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Biomedical subjects

E Young

Publications and source records attributed to E Young.

At least 181 records · Page 10Linked to original sources
PubMed1987

Use of a competitive inhibitor in a kinetic enzymatic method for measuring ethanol in serum.

We describe a kinetic enzymatic method for ethanol in serum, based on the use of pyrazole, a competitive inhibitor for alcohol dehydrogenase (EC 1.1.1.1). The method is rapid and is easily automated for the Cobas Bio centrifugal analyzer. No specimen pretreatment is necessary and the total reaction time is 120 s. The standard curve is linear up to 140 mmol/L. The within-run CV was between 1.9% and 3.5%; the between-run CV ranged from 2.6% to 4.1%. Mean analytical recovery of ethanol added to serum was 100.2%. We compared results of the kinetic enzymatic method with those from a gas-liquid chromatographic (GLC) method and another commercial alcohol dehydrogenase method (TDx REA Ethanol; Abbott Diagnostics). Linear regression analysis gave the following equations: kinetic = 0.991GLC - 0.354 mmol/L (r = 0.992, n = 110) and kinetic = 0.998TDx - 1.741 mmol/L (r = 0.993, n = 70). No interference from methanol or isopropanol was seen.

Alcohol Dehydrogenase↗
PubMed1987

Oral immunization against chlamydial eye infection.

The effects of enteric administration of different preparations of Chlamydia trachomatis prior to ocular challenge with live chlamydia were compared to the immunity that develops after recovery from ocular infection. Oral immunization with either live homologous serovar B or with formalin-killed heterologus serovar L2 did not influence the response to subsequent ocular challenge. Although oral immunization with live serovar led to protection against heterologous ocular challenge with serovar B, oral immunization with noninfectious UV-irradiated serovar L2 led to more severe and prolonged disease. An immunizing regimen designed for maximal mucosal and systemic immunity also resulted in protection against homologous ocular challenge. Although protection was correlated with the presence of serum IgA antibodies, no clear mechanism for the protective ocular immunity to chlamydial infection has emerged. These studies show that it is possible to stimulate mucosal immunity to induce protection against subsequent ocular challenge with C. trachomatis that is equal to that which follows prior ocular infection.

Acute Disease↗
PubMed1986

Constrictive pericarditis mimicking Budd-Chiari syndrome.

Budd-Chiari syndrome and constrictive pericarditis share many clinical and histologic features. Clinicians must continue to reassess patients when given histologic data that are not specific for a particular disease entity, so that subtle clinical differences are recognized, appropriate diagnosis made, and therapy instituted.

Adult↗
PubMed1986

Immunopathological and ultrastructural findings in human allergic and irritant contact dermatitis.

The histopathological features of allergic contact dermatitis were compared with those of irritant contact dermatitis in a group of 17 subjects. Each patient received simultaneous patch tests of a known allergen and a standardized irritant (benzalkonium chloride). The cellular changes occurring between 3 h and 7 days after patch test application were studied by light and electron microscopy and immunocytochemistry. No differences were observed between the induced allergic contact dermatitis (ACD) and the irritant contact dermatitis (ICD), either in the responding cell types or the sequence of cellular events. Both reactions showed a predominantly T lymphocyte infiltrate with no polymorphonuclear leukocyte involvement. Apposition of Langerhans cells to lymphocytes in the epidermis was seen in both types of response. Considerable variability in the intensity of reaction to irritant and allergen occurred within individuals. There was no statistically significant difference between the intensity of the reactions to the irritant and the allergen.

Adult↗
PubMed1986

Reactive perforating collagenosis: light, ultrastructural and immunohistological studies.

Reactive perforating collagenosis is an uncommon disorder and few accounts refer to ultrastructural features. This report includes a study by light and transmission electron microscopy of serially sectioned biopsies from early lesions in two patients. Immunohistological investigations utilizing antibodies to basement membrane, laminin, collagen and cytokeratin were also done. Collagen and elastin were demonstrated within the centre of the lesions and there was a defect in the basal lamina at the base of the lesion. The collagen, cytokeratin and the basal lamina in the lesions were antigenically similar to those in the surrounding normal skin. These results are compared with previous findings and discussed in the light of the current views on the pathogenesis of this disorder.

Basement Membrane↗
PubMed1986

ADR1-mediated regulation of ADH2 requires an inverted repeat sequence.

DNA sequence analysis of wild-type and mutant ADH2 loci suggested that two unusual features 5' of the promoter, a 22-base-pair perfect dyad sequence and a (dA)20 tract, were important for regulation of this gene (D. W. Russell, M. Smith, D. Cox, V. M. Williamson, and E. T. Young, Nature [London] 304:652-654, 1983). Oligonucleotide-directed mutagenesis was used to construct ADH2 genes lacking the 22-base-pair dyad or the (dA)20 tract (V.-L. Chan and M. Smith, Nucleic Acids Res. 12:2407-2419, 1984). These mutant genes and other ADH2 deletions constructed by BAL 31 endonuclease digestion were studied after replacing the wild-type chromosomal locus with the altered alleles by the technique of gene transplacement (T. L. Orr-Weaver, J. W. Szostak, and R. S. Rothstein, Proc. Natl. Acad. Sci. USA 78:6354-6358, 1981), using canavanine resistance as the selectable marker. Deletions lacking the dyad failed to derepress normally and did not respond to mutations at the ADR1 locus, which encodes a protein necessary to activate ADH2. Deletions of the (dA)20 tract did not have a detectable phenotype. A small deletion located just 3' to the (dA)20 tract (between positions -164 and -146) had a low amount of ADR1-dependent transcription during repressed growth conditions, indicating that the regulatory protein encoded by ADR1 is present in a potentially active form during repression and that alterations of a DNA sequence in the promoter region can unmask its latent activity.

