Niche modeling reveals life history shifts in birds at La Brea over the last twenty millennia.

A species presence at a particular site can change over time, resulting in temporally dynamic species pools. Ecological niche models provide estimates of species presence at different time intervals. The avifauna of La Brea includes approximately 120 species dating to approximately 15,000 years ago.

Evolution of rotavirus C in humans and several domestic animal species.

Rotavirus C (RVC) causes enteric disease in multiple species, including humans, swine, bovines, and canines. To date, the evolutionary relationships of RVC populations circulating in different host species are poorly understood, owing to the low availability of genetic sequence data. To address this gap, we sequenced 45 RVC complete genomes from swine samples collected in the United States and Mexico.

The Believability of Anxious Feelings and Thoughts Questionnaire (BAFT): a psychometric evaluation of cognitive fusion in a nonclinical and highly anxious community sample.

Cognitive fusion--or the tendency to buy into the literal meaning of thoughts, feelings, and bodily sensations--plays an important role in the etiology and maintenance of anxiety disorders and figures prominently in third-generation behavior therapies such as acceptance and commitment therapy (ACT). Nonetheless, there is a lack of validated self-report measures of cognitive fusion/defusion, particularly in the area of anxiety disorders. We attempted to fill this gap with the development and validation of a self-report cognitive fusion measure, the Believability of Anxious Feelings and Thoughts Questionnaire (BAFT), in both a healthy undergraduate sample (N = 432) and highly anxious community sample (N = 503) undergoing a 12-week online ACT intervention.

A truncated DNA-damage-signaling response is activated after DSB formation in the G1 phase of Saccharomyces cerevisiae.

In Saccharomyces cerevisiae, the DNA damage response (DDR) is activated by the spatio-temporal colocalization of Mec1-Ddc2 kinase and the 9-1-1 clamp. In the absence of direct means to monitor Mec1 kinase activation in vivo, activation of the checkpoint kinase Rad53 has been taken as a proxy for DDR activation. Here, we identify serine 378 of the Rad55 recombination protein as a direct target site of Mec1.

Measuring attention in the hemispheres: the lateralized attention network test (LANT).

The attention network test (ANT) is a brief computerized battery measuring three independent behavioral components of attention: Conflict resolution (ability to overcome distracting stimuli), spatial Orienting (the benefit of valid spatial pre-cues), and Alerting (the benefit of temporal pre-cues). Imaging, clinical, and behavioral evidence demonstrate hemispheric asymmetries in these attentional networks. We constructed a lateralized version of the ANT (LANT), with brief targets flashed in one or the other visual hemifield.

Phosphorylation of Rad55 on serines 2, 8, and 14 is required for efficient homologous recombination in the recovery of stalled replication forks.

DNA damage checkpoints coordinate the cellular response to genotoxic stress and arrest the cell cycle in response to DNA damage and replication fork stalling. Homologous recombination is a ubiquitous pathway for the repair of DNA double-stranded breaks and other checkpoint-inducing lesions. Moreover, homologous recombination is involved in postreplicative tolerance of DNA damage and the recovery of DNA replication after replication fork stalling.

DNA damage-induced phosphorylation of Rad55 protein as a sentinel for DNA damage checkpoint activation in S. cerevisiae.

Rad55 protein is one of two Rad51 paralogs in the budding yeast Saccharomyces cerevisiae and forms a stable heterodimer with Rad57, the other Rad51 paralog. The Rad55-Rad57 heterodimer functions in homologous recombination during the assembly of the Rad51-ssDNA filament, which is central for homology search and DNA strand exchange. Previously, we identified Rad55 protein as a terminal target of the DNA damage checkpoints, which coordinate the cellular response to genotoxic stress.

Pathogenesis of ascites tumor growth: fibrinogen influx and fibrin accumulation in tissues lining the peritoneal cavity.

In the immediately preceding paper, we demonstrated that the microvasculature supplying peritoneal lining tissues of mice bearing either of two transplantable ascites carcinomas was hyperpermeable to circulating macromolecules. Solid tumors have been shown to exhibit similar levels of microvascular hyperpermeability, leading to extravasation of plasma proteins, including fibrinogen which clots on extravasation to form an extravascular fibrin gel. To determine whether similar extravasation and clotting of plasma fibrinogen occurred in ascites tumors, we used 125I-labeled fibrinogen (125I-F) as a tracer to measure inflow of fibrinogen into the peritoneal cavities, and influx and accumulation of fibrinogen/fibrin in the peritoneal lining tissues (peritoneal wall, mesentery, and diaphragm) of mice bearing syngeneic TA3/St or MOT ascites tumors.

Pathogenesis of ascites tumor growth: vascular permeability factor, vascular hyperpermeability, and ascites fluid accumulation.

Previous studies have shown that accumulation of tumor ascites fluid results in large part from increased permeability of peritoneal lining vessels (Nagy et al., Cancer Res., 49: 5449-5458, 1989; Nagy et al.

Pathogenesis of ascites tumor growth: angiogenesis, vascular remodeling, and stroma formation in the peritoneal lining.

In the accompanying papers, we demonstrated that two murine ascites tumors (MOT and TA3/St) induced peritoneal lining blood vessels to become hyperpermeable to plasma proteins, leading to extravasation of fibrinogen and its clotting to cross-linked fibrin in peritoneal lining tissues (peritoneal wall, mesentery, and diaphragm). In solid tumors, vascular hyperpermeability and fibrin deposition lead to the generation of vascularized connective tissue. In order to determine whether fibrin had similar consequences in ascites tumors, the vasculature and stroma of peritoneal lining tissues were analyzed at successive intervals after i.

Pathogenesis of malignant ascites formation: initiating events that lead to fluid accumulation.

Initiating events leading to the accumulation of malignant ascites in the peritoneal cavity were investigated in two syngeneic transplantable murine ascites-producing tumors, MOT mouse ovarian tumor and the TA3/St mammary carcinoma. The transport of two tracers, 125I-labeled human serum albumin (125I-HSA) and 51Cr-labeled red blood cells (51Cr-RBC), into and out of the peritoneal cavity was studied at early times after i.p.

Exchange of macromolecules between plasma and peritoneal cavity in ascites tumor-bearing, normal, and serotonin-injected mice.

Fluorescein-labeled dextrans (FITC-D) from 3 to 5000 kDa (Stokes' radii from 1 to 40 nm) were used to study influx from the plasma into the peritoneum and efflux from the peritoneal cavity into the plasma in normal and ascites tumor-bearing mice and in mice whose peritoneal vessels had been rendered hyperpermeable by serotonin. Two syngeneic transplantable murine ascites tumors were studied: mouse ovarian tumor and the TA3/St breast adenocarcinoma. To control for effects of peritoneal fluid volume, influx and efflux were also analyzed in mice that had received 5 ml of 5% bovine serum albumin i.