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Biomedical subjects

D Wallach

Publications and source records attributed to D Wallach.

At least 145 records · Page 8Linked to original sources
PubMed1989

Reversion of the antichlamydial effect of tumor necrosis factor by tryptophan and antibodies to beta interferon.

Human recombinant tumor necrosis factor-alpha (TNF-alpha) inhibited the growth of Chlamydia trachomatis (L2/434/Bu) in HEp-2 cells. The effect was synergistic with that of gamma interferon (IFN-gamma). TNF-induced resistance to chlamydiae could be blocked with cycloheximide, suggesting that it involves the function of some induced proteins. Tryptophan degradation was enhanced in the TNF-treated cells and was much further increased when the cells were treated with both TNF and IFN-gamma at concentrations at which IFN-gamma by itself had very little effect. Antibodies to IFN-beta blocked the augmentation of tryptophan degradation by TNF and decreased but did not fully eliminate the antichlamydial effect of TNF. Increased concentration of tryptophan in the growth medium (greater than 100 micrograms/ml) resulted in reversion of the antichlamydial effect of TNF. This study suggests that the inhibition of chlamydial growth by TNF is mediated partly through an autocrine function of IFN-beta which, in synergism with TNF, enhances the activity of a tryptophan-degrading enzyme(s) and partly by some other activities of TNF which can be blocked by tryptophan.

Cell Line↗
PubMed1989

Detection of retrovirus particles and reverse transcriptase activity in mid-term cultured peripheral blood and lymph node cells from a French woman with Sezary syndrome.

Retrovirus particles, with an ultrastructure of type C-virus similar to HTLV-I were observed in several mid-term cultures of leukemic cells derived from a woman with a well characterised Sezary syndrome who had always resided in France. Reverse transcriptase activity was detected in supernatant fluids from day 6 to day 40 of culture. However, negative anti HTLV-I serology and the absence of specific molecular hybridization between leukemic cell DNA and two HTLV-I derived probes, argue against a HTLV-I virus.

Aged↗
PubMed1989

[Neonatal milia].

Explore the source record for details and available documents.

Diagnosis, Differential↗
PubMed1989

[The history of nosology in dermatology].

The Hippocratic texts give evidence of the first structured interest in skin diseases. Nosological preoccupations, then at their beginning, put the stress on the connections between general pathology and diseases affecting the skin, and by creating a vocabulary. The Hippocratic texts give evidence of the first structured interest in skin diseases. Nosological preoccupations, then at their beginning, put the stress on the connections between general pathology and diseases affecting the skin, and by creating a vocabulary drawn from the vegetal world initiated a long-lasting relationship between dermatology and botany. The centuries which followed witnessed a wealth of descriptions which, thanks in particular to the works of Celsus, Galen and the Arab authors, led to the formation of true medical encyclopaedias, although the diagnosis of skin diseases could not be approached. The outline of a rational dermatological thinking did not appear until the 17th century with Haffenreffer, Riolan and Willis, all influenced by Malpighi, Harvey and Sydenham. Then came the 18th century with Astruc, Turner and Lorry. But it was in fact J. Plenck who devised the first nosology that could be used in clinical practice by creating the elementary lesion principle, later revised and refined by Willan and Bateman. In contradistinction with this artificial nosology, the French school of Alibert endeavoured to set up a natural nosology unfortunately spoiled by a certain lack of pragmatism. In the second half of the 19th century three main schools of thought emerged: Hebra's, who raised the nosological approach to an anatomical level, Hardy, Bazin's, who gave predominance to diathesis, and Wilson's, who attempted a synthesis of the first two schools. At the dawn of the 20th century the dogmatism of morphological systematization seemed to wane and be superseded by an aetiological approach, then reappeared in Degos' treatise published in 1953. The latest nosologies acknowledge the importance of clinical data but give first rank to the physiopathology of diseases, sometimes replacing the anatomical systematization by a relative biological systematization which evolves with technological advances.

Dermatology↗
PubMed1989

Contact lens induced giant papillary conjunctivitis: a retrospective study.

In this retrospective epidemiological study, records from the Contact Lens Department of SUNY College of Optometry were randomly selected and reviewed. An association between contact lens induced giant papillary conjunctivitis (GPC) and a FDA classified sub-category was found. Younger patients were shown to have a higher risk of developing GPC. Gender and tear film break-up time were not found to be associated with the condition. The mean replacement time for hydrogels was 10.8 +/- 9.2 months with no significant differences among contact lens polymer types. The GPC phenomenon was almost exclusively bilateral with a mean onset time of 31.4 months after commencing lens wear. A model for the development of GPC based on tear film interactions with the hydrogel lens surface is presented. A model for the tear film's interaction with the hydrogel contact lens in situ is offered.

Adult↗
PubMed1989

Pyoderma gangrenosum with pulmonary involvement.

A 60-year-old woman had a typical pyoderma gangrenosum with monoclonal IgA gammopathy and atrophic gastritis. Two years after the onset of her skin disease, she had evidence of pulmonary abscesslike involvement. Corticosteroid therapy led to healing of skin and lung diseases. This case stresses the multisystemic manifestations of neutrophilic dermatoses with special attention to pulmonary involvement.

Drug Administration Schedule↗
PubMed1988

Dominance of resistance to the cytocidal effect of tumor necrosis factor in heterokaryons formed by fusion of resistant and sensitive cells.

The mechanisms underlying differences in vulnerability to the cytocidal effect of TNF, among various cell lines and strains, were explored by examining the response to TNF of heterokaryons formed by fusing TNF-resistant and -sensitive cells. Several combination pairs of human and murine cells, differing significantly in response to TNF toxicity, yet expressing a similar level of TNF receptors, were examined. In all combinations tested, the heterokaryons exhibited resistance to TNF toxicity, comparable, in extent, to that of the more resistant of the two parental cell lines. This dominance of resistance suggests that differences in vulnerability to TNF toxicity reflect activities which are expressed by resistant cells and are deficient in vulnerable ones, activities which perhaps protect the cell against the cytocidal effect of TNF.

