, P < 0.0001) was found: the lower the levels the more severe the clinical symptoms. No correlation was found for aldosterone. Hymenoptera venom allergic patients with repeated anaphylactic reactions during hyposensitization did not tolerate the sting of a living insect (n = 6). In these patients, renin, angiotensinogen, angiotensin I and II remained significantly lower than in healthy non-allergic controls. Patients with successful immunotherapy (n = 27) who tolerated the sting of a living insect had renin, angiotensin I and II significantly higher than patients without immunotherapy. These findings suggest a possible role of the renin angiotensin system in hymenoptera venom anaphylaxis.
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The first months of life may be an important period for allergic sensitization. Several studies suggest a relationship between the month of birth (MB) and the development of skin sensitivity to aeroallergens or the manifestation of an atopic disease. In 1988 and 1989 we investigated a population of 1066 Bavarian preschool children aged 5-6 years. Skin prick tests were performed with common aeroallergens (grass pollen, birch pollen, house-dust mite, cat epithelia). The personal history of atopic disease (atopic eczema, allergic rhinitis, bronchial asthma) was recorded by a questionnaire, and the presence of overt atopic disease was documented by a personal examination. Positive prick test reactions to the above-mentioned aeroallergens were found in 15.4%, 9.2%, 12.2%, and 10.4% of the subjects, respectively; lifetime prevalence of manifest atopic disease was 22.2% for atopic eczema, 11.7% for allergic rhinitis, and 4.5% for asthma. The MB distributions of children reacting to aeroallergens or of those with atopic diseases were compared with those of subjects with corresponding negative findings. Chi-square tests were performed for each aeroallergen and each of the atopic diseases separately. No significant differences among the MB distributions were found (P > 0.3). Thus, in this coherent group, MB correlated neither to allergic sensitization nor to manifest atopic disease.
Atopic diseases occur due to hypersensitivity to environmental antigens. A complex interaction of a variety of cell types and mediators elicits the clinical symptoms of atopic diseases. The release of histamine is increased in patients with atopic diseases. The factors regulating this release may include histamine-releasing factors, interleukin-3, the c-kit ligand, the cyclic nucleotide system, psychological factors, metabolites of arachidonic acid and cytokines. The release of histamine and the sensitivity to the release of histamine varies between individuals. Moreover, there is a circadian variation in the levels of histamine. However, atopic diseases cannot be explained by a single mediator, but involve a variety of substances. Specific antagonists can be used to elucidate the role of the various mediators in different atopic diseases.
A radioimmunoassay for histamine was used to measure histamine and 1-methylhistamine (MH) in human urine samples. The detection limit of this assay was 2 ng/ml for histamine and 0.5 ng/ml for MH. Cation exchange high performance liquid chromatography (HPLC) on a Bio-Gel TSK SP-5 PW column with gradient elution was capable of separating histamine from its precursor L-histidine and its metabolites MH and 1-methylimidazole acetic acid (MIAA). The concentration of MH-immunoreactive materials in healthy volunteers with no dietary restrictions was 202 +/- 92 micrograms/24 h (mean +/- SD; n = 14). The excretion of MH-like material, expressed as micrograms of MH per 24 h, was not significantly different before or after the intake of histamine-rich food: 217 +/- 88 vs. 276 +/- 135 micrograms/24 h (n = 10). However, in urine samples collected in individual fractions, the levels of MH immunoreactivity were significantly increased after a histamine-rich meal in comparison to the corresponding fractions which were taken a day earlier at the same time intervals after a histamine-low diet (p < 0.03). HPLC characterization of MH immunoreactivity revealed the presence of histamine, MH and a compound with the same retention time as MIAA. The ratio of histamine, MH and MIAA in controls without dietary restrictions, as determined by HPLC analysis, was 50 +/- 6, 47 +/- 5 and 3 +/- 1%, respectively. After a histamine-rich meal the ratio was 97 +/- 2% for histamine, 1% for MH and 2 +/- 1% for MIAA.
A case of chronic urticaria is presented. The case of the disease was traced back to nickel intake by food as judged from type I and IV sensitization to nickel, a positive oral challenge test and long-standing, complete healing under a nickel-restrictive diet.
The skin is in such continuous and intimate interaction with environmental influences as no other organ. Environment comes in contact with the organism in the form of substances or forces (physical, chemical, biological) and via different routes: irradiation (electromagnetic irradiation, often referred to in a simplified way as "light"), air, food, direct contact with the skin, injection, or psychosocial interactions. All these influences can lead to disease under certain conditions and in certain individuals, and especially to skin disease. The critical factors are the dose, the mode and time of contact; this is evident with regard to sunlight and its acute and chronic effects. Not only for noxious chemicals are the classification and differentiation of primary toxic reactions from hypersensitivity reactions of predisposed individuals crucial. Hypersensitivity reactions can either be immunologically mediated (allergic) or non-immunological (idiosyncrasy, pseudo-allergy). The existence of a genetic disposition does not exclude the importance of environmental factors. Atopic eczema is an example of a disease that can be influenced dramatically by a variety of environmental factors. Many toxic environmental factors are known to induce skin changes long before systemic or life-threatening diseases appear. The skin can be regarded as a "signal organ" for possible noxious environmental influences. Increased research efforts in this field are mandatory.
In human papillomavirus-associated acanthomas of the mamilla it was possible to detect DNA of HPV types 41, 6ma and a type related to type 16. The biology of HPV infection resembles that of anogenital lesions. Some of the HPV types found are rare or are thought possibly to have oncogenic potency. Possible evidence for link between HPV and carcinomas of the breast is discussed.
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The bacterial skin flora of patients with atopic eczema is different from that in healthy normal persons. In addition, such patients more often suffer from microbial infections. Differences in sebum and sweat secretion and increased bacterial adhesion to epithelial cells in atopic eczema may predispose to enhanced amounts of Staphylococcus aureus, for example, on the skin. Defective host-defence mechanisms with dysfunction of cellular and humoral immune reactions have been suggested. On the other hand, bacterial antigens may induce allergic reactions, e.g. increased IgE synthesis and enhanced expression of the low-affinity receptor for IgE (CD23, Fc epsilon RII), and the release of inflammatory mediators such as leukotrienes and histamine. The production of bacterial toxins might be important for the pathophysiology of atopic eczema. This paper summarizes the present data and tries to integrate them into a model for the induction of atopic eczema.
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