AroC, a chorismate synthase, is required for the formation of Edwardsiella tarda biofilms.

Biofilms contribute to the resistance of Edwardsiella tarda to antibiotics and host immunity. AroC in the shikimate pathway produces chorismate to synthesize crucial intermediates such as indole. In this study, the differences between biofilms produced by aroC mutants (△aroC), wild-type (WT) strains, and △aroC complementary strains (C△aroC) were detected both in vitro with 96-well plates, tubes, or coverslips and in vivo using a mouse model of subcutaneous implants.

Biomimetic smart nanoplatform for dual imaging-guided synergistic cancer therapy.

Developing an integrated multimodal diagnosis and therapeutics nanoplatform is of great importance to enhance the outcome of cancer therapy. Herein, we report a highly efficient and biocompatible nanoplatform based on the assembly of a graphene oxide (GO) and metal-organic framework (MOF) Fe-porphyrin, which was coated with a folate-functionalized erythrocyte membrane (FA-EM@GO-MOF). The nanoplatform could be targeted to cancer cells precisely, and could avoid immune elimination and had prolonged blood circulation due to the presence of FA-EM on its surface.

Target genes directly regulated by Eha are required for Edwardsiella tarda survival within macrophages.

Eha is a virulence regulator in Edwardsiella tarda (E. tarda). The present study examined how Eha regulated its target genes to affect the bacterial survival within the cells.

Hyaluronic acid-modified mesoporous silica-coated superparamagnetic FeO nanoparticles for targeted drug delivery.

The targeted delivery of anti-cancer drugs to tumor tissue has been recognized as a promising strategy to increase their therapeutic efficacy and reduce side effects. Mesoporous silica-coated superparamagnetic Fe3O4 nanoparticles (NH2-MSNs), a kind of nanocarrier, can passively enter tumor tissues to enhance the permeability and retention of drugs. However, NH2-MSNs do not specifically bind to cancer cells.

EsR240, a non-coding sRNA, is required for the resistance of Edwardsiella tarda to stresses in macrophages and for virulence.

Bacterial small non-coding RNAs (sRNAs) are gene expression modulators that respond to environmental changes and pathogenic conditions. In this study, 13 novel sRNAs were identified in the intracellular pathogen, Edwardsiella tarda (E. tarda) ET13 strain, based on RNA sequencing and bioinformatic analyses.

Eha, a regulator of Edwardsiella tarda, required for resistance to oxidative stress in macrophages.

Edwardsiella tarda is distributed widely in a variety of hosts. Eha has recently been found to be its virulence regulator. In order to explore the mechanism of its regulation, we investigated the survival rates of wild type strain ET13, and its eha mutant and complemented strains in RAW264.

The role of regulator Eha in Edwardsiella tarda pathogenesis and virulence gene transcription.

Edwardsiella tarda is a pathogen with a broad host range that infects both animals and humans. Eha is a new transcriptional regulator identified in ET13, which is involved in the bacterial hemolytic activity. This study explored the effect of the Eha in the pathogenesis of E.

Eha, a transcriptional regulator of hemolytic activity of Edwardsiella tarda.

Hemolysis causes major symptoms such as the reddening skin and systemic hemorrhagic septicemia of diseased fish infected by Edwardsiella tarda. Cytolysin A (ClyA) is a pore-forming cytotoxic protein encoded by the clyA gene in Escherichia coli K-12. In this study, we observed that the heterologous expression of the eha gene from E.

Effect of hOGG1 over-expression on cisplatin resistance in esophageal squamous carcinoma cells.

Purpose: Human 8-oxoguanine DNA glycosylase (hOGG1) is an ubiquitous protein. It initiates the DNA base excision repair (BER) pathway to repair the 8-oxoguanine lesion. This may be associated with chemotherapeutics.

Duodenal reflux leads to down regulation of DNA mismatch repair pathway in an animal model of esophageal cancer.

Background: Gastroduodenal reflux is implicated in esophageal carcinogenesis. This effect is mediated by reactive oxygen species. We hypothesized that this is mediated by DNA mismatch lesion 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxoG), which is repaired by the Mut Y homologue (MYH).

