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Biomedical subjects

E Yunis

Publications and source records attributed to E Yunis.

At least 73 records · Page 4Linked to original sources

Aging and serum immunoglobulin E levels, immediate skin tests, RAST.

The changes of the serum IgE levels, specific immediate skin-test responses, and RAST measurements with age were evaluated. A total of 331 unrelated individuals were studied, consisting of 166 subjects with ragweed allergic rhinitis and/or asthma, 67 with idiopathic (intrinsic) asthma, and 98 who appeared in good health with no clinical evidence of atopic diseases. All subjects were evaluated by history and physical examination, intradermal skin testing to the common aeroallergens, measurements of IgE antibody to common aeroallergens with the RAST, and serum IgE levels. Results demonstrated a significant decrease in serum IgE levels with aging in atopic individuals. This decline was exponential in character. In addition, a tendency for RAST and immediate type skin-test responses for selected antigens and histamine to decrease with age was observed.

Adolescent↗

Macrophage T cell interaction in man: binding of antigen-specific human proliferating and helper T cells to antigen-pulsed macrophages.

Adsorption of T cells over monolayers of autologous, but not allogeneic, macrophages (M phi) pulsed with tetanus toxoid (TT) antigen resulted in the specific depletion of the capacity of the T cells to proliferate and to release T cell helper factor in response to stimulation, with TT antigen. T cells that bound to the TT-pulsed M phi monolayers were specifically enriched in their capacity to proliferate in response to TT. Turkey antiserum to the human B cell glycoprotein p 29,34, but not turkey antiserum to human beta 2 microglobulin, inhibited the binding of TT-reactive T cells to TT-pulsed M phi. This inhibition resulted from the binding of the anti-p 29,34 antiserum to DR determinants expressed on the surface of the M phi. Immunosorbent purified IgG anti-TT, added in great excess, did not inhibit the binding of TT-reactive T cells to TT-pulsed M phi monolayers. Soluble TT antigen and rabbit antiidiotypic IgG, directed against IgG F(ab')2 anti-TT obtained from the cell donor, minimally inhibited the binding of TT-reactive T cells to TT pulsed M phi monolayers. M phi pulsed with urea-denatured TT, which contained less than 1% native TT, depleted T cell reactivity to TT to an extent almost equivalent to that achieved by M phi pulsed with native TT. These results indicate that human antigen-reactive T cells bind to the DR determinants of M phi pulsed with antigen and that the immunogenic moiety of antigen recognized by the majority of antigen reactive human T cells may differ from native antigen.

Adsorption↗

Cleidocranial dysostosis, severe micrognathism, bilateral absence of thumbs and first metatarsal bone, and distal aphalangia: a new genetic syndrome.

Five patients from three families have a new genetic syndrome. The features include cleidocranial dysostosis, bilateral absence of the thumbs and of the distal phalanges of the fingers, hypoplasia of the first metatarsus, absence of the distal phalanx and hypoplasia of the proximal phalanx of the big toe, pelvic dysplasia, bilateral hip dislocation, a constant facial dysmorphism with sparse hair, peculiar ears, severe micrognathism, and retracted and poorly delineated lips. The existence of consanguinity in two of the families, both with two affected siblings, as well as the lack of sex predilection, allow us to postulate that this syndrome is inherited in a recessive manner.

Abnormalities, Multiple↗

Full trisomy 7 and Potter syndrome.

A patient with typical Potter's syndrome and full trisomy 7 is described. All previous reports on chromosome 7 abnormalities, whether monosomic or trisomic, p or q, are reviewed and discussed, establishing two 7q trisomy syndromes: 7q22 ts leads 7q31 and 7q22, q31 leads to 7qter. Some implications of the finding of full trisomy 7 in a case of Potter's syndrome are discussed.

Autopsy↗

Histocompatibility antigen frequencies in diabetic retinopathy.

