Quantification of channel planform change on the lower Rangitikei River, New Zealand, 1949-2007: response to management?

The Rangitikei River, a large gravel‐bed wandering river located in the North Island of New Zealand, has outstanding scenic characteristics, recreational, fisheries and wildlife habitat features. Recently concerns have been raised over the potential negative impact that perceived channel changes in the latter part of the 20th century may be having on the Rangitikei River recreational fishery. This study describes and quantifies the large‐scale morphological changes that have occurred in selected reaches of the lower Rangitikei River between 1949 and 2007. This research utilised historical aerial photography and analysis in ArcGIS® to quantify channel planform change in three reaches, encompassing ~18 km of the lower Rangitikei River. This showed that the lower Rangitikei was transformed from a multi‐channelled planform to a predominantly single‐thread wandering planform, with an associated reduction in morphological complexity and active channel width of up to 74%, between 1949 and 2007. Bank protection measures instigated under the Rangitikei River Scheme have primarily driven these changes. Gravel extraction has also contributed by enhancing channel‐floodplain disconnection and exacerbating sediment deficits. The findings of this study have implications for future management of the Rangitikei. Previous lower Rangitikei River management schemes have taken a reach‐based engineering approach with a focus on bank erosion protection and flood mitigation. This study has confirmed the lower river has responded geomorphologically to these goals of river control. However questions as to the economic and ecological sustainability of this management style may encourage river managers to consider the benefits of promoting a self‐adjusting fluvial system within a catchment‐framed management approach

Role of Phospholipase Cβ3 Phosphorylation in the Desensitization of Cellular Responses to Platelet-Activating Factor

Platelet-activating factor (PAF) stimulates a diverse array of cellular responses through receptors coupled to G proteins that activate phospholipase C (PLC). Truncation of the cytoplasmic tail of the receptor to remove phosphorylation sites (mutant PAF receptor, mPAFR) results in enhancement of PAF-stimulated responses. Here we demonstrate that PAF or phorbol 12- myristate 13-acetate (PMA) pretreatment inhibited wild type PAFR-induced PLC- mediated responses by ~90%, whereas these responses to the phosphorylation- deficient mPAFR were inhibited by ~50%, despite normal G protein coupling, suggesting a distal inhibitory locus. PAF and PMA, as well as a membrane permeable cyclic AMP analog, stimulated phosphorylation of PLCβ3. A protein kinase C (PKC) inhibitor blocked phosphorylation of PLCβ3 stimulated by PAF and PMA but not by cAMP. Activation of protein kinase A (PKA) by cAMP did not result in inhibition of Ca2+ mobilization stimulated by PAF. In contrast, cAMP did inhibit the response to formylpeptide chemoattractant receptor. These data suggest that homologous desensitization of PAF-mediated responses is regulated via phosphorylation at two levels in the signaling pathway, one at the receptor and the other at PLCβ3 mediated by PKC but not by PKA. Phosphorylation of PLCβ3 by PKA could explain the inhibition of formylpeptide chemoattractant receptor signaling by cAMP. As PAF and formylpeptide chemoattractant receptors activate PLC via different G proteins, phosphorylation of PLCβ3 by PKC and PKA could provide distinct regulatory control for classes of G protein-coupled receptors

Evaluating the role of a galanin enhancer genotype on a range of metabolic, depressive and addictive phenotypes

Funded by •ERC. Grant Number: 284167 •NIH. Grant Number: 1RO1DK0921127-01 •NWO. Grant Numbers: 463-06-001, 451-04-034Peer reviewedPublisher PD

Prevalence of PTSD in Survivors of Stroke and Transient Ischemic Attack: A Meta-Analytic Review

Background and Purpose Posttraumatic stress disorder (PTSD) is common in survivors of acute life-threatening illness, but little is known about the burden of PTSD in survivors of stroke and transient ischemic attack (TIA). This study estimated the prevalence of stroke or TIA-induced posttraumatic stress disorder (PTSD) using systematic review and meta-analysis. Methods Potentially relevant peer-reviewed journal articles were identified by searching the Ovid MEDLINE, PsycINFO, PILOTS Database, The Cochrane Library and Scopus from inception to January 2013; all searches were conducted on January 31, 2013. Observational cohort studies that assessed PTSD with specific reference to a stroke or TIA that occurred at least 1 month prior to the PTSD assessment were included. PTSD rates and characteristics of the study and sample were abstracted from all included studies. The coding of all articles included demographics, sample size, study country, and method and timing of PTSD assessment. Results Nine studies (N = 1,138) met our inclusion criteria. PTSD rates varied significantly across studies by timing of PTSD assessment (i.e., within 1 year of stroke/TIA versus greater than 1 year post-stroke/TIA; 55% of heterogeneity explained; Q1 = 10.30; P = .001). Using a random effects model, the estimated rate of PTSD following stroke or TIA was 23% (95% CI, 16%–33%) within 1 year of the stroke or TIA and 11% (95% CI, 8%–14%) after 1 year. Conclusions Although PTSD is commonly thought to be triggered by external events such as combat or sexual assault, these results suggest that 1 in 4 stroke or TIA survivors develop significant PTSD symptoms due to the stroke or TIA. Screening for PTSD in a large population-based prospective cohort study with cardiovascular outcome assessments is needed to yield definitive prevalence, and determine whether stroke or TIA-induced PTSD is a risk factor for subsequent cardiovascular events or mortality

Differential Regulation of Formyl Peptide and Platelet-Activating Factor Receptors: Role of Phospholipase Cβ3 Phosphorylation by Protein Kinase A

Formylated peptides (e.g. n-formyl-Met-Leu-Phe (fMLP)) and platelet- activating factor (PAF) mediate chemotactic and cytotoxic responses in leukocytes through receptors coupled to G proteins that activate phospholipase C (PLC). In RBL-2H3 cells, fMLP utilizes a pertussis toxin (ptx)-sensitive G protein to activate PLC, whereas PAF utilizes a ptx- insensitive G protein. Here we demonstrate that fMLP, but not PAF, enhanced intracellular cAMP levels via a ptx-sensitive mechanism. Protein kinase A (PKA) inhibition by H-89 enhanced inositol phosphate formation stimulated by fMLP but not PAF. Furthermore, a membrane-permeable cAMP analog 8-(4- chlorophenylthio)-cAMP (cpt-cAMP) inhibited phosphoinositide hydrolysis and secretion stimulated by fMLP but not PAF. Both cpt-cAMP and fMLP stimulated PLCβ3 phosphorylation in intact RBL cells. The purified catalytic subunit of PKA phosphorylated PLCβ3 immunoprecipitated from RBL cell lysate. Pretreatment of intact cells with cpt-cAMP and fMLP, but not PAF, resulted in an inhibition of subsequent PLCβ3 phosphorylation by PKA in vitro. These data demonstrate that fMLP receptor, which couples to a ptx-sensitive G protein, activates both PLC and cAMP production. The resulting PKA activation phosphorylates PLCβ3 and appears to block the ability of G(βγ) to activate PLC. Thus, both fMLP and PAF generate stimulatory signals for PLCβ3, but only fMLP produces a PKA-dependent inhibitory signal. This suggests a novel mechanism for the bidirectional regulation of receptors which activate PLC by ptx-sensitive G proteins