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Biomedical subjects

M Ayub

Publications and source records attributed to M Ayub.

12 recordsLinked to original sources
PubMed1992

TGF-beta stimulation of endometrial and breast-cancer cell growth.

Growth of the human endometrial carcinoma Ishikawa cell line was stimulated by transforming growth factor-beta1 when cultured in serum-containing and chemically defined culture medium. This response was not unique to endometrial carcinoma cells, as the breast-cancer cell line, T47-D, was similarly stimulated by TGF-beta 1. TGF-beta 1 stimulated growth of MCF-7 breast-cancer cells in chemically defined medium but inhibited growth of this cell line in serum-containing medium. The data provide a demonstration of a positive growth response to TGF-beta 1 in oestrogen-receptor-positive cells and do not support the hypothesis that this growth factor is simply a negative growth regulator in epithelial-cancer cell lines.

Adenocarcinoma↗
PubMed1991

An investigation of 'functional' somatic symptoms among patients attending hospital medical clinics in Pakistan--I. Characteristics of 'non-organic' patients.

Six hundred medical clinic attenders at the Mayo Hospital, Lahore, Pakistan, were screened using the Bradford Somatic Inventory (BSI) in Urdu. The physicians' clinical diagnosis was recorded. The characteristics of mood-disordered, functional and no-diagnosis groups were compared with patients receiving organic diagnoses. Of the non-organic patients, only the mood-disordered group reported significantly more BSI symptoms than the organic group. The functional group did not have especially high scores. All groups reported a greater mean number of BSI symptoms than a student comparison group. Among the non-organic patients, there was no relationship between the number of BSI symptoms reported and sex, age, education or occupational group.

Adult↗
PubMed1991

An investigation of 'functional' somatic symptoms among patients attending hospital medical clinics in Pakistan--II. Using somatic symptoms to identify patients with psychiatric disorders.

Among 600 medical clinic attenders in Lahore, Pakistan, screened using the Bradford Somatic Inventory in Urdu, significant differences in symptom endorsement between 'organic' and 'mood-disordered' patients were found in 14 BSI items. Counting only those symptoms reported as present on more than 15 days during the previous month, significant differences in symptom endorsement were found in 21 BSI items. Another 60 patients attending the same clinics were recruited to evaluate the BSI as a screening questionnaire for mood disorders. Each patient was interviewed by a psychiatrist and a diagnosis made according to DSM III-R and ICD-9. Optimal cutting points for the 14-item, 21-item and 44-item BSI were determined by Relative Operating Characteristic (ROC) analysis. The areas under the fitted ROC curves (an index of discriminating efficiency) were similar for the three versions. Using a cut-off score of 13/14, the BSI-21 identified DSM III-R psychiatric disorders with an estimated sensitivity of 75% and specificity of 75%. Assuming a 30% prevalence in medical clinics, a positive value of around 60% can be expected when screening for psychiatric disorders.

Adult↗
PubMed1990

The inhibition of human prostatic aromatase activity by imidazole drugs including ketoconazole and 4-hydroxyandrostenedione.

Ketoconazole, an orally active imidazole drug and bifonazole, clotrimazole, econazole, isoconazole, miconazole and tioconazole are known as inhibitors of cytochrome P450 dependent steroidogenic enzymes including human placental aromatase. The aim of the present study was to investigate the effectiveness of these imidazole drugs to inhibit human prostatic aromatase activity compared with the known inhibitor of aromatase 4-hydroxyandrostenedione (4-OHA). The imidazole drugs and 4-OHA inhibited prostatic aromatase activity in a dose-dependent manner. The order of decreasing inhibitory potency determined from IC50 values (mumol/L) was: 4-OHA (1.57) greater than bifonazole (1.6) greater than tioconazole (1.69) greater than clotrimazole (1.73) greater than econazole (1.87) greater than miconazole (2.0) greater than isoconazole (2.2) greater than ketoconazole (4.7). The IC50 values for the inhibition of prostatic homogenate aromatase activity are 3-9-fold higher than that for the inhibition of human placental aromatase activity, previously reported, except that of ketoconazole which was 1.5-fold lower than that for the inhibition of placental microsomal aromatase.

Androstenedione↗
PubMed1990

Fatty acid control of growth of human cervical and endometrial cancer cells.

Stearic acid and iodo-stearic and inhibited cell growth in a cervical cancer cell line (HOG-1) in a dose-related manner, with a half maximal effect at 50 microM stearic acid. Addition of oleic acid abrogated the effect of stearic acid. EGF-stimulated DNA synthesis and growth of HOG-1 cells was inhibited in the presence of stearic acid without any apparent effect on EGF receptor number or affinity.

Cell Division↗
PubMed1990

Suppression of plasma androgens by the antiandrogen flutamide in prostatic cancer patients treated with Zoladex, a GnRH analogue.

