Five Criteria Predict Induction and Ablation of Supraventricular Tachycardia.

Introduction: Current guidelines recommend electrophysiological study (EPS) and ablation for primary treatment of supraventricular tachycardia (SVT), but there is little information to guide patient selection for the procedure. The purpose of this study was to identify preoperative features that would predict whether patients with signs or symptoms of tachycardia were likely to have SVT induced and ablated at EPS.

Methods: We performed a retrospective chart review of 1089 patients referred for EPS and ablation of SVT at 2 high volume centers.

Pericardial Decompression Syndrome After Drainage of Chronic Pericardial Effusions.

Pericardial decompression syndrome (PDS) is a potentially fatal disorder of left ventricular function that sometimes occurs after drainage of a pericardial effusion for cardiac tamponade. Patients at risk for PDS are difficult to identify. Here, we report 2 cases where PDS developed after drainage of effusions that had been present for years, suggesting that patients with chronic effusions are at higher risk for PDS.

iPSCORE: A Resource of 222 iPSC Lines Enabling Functional Characterization of Genetic Variation across a Variety of Cell Types.

Large-scale collections of induced pluripotent stem cells (iPSCs) could serve as powerful model systems for examining how genetic variation affects biology and disease. Here we describe the iPSCORE resource: a collection of systematically derived and characterized iPSC lines from 222 ethnically diverse individuals that allows for both familial and association-based genetic studies. iPSCORE lines are pluripotent with high genomic integrity (no or low numbers of somatic copy-number variants) as determined using high-throughput RNA-sequencing and genotyping arrays, respectively.

Compatibility of Radiofrequency Surgical Sponge Detection Technology with Cardiac Implantable Electronic Devices and Temporary Pacemakers.

Background: Radiofrequency (RF) technology has improved detection of retained surgical sponges with a reported 100% sensitivity and specificity. However, the potential for interactions of the RF signals emitted by the detection system with cardiac implantable electronic devices (CIEDs) or temporary pacemakers may limit its use in those patients with these devices. This study investigated whether RF detection technology causes interference or clinically significant changes in the programmed settings of implanted pacemakers and defibrillators or temporary epicardial pacemakers.

An inactive geminin mutant that binds cdt1.

The initiation of DNA replication is tightly regulated in order to ensure that the genome duplicates only once per cell cycle. In vertebrate cells, the unstable regulatory protein Geminin prevents a second round of DNA replication by inhibiting the essential replication factor Cdt1. Cdt1 recruits mini-chromosome maintenance complex (MCM2-7), the replication helicase, into the pre-replication complex (pre-RC) at origins of DNA replication.

Pocket infections of cardiac implantable electronic devices treated by negative pressure wound therapy.

Aims: Managing an infection of the pocket of a cardiac implantable electronic device (CIED) is frequently challenging. The wound is often treated with a drain or wet-to-dry dressings that allow healing by secondary intention. Such treatment can prolong the hospital stay and can frequently result in a disfiguring scar.

Geminin is required for mitotic proliferation of spermatogonia.

Spermatogonial stem cells divide throughout life, maintaining their own population and giving rise to differentiated gametes. The unstable regulatory protein Geminin is thought to be one of the factors that determine whether stem cells continue to divide or terminally differentiate. Geminin regulates the extent of DNA replication and is thought to maintain cells in an undifferentiated state by inhibiting various transcription factors and chromatin remodeling proteins.

Geminin is required for zygotic gene expression at the Xenopus mid-blastula transition.

In many organisms early development is under control of the maternal genome and zygotic gene expression is delayed until the mid-blastula transition (MBT). As zygotic transcription initiates, cell cycle checkpoints become activated and the tempo of cell division slows. The mechanisms that activate zygotic transcription at the MBT are incompletely understood, but they are of interest because they may resemble mechanisms that cause stem cells to stop dividing and terminally differentiate.

The anatomical basis of pulmonary vein reconnection after ablation for atrial fibrillation: wounds that never felt a scar?

Atrial fibrillation (AF), the most common cardiac arrhythmia, is a major cause of strokes, hospitalizations, and mortality in the United States. The toll of AF is expected to worsen in coming decades as the number of elderly Americans increases (1). This harsh demographic reality has provided an impetus to seek new strategies to prevent, control, and eliminate the arrhythmia.

Geminin-deficient neural stem cells exhibit normal cell division and normal neurogenesis.

