Enterococcus faecalis Strains with Compromised CRISPR-Cas Defense Emerge under Antibiotic Selection for a CRISPR-Targeted Plasmid.

Enterococcus faecalis is a Gram-positive bacterium that natively colonizes the human gastrointestinal tract and opportunistically causes life-threatening infections. Multidrug-resistant (MDR) E. faecalis strains have emerged that are replete with mobile genetic elements (MGEs).

Characterization of presumptive vancomycin-resistant enterococci recovered during infection control surveillance in Dallas, Texas, USA.

and are Gram-positive bacteria that normally inhabit the human gastrointestinal tract. They are also opportunistic pathogens and can cause nosocomial infection outbreaks. To prevent the spread of nosocomial infections, hospitals may rely on screening methods to identify patients colonized with multidrug-resistant organisms including vancomycin-resistant enterococci (VRE).

Enterococcus faecalis CRISPR-Cas Is a Robust Barrier to Conjugative Antibiotic Resistance Dissemination in the Murine Intestine.

CRISPR-Cas systems are barriers to horizontal gene transfer (HGT) in bacteria. Little is known about CRISPR-Cas interactions with conjugative plasmids, and studies investigating CRISPR-Cas/plasmid interactions in models relevant to infectious disease are lacking. These are significant gaps in knowledge because conjugative plasmids disseminate antibiotic resistance genes among pathogens , and it is essential to identify strategies to reduce the spread of these elements.

CRISPR-Cas and Restriction-Modification Act Additively against Conjugative Antibiotic Resistance Plasmid Transfer in Enterococcus faecalis.

Enterococcus faecalis is an opportunistic pathogen and a leading cause of nosocomial infections. Conjugative pheromone-responsive plasmids are narrow-host-range mobile genetic elements (MGEs) that are rapid disseminators of antibiotic resistance in the faecalis species. Clustered regularly interspaced short palindromic repeat (CRISPR)-Cas and restriction-modification confer acquired and innate immunity, respectively, against MGE acquisition in bacteria.

A Syllabus for Teaching Peritoneal Dialysis to Patients and Caregivers.

Being aware of controversies and lack of evidence in peritoneal dialysis (PD) training, the Nursing Liaison Committee of the International Society for Peritoneal Dialysis (ISPD) has undertaken a review of PD training programs around the world in order to develop a syllabus for PD training. This syllabus has been developed to help PD nurses train patients and caregivers based on a consensus of training program reviews, utilizing current theories and principles of adult education. It is designed as a 5-day program of about 3 hours per day, but both duration and content may be adjusted based on the learner.

Conditional deletion of histone deacetylase-4 in the central nervous system has no major effect on brain architecture or neuronal viability.

Evidence from different laboratories using cell culture and in vivo model systems indicates that histone deacetylase-4 (HDAC4) plays an essential role in maintaining neuronal survival. Indeed, HDAC4 null knockout mice, which die within 2 weeks of birth, display cerebellar degeneration, whereas RNAi-mediated knockdown of HDAC4 expression in the retina of normal mice leads to apoptosis of retinal neurons. As a step toward analyzing the role of HDAC4 in the regulation of neuronal survival in more detail, we generated two separate lines of conditional knockout mice by breeding HDAC4-flox mice with mice expressing Cre recombinase through a Thy1 or nestin promoter.

Histone deacetylase-1 (HDAC1) is a molecular switch between neuronal survival and death.

Both neuroprotective and neurotoxic roles have previously been described for histone deacetylase-1 (HDAC1). Here we report that HDAC1 expression is elevated in vulnerable brain regions of two mouse models of neurodegeneration, the R6/2 model of Huntington disease and the Ca(2+)/calmodulin-dependent protein kinase (CaMK)/p25 double-transgenic model of tauopathic degeneration, suggesting a role in promoting neuronal death. Indeed, elevating HDAC1 expression by ectopic expression promotes the death of otherwise healthy cerebellar granule neurons and cortical neurons in culture.

