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11篇 您的检索式:作者名="SAUD K"
    题名 作者 年代 出处 被引量
1Bow-tie Diagrams in Downstream Hazard Identification and Risk Assessment显示文摘Saud Y E Israni K Goddard J 2014Process Safety Progress2014,33,1:1
2The effect of a ventilated interior courtyard on the thermal performance of a house in a hot - arid region 显示文摘A1 - Hemiddi N A Megren A1 - Saud K A 2001Renewable Energy2001,24,:1
3Emission estimates of particulate matter (PM) and trace gases (SO2, NO and NO2) from biomass fuels used in rural sector of Indo-Gangetic Plain, India 显示文摘Saud T Mandal T K Gadi R 2011Atmosphere Environment2011,45,32:1
4Modulation by astrocytes of microglial cell-mediated neuroinflammation:effect on the activation of microglial signaling pathways显示文摘Tichauer J Saud K Von Bernhardi R 2006Neuroimmunomodulation2006,14,34:1
5First Report of Black Rot of Carrots Caused by Alternaria radJcina in Michigan显示文摘Saude C Hansbeck M K 2006Plant Disease2006,90,5:1
6Syndromic congenital sensorineural deafness, microtia and micredontia resulting from a novel homoallel- ic mutation in fibroblast growth factor 3 ( FGF3 ) 显示文摘Alsmadi O Meyer B F Alkuraya F Wakil S Alkayal F A1- Saud H Ramzan K A1 - Sayed M 2009Europ J Hum Genet2009,17,:1
7Knockdown of amyloid precursor protein normalizes cholinergic function in a cell line derived from the cerebral cortex of a trisomy 16 mouse: An animal model of down syndrome显示文摘Opazo P Saud K de Saint Pierre M 2006J Neurosci Res2006,84,6:1
8First report of black rot of carrots caused by Alternaria radicina in Michigan 显示文摘Saude C Hausbeck M K 2006Plant Disease2006,90,5:1
9Knockdown of amyloid precursor protein normalizes cholinergic function in a cell line derived from tile cerebral cortex of a trisomy 16 mouse: An animal model of down syndrome 显示文摘OPAZO P SAUD K de Saint Pierre M 2006J Neurosci Res2006,84,6:1
10The expressional level of tankyrase-1 gene and its regulation in colorectal cancer in a Saudi population显示文摘Tankyrase1(TNKS1)plays an essential role in cancer progression by regulating telomere length.The study aimed to determine expression of TNKS1 and its regulation in colorectal cancer(CRC)in 20 samples from Saudi patients.mRNA expression of TNKS1 in CRC and paired normal tissues was measured by qRT-PCR.Epigenetic modification of TNKS1 promoter was determined by methylation-specific PCR while somatic mutation was analyzed by Sanger sequencing in exon 10 of the gene.All cancerous and normal tissues expressed TNKS1,but level of expression in CRC tissues was significantly associated with tumor stage though no other parameters;age,gender,and tumor location,showed any correlation.Expression of TNKS1 was markedly higher in earlier(I,II)than in later(Ⅲ,Ⅳ)stages of CRC development.Both cancerous and healthy tissues had unmethylated promoters.Sanger sequencing of exon 10 masked any somatic mutation in the samples.Our findings suggest that up-regulation of TNKS1 was inversely correlated with cancer progression in CRC,indicating that TNKS1 participates in the initiation of CRC by stabilizing telomere length in the first phase of cancer progression.Mechanisms other than TNKS1 might play a role in malignant tumor progression and telomere maintenance in the late stages of CRC.HALA ABDULAZIZ M ALWARTHAN MOHAMMAD SAUD AL ANAZI NARASIMHA RPARINE RAMESA SHAFI BHAT GHADAH ALAMRO FTOON ALJARBOU SOOAD K AL-DAIHAN 2019BIOCELL2019,43,2:0
