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| 1 | p16 promoter hypermethylation:A useful serum marker for early detection of gastric cancer显示文摘AIM: To determine p16 promoter hypermethylation in gastric tumoral tissue and serum samples, its impact on p16-protein expression, and correlation with clinical and histological features. METHODS: Samples were obtained from 52 histologically confirmed cases of gastric adenocarcinoma. Gastric tissue and serum of 50 age- and sex-matched individuals with normal gastroscopy and biopsy were obtained as control samples. Methylation-specific polymerase chain reaction (MSP) was used to evaluate methylation status of p16 promoter. p16-protein expression was analyzed by immunohistochemical staining on paraffin-embedded sections. RESULTS: Methylation was detected in 44.2% (23/52) of tumoral tissues. 60.9% of them were also methylated in serum, i.e., 26.9% of all patients (14/52). Methylation was not detected in tissue and sera of control samples. p16-protein expression was decreased in 61.5% of cases (32/52), and was significantly associated with promoter hypermethylation (P < 0.001). Methylation was significantly more frequent in higher pathological grades (P < 0.05). Methylation was not associated with other clinicopathological features and environmental factors including H pylori infection and smoking. CONCLUSION: p16 promoter hypermethylation is an important event in gastric carcinogenesis. It is the principle mechanism of p16 gene silencing. It is related to malignant tumor behavior. Detection of DNA methylation in serum may be a biomarker for early detection of gastric cancer. | Mohammad Reza Abbaszadegan Omeed Moaven Hamid Reza Sima Kamran Ghafarzadegan Azadeh A'rabi Mohammad Naser Forghani Hamid Reza Raziee Ali Mashhadinejad Mostafa Jafarzadeh Ehsan Esmaili-Shandiz Ezzat Dadkhah | 2008 | World Journal of Gastroenterology2008，14，13： | 50 |
| 2 | Mycobacterium avium subspecies paratuberculosis causes Crohn's disease in some inflammatory bowel disease patients显示文摘Crohn’s disease(CD)is a chronic inflammatory condition that plagues millions all over the world.This debilitating bowel disease can start in early childhood and continue into late adulthood.Signs and symptoms are usually many and multiple tests are often required for the diagnosis and confirmation of this disease.However,little is still understood about the cause(s)of CD.As a result,several theories have been proposed over the years.One theory in particular is that Mycobacterium avium subspecies paratuberculosis(MAP)is intimately linked to the etiology of CD.This fastidious bacterium also known to cause Johne’s disease in cattle has infected the intestines of animals for years.It is believed that due to the thick,waxy cell wall of MAP it is able to survive the process of pasteurization as well as chemical processes seen in irrigation purification systems.Subsequently meat,dairy products and water serve as key vehicles in the transmission of MAP infection to humans(from farm to fork)who have a genetic predisposition,thus leading to the development of CD.The challenges faced in culturing this bacterium from CD are many.Examples include its extreme slow growth,lack of cell wall,low abundance,and its mycobactin dependency.In this review article,data from 60 studies showing the detection and isolation of MAP by PCR and culture techniques have been reviewed.Although this review may not be 100%comprehensive of all studies,clearly the majority of the studies overwhelmingly and definitively support the role of MAP in at least30%-50%of CD patients.It is very possible that lack of detection of MAP from some CD patients may be due to the absence of MAP role in these patients.The latter statement is conditional on utilization of methodology appropriate for detection of human MAP strains.Ultimately,stratification of CD and inflammatory bowel disease patients for the presence or absence of MAP is necessary for appropriate and effective treatment which may lead to a cure. | Saleh A Naser Sudesh R Sagramsingh Abed S Naser Saisathya Thanigachalam | 2014 | World Journal of Gastroenterology2014，20，23： | 9 |
