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Biomedical subjects

M Soliman

Publications and source records attributed to M Soliman.

At least 37 records · Page 2Linked to original sources
PubMed1996

Serum alpha L-fucosidase enzyme activity in ovarian and other female genital tract tumors.

OBJECTIVES: To assess the value of serum alpha-L-fucosidase as a tumor marker in the diagnosis of ovarian and other female genital tract tumors. METHODS: One-hundred fifty-one patients were studied; 101 had different genital tract tumors (malignant ovarian tumors (48), carcinoma of the cervix (13), endometrial carcinoma (6), carcinoma of the vulva (6) and benign tumors (28)). A control group of 50 healthy female patients was included. Serum alpha-L-fucosidase activity was determined in all patients and controls. Serum CA 125 level was also determined in patients with malignant ovarian tumors. RESULTS: patients with malignant ovarian tumors showed the lowest level of alpha-L-fucosidase activity in comparison to other malignant and benign tumors of the female genital tract and also in comparison to malignant ovarian tumors. RESULTS: Patients with malignant ovarian tumors showed the lowest level of alpha-L-fucosidase activity in comparison to other malignant and benign tumors of the female genital tract and also in comparison to control group. The majority of ovarian carcinoma patients (90%) had a serum level of < 275 u/ml of alpha-L-fucosidase activity, while more than 90% of the control group and other genital tumors had a serum level of > 275 u/ml. The sensitivity and specificity of serum alpha-L-fucosidase activity in diagnosing epithelial ovarian tumors were 88.5% and 98%, respectively (using a cut-off level of < 275 u/ml). The corresponding figures for CA 125 were 96.2% and 100% (using a cut-off level of > 35 u/ml). CONCLUSIONS: Serum alpha-L-fucosidase enzyme activity can be useful as a tumor marker in diagnosing advanced malignant epithelial ovarian tumors. Its sensitivity and specificity are comparable to CA 125. However, there is a lack of data to support its usefulness in the diagnosis of early stage disease (Stage 1). The cost of doing the test is one-third that of CA 125 and the test can be more widely applied in developing countries.

Adult↗
PubMed1996

T-cell recognition of residue 158-176 in thyrotropin receptor confers risk for development of thyroid autoimmunity in siblings in a family with Graves' disease.

Twenty-two subjects in a family with Graves' Disease and 20 normal subjects unrelated to the family were examined for T-cell responses to rec h TSHR-ECD and its synthetic peptides. Seven of the family members and none of the controls responded positively to rec h TSHR-ECD. Peptide 158-176 was the only residue that showed a high percentage of response among family members, no responses in spouses, and a significant difference compared to unrelated controls. Family members under age of 6 did not differ from spouses in response to rec h TSHR-ECD or any individual peptide. Family members ages 6-12 years were significantly different from spouses in response to peptides 30-49, 158-176, and 172-186. The reactivity of adult family members including 3 Graves' patients was significantly different from spouses in response to peptides 44-62, 132-150, 158-176, and 248-263. The responses of female members of the family were higher than that of the male members and significantly different for peptide 272-291. These data suggest that recognition of peptide 158-176 may be an early event in the pathogenesis of the disease and that recognition of both 158-176 and 248-263 residues may be the cornerstone for establishment of the disease.

Adolescent↗
PubMed1995

Production of thyroid-stimulating antibodies in mice by immunization with T-cell epitopes of human thyrotropin receptor.

We examined whether mice, immunized with TSH receptor (TSH-R) peptides, which are known to be T-cell epitopes in patients with Graves' disease, would show thyroid-stimulating antibody (TSAb). We immunized DBA/1J mice with TSH-R peptide amino acids 132-150, 145-163, 158-176, and 172-186 and with a pool of these four peptides. The antibodies produced in these mice were evaluated by measurement of TSAb activity using Chinese hamster ovary cells expressing human TSH-R. Seven of 20 mice showed TSAb activity that could be partially blocked with TSH-R peptides. To assess the role of T-cell epitope-specific T-cells in the production of TSAb, we transferred a T-cell line developed from a TSAb-positive mouse to other syngeneic DBA/1J mice. Two of 4 recipient mice showed TSAb activities. These findings suggest that specific T-cell epitopes of TSH-R play a crucial role in the production of TSAb.

