Volatile organic compounds (VOCs) in honey are obtained from diverse biosynthetic pathways and extracted by using various methods associated with varying degrees of selectivity and effectiveness. These compounds are grouped into chemical categories such as aldehyde, ketone, acid, alcohol, hydrocarbon, norisoprenoids, terpenes and benzene compounds and their derivatives, furan and pyran derivatives. They represent a fingerprint of a specific honey and therefore could be used to differentiate between monofloral honeys from different floral sources, thus providing valuable information concerning the honey’s botanical and geographical origin. However, only plant derived compounds and their metabolites (terpenes, norisoprenoids and benzene compounds and their derivatives) must be employed to discriminate among floral origins of honey. Notwithstanding, many authors have reported different floral markers for honey of the same floral origin, consequently sensory analysis, in conjunction with analysis of VOCs could help to clear this ambiguity. Furthermore, VOCs influence honey’s aroma described as sweet, citrus, floral, almond, rancid, etc. Clearly, the contribution of a volatile compound to honey aroma is determined by its odor activity value. Elucidation of the aroma compounds along with floral origins of a particular honey can help to standardize its quality and avoid fraudulent labeling of the product. Although only present in low concentrations, VOCS could contribute to biomedical activities of honey, especially the antioxidant effect due to their natural radical scavenging potential.

The 'intestinal' form of gastric cancer, which is the commonest type, develops against a background of chronic gastritis, atrophy, and intestinal metaplasia.1 2 Helicobacter pylori is the cause of (type B) chronic gastritis and has been shown in epidemiological studies to be a major risk factor for the development of gastric cancer.3-6 Increased mucosal cell proliferation increases the likelihood of the development of a neoplastic clone of epithelial cells7 where there is chronic epithelial injury associated with H pylori positive gastritis. However, little is known about cell proliferation in H pyloni associated gastritis. The aims of the study were, firstly, to compare antral mucosal cell proliferation in normal gastric mucosa with H pylori positive and negative chronic gastritis and, secondly, to determine the effect of H pylori eradication treatment on cell proliferation. MethodsPatients undergoing routine diagnostic endoscopy were recruited after informed consent. Those taking non-steroidal anti-inflammatory drugs, H2 antagonists, proton pump inhibitors, or bismuth salts, or those who had undergone gastric surgery, were excluded from the study. Using standard biopsy forceps, tissue specimens were taken from the gastric antrum (three) and corpus (two) for histological and immunohistochemical studies. The study was approved by the hospital ethical committee. HISTOLOGYTwo antral and two corpus biopsy specimens from each site were routinely processed, and stained with haematoxylin and eosin.H PYLORI H pylori status was determined using a modified Giemsa stain on the antral and corpus sections and a biopsy urease test (CLO/DeltaWest) on the third antral biopsy specimen. To establish eradication of the micro-organism, both tests had to be negative. IMMUNOHISTOCHEMISTRYTwo antral biopsy specimens for immunostaining were put immediately into RPMI (without L-Glutamine) (Gibco) containing bromodeoxyuridine (5 mg/10 ml). They were immersed in a waterbath for 60 minutes at 37°C then placed on filter paper and fixed in 346 on 10 May 2018 by guest. Protected by copyright.

Background: Resistance of Staphylococcus aureus to commonly used antibiotics is linked to their ability to acquire and disseminate antimicrobial-resistant determinants in nature, and the marine environment may serve as a reservoir for antibiotic-resistant bacteria. This study determined the antibiotic sensitivity profile of S. aureus isolated from selected beach water and intertidal beach sand in the Eastern Cape Province of South Africa. Methods: Two hundred and forty-nine beach sand and water samples were obtained from 10 beaches from April 2015 to April 2016. Staphylococcus aureus was isolated from the samples using standard microbiological methods and subjected to susceptibility testing to 15 antibiotics. Methicillin-resistant Staphylococcus aureus (MRSA) was detected by susceptibility to oxacillin and growth on Brilliance MRSA II agar. Antibiotic resistance genes including mecA, femA rpoB, blaZ, ermB, ermA, ermC, vanA, vanB, tetK and tetM were screened. Results: Thirty isolates (12.3%) were positive for S. aureus by PCR with over 50% showing phenotypic resistance to methicillin. Resistance of S. aureus to antibiotics varied considerably with the highest resistance recorded to ampicillin and penicillin (96.7%), rifampicin and clindamycin (80%), oxacillin (73.3%) and erythromycin (70%). S. aureus revealed varying susceptibility to imipenem (96.7%), levofloxacin (86.7%), chloramphenicol (83.3%), cefoxitin (76.7%), ciprofloxacin (66.7%), gentamycin (63.3%), tetracycline and sulfamethoxazole-trimethoprim (56.7%), and vancomycin and doxycycline (50%). All 30 (100%) S. aureus isolates showed multiple antibiotic-resistant patterns (resistant to three or more antibiotics). The mecA, femA, rpoB, blaZ, ermB and tetM genes were detected in 5 (22.7%), 16 (53.3%), 11 (45.8%), 16 (55.2%), 15 (71.4%), and 8 (72.7%) isolates respectively; Conclusions: Results from this study indicate that beach water and sand from the Eastern Cape Province of South Africa may be potential reservoirs of antibiotic-resistant S. aureus which could be transmitted to exposed humans and animals.

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