58 research outputs found
Wood Properties of Twenty Highly Ranked Radiata Pine Seed Production Parents Selected for Growth and Form
Twenty highly ranked radiata pine (Pinus radiata D. Don) seed production parent trees, grown under a commercial sawlog regime, were destructively assessed at rotation age (27 years) for wood quality traits significant to solid-wood and veneer products, including: juvenile-wood density, density variation, juvenile-wood spiral grain, compression wood, and appearance characteristics such as within-ring internal checking and resin pockets. Traits varied considerably among parents, which is reasonable since breeding efforts in New Zealand have, until recently, focused primarily on stem productivity and form. Parental information is useful for many wood properties owing to their high heritabilities in radiata pine (usually 50-80%); thus production forests established using advanced-generation genetic materials can also be expected to be variable in wood properties. Like other fastgrown pines, much of the radiata pine crop is juvenile wood, and an important challenge for tree improvement is to ensure that juvenile wood properties meet processor and end-user requirements
Genomic Fossils Calibrate the Long-Term Evolution of Hepadnaviruses
Ancient hepadnavirus sequences found in bird genomes reveal that this family of viruses, which includes the human hepatitis B virus, is much older than previously thought
The Potential Role of ORM2 in the Development of Colorectal Cancer
Colorectal cancer (CRC) is the third most common malignancy in the world. The risk of death is closely correlated to the stage of CRC at the time of primary diagnosis. Therefore, there is a compelling need for the identification of blood biomarkers that can enable early detection of CRC. We used a quantitative proteomic approach with isobaric labeling (iTRAQ) to examine changes in the plasma proteome of 10 patients with CRC compared to healthy volunteers. Enzyme-Linked Immunosorbnent Assay (ELISA) and Western blot were used for further validation. In our quantitative proteomics analysis, we detected 75 human plasma proteins with more than 95% confidence using iTRAQ labeling in conjunction with microQ-TOF MS. 9 up-regulated and 4 down-regulated proteins were observed in the CRC group. The ORM2 level in plasma was confirmed to be significantly elevated in patients suffering from CRC compared with the controls. ORM2 expression in CRC tissues was significantly increased compared with that in corresponding adjacent normal mucous tissues (P<0.001). ITRAQ together with Q-TOF/MS is a sensitive and reproducible technique of quantitative proteomics. Alteration in expression of ORM2 suggests that ORM2 could be used as a potential biomarker in the diagnosis of CRC
T2-weighted cardiovascular magnetic resonance in acute cardiac disease
Cardiovascular magnetic resonance (CMR) using T2-weighted sequences can visualize myocardial edema. When compared to previous protocols, newer pulse sequences with substantially improved image quality have increased its clinical utility. The assessment of myocardial edema provides useful incremental diagnostic and prognostic information in a variety of clinical settings associated with acute myocardial injury. In patients with acute chest pain, T2-weighted CMR is able to identify acute or recent myocardial ischemic injury and has been employed to distinguish acute coronary syndrome (ACS) from non-ACS as well as acute from chronic myocardial infarction
Translating cardioprotection for patient benefit: Position paper from the Working Group of Cellular Biology of the Heart of the European Society of Cardiology
Coronary heart disease (CHD) is the leading cause of death and disability worldwide. Despite current therapy, the morbidity and mortality for patients with CHD remains significant. The most important manifestations of CHD arise from acute myocardial ischaemia-reperfusion injury (IRI) in terms of cardiomyocyte death and its long-term consequences. As such, new therapeutic interventions are required to protect the heart against the detrimental effects of acute IRI and improve clinical outcomes. Although a large number of cardioprotective therapies discovered in pre-clinical studies have been investigated in CHD patients, few have been translated into the clinical setting, and a significant number of these have failed to show any benefit in terms of reduced myocardial infarction and improved clinical outcomes. Because of this, there is currently no effective therapy for protecting the heart against the detrimental effects of acute IRI in patients with CHD. One major factor for this lack of success in translating cardioprotective therapies into the clinical setting can be attributed to problems with the clinical study design. Many of these clinical studies have not taken into consideration the important data provided from previously published pre-clinical and clinical studies. The overall aim of this ESC Working Group Cellular Biology of the Heart Position Paper is to provide recommendations for optimizing the design of clinical cardioprotection studies, which should hopefully result in new and effective therapeutic interventions for the future benefit of CHD patients
Ischaemic conditioning and reperfusion injury
The 30-year anniversary of the discovery of 'ischaemic preconditioning' is in 2016. This endogenous phenomenon can paradoxically protect the heart from acute myocardial infarction by subjecting it to one or more brief cycles of ischaemia and reperfusion. Apart from complete reperfusion, this method is the most powerful intervention known for reducing infarct size. The concept of ischaemic preconditioning has evolved into 'ischaemic conditioning', a term that encompasses a number of related endogenous cardioprotective strategies, applied either directly to the heart (ischaemic preconditioning or postconditioning) or from afar, for example a limb (remote ischaemic preconditioning, perconditioning, or postconditioning). Investigations of signalling pathways underlying ischaemic conditioning have identified a number of therapeutic targets for pharmacological manipulation. Over the past 3 decades, a number of ischaemic and pharmacological cardioprotection strategies, discovered in experimental studies, have been examined in the clinical setting of acute myocardial infarction and CABG surgery. The results from many of the studies have been disappointing, and no effective cardioprotective therapy is currently used in clinical practice. Several large, multicentre, randomized, controlled clinical trials on cardioprotection have highlighted the challenges of translating ischaemic conditioning and pharmacological cardioprotection strategies into patient benefit. However, a number of cardioprotective therapies have shown promising results in reducing infarct size and improving clinical outcomes in patients with ischaemic heart disease