Amino Acid Sequence↗
PubMed1995

T-cell reactivity to recombinant human thyrotropin receptor extracellular domain and thyroglobulin in patients with autoimmune and nonautoimmune thyroid diseases.

Grave's disease and Hashimoto's thyroiditis are common organ-specific disorders characterized by an immune response toward a number of thyroid proteins, including TSH receptor (TSHR), thyroid peroxidase, and thyroglobulin (Tg). Although considerable progress has been made in understanding and mapping the autoantibody response to TSHR, much less is known about recognition of TSHR by pathogenic T-cells in human disease. To identify such reactions, we analyzed the T-cell proliferative responses of peripheral blood lymphocytes (PBMC) to human recombinant TSHR extracellular domain (hrecTSHR-ECD amino acids 19-417) expressed in Escherichia coli and to Tg. Forty-two patients with autoimmune thyroid disease (AITD), 13 patients with non-AITD, and 20 normal subjects were studied. PBMC from 40% of patients with AITD and 46% of patients with non-AITD reacted significantly to hrecTSHR-ECD. The reactivity to Tg was less than that to TSHR-ECD in both groups. Five percent of normal subjects showed a response to hrecTSHR-ECD and none to Tg. TSHR-specific T-cell lines were developed in 16 of 26 AITD patients and 3 of 10 non-AITD patients. CD8-positive T-cell depletion from PBMC of 8 patients with AITD by the indirect panning method did not enhance the reactivity to hrecTSHR-ECD, except in 1 patient. We conclude that TSHR-specific T-cells are present in the circulation of patients with AITD and are presumably involved in the pathogenesis of thyroid autoimmunity. The lower, but positive, reactivity to hrecTSHR-ECD found in patients with non-AITD was unexpected and may be related to lymphocytic infiltrates in the thyroid of 7 of the 11 patients.

Adult↗
PubMed1995

CTLA-4 gene polymorphism associated with Graves' disease in a Caucasian population.

Graves' disease (GD) is an autoimmune thyroid disease. Multiple genetic factors are believed to be involved in its pathogenesis, but the factors are largely unknown, except for sex (female disease preponderance) and the role of human leukocyte antigen (HLA) genes on chromosome 6. To understand the mechanisms underlying the development of GD, a search for non-HLA-linked genes is crucial, and we tested several candidate genes, including the CTLA-4 gene on chromosome 2q33. CTLA-4 molecules may either facilitate or down-regulate the second signal to T-cells, which is provided by the interaction between the two accessory molecules CD28 and B7. One hundred and thirty-three Caucasian patients (26 males) with GD and 85 local controls were included in this study. Polymerase chain reaction was used to amplify DNA containing the (AT)n repeat within the 3'-untranslated region of exon 3 of the CTLA-4 gene. The 5'-forward primer was radiolabeled, and amplified products were resolved on 5-7% sequencing gels. All subjects were previously typed for HLA class II alleles. Twenty-one alleles were observed with sizes ranging from 88-134 basepairs. In the association analysis, the genotype frequencies between GD patients and controls differed significantly (P = 0.012), and the difference was attributable to a higher frequency of the 106-basepair allele among patients (relative risk, 2.82). When the patients were subdivided with respect to sex and HLA, the phenotype frequencies of allele 106 was higher in the female patients with protective HLA specificities (DQA1*0201 positive/DQA1*0501 negative) than in those with susceptible HLA specificities (DQA1*0201 negative/DQA1*0501 positive; 81.8% vs. 45.5%; P = 0.026). The CTLA-4 gene or a closely associated gene (including CD28) confers susceptibility to GD. This association may be more important in female patients with protective HLA specificities, who otherwise would be at low risk of developing the disease.

Abatacept↗
PubMed1995

Graves' disease in severe combined immunodeficient mice.

