Two Cases of Vancomycin-Resistant Bacteremia With Development of Daptomycin-Resistant Phenotype and its Detection Using Oxford Nanopore Sequencing.

In this work, we report 2 cases of vancomycin-resistant bacteremia with development of daptomycin resistance in 2 patients with acute myeloid leukemia and myelodysplastic syndrome. Mutations related to daptomycin-nonsusceptible phenotype in genes were found in all strains of the study, including those with a minimum inhibitory concentration <1 µg/mL collected before daptomycin therapy. Epidemiological investigation using core genome single nucleotide polymorphism and core genome multilocus sequence typing revealed clonality of all the isolates.

Depth of cure of proximal composite resin restorations using a new perforated metal matrix.

The purpose of this study was to compare the depths of cure of a proximal box preparation filled in bulk with various approaches: filled with a bulk-fill or conventional composite; placed with a new perforated metal matrix, a traditional metal matrix, or a clear matrix; and polymerized with either occlusal-only or tri-sited light curing. After tri-sited curing, the use of the new perforated metal matrix band resulted in a depth of cure that was not significantly different from that achieved with the use of metal bands (removed during curing) or transparent matrix bands. Adequate polymerization was obtained at depths of more than 5.

Microleakage and shear bond strength of a new sealant containing prereacted glass ionomer particles.

A new fluoride-releasing sealant system is claimed to allow easier and faster placement while providing high bond strengths without the need for phosphoric acid etching. A study was designed to compare the microleakage and shear bond strength of a self-etching, Giomer-based sealant system with those of a traditional resin sealant. Group 1 received traditional sealant applied after use of a 35% phosphoric acid etchant; group 2 received Giomer sealant after use of a self-etching primer; and group 3 received Giomer sealant after the addition of an initial phosphoric acid etching step and placement of the primer.

Effect of surface treatments on the mechanical properties and antimicrobial activity of desiccated glass ionomers.

Objectives: The purpose of this study was to evaluate the effect of various surface treatments on the mechanical properties and antibacterial activity of desiccated glass-ionomer (GI) and resin-modified glass-ionomer (RMGI) materials.

Methods: One hundred GI and RMGI specimens were fabricated in a mold, stored in 100% humidity for 24h, placed in air to desiccate for 24h, and then stored for one week in one of the five media [casein phosphopeptide-amorphous calcium phosphate (CPP-ACP), chlorhexidine (CHX), sodium fluoride (NaF), cetylpyridinium chloride (CPC), or 100% humidity (control)]. Fifty GI and RMGI specimens were tested in flexure to determine flexural strength and modulus, with the fragments used for Knoop hardness testing.

Effect of a new salivary-contaminant removal method on bond strength.

The study evaluated the effect of salivary-contaminant removal methods on the bond strength of resin cement to hydrofluoric acid-etched ceramic. Treatment with a new cleaning paste resulted in bond strengths not significantly different from those obtained in phosphoric acid-treated, hydrofluoric acid-treated, and uncontaminated control groups; thus the paste may be considered an alternative to phosphoric acid or hydrofluoric acid for removal of salivary contaminants.

An FGF autocrine loop initiated in second heart field mesoderm regulates morphogenesis at the arterial pole of the heart.

In order to understand how secreted signals regulate complex morphogenetic events, it is crucial to identify their cellular targets. By conditional inactivation of Fgfr1 and Fgfr2 and overexpression of the FGF antagonist sprouty 2 in different cell types, we have dissected the role of FGF signaling during heart outflow tract development in mouse. Contrary to expectation, cardiac neural crest and endothelial cells are not primary paracrine targets.

Intracardiac septation requires hedgehog-dependent cellular contributions from outside the heart.

Septation of the mammalian heart into four chambers requires the orchestration of multiple tissue progenitors. Abnormalities in this process can result in potentially fatal atrioventricular septation defects (AVSD). The contribution of extracardiac cells to atrial septation has recently been recognized.

Independent requirements for Hedgehog signaling by both the anterior heart field and neural crest cells for outflow tract development.

Cardiac outflow tract (OFT) septation is crucial to the formation of the aortic and pulmonary arteries. Defects in the formation of the OFT can result in serious congenital heart defects. Two cell populations, the anterior heart field (AHF) and cardiac neural crest cells (CNCCs), are crucial for OFT development and septation.

The bone morphogenetic protein antagonist noggin regulates mammalian cardiac morphogenesis.

Bone morphogenetic proteins (BMPs) play many roles in mammalian cardiac development. Here we address the functions of Noggin, a dedicated BMP antagonist, in the developing mouse heart. In early cardiac tissues, the Noggin gene is mainly expressed in the myocardial cells of the outflow tract, atrioventricular canal, and future right ventricle.

Fgf8 is required for anterior heart field development.

