Prevention Funding Project: Synthesis of Research on Economic Change, Welfare Reform, and Child Maltreatment

This study concludes with a fair amount of certainty that there is a relationship between child maltreatment and economic decline. Stated differently, there is substantial evidence that economic decline affects the treatment of children by their parents. However, it is important to note that the data presented on the link between economic decline and child maltreatment in this synthesis is outdated, and thus limited. That is, most of the studies presented as supporting evidence for the relationship between child abuse and economic decline date from the Great Depression to the 1990's. No recent evidence (i.e., within the last 10 years) was found to lend support for the relationship between child maltreatment and economic decline. At best, one can conclude that a number of economic and social changes occurring since the Depression (e.g., unemployment compensation, severance pay, employment of spouse, unemployment precipitated by job loss) probably lessen the negative impact of job and income loss in the early 90's context. And, although the magnitude of effects may differ, the direction of effects and the mechanisms by which economic loss affects children are similar for these two periods. Unfortunately, no comparable data was found to extend this conclusion to more recent years. Second, with respect to the link between TANF and child maltreatment, it can be concluded that higher welfare benefits are associated with lower rates of neglect and out-of-home care. It is critical to note that the welfare reforms discussed in this synthesis have taken place against the backdrop of a very strong economy! Therefore, welfare reforms may have larger long-run effects on maltreatment than the evidence presented here

Laparoscopic Management of Sigmoidorectal Intussusception

This case of sigmoidorectal intussusception was caused by a large tubovillous adenoma and managed with laparoscopic sigmoidectomy

Identification of gender differences in ultrasound milestone assessments during emergency medicine residency training: a pilot study

Objectives: Prior literature suggests that incongruities between male and female resident's procedural competency may be explained by gender bias during the evaluation process. There are no known studies investigating gender differences in the assessment of ultrasound-based procedural skills among emergency medicine (EM) residents. The purpose of this study was to evaluate for gender differences in ultrasound milestone assessments among EM residents. Methods: This is a retrospective study including EM residents. Milestone assessment data were collected from a total of 3 Accreditation Council for Graduate Medical Education (ACGME) EM residency programs representing a 3-year period The outcome measures included mean milestone levels, milestone levels at baseline and graduation and differences in milestone achievement between female and male EM residents. An unpaired Student's t-test was used to compare milestone scores between female and male residents. Results: A total of 456 ultrasound milestone evaluations were collected from 91 EM residents (34 females [37%] and 57 males [63%]). No significant differences were noted in the overall mean milestone level between females (2.3 +/- 0.6) and males (2.2 +/- 0.6) (P=0.387). There were no significant differences noted in the ultrasound milestone level between females (0.8 +/- 0.6) and males (0.7 +/- 0.7) at baseline (P=0.754). Although it did not reach statistical significance (P=0.197), the increase in the mean ultrasound milestone level from baseline to graduation was greater in males (3.4 +/- 0.7) compared to females (3.1 +/- 0.7). Conclusion: Overall, there were no statistically significant differences in the mean ultrasound milestone levels between females and males. The rate of ultrasound milestone level achievement during EM residency training at our institution had a slight tendency to be higher for males than females in the observed residency programs; however, this also did not reach statistical significance. Possible gender bias while evaluating ultrasound milestone levels needs to be further studied on a larger scale.Open access journal.This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]

Ligand-Independent HER2/HER3/PI3K Complex Is Disrupted by Trastuzumab and Is Effectively Inhibited by the PI3K Inhibitor GDC-0941

SummaryHerceptin (trastuzumab) is the backbone of HER2-directed breast cancer therapy and benefits patients in both the adjuvant and metastatic settings. Here, we describe a mechanism of action for trastuzumab whereby antibody treatment disrupts ligand-independent HER2/HER3 interactions in HER2-amplified cells. The kinetics of dissociation parallels HER3 dephosphorylation and uncoupling from PI3K activity, leading to downregulation of proximal and distal AKT signaling, and correlates with the antiproliferative effects of trastuzumab. A selective and potent PI3K inhibitor, GDC-0941, is highly efficacious both in combination with trastuzumab and in the treatment of trastuzumab-resistant cells and tumors

p21-activated kinase 1: PAK'ed with potential

The p21-activated kinases (PAKs) are central players in growth factor signaling networks and morphogenetic processes that control proliferation, cell polarity, invasion and actin cytoskeleton organization. This raises the possibility that interfering with PAK activity may produce significant anti-tumor activity. In this perspective, we summarize recent data concerning the contribution of the PAK family member, PAK1, in growth factor signaling and tumorigenesis. We further discuss mechanisms by which inhibition of PAK1 can arrest tumor growth and promote cell apoptosis, and the types of cancers in which PAK1 inhibition may hold promise

Inhibition of the p110α isoform of PI 3-kinase stimulates nonfunctional tumor angiogenesis

Understanding the direct, tumor cell–intrinsic effects of PI 3-kinase (PI3K) has been a key focus of research to date. Here, we report that cancer cell–extrinsic PI3K activity, mediated by the p110α isoform of PI3K, contributes in an unexpected way to tumor angiogenesis. In syngeneic mouse models, inactivation of stromal p110α led to increased vascular density, reduced vessel size, and altered pericyte coverage. This increased vascularity lacked functionality, correlating with enhanced tumor hypoxia and necrosis, and reduced tumor growth. The role of p110α in tumor angiogenesis is multifactorial, and includes regulation of proliferation and DLL4 expression in endothelial cells. p110α in the tumor stroma is thus a regulator of vessel formation, with p110α inactivation giving rise to nonfunctional angiogenesis, which can stunt tumor growth. This type of vascular aberration differs from vascular endothelial growth factor–centered antiangiogenesis therapies, which mainly lead to vascular pruning. Inhibition of p110α may thus offer a new antiangiogenic therapeutic opportunity in cancer