Graves' disease (GD) is an autoimmune thyroid disorder involving an antibody (TSAb) directed against the TSH receptor (TSHR) producing thyroid stimulation. We have developed an animal model of GD by engrafting peripheral blood mononuclear cells or T cell lines plus autologous thyroid tissue into severe combined immunodeficient (SCID) mice. We xenografted Graves' thyroid tissue from six patients into six groups of SCID mice. Autologous PBMC and T cell lines reactive to recombinant human TSHR extracellular domain and non-TSHR lines were injected ip into the designated groups. In some of the studies, thyroid tissue was irradiated with 2000 rads before xenografting. Irradiation of xenografts induced thyroid tissue damage and release of thyroid antigens and hormones. Mice reconstituted with peripheral blood mononuclear cells or nonspecific T cell lines did not simulate GD. However, we achieved production of TSAb, elevation of serum T3, and TSAb-dependent survival and function of human Graves' thyroid tissue in SCID mice reconstituted with TSHR-specific T cell lines. We reconstituted SCID mice with PBMC and TSHR-specific T cell lines that recognized TSHR peptide 158-176. This may be in vivo evidence of the importance of peptide 158-176 as an immunodominant epitope on the TSHR extracellular domain.

Adult↗
PubMed1995

T-cells recognize multiple epitopes in the human thyrotropin receptor extracellular domain.

In Graves' disease (GD), the TSH receptor (TSHR) is believed to be the major target of an autoimmune response. T-Lymphocytes regulate the immune system. To assess the interaction of T-cells with TSHR in the pathogenesis of GD, we tested the T-cell response of peripheral blood mononuclear cells and T-cell lines to the recombinant human TSHR extracellular domain (rhTSHR-ECD) and 31 synthetic peptides corresponding to the entire TSHR-ECD in 20 patients with GD, 8 patients with Hashimoto's thyroiditis, 7 with colloid nodular goiter (CNG), and 20 normal controls. Comparing patients from different groups with normal subjects, there was a significant response to rhTSHR-ECD and thyroglobulin in GD patients (P < 0.001) and HT patients (P < 0.05), but not in CNG patients (P > 0.1). All 20 patients with GD responded to at least one peptide. The reactivity in GD patients was heterogeneous and spanned the entire TSHR-ECD. However, the reactivity was significantly different from that in controls for peptide regions 44-88, 119-176, 227-263, and 343-376, and the stimulation index (SI) values were significantly different for peptides 272-291 and 301-320. Significant differences were confined to peptides 158-176 and 343-362 and the region 227-263 for comparison of the number of positive responses in patients and controls to individual peptides. Forty-six percent of human leukocyte antigen-DQA1 0501 allele-positive Graves' patients responded to peptides 158-176 and 248-263 (SI = 3 or more) compared to 14% of allele-negative patients. In HT and CNG patients, the response was mainly to peptides in the carboxy-terminal half of the TSHR-ECD. Concordance of the reactivity in T-cell lines and peripheral blood mononuclear cells was observed in 36% of direct comparisons in GD. Eighty-five percent and 90% of GD patients were positive for microsomal antibody and TSHR antibody, respectively, and 59% of microsomal antibody-positive and 67% of TSHR antibody-positive patients responded to rhTSHR-ECD (SI = 2 or more). However, there was no significant correlation between antibody-positive patients and reactivity to specific peptides. Using multiple criteria to define immunodominance, peptides 158-176, 237-252, 248-263, and 343-362 seem to be important epitopes and may be critical for T-cell triggering in GD.

Adult↗
PubMed1995

Proliferative responses of T-cells to thyroid antigens and synthetic thyroid peroxidase peptides in autoimmune thyroid disease.