Alcohol Dehydrogenase↗
PubMed1986

Treatment of psoriasis with dithranol cream compared with dithranol paste.

In a paired-comparison study in 15 hospitalized patients suffering from psoriasis, Dithrocream was compared with dithranol in Lassar's paste. The therapeutic effectiveness of the two preparations was about the same, but Dithrocream gave fewer side effects in the form of staining and irritation.

Administration, Topical↗
PubMed1986

'Lymphocyte-defined' antigens on corneal fibroblasts.

Human stromal (fibroblast) cultures were established from random, normal corneas obtained from the International Eye Bank in Baltimore. Cultures were assessed for the expression of Class I, Class II, monocyte/granulocyte and T-cell antigens before and after treatment with gamma or alpha interferon (IFN), interleukin 2, and 4 beta-phorbol 12 beta-myristate 13 alpha-acetate (PMA). Class I (B2 microglobulin) and monocyte/granulocyte (Leu M-1) antigens were evident before induction, natural killer cell (Leu 7) antigens were transiently expressed, and Class II (HLA-DR, Leu 10) antigens were not expressed until after induction with gamma IFN. PMA reduced the numbers of cells positive for Leu M-1 while alpha IFN and interleukin 2 had no effect on antigen expression. Kinetic studies of HLA-DR induction indicated that as little as 12 hours exposure to gamma IFN was sufficient to initiate induction and that 30% of the population was still expressing HLA-DR 7 days after removal of gamma IFN. The inducible expression of Class II antigens following lymphokine exposure may play a critical role in rejection of allografted corneas.

Adult↗
PubMed1986

Immune mechanisms in chlamydial eye infection. Development of T suppressor cells.

In vitro proliferation assays of whole peripheral blood mononuclear leukocytes (PBML) and PBML depleted of suppressor T cells were performed in cynomolgus monkeys after they had received one, two, or repeated ocular inoculations with Chlamydia trachomatis. Whole PBML responded only weakly to chlamydial antigen, and responses to concanavalin A were depressed for 12 wk following ocular infection. Depletion of the suppressor T cell population did not result in increased chlamydia-specific proliferation until 14-20 wk after initial antigen contact, suggesting that circulating suppressor T cells are not responsible for the initiation of the chronic state.

Animals↗
PubMed1986

Clinical and immunological results of corneal allograft rejection.

Of 111 episodes of graft rejection in 66 patients, 62 responded to therapy with graft clearing (responders); 49 did not (non-responders). Both groups were of similar age, sex, and etiology; both had a similar rate of glaucoma and a similar rate of previous grafting. In responders the graft reaction was shorter in duration (2.2 vs. 5.6 wks. p less than 0.005), and it was necessary to increase the number of glaucoma medications more often in non-responders compared to responders (41% vs. 19%, p less than 0.02). The interval from surgery to reaction was similar in responders and non-responders (18.2 vs. 13.3 mos., p greater than 0.1). An epithelial rejection line was present in 11% of responders, but was not present in non-responders (p less than 0.05). Lymphocytotoxic antibody development correlated with rejection in 16 of 64 episodes. Patients who responded to treatment were more frequently asymptomatic (p less than 0.05) or were treated earlier following the onset of symptoms compared to non-responders (p less than 0.0001).

Adult↗
PubMed1986

Experimental ocular onchocerciasis in cynomolgus monkeys.

Infection of cynomolgus monkeys with microfilariae (Mf) of Onchocerca lienalis was studied as a model for human ocular onchocerciasis. Normal monkeys and immunized monkeys were given intracorneal/subconjunctival, intracameral, or intravitreal injections of Mf or bovine serum albumin (control). Selected animals were given diethylcarbamazine citrate (DEC) orally (15 mg/kg) daily after the ocular infection. Following intravitreal challenge, living Mf and fibrinous exudates were visible by slit-lamp in both the anterior chamber and vitreous. Eosinophils and macrophages surrounded the Mf in the vitreous, with degranulated eosinophils adherent to the Mf. Eosinophils infiltrated the uvea and surrounded the retinal vessels. After intracorneal injection of Mf, living Mf were visible by slit-lamp biomicroscopy in the cornea for 3 days, with minimal inflammation of the corneas occurring over the 7 days after injection. Intracamerally injected Mf induced anterior uveitis. The extent of the inflammatory reactions was not substantially altered by DEC treatment following intraocular injection of Mf. In vitro proliferative responses of peripheral blood leukocytes to a crude Mf antigen were not observed in infected monkeys and proliferative responses to mitogen declined in these animals. Responses to mitogen were inhibited by addition of Mf antigen in vitro in normal monkeys. Circulating IgG antibodies were present in the sensitized, intracorneally, and intravitreally challenged animals. No obvious correlations were present between IgG antibody level and ocular inflammation.

Animals↗