Novel targets and future strategies for acute cardioprotection: Position Paper of the European Society of Cardiology Working Group on Cellular Biology of the Heart
Ischaemic heart disease and the heart failure that often results, remain the leading causes of death and disability in Europe and worldwide. As such, in order to prevent heart failure and improve clinical outcomes in patients presenting with an acute ST-segment elevation myocardial infarction and patients undergoing coronary artery bypass graft surgery, novel therapies are required to protect the heart against the detrimental effects of acute ischaemia/reperfusion injury. During the last three decades, a wide variety of ischaemic conditioning strategies and pharmacological treatments have been tested in the clinic - however, their translation from experimental to clinical studies for improving patient outcomes has been both challenging and disappointing. Therefore, in this Position Paper of the European Society of Cardiology Working Group on Cellular Biology of the Heart, we critically analyse the current state of ischaemic conditioning in both the experimental and clinical settings, provide recommendations for improving its translation into the clinical setting, and highlight novel therapeutic targets and new treatment strategies for reducing acute myocardial ischaemia/reperfusion injury
Involvement of nerves and calcium channels in the intestinal response to Clostridium difficile toxin A: an experimental study in rats in vivo
BACKGROUND—The involvement of nerves and calcium channels in the intestinal response to Clostridium difficile toxin A (luminal concentration 1 or 15 µg/ml) was studied in the small intestine of rats in vivo.
METHODS—Inflammation was quantified by estimating myeloperoxidase (MPO) activity in the intestinal lumen, extravascular accumulation of Evan's blue (EB) in the intestine, and number of red blood cells (RBCs) in veins in histological sections. Intestinal damage was estimated using a histological grading system. In some experiments net fluid transport was recorded using a gravimetric technique.
RESULTS—In acutely denervated intestines, toxin A caused marked destruction of the villi, increased luminal release of MPO activity, and augmentation of intestinal content of EB and venous RBCs. Denervating the intestine 3-4 weeks prior to the actual experiment prevented the development of villus damage and significantly decreased the number of RBCs in intestinal veins in experiments with a low toxin concentration, whereas no effect was demonstrated on luminal MPO activity. Using a high toxin concentration, chronic denervation decreased only the number of RBCs. Pretreatment with hexamethonium (low toxin concentration; acute denervation) attenuated the effect of toxin A on morphology, luminal MPO activity, and number of RBCs. Pretreatment with nifedipine (low toxin concentration; acute denervation) significantly decreased intestinal MPO activity and number of RBCs. Tissue accumulation of EB was not influenced by experimental manipulation. Net fluid transport was measured in experiments exposing the intestinal mucosa to a high toxin concentration. Fluid secretion caused by the toxin was significantly attenuated by intravenous hexamethonium whereas no effect was observed after administration of nifedipine or granisetron.
CONCLUSIONS—At a low toxin concentration, intramural reflexes are involved in the inflammatory response whereas axon reflexes contribute to tissue damage. At a high toxin concentration no nervous involvement in the toxin A response was demonstrated except for fluid secretion evoked by the toxin.


Keywords: cholera toxin; enteric nervous system; 5-hydroxytryptamine; myeloperoxidase; red blood cell
Forage dry matter yields and psyllid resistance of thirty-one leucaena selections in Hawaii
Forage yields of L. leucocephala (Lam). de Wit have been reduced as the result of psyllid damage since Heteropsylla cubana Crawford invaded the Hawaiian Islands in 1984. The forage productivity and psyllid resistance of 31 Leucaena species and interspecific hybrids were assessed from 5 harvests in Hawaii during 1991 and 1992. The trial consisted of an augmented randomized complete block with 22 Leucaena selections in all 4 replicates, 2 selections in 3 replicates and 7 selections in 1 or 2 replicates. Forage (leaves and stems < 6 mm diam.) dry matter (DM) biomass yield over a 13-month period ranged from 1.4 to 34 Mg ha from total DM ranging from 1.9 to 63.7 Mg ha. Percent forage fractions ranged from 49 to 78% (forage DM/total DM). The 10 selections in this trial of either L. pallida Britton & Rose, and its hybrids with L. leucocephala consistently produced both the highest forage and total DM yields averaging 22 and 40 Mg ha, respectively. This represented a three-fold increase in forage production when compared to L. leucocephala K636 (a standard around the world). The excellent performance of the L. pallida lines was attributed to high psyllid resistance and seedling vigor. All L. pallida selections with the exception of K953 exhibited good psyllid resistance. Leucaena diversifolia Benth. K749, L. pallida K376, and L. esculenta (Moc. & Sesse) Benth. K950 had the highest psyllid resistance (
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