Selective decrease in the DNA base excision repair pathway in squamous cell cancer of the esophagus.

Objectives: Oxidative damage can lead to a highly mutagenic 8-oxoguanine lesion, which mispairs with adenosine residues, leading to G:C-->T:A transversions. In mammalian cells 8-oxoguanine glycosylase initiates the DNA base excision repair pathway to repair the 8-oxoguanine lesion. To date, there is no information regarding oxidative DNA damage and repair pathways in esophageal cancer.

pKa of acetate in water: a computational study.

Several computational methods including the conductor-like polarizable continuum model, CPCM with both UAKS and UAHF cavities, Cramer and Truhlar's generalized Born solvation model, SM5.4(AM1), SM5.4(PM3), and SM5.

The mitochondrial K-ATP channel opener, diazoxide, prevents ischemia-reperfusion injury in the rabbit spinal cord.

Paraplegia resulting from ischemia is a catastrophic complication of thoracoabdominal aortic surgery. The current study was designed to investigate the effects of diazoxide (DZ) on mitochondrial structure, neurological function, DNA damage-repair, and apoptosis in spinal cord ischemia-reperfusion injury. Rabbits were subjected to 30 minutes of spinal cord ischemia and reperfusion (1 hour) with or without diazoxide (n = 6 in each group) by clamping and releasing the infrarenal aorta.

Increased mitochondrial reactive oxygen species production in newborn brain during hypoglycemia.

Hypoglycemia is associated with gray and white matter injury in immature brain, but the specific mechanisms responsible for hypoglycemic brain injury remain poorly defined. We postulated that mitochondrial electron transport chain function is altered during hypoglycemia due to the decreased availability of reducing equivalents, and that altered activity of the electron transport chain would increase mitochondrial production of free radicals and lead to mitochondrial oxidant injury. The present study tests the hypothesis that production of reactive oxygen species (ROS) by cerebral mitochondria is increased during acute hypoglycemia.

beta(2)-Adrenergic stimulation attenuates left ventricular remodeling, decreases apoptosis, and improves calcium homeostasis in a rodent model of ischemic cardiomyopathy.

The benefit of the beta(2)-adrenergic agonist, clenbuterol, in left ventricular assist device patients with dilated cardiomyopathy has been reported, but its effect on ischemic heart failure (HF) is unknown. We investigated whether clenbuterol improves left ventricular remodeling, myocardial apoptosis and has synergy with a beta(1) antagonist, metoprolol, in a model of ischemic HF. Rats were randomized to: 1) HF only; 2) HF + clenbuterol; 3) HF + metoprolol; 4) HF + clenbuterol + metoprolol; and 5) rats with sham surgery.

Cardiac myocyte apoptosis is associated with increased DNA damage and decreased survival in murine models of obesity.

Disruption of leptin signaling is associated with obesity, heart failure, and cardiac hypertrophy, but the role of leptin in cardiac myocyte apoptosis is unknown. We tested the hypothesis that apoptosis increases in leptin-deficient ob/ob and leptin-resistant db/db mice and is associated with aging and left ventricular hypertrophy, increased DNA damage, and decreased survival. We studied young (2- to 3-month-old) and old (12- to 14-month-old) ob/ob and db/db mice and wild-type (WT) controls (n=2 to 4 per group).

Oxidative DNA damage and DNA repair enzyme expression are inversely related in murine models of fatty liver disease.

Mitochondrial generation of reactive oxygen species (ROS) is increased in mice with fatty livers induced by genetic obesity, chronic consumption of ethanol, or methionine/choline-deficient diets. Both nuclear and mitochondrial (mt) DNA are targets for ROS-induced damage and accumulate hydroxylated bases, such as 8-hydroxy-2'-deoxyguanosine (8-oxoG) and base substitution of adenine with 8-oxoG (A*8-oxoG), that introduce mutations that promote cancer as well as cell death. The mammalian homolog of the bacterial DNA mismatch repair enzyme MutY (MYH) removes A*8-oxoG from nuclear and mtDNA, reduces 8-oxoG accumulation, and restores genomic stability after ROS exposure.