| 3 | Role of ATG16L,NOD2 and IL23R in Crohn's disease pathogenesis显示文摘Inflammatory bowel disease is a group of diseases that includes Crohn's disease (CD) and ulcerative colitis.CD is characterized as a chronic inflammatory disease of the gastrointestinal tract,ranging from the mouth to the anus.Although there are gross pathological and histological similarities between CD and Johne's disease of cattle,the cause of CD remains controversial.It is vital to understand fully the cause of this disease because it affects approximately 500 000 people in North America and Europe.It ranges from 27 to 48 cases per 100 000 people.There are many theories on the cause of CD ranging from possible association with environmental factors including microorganisms to imbalance in the intestinal normal flora of the patients.Regardless of the environmental trigger,there is strong evidence that a genetic disposition is a major key in acquiring CD.Many studies have proven the link between mutations in the ATG16L,NOD2/CARD15,IBD5,CTLA4,TNFSF15 and IL23R genes,and CD.The purpose of this review is to examine all genetic aspects and theories of CD,including up to date multiple population studies performed worldwide. | Saleh A Naser Melissa Arce Anam Khaja Marlene Fernandez Najih Naser Sammer Elwasila Saisathya Thanigachalam | 2012 | World Journal of Gastroenterology2012，18，5： | 5 |
| 4 | Systematic review and meta-analysis on the association of tuberculosis in Crohn's disease patients treated with tumor necrosis factor-α inhibitors(Anti-TNFα)显示文摘AIM To perform a meta-analysis on the risk of developing Mycobacterium tuberculosis(TB) infection in Crohn's disease(CD) patients treated with tumor necrosis factoralpha(TNFα) inhibitors.METHODS A meta-analysis of randomized, double-blind, placebocontrolled trials of TNFα inhibitors for treatment of CD in adults was conducted. Arcsine transformation of TB incidence was performed to estimate risk difference. A novel epidemiologically-based correction(EBC) enabling inclusions of studies reporting no TB infection cases in placebo and treatment groups was developed to estimate relative odds.RESULTS Twenty-three clinical trial studies were identified, including 5669 patients. Six TB infection cases were reported across 5 studies, all from patients receiving TNFα inhibitors. Eighteen studies reported no TB infection cases in placebo and TNFα inhibitor treatment arms. TB infection risk was significantly increased among patients receiving TNFα inhibitors, with a risk difference of 0.028(95%CI: 0.0011-0.055). The odds ratio was 4.85(95%CI: 1.02-22.99) with EBC and 5.85(95%CI: 1.13-30.38) without EBC.CONCLUSION The risk of TB infection is higher among CD patients receiving TNFα inhibitors. Understanding the immunopathogenesis of CD is crucial, since using TNFα inhibitors in these patients could favor mycobacterial infections, particularly Mycobacterium avium subspecies paratuberculosis, which ultimately could worsen their clinical condition. | Brent L Cao Ahmad Qasem Robert C Sharp Latifa S Abdelli Saleh A Naser | 2018 | World Journal of Gastroenterology2018，24，25： | 4 |
| 5 | Pathophysiology of autism spectrum disorders:Revisiting gastrointestinal involvement and immune imbalance显示文摘Autism spectrum disorders(ASD)comprise a group of neurodevelopmental abnormalities that begin in early childhood and are characterized by impairment of social communication and behavioral problems including restricted interests and repetitive behaviors.Several genes have been implicated in the pathogenesis of ASD,most of them are involved in neuronal synaptogenesis.A number of environmental factors and associated conditions such as gastrointestinal(GI)abnormalities and immune imbalance have been linked to the pathophysiology of ASD.According to the March 2012 report released by United States Centers for Disease Control and Prevention,the prevalence of ASD has sharply increased during the recent years and one out of 88 children suffers now from ASD symptoms.Although there is a strong genetic base for the disease,several associated factors could have a direct link to the pathogenesis of ASD or act as modifiers