Biomedical subjects

I Osman

Publications and source records attributed to I Osman.

26 records · Page 2Linked to original sources

PubMed1998

[Characteristics of development and morphology of Echinococcus granulosus of camel origin in north Xinjiang].

AIM: To study the characteristics of development and morphology of E. granulosus of camel origin in north Xinjiang. METHODS: Six dogs were infected with protoscolices and then purged with arecoline at days 35 and 45 p.i. RESULTS: Six dogs were heavily infected, the worm burden were 14,780 to 135,900 at days 35 and 45 p.i. At day 35 p.i. 77% of the had developed three segments, 10% contained mature eggs with fully developed "thickshelled" embryophores. Morphological studies revealed the following characteristics for 35-day-old worms; the mean length of the terminal segment accounted for 56% of the total worm length; the position of the sexually mature segment was always terminal (77%); the female reproductive system possessed an enlongated ovary with compact lobules; the Mehlis gland was covered by the vitelline gland and the testes were distributed throughout the segment arranging in a row posterior to the vitelline gland. CONCLUSION: The E. granulosus of camel isolate in north Xinjiang can readily be distinguished from the horse, sheep, cattle and pig strains, but is similar to the camel (Camelus dromedarius) strain distributed in North Africa.

Animals↗

PubMed1997

Chromosome 16 in primary prostate cancer: a microsatellite analysis.

Cytogenetic and molecular genetic analyses of prostate cancer specimens have revealed nonrandom chromosomal deletions, affecting chromosomes 7q, 8p, 10q and 16q. Based on these data, we designed this study to further characterize the altered region(s) on chromosome 16 by evaluating 16 microsatellite markers on a population composed of 32 paired normal and primary prostatic tumor samples. The 16 microsatellites selected mapped to 11 distinct loci on 16q and 5 loci on 16p. No alterations were identified affecting 16p. However, 16 of 31 (51%) informative cases showed molecular alterations in at least one of the loci analyzed on 16q, consisting of 18 deletions and 11 bandshifts. Moreover, most of the deletions clustered at 6 microsatellite loci, mapping to the 16q22.1-23.1 region. Our results suggest that microsatellite alterations on the long arm of chromosome 16 are frequent events in prostate cancer, and that the 16q22.1-23.1 region might harbor a tumor suppressor gene involved in prostate cancer.

Adenocarcinoma↗

PubMed1997

The effect of growth hormone replacement therapy for up to 12 months on lipoprotein composition and lipoprotein(a) in growth hormone-deficient adults.

The effect of growth hormone replacement therapy in near physiological doses on lipoprotein composition and serum lipoprotein(a) concentrations was investigated in growth hormone-deficient subjects. A randomised, double-blind, placebo-controlled trial of recombinant growth hormone was undertaken for 6 months followed by an open extension for a further 6 months (0.125 IU/kg per week for the first 4 weeks of each 6 month period and thereafter 0.25 IU/kg per week). A total of 18 patients with isolated growth hormone deficiency or hypopituitarism were studied. Lipid concentrations were estimated in lipoprotein fractions and protein concentrations were measured in low density lipoprotein (LDL). Glucose and glycated haemoglobin in blood and insulin, cholesterol, triglyceride, apolipoproteins A-I and B and lipoprotein(a) concentrations were measured in serum. In the placebo-controlled phase fasting blood glucose concentrations increased with growth hormone treatment from 5.0 +/- 0.2 to 5.8 +/- 0.2 mmol/l (P = 0.02) (mean +/- S.E.M.), although no significant changes were seen in lipids or lipoproteins. In the group receiving active treatment total serum cholesterol decreased from 6.0 +/- 0.4 to 5.2 +/- 0.3 mmol/l (P = 0.002) after 6 months, due to reduced LDL cholesterol concentrations. Low density lipoprotein protein concentrations fell (0.8 +/- 0.1 versus 0.7 +/- 0.1 g/l) (P = 0.005), and LDL phospholipid levels decreased from 0.9 +/- 0.1 to 0.7 +/- 0.1 mmol/l (P = 0.007). Serum cholesterol and LDL composition reverted to pre-treatment values by 12 months. Fasting blood glucose remained above pre-treatment values (P = 0.036) and fasting insulin was significantly increased (P = 0.044). There was no effect of growth hormone therapy on serum triglyceride, apolipoprotein or lipoprotein(a) concentrations. In conclusion, growth hormone therapy with near physiological doses has no long term effects on serum lipoprotein(a) concentrations or lipoprotein composition.

Adult↗

PubMed1997

Expression of cyclin D1, but not cyclins E and A, is related to progression in bilharzial bladder cancer.