Isoform-specific toxicity of Mecp2 in postmitotic neurons: suppression of neurotoxicity by FoxG1.

The methyl-CpG binding protein 2 (MeCP2) is a widely expressed protein, the mutations of which cause Rett syndrome. The level of MeCP2 is highest in the brain where it is expressed selectively in mature neurons. Its functions in postmitotic neurons are not known.

Characterisation and carriage ratio of Clostridium difficile strains isolated from a community-dwelling elderly population in the United Kingdom.

Background: Community-associated Clostridium difficile infection (CDI) appears to be an increasing problem. Reported carriage rates by C. difficile are debatable with suggestions that primary asymptomatic carriage is associated with decreased risk of subsequent diarrhoea.

Neuron-selective toxicity of tau peptide in a cell culture model of neurodegenerative tauopathy: essential role for aggregation in neurotoxicity.

Intracellular aggregation of tau is a pathological hallmark in Alzheimer's disease and other tauopathies. The mechanisms underlying tau aggregation and the role that these aggregates play in neuronal death have remained controversial. To study these issues, we established a cell culture model of tauopathy using a hexameric peptide with the sequence (306)VQIVYK(311) located within the third microtubule-binding repeat of tau, rendered cell-permeable by a tag of nine arginine residues (R(9)).

Identification of novel 1,4-benzoxazine compounds that are protective in tissue culture and in vivo models of neurodegeneration.

Neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and Huntington's disease and conditions such as ischemic stroke affect millions of individuals annually and exert an enormous financial burden on society. A hallmark of these conditions is the abnormal loss of neurons. Currently, there are no effective strategies to prevent neuronal death in these pathologies.

International survey of peritoneal dialysis training programs.

Objective: To survey nurses around the world about current practices for peritoneal dialysis (PD) home training programs.

Design: Random sampling of nurses to complete a written survey from the International Society for Peritoneal Dialysis Nursing Liaison Committee.

Settings: United States, Canada, South America (Brazil, Columbia), The Netherlands, Hong Kong.

Anesthesia and blood sampling of wild big brown bats (eptesicus fuscus) with an assessment of impacts on survival.

We anesthetized and blood sampled wild big brown bats (Eptesicus fuscus) in Fort Collins, Colorado (USA) in 2001 and 2002 and assessed effects on survival. Inhalant anesthesia was delivered into a specially designed restraint and inhalation capsule that minimized handling and bite exposures. Bats were immobilized an average of 9.

Increasing self-efficacy and knowledge through a seizure education program for special education teachers.

Since the passage of the 1975 Education for All Handicapped Children Act and the 1986 PL99-457 amendment, many children aged birth to 3 years with special health care needs are enrolled in early intervention programs. Educators working in early intervention services often need to respond to and manage seizure activity and medical emergencies for special needs children. To do so, they need to have knowledge and confidence in their ability to intervene effectively.

Chemical anoxia of tubular cells induces activation of c-Src and its translocation to the zonula adherens.

Cyanide (CN)-induced chemical anoxia of cultured mouse proximal tubular (MPT) cells increased the kinase activity of c-Src by approximately threefold. 4-Amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine (PP2), a specific inhibitor of c-Src, prevented Src activation. CN also increased the permeability of MPT cell monolayers, an event ameliorated by PP2.

ATP depletion of tubular cells causes dissociation of the zonula adherens and nuclear translocation of beta-catenin and LEF-1.

This study examined the events associated with the reversible disruption of the structural and functional integrity of the zonula occludens (ZA) induced by ATP depletion of renal tubular cells. It shows that loss of the ZA after ATP depletion is associated with the withdrawal of E-cadherin, alpha-catenin, and beta-catenin, probably as intact cadherin-catenin complexes from the basolateral membrane of tubular cells. The relative amounts of all three proteins increased in the Triton X-100-insoluble fraction of cell lysates and decreased in the Triton X-100-soluble pool.