of the genes thus aggravating the initial problem.Many children suffering from ASD have GI problems such as abdominal pain,chronic diarrhea,constipation,vomiting,gastroesophageal reflux,and intestinal infections.A number of studies focusing on the intestinal mucosa,its permeability,abnormal gut development,leaky gut,and other GI problem raised many questions but studies were somehow inconclusive and an expert panel of American Academy of Pediatrics has strongly recommended further investigation in these areas.GI tract has a direct connection with the immune system and an imbalanced immune response is usually seen in ASD children.Maternal infection or autoimmune diseases have been suspected.Activation of the immune system during early development may have deleterious effect on various organs including the nervous system.In this review we revisited briefly the GI and immune system abnormalities and neuropeptide imbalance and their role in the pathophysiology of ASD and discussed some future research directions. | Mohtashem Samsam Raheleh Ahangari Saleh A Naser | 2014 | World Journal of Gastroenterology2014，20，29： | 3 |
| 6 | Correlation between rpoB gene mutation in Mycobacterium avium subspecies paratuberculosis and clinical rifabutin and rifampicin resistance for treatment of Crohn’s disease显示文摘AIM: To investigate overlapping regions of the rpoB gene previously involved with rifamycin resistance in M. tuberculosis and seek correlation between rpoB mutations in clinical MAP strains with susceptibility to RIF and RFB. METHODS: We designed a molecular-based PCR method for the evaluation of rifabutin (RFB) and rifampicin (RIF) resistance based on probable determinant regions within the rpoB gene of MAP, including the 81 bp variable site located between nucleotides 1363 and 1443. The minimum inhibitory concentration (MIC) for RIF was also determined against 11 MAP isolates in attempt to seek correlation with rpoB sequences. RESULTS: We determined that MAP strain 18 had an MIC of > 30 mg/L and ≤ 5 mg/L for RIF and RFB respectively, and a significant and novel rpoB mutation C1367T, compared to an MIC of ≤ 1.0 mg/L for both drugs in the wild type MAP. The 30-fold increase in the MIC was a direct result of the rpoB mutation C1367T, which caused an amino acid change Thr456 to Ile456 in the drug’s binding site. In addition, MAP strain 185 contained five silent rpoB mutations and exhibited an MIC comparable to the wild-type. Moreover, our in vitroselected mutation in MAP strain UCF5 resulted in the generation of a new resistant strain (UCF5-RIF16r) that possessed T1442C rpoB mutation and an MIC > 30 mg/L and > 10 mg/L for RIF and RFB respectively. Sequencing of the entire rpoB gene in MAP strains UCF4, 18, and UCF5-RIF16r revealed an rpoB mutation A2284C further downstream of the 81 bp variable region in UCF4, accounting for observed slight increase in MIC. In addition, no other significant mutations were found in strains 18 and UCF-RIF16r. CONCLUSION: The data clearly illustrates that clinical and in vitro-selected MAP mutants with rpoB mutations result in resistance to RIF and RFB, and that a single amino acid change in the beta subunit may have a significant impact on RIF resistance. Unconventional drug susceptibility testing such as our molecular approach will be beneficial for evaluation of antibiotic effectiveness. This molecular approach may also serve as a model for other drugs used for treatment of MAP infections. | Daniel R Beckler Sammer Elwasila George Ghobrial John F Valentine Saleh A Naser | 2008 | World Journal of Gastroenterology2008，14，17： | 2 |