The present study was conducted to analyze the alterations affecting cyclins D1, E, and A in bilharzial bladder cancer and to assess their potential clinical significance. A total of 125 cases were examined. Histopathological subtypes included 68 squamous cell carcinomas, 55 transitional cell carcinomas, and 2 adenocarcinomas. Immunohistochemical analyses were performed using a panel of well-characterized antibodies. The results were correlated with proliferative index, as assessed by Ki67 antigen expression. The cyclin D1-positive phenotype, defined as the identification of positive immunoreactivity in the nuclei of >/=20% of tumor cells, was found in 33 of 107 (31%) evaluable cases. A significant association was observed between the cyclin D1-positive phenotype and deep muscle invasion (P = 0.02), high tumor grade (P = 0.02), and Ki67 high proliferative index (P = 0.03). The cyclin E-positive phenotype, defined as per cyclin D1, was found in 79 of 106 (75%) evaluable cases. The cyclin A-positive phenotype, defined using the above criteria, was identified in 60 of 108 (56%) evaluable cases. No statistically significant association was found between cyclins E or A and clinicopathological parameters or proliferative index. However, there was a strong association between the expression of cyclin D1 and the coexpression of cyclins A and/or E (P = 0.05). Ki67 proliferative index was considered high when >/=20% of tumor cells displayed positive nuclear staining, a phenotype that was observed in 99 of 115 (86%) cases. These data support the hypothesis that cyclin D1 activation determines the evolution of a particular subset of aggressive bladder tumors. In addition, cyclins E and A seem to follow an unscheduled pattern of expression, based on the high frequency of identifying a positive phenotype for these cyclins and the lack of correlation between their expression and Ki67 high proliferative index. It may be postulated that the expression of G1 cyclin genes is deregulated in bilharzial bladder cancer, and that cyclin D1 acts as an oncogenic event in these neoplasms. Moreover, the moderate number of tumors displaying the cyclin D1-positive phenotype (31%) versus the high frequency observed for both cyclins E (75%) and A (56%), suggests a short G1 disbalanced by a long S phase and a rapid transversal of the cell cycle, as evidenced by a high Ki67 index observed in 86% of these cases. This imbalance in the cell cycle, together with alterations reported on the p53 pathway, might underline the accumulation of DNA damage and the aggressive clinical course of bilharzial bladder cancer.

Adenocarcinoma↗

PubMed1997

Alterations affecting the p53 control pathway in bilharzial-related bladder cancer.

Bilharzial-related bladder carcinoma (BBC) is the most common malignant neoplasm in Egypt, also occurring with a high incidence in other regions of the Middle East and East Africa. The clinical and pathological features of BBC are different than those described for the conventional transitional cell carcinoma of the bladder, including the high incidence of squamous cell carcinoma reported in BBC and the fact that over 90% of BBC cases at presentation are advanced-stage tumors (P3 and P4). This study was conducted to better define the phenotypic alterations associated with BBC affecting the p53 cell cycle control pathway, including altered patterns of expression of downstream effector proteins such as mdm2 and p21/WAF1. A well-characterized cohort of 125 patients affected with bilharzial-related bladder tumors was studied. Tumors were classified as squamous carcinomas (n = 68), transitional cell carcinomas (n = 55), or adenocarcinomas (n = 2). The products encoded by TP53, mdm2, and p21/WAF1 genes were analyzed by immunohistochemistry. Furthermore, the patterns of expression of these molecules were correlated with the Ki67 proliferative index. In addition, the microanatomical distribution of programmed cell death was assessed in a subset of tumors, using the so-called terminal deoxynucleotidyl transferase-mediated nick end labeling method. p53 nuclear overexpression was identified in 25 (20%) of 125 cases. Nuclear overexpression of mdm2 was detected in 74 (59.2%) of 125 cases. There was a statistically significant association between coexpression of both p53 and mdm2 and detection of lymph node metastases (P = 0.04). p21/WAF1 expression was detected in 87 (72%) of 121 evaluable cases. A high Ki67 proliferative index was observed in 99 (86%) of 115 evaluable cases. There was a statistically significant association between high Ki67 proliferative index and mdm2-positive phenotype (P = 0.005) and deep muscle invasion (P3b; P = 0.026) as well as lymph node metastases (P = 0.039). Apoptosis was observed in terminally differentiated tumor cells identified in the superficial layers of well-differentiated squamous carcinoma or exfoliating cells in transitional lesions. However, only rare apoptotic tumor cells were found in basal or suprabasal layers as well as in the invasive elements of the neoplasms studied. These results suggest that the frequency of p53 nuclear overexpression in BBC is lower than that reported for conventional transitional cell carcinoma. Nevertheless, tumors with p53 alterations have a greater propensity to progress. The prominent number of cases displaying an mdm2-positive phenotype suggests that this may be an early incident in BBC and should be regarded as a potential oncogenic phenomenon. This is supported by the significant correlation between high Ki67 proliferative index and mdm2 overexpression. The association of an aggressive clinical course with the coexpression of both p53 and mdm2 products might be viewed as a cooperative effect that develops in tumor progression.

