ABSTRACT
Helicobacter pylori [H .pylori] has been considered as a most important risk factor for gastric cancer by inducing chronic inflammation. CagA positive H.pylori strain is associated with higher levels of gastric inflammation, however there is no universal agreement on the link between H. pylori harboring CagA and the reportedly risk of precancerous lesions. To ascertain whether CagA positive H. pylori infection correlates with higher gastric epithelial cells oxidative DNA damage and precancerous changes. Sixty two dyspeptic patients attending for diagnostic GIT endoscopy were enrolled in this study .10 patients had normal endoscopic findings [group I], 10 cases had non ulcerative gastritis with H. pylori negative [group II], while 25 patients presented with non ulcerative gastritis were positive for H. pylori [group III], and 17 cases had ulcerative gastritis with H. pylori positive [group IV]. All involved individuals were subjected to clinical examination, abdominal ultrasonographic examination, histopathological examination of gastric mucosa and culturing of mucosal biopsies for H. pylori detection. Seroprevalence of H. pylori strains bearing the cytotoxin associated gene A [CagA] in the serum were assessed by ELISA. DNA damage in gastric epithelial cells was investigated by comet assay. H. pylori CagA was detected in 10 cases of group III and 13 cases of group IV. Gastric epithelial cells DNA damage was significantly increased in H. pylori positive groups [III, IV than H. pylori negative group II] [P< 0.001] with the highest values in group IV [P<0.001], also in CagA positive cases either in group III [P< 0.001] and group IV [P<0.001] compared to CagA negative cases with a significant correlation with more severe grade of gastric atrophy [P< 0.001] and intestinal metaplasia [P< 0.001] as precancerous lesions. CagA H. pylori strains sero-positivity was related to more advanced gastric pathology and precancerous changes with increased oxidative DNA damage in the epithelial cells which could represent as cancer prone biological context
ABSTRACT
Group A beta-hemolytic streptococcus [GABHS], which is the most common cause of pharyngeotonsilitis, is the target of most diagnostic and therapeutic strategies. Pyrogenic exotoxin B [speB] is one of the most important virulence factors of GAS as it cause destruction of host defense system proteins .Early and appropriate treatment of GABHS significantly reduces the risk of development of acute rheumatic fever which can be prevented if an early and adequate course of antibiotic is received. To evaluate the role of speB as an early genetic marker for diagnosis of S. pyogenes [GABHS] in comparison with other methods and its correlation with the post-infectious sequelae. 80 patients were included in this study, they were selected from those attending Pediatric Outpatient Clinic. They were divided into two groups: 48 patients with acute follicular tonsillitis [Group I] and 32 patients with rheumatic fever or rheumatic heart disease [Group II]. They were subjected to complete clinical examination and throat swabs were collected from each patients and tested for: Culture, Rapid antigen detection test [RADT] and for the expression of speB gene using PCR technique. GABHS were detected by culture in [50.0% and 71.88%] of group I and group II respectively, while by using RADT, were detected in [52.08% and 84.38%] of group I and group II respectively. speB gene were detected in [50% and 93.75%] of group I and group II respectively with significant deference [P<0.001]. In comparison to culture, PCR showed 97.87% sensitivity and 75.75% specificity, while RADT showed 91.48% sensitivity and 72.72% specificity. Detection of speB gene shows high sensitivity and specificity in comparison with other detection methods and can be used as an early marker for diagnosis of GABHS and predicting the post- infectious sequelae
ABSTRACT
COPD is characterized by air flow limitation that is not fully reversed and associated with an influx of neutrophils, macrophages and CD8 T lymphocytes in the airways. The disease is characterized by airflow limitation and is associated with an abnormal inflammatory response of the lungs in response to noxious particles or gases and associated with systemic manifestation. Sixty consecutive patients with COPD and 40 normal healthy individuals were included. All cases and controls were subjected to detection of 2 polymorphic loci [S1 AND Q1] of ADAM33 by PCR-RFLP technique. The percentage of S1 and Q1 AA genotype and A allele were significantly increased in control than in COPD patients while there was significant increase in S1 and Q1 GG genotype and G allele in COPD patients than in control [p < 0.001]. No significant difference was found between smoker and non-smoker among the two studied groups in genotype and alleles distribution of ADAM33 SNPs S1 and Q1 p > 0.05, whereas there was significant increase in ADAM33 S1 G allele and Q1 G allele in smoker and non-smoker in COPD patients as compared to their corresponding fellows in control group [p < 0.05]. As regard to Pulmonary function test there was significant decrease in% of FEV1 in COPD patients as compared to control group for both smokers and non-smokers [p < 0.001]. Within both control and COPD groups smokers had significant decrease in FEV1% as compared to non-smokers [p < 0.001]. There was a significant decrease in FEV1% among all genotypes in smoker as compared to non-smoker COPD patients [p < 0.001], the most prominent decrease was found in smoker GG genotype for both ADAM33 S1 and Q1 in COPD patients. In conclusion, we found that polymorphisms in the SNPs [Q1 and S1] of ADAM33 gene are associated with COPD in the general population. In addition, smoker patients with GG genotype in [S1 and Q1] ADAM33 will have more pronounced decline in the pulmonary function test [FEV1]
Subject(s)
Humans , Male , Female , Polymorphism, Genetic/genetics , Smoking/genetics , Pulmonary Disease, Chronic Obstructive/geneticsABSTRACT
Pulmonary arterial hypertension [PAH] is an important risk factor for morbidity and mortality in patients with mitral valve disease. Recent studies highlighted the possible influence of inflammatory mechanisms in several types of PAH but data about PAH in rheumatic heart disease [RHD] are lacking. The aim of this study was to investigate the circulating level of the chemokine regulated upon activation, normal T-cell expressed and secreted [RANTES] and the cytokine interleukine-6 [IL-6] in patients with rheumatic mitral valve disease associated with pulmonary hypertension. Serum'level of [RANTES] and [IL-6] were measured by enzyme-linked immunosorbent assay [ELISA] in 18 patients with mitral valve disease and 10 matched healthy subjects [control group], All patients had PAH and 7 only [38.9%] had severe pulmonary hypertension. The serum level of RANTES in the patients' group was not statistically different from that in the control group. However, patients with severe pulmonary hypertension have a mean serum level of RANTES of [6138.6 +/- 1572.5 pg/ml] that is significantly greater than that of patients without severe pulmonary hypertension [1818.2 +/- 153,6 pg/ml] [p=0.029]. On the other hand, the serum level of lL-6 in the patients was statistically different from that-of the control [378 +/- 12.7 vs. 262 +/- 28.6 respectively, p<0.005]. Comparison of IL-6 serum level in patients with and without severe pulmonary hypertension showed that the level is higher in patients with severe pulmonary hypertension but without statistical significance [410 +/- 5.77 vs. 370 +/- 15.1 pg/ml respectively p=0.71]. Clarification of the role of inflammatory mediators in the pathobiology of pulmonary hypertension in RHD is required in other studies on a wide scale. Despite of the multifactorial nature and complex mechanisms of pulmonary hypertension in RHD, RANTES and IL-6 should be investigated as potential therapeutic targets in the control of rheumatic severe pulmonary hypertension