We studied the immune responses of 33 patients with autoimmune thyroid disease (AITD; including 17 with Hashimoto's thyroiditis and 16 with Graves' disease), 5 patients with non-AITD, 12 control subjects (CS), and 2 subjects with a family history of autoimmunity to the main thyroid antigens. These antigens included thyroid peroxidase (TPO), thyroglobulin (Tg), TSH receptor (TSH-R), and 13 overlapping TPO peptides. T-cell lines (TCL) were isolated from peripheral blood mononuclear cells (PBMC) after incubation with TPO, Tg, or a protein derivative of tuberculin (PPD). PBMC and TCL were used in a 3- to 5-day microproliferation assay. Peripheral lymphocytes from most AITD patients responded with a stimulation index of 3 or more to TPO, Tg, and/or TSH-R (60-88%) as well as to two or more TPO peptides. Lymphocytes from 3 of 5 patients with non-AITD and 2 subjects with a family history of autoimmunity were also reactive to thyroid antigens. TPO TCL showed a high proliferative response to TPO and its peptides, whereas Tg TCL were less reactive and PPD TCL were nonreactive to these antigens. Six of the 13 peptides tested produced highly significant stimulation in PBMC (CS, 0-17%; AITD, 60-92%) and TPO TCL (73-91%). The amino acid sequences of these putative epitopes were located in TPO regions 100-119, 211-223, 261-275, 420-434, 625-644, and 882-901. These results demonstrate T-cell responses to the main thyroid antigens, including TPO, Tg, and TSH-R, and confirm the heterogeneity of TPO T-cell epitopes in patients with AITD. Amino acid residues 100-119, 420-434, 625-644, and 882-901 are the most common sites recognized by TPO TCL, indicating that they may be immunogenic epitopes in AITD.

Adult↗
PubMed1995

Does thyroidectomy, radioactive iodine therapy, or antithyroid drug treatment alter reactivity of patients' T cells to epitopes of thyrotropin receptor in autoimmune thyroid diseases?

The effect of treatment on thyroid antibody production and T cell reactivity to thyroid antigens was studied in 15 patients with Graves' disease (GD) before and after thyroidectomy, 19 patients with GD before and after radioactive iodine (RAI) therapy, and 9 patients maintained euthyroid on antithyroid drugs (ATD). Twenty subjects matched for age and sex without known thyroid disease served as controls. In GD patients, the responses of peripheral blood mononuclear cells (PBMC) and TSH receptor (TSHR)-specific T cell lines to recombinant human TSHR extracellular domain, thyroglobulin, and TSHR peptides were examined on the day of surgery or RAI therapy (day 0) and also 6-8 weeks and 3-6 months thereafter. Reactivity to TSHR peptides before surgery was heterogeneous and spanned the entire extracellular domain. Six to 8 weeks after subtotal thyroidectomy, the number of patients' PBMC responding to any peptide and the average number of recognized peptides decreased. A further decrease in the T cell reactivity to TSHR peptides was observed 3-6 months after surgery. The responses of PBMC from Graves' patients before RAI therapy were less than those in the presurgical group. Six to 8 weeks after RAI therapy, the number of patients responding to any peptide and the average number of recognized peptides increased. Three to 6 months after RAI, T cell responses to TSHR peptides were less than those 6-8 weeks after RAI therapy, but still higher than the values on day 0. Responses of PBMC from patients with GD, maintained euthyroid on ATD, were lower than those before surgery or RAI therapy. The reactivity of T cell lines in different groups reflected a pattern similar to PBMC after treatment. TSHR antibody and microsomal antibody levels decreased after surgery, but increased after RAI therapy. The difference in the number of recognized peptides by patients' PBMC before RAI and surgery may reflect the effect of long term therapy with ATD in the patients before RAI vs. the shorter period in patients before surgery. The decreased T cell reactivity to thyroid antigens after thyroidectomy could be the result of removal of a major part of the thyroid gland or redistribution of suppressor-inducer T cells. The increased T cell response after RAI therapy is probably epitope specific, rather than a response to the whole TSHR molecule. Synchronous recognition of peptides 158-176 and 248-263 is important for the development of GD, and the loss of recognition of one of these epitopes may be an early sign of immune remission and a predictor of euthyroidism.

Adult↗
PubMed1993

Characterization of T-cell clones generated from skin of patients with psoriasis.

BACKGROUND: The infiltrating cells in psoriasis include a subpopulation of autoreactive T cells. OBJECTIVE: The aim of this study was to further characterize skin-infiltrating T lymphocytes in patients with psoriasis. METHODS: Forty-five T-cell clones were generated from skin biopsy specimens from two patients. RESULTS: Phenotypic studies on 25 of 45 clones revealed that 19 (76%) of the clones were CD4+, 5 (20%) were CD8+, and 1 (4%) clone was CD4- and CD8-. Twenty-three clones were stained for identification of T-cell receptors. Twenty-two clones expressed alpha/beta T-cell receptors and one clone (CD4-/CD8-) expressed no T-cell receptor. Nineteen clones (42%) were autoreactive with no restriction to class I or class II HLA antigens. By contrast, proliferation of two of the seven clones was inhibited by class I monoclonal antibody, whereas proliferation of four of seven clones was inhibited by class II monoclonal antibody. CONCLUSION: These data suggest that skin-infiltrating lymphocytes in patients with psoriasis may recognize HLA-associated molecules, perhaps the peptide of the HLA groove. The recognition of the peptide is presumably inhibited when monoclonal antibody is bound to the HLA molecule.