Adenocarcinoma↗

PubMed1996

Mitoxantrone and cytosine arabinoside in previously untreated adult patients with acute non-lymphocytic leukemia.

Twenty-five adult patients with previously untreated acute non-lymphocytic leukemia (ANLL) were treated with mitoxantrone (Mto) 12 mg/m2 daily by 30 minutes intravenous (IV) infusion for 3 days and cytosine arabinoside (Ara-C) 200 mg/m2 daily by continuous infusion for 7 days, as an induction therapy. After complete remission (CR) was observed, they were given two more courses of consolidation therapy which was as Mto 12 mg/m2 daily by 30 minutes IV infusion for one day, and Ara-C 200 mg/m2 daily by 30 minutes IV infusion for 5 days. CR was obtained in 18 of 25 patients (72%). Median remission duration was 294 days and length of survival was 366 days. 11 patients (44%) are still in remission. Myelosupression developed in all patients following induction therapy, but it was not observed after consolidation therapies. Non-hematological side-effects consisted of nausea, vomiting, alopecia, stomatitis, and transient elevation in liver enzymes. Our therapeutic responses are similar to those obtained by others.

Adolescent↗

PubMed1995

A sensitive time-resolved immunofluorometric assay for the measurement of apolipoprotein B in cerebrospinal fluid. Application to multiple sclerosis and other neurological diseases.

Although low density lipoprotein receptors have been described on oligodendrocytes, apolipoprotein B was thought to be absent or present in only very small amounts in cerebrospinal fluid (CSF). Several immunoassays have been used for the measurement of apolipoprotein B in serum. However, the majority of methods cannot be used to measure small amounts of apolipoprotein B in CSF. In this study, we describe a highly sensitive time resolved immunofluorometric assay (TR-IFMA) using europium as label (detection limit: 0.3 microgram/l). The reliability of the TR-IFMA for the measurement of apolipoprotein B was first studied in serum. Serum and CSF apolipoprotein B concentrations were then determined in subjects free of neurological disorders and in patients with multiple sclerosis. Local intrathecal apolipoprotein B synthesis was calculated. Although the high sensitivity of the TR-IFMA allowed low amounts of apolipoprotein B in CSF to be detected (0.11 +/- 0.06; 0.12 +/- 0.06 mg/l in controls and multiple sclerosis patients, respectively), no apolipoprotein B could be detected in CSF by electroimmunodiffusion. As suggested by the blood/CSF apolipoprotein B ratio (about 6000), no apolipoprotein B synthesis was observed by both using apolipoprotein B index and formula. This indicates its probable serum origin. Moreover, there was no difference between controls and multiple sclerosis patients in CSF, serum, blood/CSF, index, and local intrathecal apoliprotein B synthesis. Finally, these results suggest that the role of apolipoprotein B in lipid transport in the central nervous system may be questionable.

Adult↗

PubMed1995

Combined immunosuppressive therapy in aplastic anaemia.

Fifteen patients with aplastic anaemia (AA) were treated combined immunosuppressive treatment (9 of them had severe, the others had less severe AA). Cyclosporin A(CsA) was given as 12 mg/kg/daily intravenous infusions for 90 days with serum levels being monitored weekly by radioimmunoassay. Antilymphocyte globulin serum (ALG) was administered by intravenous infusion through eight hours at a dosage of 20 mg/kg/daily for eight days. Methylprednisolone (MP) was given orally as 5 mg/kg/daily, tapered every three days, for 29 days. Complete remission (CR) was observed in five severe AA patients and two less severe AA patients with therapy. Partial remission (PR) was observed in one severe AA and two less severe AA patients. No remissions were reached in four patients, two of whom had severe AA, the others had less severe AA. Replace was observed in two patients as sixth and ninth month. Haemolysis occurred in one patient and MP was started. Only one patient died during the treatment because of infection due to febrile neutropaenia. Toxicities were reversible. Combined immunosuppressive treatment may be the treatment of choice for patients who are not eligible for bone marrow transplantation.

Adolescent↗