In the mouse embryo, the splanchnic mesodermal cells of the anterior heart field (AHF) migrate from the pharynx to contribute to the early myocardium of the outflow tract (OT) and right ventricle (RV). Recent studies have attempted to distinguish the AHF from other precardiac populations, and to determine the genetic and molecular mechanisms that regulate its development. Here, we have used an Fgf8lacZ allele to demonstrate that Fgf8 is expressed within the developing AHF.

FGF8 is required for cell survival at distinct stages of nephrogenesis and for regulation of gene expression in nascent nephrons.

During kidney morphogenesis, the formation of nephrons begins when mesenchymal nephron progenitor cells aggregate and transform into epithelial vesicles that elongate and assume an S-shape. Cells in different regions of the S-shaped body subsequently differentiate into the morphologically and functionally distinct segments of the mature nephron. Here, we have used an allelic series of mutations to determine the role of the secreted signaling molecule FGF8 in nephrogenesis.

Loss of Gbx2 results in neural crest cell patterning and pharyngeal arch artery defects in the mouse embryo.

Several syndromes characterized by defects in cardiovascular and craniofacial development are associated with a hemizygous deletion of chromosome 22q11 in humans and involve defects in pharyngeal arch and neural crest cell development. Recent efforts have focused on identifying 22q11 deletion syndrome modifying loci. In this study, we show that mouse embryos deficient for Gbx2 display aberrant neural crest cell patterning and defects in pharyngeal arch-derived structures.

Chorioallantoic fusion defects and embryonic lethality resulting from disruption of Zfp36L1, a gene encoding a CCCH tandem zinc finger protein of the Tristetraprolin family.

The mouse gene Zfp36L1 encodes zinc finger protein 36-like 1 (Zfp36L1), a member of the tristetraprolin (TTP) family of tandem CCCH finger proteins. TTP can bind to AU-rich elements within the 3'-untranslated regions of the mRNAs encoding tumor necrosis factor (TNF) and granulocyte-macrophage colony-stimulating factor (GM-CSF), leading to accelerated mRNA degradation. TTP knockout mice exhibit an inflammatory phenotype that is largely due to increased TNF secretion.

BMP receptor IA is required in mammalian neural crest cells for development of the cardiac outflow tract and ventricular myocardium.

The neural crest is a multipotent, migratory cell population arising from the border of the neural and surface ectoderm. In mouse, the initial migratory neural crest cells occur at the five-somite stage. Bone morphogenetic proteins (BMPs), particularly BMP2 and BMP4, have been implicated as regulators of neural crest cell induction, maintenance, migration, differentiation and survival.

Cre-mediated excision of Fgf8 in the Tbx1 expression domain reveals a critical role for Fgf8 in cardiovascular development in the mouse.

Tbx1 has been implicated as a candidate gene responsible for defective pharyngeal arch remodeling in DiGeorge/Velocardiofacial syndrome. Tbx1(+/-) mice mimic aspects of the DiGeorge phenotype with variable penetrance, and null mice display severe pharyngeal hypoplasia. Here, we identify enhancer elements in the Tbx1 gene that are conserved through evolution and mediate tissue-specific expression.

Tbx1 is regulated by tissue-specific forkhead proteins through a common Sonic hedgehog-responsive enhancer.

Haploinsufficiency of Tbx1 is likely a major determinant of cardiac and craniofacial birth defects associated with DiGeorge syndrome. Although mice deficient in Tbx1 exhibit pharyngeal and aortic arch defects, the developmental program and mechanisms through which Tbx1 functions are relatively unknown. We identified a single cis-element upstream of Tbx1 that recognized winged helix/forkhead box (Fox)-containing transcription factors and was essential for regulation of Tbx1 transcription in the pharyngeal endoderm and head mesenchyme.

Fgf8 is required for pharyngeal arch and cardiovascular development in the mouse.

We present here an analysis of cardiovascular and pharyngeal arch development in mouse embryos hypomorphic for Fgf8. Previously, we have described the generation of Fgf8 compound heterozygous (Fgf8(neo/-)) embryos. Although early analysis demonstrated that some of these embryos have abnormal left-right (LR) axis specification and cardiac looping reversals, the number and type of cardiac defects present at term suggested an additional role for Fgf8 in cardiovascular development.

A genetic link between Tbx1 and fibroblast growth factor signaling.

Tbx1 haploinsufficiency causes aortic arch abnormalities in mice because of early growth and remodeling defects of the fourth pharyngeal arch arteries. The function of Tbx1 in the development of these arteries is probably cell non-autonomous, as the gene is not expressed in structural components of the artery but in the surrounding pharyngeal endoderm. We hypothesized that Tbx1 may trigger signals from the pharyngeal endoderm directed to the underlying mesenchyme.