Sunitinib as initial therapy in patients with locally advanced features of the primary tumor was feasible and resulted in an antitumor effect that enabled subsequent surgery in a subset of patients. Further prospective study is required to refine the most suitable application of this approach.
Human epidermal growth factor receptors (HER) play a critical role in the branching morphogenesis of renal tubules. In the current study, we analyzed the expression of HER2 in Wilms tumor and assessed the role of this gene in the tumorgenesis of Wilms tumor. During the period from 1960 to 2005, 40 patients with Wilms tumor were treated in our department. Twenty-four of those patients (except those with clear cell sarcoma of the kidney and malignant rhabdoid tumor of the kidney) were collected and assessed. The histological component of each Wilms tumor was divided into three categories (epithelial, blastemal, and mesenchymal) and the extent of HER2 protein expression was analyzed immunohistochemically. The normal kidney tissue accompanied with 12 cases of Wilms tumor was also examined. In the normal kidney, HER2 showed a strong immunoreactivity in the cell membranes of the collecting tubules and in the endothelial cells. Of 24 cases, 15 cases showed an epithelial component, while 24 cases had a blastemal component and 21 cases had a mesenchymal component, respectively. Among the 15 specimens with epithelial cell differentiation, eight (53.3%) showed HER2 immunoreactive epithelial cells. HER2 immunoreactive blastemal cells were present in 11 (45.8%) of 24 specimens with blastemal cells. On the other hand, only 3 (14.3%) of 21 specimens containing mesenchymal cells showed HER2 immunoreactivity. These results suggest that the extent of HER2 expression is associated with epithelial differentiation in Wilms tumor. These histological findings may therefore help to explain the development of Wilms tumor from the standpoint of histological differentiation.
Coronary artery ectasia (CAE) is usually considered a variant of coronary artery atherosclerosis; however, a definite link has not yet been confirmed. As not all patients with CAE are symptomatic, the real incidence is unknown. The aim of this study was to evaluate the prevalence of CAE and its clinical and angiographic characteristics as well as its relation to coronary artery calcification and any associated vascular abnormality by using multidetector computed tomography (MDCT). We prospectively enrolled 2,600 patients (mean age 55 ± 10 years) who were scheduled for computed tomography coronary angiography (CTCA). CTCA was performed using 64-MDCT with dedicated software for calcium measurement. CAE was defined as an arterial segment with a diameter of >1.5 times the diameter of the adjacent normal segment. The presence of ≥70 % diameter stenosis of any major epicardial vessel was considered an obstructive lesion. CAE was encountered in 192 (7.4 %) patients and showed gender predominance in men (88 %). Patients with CAE were more hypertensive but less diabetic. Left anterior descending artery was the most commonly affected vessel. Only 16 % of CAE patients had no atherosclerotic lesion. Coronary artery calcium score (CACS) and prevalence of ascending aorta aneurysm were shown to be significantly higher in CAE patients compared to patients having no ectasia. A significant negative correlation was noted between CACS and Markis classification. CTCA is a feasible technique to identify and evaluate morphology of CAE. The link between CACS and CAE may favor the consideration that ectasia is an advanced form of atherosclerosis.
In opposite to most countries, avian influenza virus H5N1 became endemic in Egypt. Since, its first emerge in 2006 in Egypt, the virus could infect different species of birds and animals and even human. Beside the great economic losses to the local poultry industry in Egypt, the virus infected 166 confirmed human cases, 59 cases ended fatally. In the present study, the persistence of the avian influenza in the Egyptian environment was studied. For this purpose, serum samples were collected from human, cattle, buffaloes, sheep, goat, horses, donkeys, swine, sewage rats, stray dogs and stray cats. The sera were collected from Cairo and the surrounding governorates to be examined for the presence of anti-H5N1 antibodies by Haemagglutination Inhibition Test (HI) and ELISA test. Clear differences in the seroprevalence were noticed among different species and also between the results obtained by both techniques indicating the difference in test accuracy. The present data indicate wide spread of the H5N1 virus in the Egyptian environment.
In this study, we further established the role of interleukin-1 (IL-1) alpha and IL-1 beta as regulators of proliferation of acute myeloid leukemia (AML) cells. IL-1 stimulated tritiated thymidine (3H-TdR) uptake of AML cells in 13 of 28 cases. Cytogenetic analysis confirmed the leukemic clonality of the IL-1-stimulated cells. Most likely, IL-1 exerted these stimulative effects directly on AML blast cells because IL-1 effectively induced 3H-TdR uptake of CD34-positive AML blasts (separated following cell sorting). Furthermore, adherent cell-depleted AML samples of three patients were more effectively stimulated than nondepleted AML fractions. Cluster and colony formation from adherent cell depleted AML samples could also be stimulated with IL-1, ie, in seven of ten cases analyzed. Subsequent experiments indicated that IL-1 stimulation depended on the release of GM-CSF because (1) induction of DNA synthesis of AML cells by IL-1 could be abrogated with antigranulocyte-macrophage colony-stimulating factor (GM-CSF) antibody, (2) conditioned media (CM) prepared from IL-1 stimulated AML blasts (adherent cell depleted) could stimulate the proliferation of purified normal bone marrow progenitors whereas supernatants from nonstimulated AML blasts did not, and (3) GM-CSF was demonstrated in IL-1/AML-CM with a specific radioimmunoassay, while GM-CSF was not detectable in nonstimulated supernatants. In one case of AML showing significant 3H- TdR uptake in the absence of CSFs, this spontaneous DNA synthesis was found to depend on autocrine IL-1 beta release as it could be suppressed with anti-IL-1 beta antibody or anti-GM-CSF. The blockade by anti-IL-1 beta could be overcome by the addition of high concentrations of IL-1 beta as well as GM-CSF. Thus, in this particular case, endogenously produced IL-1 beta had stimulated the release of GM-CSF which resulted in GM-CSF-dependent proliferation. The results indicate that GM-CSF production by AML blasts is often regulated by IL-1 rather than being constitutive.
By conducting a case-control study in two university hospitals, we explored the association between modifiable risk behaviours and diarrhoea. Children aged <5 years attending outpatient clinics for diarrhoea were matched by age and sex with controls. Data were collected on family demographics, socioeconomic indicators, and risk behaviour practices. Two rectal swabs and a stool specimen were collected from cases and controls. Samples were cultured for bacterial pathogens using standard techniques and tested by ELISA to detect rotavirus and Cryptosporidium spp. Four hundred cases and controls were enrolled between 2007 and 2009. The strongest independent risk factors for diarrhoea were: presence of another household member with diarrhoea [matched odds ratio (mOR) 4.9, 95% CI 2.8-8.4] in the week preceding the survey, introduction to a new kind of food (mOR 3, 95% CI 1.7-5.4), and the child being cared for outside home (mOR 2.6, 95% CI 1.3-5.2). While these risk factors are not identifiable, in some age groups more easily modifiable risk factors were identified including: having no soap for handwashing (mOR 6.3, 95% CI 1.2-33.9) for children aged 7-12 months, and pacifier use (mOR 1.9, 95% CI 1.0-3.5) in children aged 0-6 months. In total, the findings of this study suggest that community-based interventions to improve practices related to sanitation and hygiene, handwashing and food could be utilized to reduce the burden of diarrhoea in Egyptian children aged <5 years.
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