CD4 Antigens↗
PubMed1993

Myocardial texture and cardiac calcification in uremia.

Seventy patients with advanced chronic renal failure were examined by 2D echocardiography in an effort to determine the prevalence of changes in myocardial texture and of valvular calcification. Changes in myocardial texture may be due to calcium deposition in the myocardium, the relationship between changes in myocardial texture and factors that may enhance myocardial calcification (blood levels of parathyroid hormone, PTH, and calcium-phosphorus product) were also evaluated. Myocardial texture was abnormal in 36 patients. In 68 patients, structural calcification could be assessed; a high degree of calcification was found. No correlation was found between either the echocardiographic parameter and blood levels of PTH or calcium-phosphorus product. We conclude that myocardial textural changes and intracardiac calcification are common in chronic renal failure and that these abnormalities do not correlate with blood PTH levels or calcium-phosphorus product.

Adult↗
PubMed1991

Some immunological aspects of chronic liver diseases in Egyptian children.

This study was conducted on 40 Egyptian children (21 males and 19 females) with various chronic liver diseases, selected from the out-patient Pediatric Hepatology Clinic of Ain Shams University Hospital. Their ages ranged from 1.5 to 13 years with a mean of 5.98 +/- 3.72 years. Twenty healthy children of comparable age and sex to the patients were chosen as controls. All children were subjected to detailed history taking, thorough clinical examination and laboratory investigations including full blood picture, urine and stool examination, liver function tests, prothrombin time and hepatitis B surface antigen in addition to sigmoidoscopy with rectal snip examination, abdominal ultrasonography and liver biopsy. Moreover, immunological investigations were done, that included estimation of the serum complement levels of C3 and C4 by using single radial immunodiffusion method, assessment of the phagocytic and intracellular killing activity of polymorphonuclear leucocytes by living Candida albicans uptake and detection of non organ specific autoantibodies in the serum by indirect immunofluorescence technique. This study showed that the serum level of C3 was increased and C4 was decreased significantly in patients with chronic liver disease, especially in chronic active hepatitis. Regarding phagocytosis, there was significant impairment of the neutrophil phagocytic function but not the intracellular lytic activity of candida albicans. This reduced phagocytic function was more pronounced in patients having chronic hepatitis and cirrhosis than in bilharzial and other cases. Serum autoantibodies; antinuclear and antimitochondrial antibodies were absent in the sera of both patients and controls, while antismooth muscle antibodies were found in the sera of 47.5% of patients with chronic liver diseases and non of the control sera. The highest incidence of these antibodies was present in HBs Ag negative patients with chronic active hepatitis (80%). We concluded that patients with chronic liver diseases have disturbed functions of both complement and phagocytic systems that may lead to increased susceptibility to recurrent infections. So, routine assessment of immunological status with early diagnosis and treatment of infections are important in the proper management of these patients. In addition, detection of serum auto-antibodies in these patients is helpful in the early diagnosis of auto-immune liver diseases.

Child↗
PubMed1989

Detection of steroid hormone (estrogen) residues in imported red meat.

28 immature female albino mice were utilized to clarify if there was a sufficient amount of the hormonal agent used in the production of meat for human consumption, such as estrogen, can remain in meat cut from carcasses of animals administered hormones during finishing to have deletorious effects on human ingestors. The animals were divided into 4 equal groups, group A: control, fed on normal ration, group B: each mouse were injected with 0.2 microgram of estradiol propionate i. p. daily, group C: were fed on normal ration mixed with imported minced meat, 5 g/mouse/day, group D: were fed as in group C, but we used local minced meat. Sera were collected after one week. There were significant increase in both FSH and LH in group B, slight rise in both FSH and LH in groups C and D but group A have the lower level of both FSH and LH. The number of Graafian follicle were significantly higher in group B, also the body weight of group B, were rapidly increased more than other groups. Both of groups C and D nearly inclose to each other, in body weight, indicating that imported meat were free from any estrogenic residues in comparison to our local meat.

