A study of RUNX3, E-cadherin and ß-catenin in CagA-positive Helicobacter pylori associated chronic gastritis in Saudi patients.

OBJECTIVE: H. pylori is the most important risk factor for gastric carcinoma. CagA-positive H. pylori is associated with an increased risk for gastric cancer compared with negative strains. RUNX3 is a tumor suppressor gene, which is related to the genesis of gastric cancer. ß-catenin is integrated with E-cadherin in the cell membrane, and aberrant expression of the complex was reported in gastric carcinoma. Aim of this paper is to determine of the relation between RUNX3, E-cadherin and ß-catenin in chronic gastritis associated with cagA-positive H. pylori infection. PATIENTS AND METHODS: Retrospective study was done on formalin fixed paraffin embedded gastric biopsies blocks of 90 patients diagnosed as H. pylori associated chronic gastritis. H. pylori was detected using modified Giemsa stain. Nested PCR was used for detection of cagA, reverse transcription-PCR for detection of RUNX3 and immunohistochemistry for detection of E-cadherin and ß-catenin. RESULTS: Fifty percent of cases were found to be cagA positive. CagA was significantly associated with the intensity of mononuclear inflammation, the intensity of neutrophilic inflammation, the degree of mucosal atrophy and loss of RUNX3 but not with the density of H. pylori, intestinal metaplasia, E-cadherin or ß-catenin. There was significant relation between loss of RUNX3 and increasing density of H. pylori, intensity of neutrophilic inflammation, mucosal atrophy and intestinal metaplasia. RUNX3 was found to be significantly correlated with E-cadherin but not with ß-catenin. E-cadherin showed decreased expression in 36.7% of biopsies while, ß-catenin was decreased in 33% of biopsies. CONCLUSIONS: Loss of RUNX3, E-cadherin and ß-catenin was considered early events in the cascade of gastric carcinoma development. Loss of RUNX3 but neither E-cadherin nor ß-catenin was related to cagA positive H. pylori strains.

Epidemiological investigation of nosocomial infection with multidrug-resistant Acinetobacter baumannii.

BACKGROUND: Multidrug resistant Acinetobacter baumannii, (MRAB) is an important cause of hospital acquired infection. AIM: To document the emergence of MRAB in an Intensive Care Unit (ICU); and to characterize its hospital-wide outbreak by investigating antibiotypes and genotypes. MATERIALS AND METHODS: A six-month prospective study for the presence of MRAB infection or colonization on inpatients, health care workers and environmental sites was done at an ICU in Fahd Hospital, Saudi Arabia. For all the collected specimens, microbiological analysis and antimicrobial susceptibility testing using an automated system (Phoenix, Becton Dickinson, USA) were performed. Pulsed-Field Gel Electrophoresis (PFGE) analysis was done to determine the clonal relationship between isolates. RESULTS: A total 18 MRAB were isolated from 12 patients and 3 environmental samples. The risk factors for the acquisition of infection were age less than 60 years, mechanical ventilation, surgical interference and co-morbidity. Five PFGE profiles; pulsotype A to E, were identified. Pulsotype C isolates were further separated into 5 subtypes with predominance of subtype C3. CONCLUSIONS: The study revealed a causal link between the contaminated ventilator and the subsequent MRAB. A correct antibiotic strategy should be addressed; and strict compliance with basic and potential control measures for the containment of infection should be achieved.

Anti-inflammatory effects of the chloroform extract of Pulicaria guestii ameliorated the neutrophil infiltration and nitric oxide generation in rats.

Pulicaria guestii Rech.f. & Rawi is a fragrant, perennial herb, which grows wild, west of Al-Madinah, Saudi Arabia. Several reports were published on the anti-inflammatory activity of the sesquiterpene lactones, phenolics and flavonoids, which constitute the main active constituents of the members of the genus Pulicaria. The present study was designed to explore the potential anti-inflammatory effect of P. guestii in several experimental models. The methanol extract of the dried aerial parts of P. guestii was extracted with petroleum ether, chloroform and n-butanol. The chloroform extract was analysed on TLC and examined under UV and visible light in presence of AlCl(3) spray. The free radical scavenging activity and the total phenolic content in the CHCl(3) extract were estimated. The crude methanol extract and the CHCl(3) fraction were examined against carrageenin-induced paw edema and ear edema induced by croton oil application. The crude methanolic extract significantly reduced carrageenin-induced rat paw edema. After fractionation, the chloroform fraction caused significant reduction in carrageenin-induced rat paw edema in addition to diminishing prostaglandin E(2) (PGE(2)) in the inflammatory exudates. Topical application of chloroform fraction significantly reduced rat ear edema induced by croton oil application. In the same model, chloroform fraction reduced neutrophil infiltration, as indicated by the significant decrease in myeloperoxidase activity, and ameliorated histopathological changes induced by croton oil application. In lipopolysaccharide-induced inflammation in rat air pouch, chloroform fraction significantly reduced the nitric oxide level and tumor necrosis factor-α release. In conclusion, the chloroform fraction of P. guestii extract possesses anti-inflammatory activity in several experimental models. Further investigations are needed to identify the active constituents responsible for this anti-inflammatory activity.

Nasal carriage and antibiotic resistance of Staphylococcus aureus isolates from hospital and non-hospital personnel in Abha, Saudi Arabia.

The prevalence of nasal carriage of Staphylococcus aureus, antibiograms and prevalence of methicillin-resistant S. aureus (MRSA) were studied in 1999 among healthy hospital and non-hospital personnel in Abha, Saudi Arabia. S. aureus was isolated from 26.1% of 299 adults in the community and 25.4% of 279 hospital personnel. No isolate was resistant to vancomycin. Antibiotic resistance rates, for all other antibiotics tested except cephalothin, were significantly higher for strains from hospital personnel (P values < 0.001-0.04) compared to non-hospital adults. The antibiograms were also compared with those of 140 clinical isolates. The rates of resistance of the inpatient strains to all the antibiotics tested were significantly higher than those of hospital nasal carrier strains (P < 0.001-0.05). MRSA was isolated, respectively, from 5.1% and 18.3% of non-hospital and hospital carriers; MRSA carriage rates were 1.3% and 4.7%, respectively, for non-hospital and hospital carriers, and 61% of S. aureus isolates from infected patients were MRSA. Only 8% of non-hospital but 44% of hospital carrier strains were multiply resistant (P < 0.001). Multiple resistance among inpatient strains (89%) was significantly higher than that among hospital nasal strains (44%) (P < 0.001). Such rates of multiple resistance and endemic MRSA prevalence among healthy carriers (11%) at a much higher rate than those reported in the literature should raise concern in a region with unrestricted availability of antibiotics.