We studied the histocompatibility antigens A and B in 300 insulin-dependent diabetics: 200 had proliferative retinopathy and 100 did not. The two groups were matched for known duration of diabetes and other clinical features. In both groups the frequencies of HLA-B8, HLA-B18, and HLA-B8/HLA-B15 were significantly higher, and those of HLA-B7 and HLA-B12 were significantly lower than in healthy controls. The patients with proliferative retinopathy were significantly less often positive for HLA-B7 (X2 = 10.0; Pc < .03) than patients with nonproliferative retinopathy. When both groups were stratified for age at diagnosis, there were additional differences. HLA-B15 was significantly more frequent in the proliferative retinopathy group with age at diagnosis between 15 and 40 years (nonproliferative retinopathy = 16.4%; proliferative retinopathy = 39.4%; X2 = 7.89, Pc < .03; relative risk = 3.32) and HLA-B7 significantly less frequent (nonproliferative retinopathy = 23.6%; proliferative retinopathy = 5.6%; X2 = 8.0, Pc < .03; relative risk = 0.19). These differences in histocompatibility frequencies between patients with and without proliferative retinopathy indicate a genetic contribution to diabetic retinopathy.

Adolescent↗

X-linked Dyggve-Melchior-Clausen syndrome.

Ten affected males studied from four generations of a Colombian family with Dyggve-Melchior-Clausen (DMC) syndrome are described. The ages of the affected males varied from 13 to 50 years and they presented with typical clinical and radiological manifestations of the syndrome. The association of normal intelligence and a clear X-linked recessive inheritance in this family is evidence of heterogeneity in the Dyggve-Melchior-Clausen syndrome. In agreement with previous reports for DMC dwarfism, this new form has normal mucopolysaccharide excretion.

Abnormalities, Multiple↗

Use of monocytes in HLA-A, B, C and DR typings.

A simple method of improved serologic typing of monocytes for HLA-A, B, C and DR specificities is described. The method employs monocytes recovered from frozen samples of peripheral blood mononuclear cells; it chiefly involves pretreatment of monocytes with 0.01% iodoacetamide (IAA) prior to typing. The advantage of this method lies principally in the lowering of the background nonspecific cytotoxicities and false positive readings upon IAA addition to the monocyte preparations. Using this method monocytes can be typed for HLA-A, B, C determinants. Although the addition of IAA results in substantial typing improvements, we found the assignment of A, B, C specificities difficult due to the presence of extra positive reactions when monocytes were compared to T lymphocyte typings. probably due to the presence of DR or monocyte specific antibodies in the routinely used HLA antisera. This method proved to be most useful in DR typings where mono cytes in the presence of IAA were compared with autologous B cells in the absence of IAA. The differences in typings due to a decrease in false positive cytotoxic readings were significantly in favor of using IAA treated monocytes in DR typings (P < 0.0001). The use of IAA in the course of B cell or T cell typings bad no adverse consequences on either A, B, C or DR typings, respectively. Our results indicate a potential usefulness for the use of IAA in typing monocytes HLA determinants in general and for the DR determinants in particular.

Enzyme Inhibitors↗

Partial trisomy 3q.

A new case of partial trisomy 3q is reported in a 5-year-old female with severe congenital malformations and psychomotor retardation. A review of the literature, with a total of 11 patients, allows us to conclude that the clinical picture reminiscent of the Cornelia de Lange syndrome is caused by the trisomic state.

Abnormalities, Multiple↗

Direct duplication 2p14 to 2p23.

A malformed male newborn was first diagnosed as having Smith-Lemli-Opitz syndrome. Extensive cytogenetic studies, including Q, G, C, R and T banding and BudR treatment, were applied, finally leading the authors to conclude that the patient had a partial 2p trisomy caused by direct duplication 2p14 to 2p23. This was a de novo chromosome abnormality, as both parents had normal karyotypes.

Abnormalities, Multiple↗

Partial trisomy-5p.

Two sibs with partial trisomy-5p are reported. Their father is the carrier of a balanced translocation 46,XY,t(4q+;5p-). Twelve cases of partial trisomy-5p--including our two patients--have been reported. The most common abnormalities found were mental retardation, short stature, dolichocephaly, prominent nasal bridge, prognathism, seizures, hypotonia, ear abnormalities, increased ulnar loops on the fingertips, and cryptorchidism in affected males.

Abnormalities, Multiple↗