A new approach against Helicobacter pylori using plants and its constituents: A review study.

Helicobacter pylori is a Gram-negative, spiral-shaped bacillus that colonizes 50% of the world population and is considered a class 1 carcinogen by the World Health Organization. This pathogen is the most common cause of infection-related cancers. Apart from cancer, it also causes several gastric and extra gastric diseases. Eradication of H. pylori using antibiotics is a global challenge because of its drug resistance. Alternative treatment options are gaining more attention to tackle drug-resistant H. pylori infections. Several medicinal plants and their isolated compounds have been reported for their antimicrobial activity against H. pylori. The mechanism of action of many of these plant extracts and plant-derived compounds is different from that of conventional antibiotics. Therefore they are shown to be effective against drug-resistant strains of H. pylori. They act by inhibiting bacterial enzymes, adhesions with gastric mucosa, suppression of nuclear factor-κB and by inhibition of oxidative stress. Extracts from Pistacia lentiscus, Brassica oleracea, Glycyrrhiza glabra, Camellia sinensis, Cinnamomum cassia, Allium sativum and Nigella sativa plants and isolated phyto-compounds such as curcumin, resveratrol, quercetin, allicin and ellagic acid demonstrated antimicrobial activity against H. pylori under in vivo conditions. The plant extracts of Zingiber officinale, Glycyrrhiza glabra; and phytochemical allicin and berberine when combined with standard treatment, result in a dramatic increase in H. pylori eradication. In this review, we highlighted the therapeutic efficacy of different plant extracts and isolated phyto compounds against H. pylori infection and described their role in tackling H. pylori resistance to antibiotics.

Structural Modifications on Chalcone Framework for Developing New Class of Cholinesterase Inhibitors.

Due to the multifaceted pharmacological activities of chalcones, these scaffolds have been considered one of the most privileged frameworks in the drug discovery process. Structurally, chalcones are α, ß-unsaturated carbonyl functionalities with two aryl or heteroaryl units. Amongst the numerous pharmacological activities explored for chalcone derivatives, the development of novel chalcone analogs for the treatment of Alzheimer's disease (AD) is among the research topics of most interest. Chalcones possess numerous advantages, such as smaller molecular size, opportunities for further structural modification thereby altering the physicochemical properties, cost-effectiveness, and convenient synthetic methodology. The present review highlights the recent evidence of chalcones as a privileged structure in AD drug development processes. Different classes of chalcone-derived analogs are summarized for the easy understanding of the previously reported analogs as well as the importance of certain functionalities in exhibiting cholinesterase inhibition. In this way, this review will shed light on the medicinal chemistry fraternity for the design and development of novel promising chalcone candidates for the treatment of AD.

Pannexins form gap junctions with electrophysiological and pharmacological properties distinct from connexins.

Stable expression of pannexin 1 (Panx1) and pannexin 3 (Panx3) resulted in functional gap junctions (GJs) in HeLa cells, but not in Neuro-2a (N2a) or PC-12 cells. The glycosylation pattern of expressed Panx1 varied greatly among different cell lines. In contrast to connexin (Cx) containing GJs (Cx-GJs), junctional conductance (Gj) of pannexin GJs (Panx-GJs) is very less sensitive to junctional voltage. Both Panx1 and Panx3 junctions favoured anionic dyes over cations to permeate. Though, carbenoxolone (CBX) and probenecid blocked Panx1 hemichannel activity, they had no effect on Panx1-GJs or Panx3-GJs. Extracellular loop 1 (E1) of Panx1 possibly bears the binding pocket. The Cx-GJ blocker heptanol blocked neither Panx1 hemichannel nor Panx-GJs. Unlike the GJs formed by most Cxs, CO2 did not uncouple Panx-GJs completely. Oxygen and glucose deprivation (OGD) caused lesser uncoupling of Panx-GJs compared to Cx43-GJs. These findings demonstrate properties of Panx-GJs that are distinctly different from Cx-GJs.

Morbidities of lung cancer surgery in obese patients.

BACKGROUND: Obesity is a risk factor for increased perioperative morbidity and mortality in surgical patients. There have been limited studies to correlate the morbidity of lung cancer resection with obesity. METHODS: We performed a retrospective study of patients who underwent surgical resection for lung cancer at the Medical College of Wisconsin, Milwaukee, from 2006 to 2010. Data on patient demographics, weight, pathological findings, and hospital course were abstracted after appropriate institutional review board approval. Perioperative morbidity was defined as atrial fibrillation, heart failure, respiratory failure, pulmonary embolism, or any medical complications arising within 30 days after surgery. The Fisher exact test was used to test the association between body mass index (BMI) and perioperative morbidities. RESULTS: Between 2006 and 2010, 320 lung resections were performed for lung cancer. The median age was 67 (interquartile range, 59-75) years, and 185 (57.8%) were females. A total of 121 (37.8%) of patients had a BMI lower than 25, and 199 (62.18%) patients had a BMI of 25 or higher. The 30-day mortality rate was 1.8% (n = 6) in the whole group; only 2 of these patients had a BMI of 25 or higher. Perioperative morbidity occurred in 28 (23.14%) of patients with a normal BMI and in 47 (23.61%) of patients with a BMI of 25 or higher (P = .54). Specific morbidities encountered by patients with normal versus BMI of 25 or higher were as follows: atrial fibrillation, 11 (9.09%) versus 24 (12.06%) (P = .46); pulmonary embolism, 1 (0.83%) versus 3 (1.51%) (P = 1.0); congestive heart failure, 2 (1.65%) versus 2 (1.01%) (P = .63); renal failure, 4 (3.3%) versus 2 (1.0%) (P = .29); respiratory failure, 12 (9.92%) versus 17 (8.54%) (P = .69); and acute respiratory distress syndrome, 2 (1.65%) versus 1 (0.50%) (P = .55). The median hospital stay was 5 days in the lower BMI group and 4 days in the BMI of 25 or higher group (P = .52). CONCLUSIONS: Overweight and normal weight patients do not differ significantly in rates of perioperative morbidities, 30-day mortality, and length of stay. Our study indicates that potential curative surgical resections can be offered to even significantly overweight patients.

The cytoplasmic C2A domain of synaptotagmin shows sequence specific interaction with its own mRNA.

Synaptotagmin-1 (Syt1) is essential in Ca(2+)-dependent neurotransmitter release, but its expression regulation is unknown. Here we report that the cytoplasmic Syt1 fragment forms ribonucleoprotein complex by interacting with the 3' untranslated region (3(')UTR) of its own mRNA. Two protein-binding domains, GU(15) repeat and GUCAAUG, within the Syt 3'UTR and the C2 domains in Syt1, especially C2A, are essential in this ribonucleoprotein complex formation. Furthermore, in in vitro assay the translation efficiency of Syt1 mRNA was downregulated in presence of 3'UTR. These results demonstrate for the fist time that the soluble fraction of Syt1 can interact with its own mRNA in a highly sequence specific manner.

Sickle cell patient with an acute chest syndrome and a negative chest X-ray: potential role of the ventilation and perfusion (V/Q) lung scan.

Acute chest syndrome (ACS) in sickle cell disease is caused by thromboemboli in the pulmonary vasculature. The diagnostic criteria include the presence of pulmonary infiltrate(s) on chest x-ray. This case report suggests that a V/Q scan may play a diagnostic role in sickle cell patients with symptoms of ACS and a negative chest x-ray.