Animals↗
PubMed1988

Sensitization and desensitization to lethal effects of tumor necrosis factor and IL-1.

BALB/c mice were sensitized to lethal effects of human rTNF-alpha and of human rIL-1 alpha by simultaneous treatment with sublethal doses of actinomycin D (Act D) or D-galactosamine (GalN). In contrast, treatment with sublethal doses of TNF or IL-1 themselves resulted in desensitization of the mice to the lethal effect of these cytokines: mice injected with TNF or IL-1 in the absence of Act D or GalN responded to a second injection of TNF or IL-1, this time together with Act D or GalN, by a significantly delayed death, or even survived. Desensitization developed rapidly (0.5-1.0 h) and abated 24 to 48 h postinjection. Each of the two cytokines induced hyporesponsiveness to its own lethal effect as well as to that of the other. Injection of TNF or IL-1 at sublethal doses resulted also in hyporesponsiveness to the lethal effect of LPS on mice primed with bacillus Calmette-Guérin, an effect which most likely is mediated by TNF and IL-1 produced in those mice in response to the LPS. TNF and IL-1 in combination had an additive effect both in lethality and in desensitization of the mice. These findings suggest that some of the deleterious effects of TNF and IL-1 are modulated by antagonistic mechanisms; mechanisms which can be suppressed by sensitizing agents, specifically by agents inhibiting the synthesis of RNA or protein; but which, in the absence of such agents, are found to be augmented in response to TNF and IL-1, thus resulting in desensitization.

Animals↗
PubMed1988

Tumor necrosis factor in middle ear effusions.

The presence of tumor necrosis factor (TNF) was determined in middle ear effusions from 27 ears of children with chronic otitis media with effusion. Cytotoxic activity was assessed by quantitation of target (HeLa) cell death after incubation with the aspirate. Moderate cytotoxic activity was found in 17 of 27 samples (mean cell death of 53% and 32% at 1:2 and 1:4 dilutions, respectively). In ten (37%) of the middle ear effusion aspirates no cytotoxic activity was detected. To confirm that cytotoxicity was due to TNF, 13 of the samples with cytotoxic activity were incubated with a monoclonal anti-TNF antibody and retested. Cytotoxicity was blocked by the anti-TNF antibodies in all cases. Tumor necrosis factor, derived most probably from macrophages or mast cells in the middle ear, may mediate various pathologic processes associated with otitis media, such as generation of mucoid effusion, fibroblast proliferation, and bone resorption.

Child↗
PubMed1988

Interrelated effects of tumor necrosis factor and interleukin 1 on cell viability.

Cells are sensitized to the cytolytic effect of tumor necrosis factor (TNF) by simultaneous application of inhibitors of RNA or protein synthesis. Treating cells, in the absence of such inhibitors, with cytokine preparations produced by stimulated mononuclear leukocytes may render them resistant to the cytolytic effect of TNF + the inhibitors. One of the cytokines which induces that resistance was identified as TNF itself (17). As shown in the present study, similar resistance against TNF-mediated killing can be effectively induced also with preparations of cytokines which are depleted of TNF. Fractionation of such TNF-free preparations revealed that their resistance-inducing activity is mediated by interleukin 1 (IL 1). In part of the cell lines in which IL 1 induced resistance to TNF killing, when applied without inhibitors of protein/RNA synthesis, it was found to exert cytolytic effect in the presence of such inhibitors, however, less effectively than TNF. Both TNF and IL 1 thus appear to activate in cells cytolytic mechanisms as well as antagonizing mechanisms which can protect cells from cytolysis.

Cell Line↗
PubMed1988

Congenital dyschromia with erythrocyte, platelet, and tryptophan metabolism abnormalities.

The case of a female child with a unique generalized congenital dyschromia is reported. She had hypopimented skin, with hypomelanosis and hypomelanocytosis, and many pigmented macules, which consisted of epidermal and dermal hypermelanosis without hypermelanocytosis. Biochemical investigations revealed normal catecholamine metabolism but abnormal tryptophan metabolism, including a decrease in blood serotonin and melatonin. A slight platelet storage pool disease was demonstrated, and a recurrent megaloblastic folate-related anemia occurred. The possible relationship between the pigmentary disease and the biochemical abnormalities is discussed. We suggest that this case represents a previously undescribed association of dyschromia, erythrocyte, platelet, and tryptophan metabolism abnormalities.

Blood Platelets↗
PubMed1988

Erythema multiforme is associated to HLA-Aw33 and DRw53.

Erythema multiforme is an acute eruption of the skin and mucous membranes of various aetiologies. Forty-one unrelated patients were HLA typed for 53 specificities of the HLA-A, B, C, DR and DQ series. Frequencies of Aw33 and DRw53 were significantly increased: Aw33, 17.0% in patients vs 2.8% in controls (corrected p = 0.01, relative risk = 7.2); DRw53, 70.7% in patients vs 30.5% in controls (corrected p = 0.0005, relative risk = 5.5).

Adult↗
PubMed1988

Inhibition of Chlamydia trachomatis growth by recombinant tumor necrosis factor.

Purified human recombinant tumor necrosis factor (rTNF) alpha inhibited the growth of Chlamydia trachomatis (L2/434/Bu) in HEp-2 cell cultures. The inhibition of C. trachomatis yield could be achieved even when the rTNF alpha (200 ng/ml) was added up to 12 h after infection. The effect of rTNF alpha on chlamydial infection was synergistic with that of gamma interferon.

Carcinoma↗