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6 result(s) for "Abd El-Kader, Nour M."
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Detection of Cryptosporidium parvum and Cryptosporidium hominis in human patients in Cairo, Egypt
Cryptosporidium is a significant cause of diarrheal disease in developing and industrialized nations. Cryptosporidium hominis and Cryptosporidium parvum are the main agents of cryptosporidiosis in humans. In Egypt, very little is known about genetic structure of Cryptosporidium spp. Therefore, this study was designed to examine samples from sporadic cases of cryptosporidiosis in Egyptians in order to identify the species involved in infection as well as the transmission dynamics and distribution of the parasite in the Great Cairo area. A total of 391 human faecal samples were collected, between May 2008 and March 2009, from ten public hospitals in Great Cairo. Initial screening by immunochromatographic detection kit “the Stick Crypto-Giardia; Operon” showed 23 possible positive cases. Twenty of them were confirmed by microscopic examination. PCR was performed by amplification of the oocyst wall protein (COWP) gene where 18 out of 23 samples were positive, one not detected by microscopy. Cryptosporidium genotyping was performed by RFLP analysis of PCR products of the diagnosis PCR. Only 15 samples rendered a digestion pattern. The genotyping distribution was nine cases showing C. hominis genotype, three showing C. parvum genotype and three showing mixed infection by C. hominis and C. parvum. The data showed an elevated prevalence of C. hominis (80.0%), the most anthroponotic species, suggesting a human–human transmission. Furthermore, the presence of up to 40% of samples infected with C. parvum shows that further investigations are required to determine the subgenotypes of C. parvum to clarify the mode of transmission in order to improve the control measures.
Molecular diagnosis of Entamoeba spp. versus microscopy in the Great Cairo
Amoebiasis is a human disease produced by Entamoeba histolytica which causes widespread mortality and morbidity worldwide through diarrheal disease and abscess establishment in parenchymal tissues such as liver, lung, and brain. The true prevalence of infection is unknown for most areas of the world due to the difficulty to characterise Entamoeba histolytica versus other non-pathogenic amoebas with identical morphology, as E ntamoeba dispar , and E ntamoeba moshkovskii . To overcome microscopy misidentification issues, we tested a nested multiplex polymerase chain reaction (PCR) and a real-time PCR on 194 stool samples collected from incoming dysentery patients in Cairo hospitals diagnosed with E. histolytica by microscopy. Nested PCR showed only 20 (10.3%) samples positive to E. histolytica and 17 (8.7%) to E. dispar . The real-time PCR detected only 19 and 11 samples positive to E. histolytica and E. dispar respectively, showing less sensitivity than the nested PCR. The data show that prevalence of E. histolytica in Cairo is lower when specific diagnosis methods are used instead of traditional microscopy, allowing to differentiate between morphologically identical human amoebas species.
Hepatic restorative potential of Portulaca oleracea ethanolic extract and/or metformin in type II diabetes mellitus model induced by high-fat diet and STZ
Background The risk of liver injury is increased by persistent hyperglycemia. Diabetes-related liver damage involves both oxidative stress and an abnormal inflammatory response. Nevertheless, many plants possess notable pharmaceutical properties, such as Portulaca oleracea (purslane, PE), which stands out for its wide range of potential medicinal applications globally. Consequently, this research sought to investigate the possibilities of purslane ethanolic extract in protecting against liver damage, oxidative stress, and the inflammatory response associated with diabetes. Methods Diabetes was induced in rats through a high-fat diet, followed by a single intraperitoneal injection of 35 mg/kg of streptozotocin (STZ). The diabetic rats were treated with PE at dose of (100 mg/kg), metformin (MT) at dose of (100 mg/kg) or combination therapy of (50 mg/kg) PE plus (50 mg/kg) MT for 4 weeks. Prooxidants (TBARS, XO, and NO) levels, antioxidant enzymes activity (SOD and GPx), inflammatory markers (TNF-α, IL-1β, and IFN-γ), and hepatic architecture abnormalities were measured by using standardized protocols. Results Rats treated with STZ exhibited notable elevations in tissue prooxidants (TBARS, XO, and NO), and inflammatory markers (TNF-α, IL-1β, and IFN-γ), with a parallel reduction in the activity of tissue antioxidants (SOD and GPx). Severe histopathological include vacuolated hepatocytes, dilated congested central veins, and numerous apoptotic signs, in addition to histochemical alterations in the liver tissue, were noted. When diabetic animals were treated with MT, PE ethanolic extract, or a combination of MT plus PE, these deleterious effects were improved. Conclusion All together the obtained data confirmed that PE displayed an ameliorating effect against the liver damage, inflammatory response, and oxidative damage linked to diabetic mellitus.
Levels of monochloropropane-diol and glycidyl esters in heated palm oil and assessment of their risk in the animal model
3-monochloropropane-1,2-diol esters (3-MCPD-Es) , 2-monochloropropane-1,3-diol esters (2-MCPD-Es), and glycidyl esters (G-Es) are heat-induced pollutants that formed during the vegetable oil refining process. The current study investigated the effects of heated palm oil containing measured amounts of MCPD-Es and G-Es on rats' lipid profile, liver and kidney functions. Using gas chromatography-mass spectrometry, 3-MCPD-Es, 2-MCPD-Es, and G-Es concentrations in heated palm oil were determined at various intervals. Forty healthy male Sprague–Dawley rats (200–250 g) were divided into four groups (I to IV). Group I was fed a regular diet (negative control). Groups II, III and IV were fed a regular diet fortified with 15% (w/w) of unheated palm oil, palm oil heated at 200 °C for 15 min, and palm oil heated at 200 °C for 30 min, respectively, for 8 weeks. The rats were fed an ordinary diet with nutritional pellets and given water ad libitum. The animal groups were sacrificed, blood samples taken, and the tissues stained with hematoxylin and eosin. The results showed that 3-MCPD-Es, 2-MCPD-Es and G-Es in heated palm oil were 5.4, 3.3 and 2.1 mg kg −1 oil, respectively, and formed at the mildest tested conditions (200 °C, 30 min). Palm oil heated at 200 °C for 30 min increased liver enzymes (alanine transaminase, aspartate transaminase, and alkaline phosphatase), serum kidney functions (uric acid, urea, and creatinine) and lipid profile (plasma cholesterol, plasma triglycerides, LDL-cholesterol, and VLDL-cholesterol) while decreasing HDL-cholesterol compared to rats fed a regular diet. Histological changes occurred in the liver and kidney of rats. It could be concluded that levels of MCPD-Es and G-Es in heated palm oil may pose a potential risk to the health of consumers and need to be constantly monitored.