Morphine stimulates tumor angiogenesis and cancer progression in mice. We examined if morphine influences endothelial-pericyte interaction via platelet-derived growth factor-BB (PDGF-BB) and PDGF receptor-β (PDGFR-β). Clinically relevant doses of morphine stimulated PDGF-BB secretion from human umbilical vein endothelial cells and activated PDGFR-β and mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) phosphorylation in human pericytes. These in vitro effects of morphine were translated into promotion of tumor angiogenesis in a transgenic mice model of breast cancer when treated with clinically used dose of morphine. Increased vessel-associated immunoreactivity of desmin and PDGFR-β was observed on pericytes in tumors of morphine-treated mice. These data suggest that morphine potentiates endothelial-pericyte interaction via PDGF-BB/PDGFR-β signaling and promotes tumor angiogenesis, pericyte recruitment, and coverage of tumor vessels. We speculate that morphine may impair the effectiveness of antiangiogenic therapy by influencing vascular pericyte coverage.

Hyperprogression and pseudoprogression are two atypical responses to immune checkpoint inhibitor therapy that affect therapeutic decisions and prognosis. Identification of predictive biomarkers for atypical responses either before or during treatment remains a huge unmet need in cancer immunotherapy. Many studies have looked at potential biomarkers, including clinical factors and laboratory findings (e.g., peripheral blood counts, circulating tumor DNA, cytokine levels). The results of these studies have been inconsistent, possibly due to small sample sizes, different tumor types and heterogeneity of the definition of these atypical responses.

Disaster Medicine is a relatively new discipline. Understanding of the current status of its science is needed in order to develop a roadmap for the direction and structure of future studies that will contribute to building the science of the health aspects of disasters (HADs). The objective of this study was to examine the existing, peer-reviewed literature relevant to the HADs to determine the status of the currently available literature underlying the science of the HADs. A total of 709 consecutive, peer-reviewed articles published from 2009-2014 in two disaster-health-related medical journals, Prehospital and Disaster Medicine (PDM) and Disaster Medicine and Public Health Preparedness (DMPHP), were examined. Of these, 495 were disaster-related (PDM, 248; DMPHP, 247). Three major categories defined these disaster-related research articles: (1) Epidemiological studies comprised 50.5%; (2) Interventional, 20.3%; and (3) Syntheses, 26.9%. Interventional studies were sub-categorized into: (a) Relief Responses, 23.0%; (b) Recovery Responses, 2.0%; or (c) Risk-Reduction Interventions, 75.0%. Basically, the inventories were consistent within the two journals. Reported indicators of outcomes related to the responses were constrained to achievement indicators (numbers accomplished). Syntheses articles were sub-categorized into: (a) Literature Reviews, 17.6%; (b) Opinions, 25.2%; (c) Models, 24.4%; (d) Frameworks, 6.9%; (e) Guidelines, 13.0%; (f) Tools, 3.0%; (g) Protocols, Policies, or Criteria, 2.3%; or (h) Conference Summaries, 7.6%. Trend analyses indicated that the relative proportions of articles in each category and sub-category remained relatively constant over the five years. No randomized controlled trials (RTCs), non-randomized, comparative controlled trials (CCTs), or systematic reviews were published in these journals during the period examined. Each article also was examined qualitatively for objectives, study type, content, language, and structure. There was no common structure used for any category or sub-categories. In addition, the terminology used was inconsistent and often confusing. This categorization process should be applied to other peer-reviewed journals that publish research related to HADs. As evidenced in the current study, the evidence base for HADs is far from robust and is disorganized, making the development of scientific evidence on which to base best practices difficult. A stronger evidence base is needed to develop the science associated with the HADs. This will require a common structure and terminology to facilitate comparisons. Greater depth of reporting is needed in order to render the Epidemiological studies more useful in mitigating the negative health impacts of hazard-related events. Interventional studies must be structured and include outcomes, impacts, benefits, and costs with robust indicators. The outcomes and impacts of Risk-Reduction Interventions will require the evaluation of changes in the epidemiology documented in future events or exercises. Birnbaum ML , Adibhatla...

Miconia machinazana C.Ulloa & D.A. Neill, sp. nov.,a new species of Melastomataceae from the Ecuador-Peru border is described and illustrated. It is characterized by the narrow, decussate leaves, dense reddish brown indument, small flowers in short panicles, pale yellow petals, and anthers opening by two large terminal pores.

Background: Angiogenesis is a process involved in the formation of new vessels, and is essential for tumor growth and metastases. Angiogenic factors are critical for the initiation of angiogenesis and maintenance of the vascular network. VG5Q is a newly discovered protein that acts as a potent angiogenic factor in promoting angiogenesis and has also been implicated in the vascular pathophysiology of Klippel-Trenaunay syndrome. However, little is known about its role in cancer progression. Method: In this study, VG5Q expression was screened using RT-PCR and Western blotting in the following cancer cell lines: breast (MCF-7), renal (Caki, ACHN), mesothelioma (H2373, H2596), ovarian (OVCAR5), lung (H226, A549) and pancreatic (Panc-1, MiaPaCa). Human umbilical vein endothelial cells (HUVEC) and blood outgrowth endothelial cells (BOEC) were also screened. Results: All cancer cell lines expressed high levels of VG5Q that were comparable to the levels expressed in endothelial cells. The only exception was MiaPaCa cells. In order to understand the biology of VG5Q in cancer cells, we used siRNA knockdown of VG5Q expression in the mesothelioma cell lines H2373 and H2596. Gene-specific silencing of VG5Q resulted in markedly decreased proliferation, invasion, and soft-agar colony formation in these cells. Furthermore, VG5Q silencing increased apoptosis as seen by an increase in annexin levels. Conclusion: VG5Q silencing has profound effects on cancer cell biology, suggesting the hypothesis that the role of VG5Q may not be limited to angiogenic signaling in endothelial cells.