| 7 | Role of PTPN2/22 polymorphisms in pathophysiology of Crohn's disease显示文摘AIM To establish the relationship of protein tyrosine phosphatase non-receptor type 2 and 22(PTPN2/22) polymorphisms and mycobacterial infections in Crohn's disease(CD). METHODS All 133 subjects' blood samples were genotyped for nine single nucleotide polymorphisms(SNPs) in PTPN2/22 using TaqMan^(?) genotyping, while the effect of the SNPs on PTPN2/22 and IFN-γ gene expression was determined using RT-PCR. Detection of Mycobacterium avium subspecies paratuberculosis(MAP) IS900 gene was done by nPCR after DNA extraction from the isolated leukocytes of each subjects' blood samples. T-cells isolated from the patient samples were tested for response to phytohematoagglutonin(PHA) mitogen or mycobacterial antigens by Brd U proliferation assays for T-cell activity. RESULTS Out of the nine SNPs examined, subjects with either heterozygous(TC)/minor(CC) alleles in PTPN2:rs478582 occurred in 83% of CD subjects compared to 61% healthy controls(P-values < 0.05; OR = 3.03). Subjects with either heterozygous(GA)/minor(AA) alleles in PTPN22:rs2476601 occurred in 16% of CD compared to 6% healthy controls(OR = 2.7). Gene expression in PTPN2/22 in CD subjects was significantly decreased by 2 folds compared to healthy controls(P-values < 0.05). IFN-γ expression levels were found to be significantly increased by approxiately 2 folds in subjects when either heterozygous or minor alleles in PTPN2:rs478582 and/or PTPN22:rs2476601 were found(P-values < 0.05). MAP DNA was detected in 61% of CD compared to only 8% of healthy controls(P-values < 0.05, OR = 17.52), where subjects with either heterozygous or minor alleles in PTPN2:rs478582 and/or PTPN22:rs2476601 had more MAPbacteremia presence than subjects without SNPs did. T h e average T-cell proliferation in CD treated with PHA or mycobacteria antigens was, respectively, 1.3 folds and 1.5 folds higher than healthy controls without any significant SNP. CONCLUSION The data suggests that SNPs in PTPN2/22 affect the negative regulation of the immune response in CD patients, thus leading to an increase in inflammation/apoptosis and susceptibility of mycobacteria. | Robert C Sharp Shazia A Beg Saleh A Naser | 2018 | World Journal of Gastroenterology2018，24，6： | 2 |
| 8 | Stability of vertically bent pipelines buried insand 显示文摘 | Sahel N A Hamdan N A Junaid A S Ibrahim M A Naser A A | 2004 | Journal of Pressure Vessel Technology Transactions of the ASME2004，126，3： | 1 |
| 9 | Activated clotting time level with weight based heparin dosing during percutaneous coronary intervention and its de- terminant factors 显示文摘 | Majid S Naser A Bahram S | 2014 | J Cardiovasc Thorac Res2014，6，2： | 1 |
| 10 | Life cycle analysis of UK coal fired power plants显示文摘 | Naser A Timothy T | 2008 | Energy Conversion and Management2008，49，2： | 1 |
| 11 | A review of drought indices显示文摘 | Zargar A Sadiq R Naser B | 2011 | Environmental Reviews2011，，： | 1 |
| 12 | Umbilical hernia in cirrhotic patients:outcome of elective repair显示文摘 | Lasheen A Naser H M Abohassan A | 2013 | J Egypt Soc Parasitol2013，43，： | 1 |
| 13 | The effect of replacement feeding of some protein sources with pollen on honey bee population and colony performance显示文摘 | MOHAMMAD R D NASER M S ABOLFAZL A G | 2007 | Journal of Animal and Veterinary Advances2007，6，11： | 1 |
| 14 | Aerodynamics of an isolated slot-burner from a tangentially-fired boiler显示文摘 | Hart J T Naser J A Witt P J | | 0，，9： | 1 |
| 15 | Computational fluid dynamic modeling of zinc slag fuming process in top-submerged lance smelting furnace显示文摘 | HUDA N NASER J BROOKS G REUTER M A MATUSEW1CZ R W | 2012 | Metallurgical and Materials Transactions B2012，43，1： | 1 |
| 16 | The emerging panclem,e o5 o besity and diabetes: Are we doing enough to prevent a disaster? 显示文摘 | Naser KA Gruber A Thomson GA | 2006 | Int J Clin Proct2006，60，9： | 1 |
| 17 | Analysis and Design of a Multiple Feedback Loop Control Strategy for Single-Phase Voltage-Source UPS Inverters 显示文摘 | Naser M A R John E Q | 1996 | IEEE Trans on PE1996，11，4： | 1 |
| 18 | Rapid and sensitive static headspace gas chromatograthy-mass spectrometry method for the analysis of ethanol and abused inhalants in blood显示文摘 | Ahmed Hassan Al-Awadhi Zainat Naser Al-Hatali et | 2004 | Journal of chromatography b2004，799，： | 1 |
| 19 | Modeling of insulated CFRP-strengthened reinforced concrete T- beam exposed to fire 显示文摘 | Hawileh R A Naser M Zaidan W | 2009 | Engineering Structures2009，31，12： | 1 |
| 20 | Evaluation of plyometric,weight training and their combination on angular velocity显示文摘 | RAHMAN R PARVIN A NASER B | | 0，，01： | 1 |
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