Neural stem cells (NSCs) are the progenitors of neurons and glial cells during both embryonic development and adult life. The unstable regulatory protein Geminin (Gmnn) is thought to maintain neural stem cells in an undifferentiated state while they proliferate. Geminin inhibits neuronal differentiation in cultured cells by antagonizing interactions between the chromatin remodeling protein Brg1 and the neural-specific transcription factors Neurogenin and NeuroD.

Geminin deletion from hematopoietic cells causes anemia and thrombocytosis in mice.

HSCs maintain the circulating blood cell population. Defects in the orderly pattern of hematopoietic cell division and differentiation can lead to leukemia, myeloproliferative disorders, or marrow failure; however, the factors that control this pattern are incompletely understood. Geminin is an unstable regulatory protein that regulates the extent of DNA replication and is thought to coordinate cell division with cell differentiation.

Therapy-related myelodysplastic syndrome presenting as fulminant heart failure secondary to myeloid sarcoma.

Rapidly progressive heart failure is commonly caused by an extensive myocardial infarction, a mechanical complication of infarction, myocarditis, or acute valvular insufficiency. We present an unusual case that was caused by a diffuse infiltration of the myocardium with leukemic cells (myeloid sarcoma). The patient presented with episodic shortness of breath, he was anemic and thrombocytopenic, and his bone marrow biopsy revealed myelodysplastic syndrome from treatment for oligodendroglioma.

Enucleation of feeder cells and egg cells with psoralens.

The cell nucleus must be inactivated or destroyed in order to generate feeder layers for cultured cells or to prepare recipient egg cells for nuclear transfer. Existing enucleation techniques are either cumbersome or employ toxic chemicals. Here we report a new method to enucleate cells by treatment with a psoralen and long-wave ultraviolet light.

An integrated genome screen identifies the Wnt signaling pathway as a major target of WT1.

WT1, a critical regulator of kidney development, is a tumor suppressor for nephroblastoma but in some contexts functions as an oncogene. A limited number of direct transcriptional targets of WT1 have been identified to explain its complex roles in tumorigenesis and organogenesis. In this study we performed genome-wide screening for direct WT1 targets, using a combination of ChIP-ChIP and expression arrays.

Identifying the aesthetic and functional determinants in the collapsed dentition.

This patient's treatment involved a complex diagnostic challenge, as well as a challenging clinical sequence due to the utilization of immediate implant placement and restoration after extraction along with immediate prosthodontic restoration with sinus elevation with bone grafting. The inability to have diagnostic patient wax try-ins required a detailed and exacting diagnostic work-up which included significant laboratory diagnostic wax-ups. The utilization of the ACP Parameters of Care for Partial Edentulism for a PDI Class IV patient provided a framework in which care could be planned and executed with confidence.

Geminin is overexpressed in human pancreatic cancer and downregulated by the bioflavanoid apigenin in pancreatic cancer cell lines.

Pancreatic adeniocarcinoma is among the deadliest of human cancers. Apigenin, an antitumor flavonoid, inhibits pancreatic cancer cell proliferation in vitro. Geminin is a recently identified novel protein that plays a critical role in preventing abnormal DNA replication by binding to and inhibiting the essential replication factor Cdt1.

Geminin prevents rereplication during xenopus development.

To maintain a stable genome, it is essential that replication origins fire only once per cell cycle. The protein Geminin is thought to prevent a second round of DNA replication by inhibiting the essential replication factor Cdt1. Geminin also affects the development of several different organs by binding and inhibiting transcription factors and chromatin-remodeling proteins.

Measurement of geminin activity in Xenopus egg extracts.

Geminin is an unstable protein that inhibits DNA replication by interfering with the assembly of prereplication complex at replication origins. Geminin is thought to prevent a second round of replication during late S- or G2-phase. The protein is destroyed by ubiquitin-dependent proteolysis during mitosis, allowing a new round of replication in the next cell cycle.

Geminin has dimerization, Cdt1-binding, and destruction domains that are required for biological activity.

Geminin is an unstable regulatory protein that affects both cell division and cell differentiation. Geminin inhibits a second round of DNA synthesis during S and G(2) phase by binding the essential replication protein Cdt1. Geminin is also required for entry into mitosis, either by preventing replication abnormalities or by down-regulating the checkpoint kinase Chk1.