11Gastric antisecretory and antiulcer activity of bovine hemoglobin显示文摘AIM: To investigate gastric antisecretory and gastro- protective activity of bovine hemoglobin (B-Hb) in rats. METHODS: Adult Albino-Wistar rats were divided into groups of 6 animals each. B-Hb in doses of 100, 300 and 900 mg/kg body weight was tested for gastric acid secretion and antiulcer activity. Gastric secretions were measured 6 h after pylorus ligation in rats pretreated with B-Hb. The acidity was measured by titrating gastric contents against 0.01 mol/L NaOH to pH 7. Indomethacin ulcers were produced by oral administration of 30 mg/kg bw in the rats pretreated with B-Hb one hour before indomethacin. Six hours after indomethacin stomach removed and ulcer index was recorded. Ethanol ulcer were produced by 1 mL of ethanol in the rats pretreated with B-Hb 30 min before the ethanol.One hour after ethanol stomach were cut open to score ulcers. Histological examination and analysis of gastric wall mucus, non-protein sulfhydryl groups (NP-SH), and myeloperoxidase (MPO) were carried in gastric tissue following ethanol administration. RESULTS: In control rats pylorus ligation for 6 h resulted in the accumulation of 8.1 ± 0.61 mL of gastric secretion. The treatment of the rats with 100, 300 and 900 mg/kg of B-Hb produced a significant decrease in the volume of gastric secretion 5.6 ± 0.63, 5.5 ± 0.75 and 4.7 ± 0.58 mL respectively as compared to the control group [analysis of variance (ANOVA) F = 4.77, P < 0.05]. The lesion area in the control group was found to be 22.4 ± 3.2 mm2 six hours after the administration of indomethacin. Treatment of rats with B-Hb at doses of 100 mg/kg (24.3 ± 3.29 mm2), 300 mg/kg (16.2 ± 1.45 mm2) and 900 mg/kg (12.6 ± 1.85 mm2) produced a dose dependent decreased the lesion scores (ANOVA F = 4.50, P < 0.05). The ulcer index following one hour after 1 mL ethanol was 7.1 ± 0.31. Pretreatment of rats with B-Hb at the doses of 100 mg/kg (2.5 ± 0.42), 300 mg/kg (2.1 ± 0.4) and 900 mg/kg (0.7 ± 0.21) significantly inhibited the formation of gastric lesions (ANOVA F = 63.26, P < 0.0001). Histological examination of gastric mucosa following ethanol showed significant lesions in the form of gastric pits with detachment of the surface epithelium; vacuolation of epithelial cells and elongation of microvessels. The changes were dose-dependently attenuated by B-Hb. The treatment of rats with ethanol significantly decreased the Alcian blue binding capacity of gastric wall mucus (480 ± 25.6 μg Alcian blue/g of tissue) as compared to control rats (667 ± 25.8 μg). Pretreatment of rats with B-Hb at the doses of 100 mg/kg (516 ± 31.6 μg/g), 300 mg/kg (558 ± 28.8 μg/g) and 900 mg/kg (654 ± 33.8 μg/g) significantly attenuated ethanol induced depletion of gastric wall mucus (ANOVA F = 8.05, P < 0.005). A significant and dose dependent increase of gastric mucosal NP-SH (ANOVA F = 19.62, P < 0.001) and decrease in MPO activity (ANOVA F =3.1, P < 0.05) was observed in B-Hb treated rats. CONCLUSION: B-Hb possesses significant gastric antisecretory and gastroprotective activity against experimentally induced gastric lesion. The gastroprotective effects of B-Hb are accompanied by inhibition of neutrophils activity, reduction of oxidative stress and maintenance of mucosal integrity.Abdulrahman K Al Asmari Saud Al Omani Ibrahim Elfaki Mohammad Tariq Ahmed Al Malki Saeed Al Asmary 2013World Journal of Gastroenterology2013,19,21:0
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