Chronic treatment with the GnRH (gonadotrophin hormone releasing hormone) agonist Zoladex causes suppression of testicular androgens. Use of antiandrogens has been advocated to block the effects of the initial surge of androgens, and to block any presumed effects of adrenal androgens. We have measured plasma concentrations of androgens and possible precursors before and during treatment in the following prostate cancer patients: 10 who received Zoladex alone (Z), nine who received Zoladex + the anti-androgen flutamide (Z + F) and five who were orchidectomized (O). Testosterone fell in the Z + F group to 0.84 +/- 0.21 nmol/l (mean +/- SD) significantly lower (Wilcoxon P less than 0.05) than after Z (1.58 +/- 1.84 nmol/l) alone. Progesterone and 17 alpha-hydryxyprogesterone did not change significantly in any group. Androstenedione and dehydroepiandrosterone sulphate (DHAS) showed significant falls in Z + F (from 3.44 +/- 0.34 to 1.92 +/- 0.18 mumol/l and from 3.88 +/- 0.64 to 1.92 +/- 0.36 mumol/l respectively) but not in other groups. These results are consistent with our demonstration of an inhibitory effect of flutamide, hydroxyflutamide and other antiandrogens on human adrenal microsomal 17 alpha-hydroxylase and 17,20-lyase activities in vitro.

17-alpha-Hydroxyprogesterone↗
PubMed1990

Absence of specific cell-surface binding of tissue plasminogen activator in uterine cells.

Tissue plasminogen activator (tPA), an arginine-specific serine protease, is an oestrogen-regulated protein in uterine and breast cancer tissue. It contains a domain which shares homology with epidermal growth factor (EGF). The aim of the present study was to determine whether specific tPA receptors or EGF receptors mediate the binding of tPA to cells and whether tPA possesses intrinsic mitogenic activity. The binding of 125I-labelled tPA to rat uterine and liver membranes was shown to be non-specific and could not be displaced by unlabelled tPA or EGF. Furthermore, acid washing of cell membranes did not unmask specific tPA-binding sites. In contrast, 125I-labelled EGF binding to both rat uterine and liver membranes was displaced in a dose-dependent manner by unlabelled EGF, and Scatchard analysis of the binding data revealed dissociation constant (Kd) values of 2.4 and 0.71 nM respectively. Unlabelled tPA (up to 20,000-fold excess) did not displace 125I-labelled EGF binding to these membranes. A study of the binding of 125I-labelled tPA and 125I-labelled EGF to endometrial carcinoma cells (Ishikawa), cervical carcinoma cells (HOG-1) and vulval carcinoma cells (A431) showed that up to a 100-fold excess of EGF or a 1000-fold excess of tPA did not displace 125I-labelled tPA binding to these cells. In contrast, 125I-labelled EGF binding was displaced by unlabelled EGF (Kd values for Ishikawa and HOG-1 cells were 2.72 and 1.92 nM respectively) but not by unlabelled tPA (1000-fold excess).(ABSTRACT TRUNCATED AT 250 WORDS)

Acids↗
PubMed1979

Evidence for a thyrotropin inhibitory effect of histamine in man.

Because of certain side effects of cimetidine therapy which may be hormonally mediated (e.g. gynecomastia), there has been recent interest in the possible endocrine effects of this H2 histamine receptor-blocking agent used in the treatment of peptic ulcer disease. Accordingly, the effect of chronic cimetidine therapy on anterior pituitary function was examined in 12 adult men with mild peptic ulcer disease. TRH and insulin-hypolycemic stimulation tests were performed by standard methods. Serum for TSH and PRL RIA was obtained after TRH; serum for GH, cortisol, and PRL RIA was obtained after insulin-induced hypoglycemia. In addition, serum for LH, FSH, testosterone, and PRL was obtained every 4 h for 24 h. After these baseline studies, 300 mg cimetidine were administered orally 4 times a day for 4--8 weeks and the studies were repeated as before. Chronic treatment with cimetidine caused a significant increase in the peak TSH response to TRH at 30 min (mean peak TSH value before cimetidine, 7.0 microU/ml; after cimetidine, 10.2 microU/ml; P less than 0.05) as well as a significant increase in the TSH area under the curve. There was no statistically significant effect of cimetidine on basal TSH or basal or stimulated PRL secretion. Cimetidine had no effect on the GH, PRL, or cortisol response to insulin-induced hypolycemia or the 24-h secretion of LH, FSH, testosterone, or PRL.

Adult↗
PubMedDate not supplied

Diet therapy in severe clinical expression of debrancher deficiency.

An eleven year old boy was referred because of sudden loss of consciousness, muscular weakness, poor general health, severe hypoglycemia with seizures and hepatomegaly. Response to oral glucose and galactose increased blood lactic acid and glucose at different times. Fasting values of blood lactic was normal, but glucose was found at 33 mg/dl. Similar test made up two hours after feeding revealed hyperlactatemia (35-50 mg/dL) and hyperglycemia (129 mg/dL). Glucagon did not result in a rise of glucose at fasting or feeding. Hepatic glycogen content was found 15 gm/100 mg of tissue. The enzyme activities revealed a deficiency of the liver debranching enzyme while leukocytes had normal enzyme activity. Hepatic biopsy showed liver fibrosis. The present case had the clinical characteristics of severe form of glycogen storage disease. A low carbohydrate and high protein diet was indicated in order to increase the gluconeogenic precursors. Although debranching enzyme deficiency is almost always benign a high carbohydrate diet induced a more severe expression of the disease.

Child↗