Variation of antibiotic resistance in Salmonella Enteritidis,Escherichia coli O157:H7, and Listeria monocytogenes after exposure to acid,salt, and cold stress

Bacteria with antibiotic-resistant could seriously threaten to human health, increasing the treatment cost for infections and negatively affecting treatment outcomes. Stress adaptation is one possible mechanism for the acquisition or enhancement of antibiotic resistance in bacteria as a result of cross-protection. In this study, the effects of acid, salt, and cold stress on the antibiotic resistance of Salmonella Enteritidis, Listeria monocytogenes, and Escherichia coli O157:H7 were investigated using the disc diffusion method. For S. Enteritidis, acidic growth conditions increased resistance to ciprofloxacin and erythromycin (p < .05), and addition of 4% NaCl to growth media decreased resistance to chloramphenicol (p < .05). Irrespective of pH and the NaCl concentration of the growth medium, refrigerated E. coli O157:H7 showed increased resistance to amoxycillin, ciprofloxacin, gentamicin, streptomycin, and erythromycin (p < .05). Acid-adapted L. monocytogenes showed decreased the resistance to amoxycillin, ampicillin, chloramphenicol, ciprofloxacin, erythromycin, gentamicin, streptomycin, and tetracycline (p < .05). In conclusion, prolonged exposure of foodborne pathogens to acid, salt, and cold stress alters their antibiotic resistance. However, the effect of acid, salt, and cold stress on bacterial antibiotic resistance depend on both the bacterial species and the specific antibiotic. Therefore, multiple factors need to be considered for a foodborne antimicrobial resistant risk assessment.     

Deliberately Losing Control of C−H Activation Processes in the Design of Small-Molecule-Fragment Arrays Targeting Peroxisomal Metabolism

Combined photochemical arylation, “nuisance effect” (S_NAr) reaction sequences have been employed in the design of small arrays for immediate deployment in medium-throughput X-ray protein–ligand structure determination. Reactions were deliberately allowed to run “out of control” in terms of selectivity; for example the ortho-arylation of 2-phenylpyridine gave five products resulting from mono- and bisarylations combined with S_NAr processes. As a result, a number of crystallographic hits against NUDT7, a key peroxisomal CoA ester hydrolase, have been identified.     

Tensile testing and fracture mechanism analysis of polyvinyl alcohol nanofibrous webs

A tensile properties testing study was conducted to understand the influence of thickness, cross-head speed (speed of testing), gauge length (GL; specimen test length), and sample shape on important tensile properties of polyvinyl alcohol (PVA) nanofiber webs. The effects of each testing parameter on load at break, extension at break, Young's modulus, and tensile stress–strain curve of PVA nanofiber webs are analyzed. The Welch two sample t-tests show the significant difference among tested data. Using interaction plots, two-way analysis of variance, and margin mean plots, the interaction effects among testing parameters have been analyzed. Of all the factors, cross-head speed, the interaction among GL, and sample thickness (GL: Thickness) and the interaction among GL, testing speed and sample thickness (GL: Speed: Thickness) have significant influence on the tensile properties of PVA nanofiber webs. Moreover, the hypothesized model of mechanism of tensile strain–stress curve of PVA nanofiber webs has been proposed. Based on the model, the tensile strain–stress curve can be split into three stages: linear elastic, partial break up, and complete breakage. This study will provide a better understanding of tensile testing parameters' effects and their interaction effects on the tensile properties of nanowebs.     

Glibenclamide for the Treatment of Ischemic and Hemorrhagic Stroke

Ischemic and hemorrhagic strokes are associated with severe functional disability and high mortality. Except for recombinant tissue plasminogen activator, therapies targeting the underlying pathophysiology of central nervous system (CNS) ischemia and hemorrhage are strikingly lacking. Sur1-regulated channels play essential roles in necrotic cell death and cerebral edema following ischemic insults, and in neuroinflammation after hemorrhagic injuries. Inhibiting endothelial, neuronal, astrocytic and oligodendroglial sulfonylurea receptor 1–transient receptor potential melastatin 4 (Sur1–Trpm4) channels and, in some cases, microglial K_ATP (Sur1–Kir6.2) channels, with glibenclamide is protective in a variety of contexts. Robust preclinical studies have shown that glibenclamide and other sulfonylurea agents reduce infarct volumes, edema and hemorrhagic conversion, and improve outcomes in rodent models of ischemic stroke. Retrospective studies suggest that diabetic patients on sulfonylurea drugs at stroke presentation fare better if they continue on drug. Additional laboratory investigations have implicated Sur1 in the pathophysiology of hemorrhagic CNS insults. In clinically relevant models of subarachnoid hemorrhage, glibenclamide reduces adverse neuroinflammatory and behavioral outcomes. Here, we provide an overview of the preclinical studies of glibenclamide therapy for CNS ischemia and hemorrhage, discuss the available data from clinical investigations, and conclude with promising preclinical results that suggest glibenclamide may be an effective therapeutic option for ischemic and hemorrhagic stroke.