Animals↗
PubMed1988

Hepatic macrophage function in schistosomal glomerulopathy.

Hepatic fibrosis in the pathogenesis of schistosomal glomerulopathy cannot be explained by any positive influence of hepatocellular injury. In order to examine the potential role of impairment of hepatic macrophage function, the t1/2 plasma clearance of 99mTc-sulphur colloid was studied in 30 patients with schistosomal glomerulopathy, ten normal volunteers, ten cases of uncomplicated intestinal schistosomiasis, ten non-schistosomal cirrhotic patients and ten non-schistosomal nephrotic patients. Liver and renal biopsies were obtained from appropriate groups and examined by light microscopy and glomerular immunofluorescence. There was a significant correlation between t1/2 of sulphur colloid clearance and proteinuria, mesangial hypercellularity, and predominance of IgA glomerular deposits. These data indicate that hepatic macrophage dysfunction is an important factor in the pathogenesis of schistosomal glomerulopathy, and that IgA plays a major role in advanced glomerular lesions. The degree of impairment of hepatic macrophage function may influence the pattern and severity of glomerular lesions depending upon the affection of IgA clearance mechanisms.

Adult↗
PubMed1985

Serum gastrin in chronic renal failure: morphological and physiological correlations.

Elevated serum gastrin (SG) has been reported in chronic renal failure (CRF). We studied SG levels in relation to various humoral and gastroduodenal histopathologic findings in 20 controls, 12 uremics under conservative therapy (CT), 27 patients on regular dialysis (RDT) and 8 transplanted patients (Tx). SG and parathyroid hormone (PTH) levels were estimated by radioimmunoassay (RIA), in addition serum BUN, creatinine, Ca++PO4---and alkaline phosphatase (predialysis in RDT) were determined. 20 patients (12 on CT and 8 on RDT) underwent pentagastrin (PG) stimulation test and upper gastrointestinal endoscopy with biopsy of gastric and duodenal mucosa. The mucosal samples were stained for mucopolysaccharides (MPS), nucleic acid (NA) and alkaline phosphatase (AP), and divided into intense, normal or faint staining. Mean SG was 688.71 pg/ml (CT cases), 636.2 pg/ml (RDT cases) and 280.6 pg/ml (Tx cases), all values being significantly higher than controls (118.46 pg/ml). SG level had a linear correlation with serum creatinine in CT patients and predialysis creatinine in RDT patients, but not with other parameters studied (BUN, Ca++,PTH,PO4---AP). The incidence of gastroduodenal erosions (40%) had a significant negative correlation with SG. They were more frequent with normal MPS stain (p = 0.01) and NA staining (p less than 0.001) than faint staining of gastric mucosa biopsy. The acid response to PG stimulation was inversely correlated with SG. We believe that elevated SG is compensatory to a decreased response of the gastroduodenal mucosa to PG. Mere retention of SG does not explain its elevation as its correlation with serum creatinine existed not only in patients on CT, but also in RDT patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaline Phosphatase↗
PubMed1984

Immunofluorescent analysis of renal biopsies in uncomplicated Schistosoma haematobium infections in children.

Renal biopsies were studied by light and immunofluorescent microscopy in 13 young individuals with uncomplicated Schistosoma haematobium infections. Slight mesangial cell proliferation and matrix increase were found in three biopsies and focal interstitial inflammatory infiltrates were noted in six. However extensive IgG (nine cases) and IgM (seven cases) granular deposits were found in the mesangial areas. C3 was found in only three of these cases. Clq, fibrinogen, IgA and IgE were not found deposited except for one case with IgE. Schistosome antigen was identified in mesangial areas in four biopsies after acid treatment of the sections. It appears the immune complexes are deposited consistently in the renal glomeruli in S. haematobium infections but their role in inducing clinical renal disease is minimal.

Biopsy↗