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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Patients who have undergone gastric resection are at higher risk of developing gastric carcinoma than normal subjects, and bile reflux is believed to play a role in carcinogenesis. An Little is known of the cell kinetics of the gastric corpus mucosa in H pylori gastritis or after gastric resection. This study aimed to measure mucosal cell proliferation in H pylori gastritis affecting the corpus and to compare this with cell proliferation in the gastric corpus after surgical resection. MethodsPatients undergoing routine diagnostic endoscopy were recruited after they had given informed consent. Those taking H2 antagonists, proton pump inhibitors, non-steroidal anti-inflammatory drugs, antibiotics, or bismuth salts were excluded from the study. At endoscopy, using standard forceps, biopsy specimens were taken from the antrum (2) and corpus (3) of the intact stomach. In patients who had undergone gastric resection, biopsy specimens (3) were taken from a point approximately 5-10 cm from the anastomosis, or 10 cm from the pylorus in the intact resected stomach, on the greater curve. Two biopsy specimens from each site were placed in 10% formalin, routinely processed, and stained with haematoxylin and eosin. A modified Giemsa stain was used to detect H pylori. The third biopsy from the corpus or gastric remnant was taken for in vitro bromodeoxyuridine labelling. Only biopsy specimens of the gastric remnant that were of body type mucosa were included in the study. The study was approved by the hospital ethics committee. BROMODEOXYURIDINE LABELLINGThe corpus/remnant biopsy specimen for immunostaining was put immediately into RPMI 1640 (without L-Glutamine) (Gibco) containing bromodeoxyuridine (5 mg/10 ml), incubated in a waterbath for 60 minutes at 370C, then placed on filter paper and fixed in formalin. Using a three step immunoperoxidase technique, sections were stained with anti-bromodeoxyuridine (DAKOPATT) antibody (1:20 dilution) for 60 minutes. Only sections that were complete and orientated were counted. For the purpose of counting, the gastric mucosa was divided into three zones: zone 1=surface and gastric pit; zone 2 = isthmus; zone 3=gland base. The number of cells to be counted was determined by counting consecutive high power fields until the continuous mean varied by less than 5%. Five hundred cells were found to be necessary.

Background The global prevalence of H. pylori approaches 50%, with prevalence rates between 20 and 40% in developed countries and up to 90% in Africa and other developing nations of the world. Development of H. pylori -associated diseases is determined by a number of virulence factors. This study aimed at determining the prevalence of H. pylori infections and virulence genes ( cag A , dup A , and vac A); the relationship between virulence factors and gastroduodenal diseases among patients. Methods Gastric biopsies were obtained from patients and cultured, DNA was extracted from cultured isolates and biopsies for PCR assay after which samples were investigated using standard laboratory procedures. Data of associated risk factors were obtained with the aid of questionnaires. Results Of the 444 participants, H. pylori was detected in 115 (25.9%) from culture analysis and 217 (48.9%) by direct PCR method. Ninety-eight (85.2%) of the culture-positive patients were also detected by PCR giving an overall prevalence of 52.7% (234/444). The highest number of H. pylori isolates 76.9% (180/234) was obtained from patients suffering from pangastritis. The Cag A virulence gene was found in 62% (145/234), dup A in 53.4% (125/234) and vac A in 90.6% (212/234). Vac A genotype s1 m1 was the most prevalent [56.4% (132)] followed by s2 m2 [11.5% (27)], s2 m1 [10.3% (24)] and [s1 m2 9.4% (22)]. There was a significant association observed in vac A s1 and peptic ulcer disease, as well as vac A s1/m2 and gastric erosion ( P < 0.05). Conclusion The study revealed a significant association between virulence genes and the development of certain forms of gastric infections while the variations in H. pylori detection and the associated risk factors investigated in the study were not significantly related. Electronic supplementary material The online version of this article (10.1186/s12876-019-0986-0) contains supplementary material, which is available to authorized users.

Helicobacter pylori is a Gram-negative, micro-aerophilic, motile, curved rod that inhabits the gastric mucosa of the human stomach. It chronically infects thousands of millions of people world-wide, and is one of the most genetically diverse of bacterial species. Infection with the bacterium leads to chronic gastritis, peptic ulceration, gastric cancers and gastric mucosa-associated lymphoid-tissue (MALT) lymphoma. The prevalence of infection appears to be partly determined by geographical and socio-demographic factors, being higher in Africa than elsewhere. Current treatment, based on potent combinations that each consist of a proton-pump inhibitor and two antibiotics, is successful in 80%-90% of patients. Some undesirable side-effects, poor patient compliance and drug resistance are, however, associated with significant levels of treatment failure and with contra-indications for some patients. Antibiotic resistance in H. pylori is a growing global concern that merits the urgent attention of public-health authorities. Numerous pieces of clinical evidence have revealed that eradication of the organism from a patient results in improvement of gastritis and drastically decreases the frequency of relapse of gastric and duodenal ulcers. Natural products, including medicinal plants and honey, may offer useful alternatives in the treatment of H. pylori-related infections.

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