Effects of lameness treatment for claw horn lesions on lying behaviour in dairy cows

Lameness affects lying behaviour in dairy cattle, increasing total lying time and the number of lying bouts. However, there is limited information about the effect of lameness treatment on dairy cow behaviour. This study investigated the effect of four lameness treatments on lying behaviour (total lying time, number of bouts, average bout duration and laterality of lying) in dairy cows. Forty-four newly lame cows were treated randomly with one of four treatment protocols: trim only, trim + block, trim + NSAID, and trim + block + NSAID. Thirty-four non-lame control cows were matched by parity, days in milk, and farm-pen. Each cow had an accelerometer attached to the hind leg, lying behaviour data was collected over 5 days immediately after treatment and analysed using multilevel regression models. Lame cows in three of the four treatment groups demonstrated no increase in lying time compared to non-lame controls. This finding is contrary to previous work and may reflect the enrolment criteria which favoured the selection of cows with mild disease i.e. before the behavioural impacts of lameness had manifested. Only cows in the treatment group which received a therapeutic trim and a foot block saw higher lying times post treatment. As this effect was not apparent in the group which received a NSAID in addition to a trim and a foot block, we hypothesise that this effect is caused by discomfort associated with the block. Where foot blocks are administered as part of treatment protocols, we propose that NSAIDs should be administered concurrently to alleviate the behavioural changes and likely discomfort associated with this treatment

White matter disturbances in major depressive disorder : a coordinated analysis across 20 international cohorts in the ENIGMA MDD working group

Altres ajuts: The ENIGMA-Major Depressive Disorder working group gratefully acknowledges support from the NIH Big Data to Knowledge (BD2K) award (U54 EB020403 to PMT) and NIH grant R01 MH116147 (PMT). LS is supported by an NHMRC MRFF Career Development Fellowship (APP1140764). We wish to acknowledge the patients and control subjects that have particiaped int the study. We thank Rosa Schirmer, Elke Schreiter, Reinhold Borschke and Ines Eidner for image acquisition and data preparation, and Anna Oliynyk for quality checks. We thank Dorothee P. Auer and F. Holsboer for initiation of the RUD study. We wish to acknowledge the patients and control subjects that have particiaped int the study. We thank Rosa Schirmer, Elke Schreiter, Reinhold Borschke and Ines Eidner for image acquisition and data preparation, and Anna Oliynyk for quality checks. We thank Dorothee P. Auer and F. Holsboer for initiation of the RUD study. NESDA: The infrastructure for the NESDA study (www.nesda.nl) is funded through the Geestkracht program of the Netherlands Organisation for Health Research and Development (Zon-Mw, grant number 10-000-1002) and is supported by participating universities (VU University Medical Center, GGZ inGeest, Arkin, Leiden University Medical Center, GGZ Rivierduinen, University Medical Center Groningen) and mental health care organizations, see www.nesda.nl. M-JvT was supported by a VENI grant (NWO grant number 016.156.077). UCSF: This work was supported by the Brain and Behavior Research Foundation (formerly NARSAD) to TTY; the National Institute of Mental Health (R01MH085734 to TTY; K01MH117442 to TCH) and by the American Foundation for Suicide Prevention (PDF-1-064-13) to TCH. Stanford: This work was supported by NIMH Grants R01MH59259 and R37101495 to IHG. MS is partially supported by an award funded by the Phyllis and Jerome Lyle Rappaport Foundation. Muenster: This work was funded by the German Research Foundation (SFB-TRR58, Projects C09 and Z02 to UD) and the Interdisciplinary Center for Clinical Research (IZKF) of the medical faculty of Münster (grant Dan3/012/17 to UD). Marburg: This work was funded by the German Research Foundation (DFG, grant FOR2107 DA1151/5-1 and DA1151/5-2 to UD; KI 588/ 14-1, KI 588/14-2 to TK; KR 3822/7-1, KR 3822/7-2 to AK; JA 1890/ 7-1, JA 1890/7-2 to AJ). IMH-MDD: This work was supported by the National Healthcare Group Research Grant (SIG/15012) awarded to KS. Barcelona: This study was funded by two grants of the Fondo de Investigación Sanitaria from the Instituto de Salud Carlos III, by the Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM). The author is funded through 'Miguel Servet' research contract (CP16-0020), co-financed by the European Regional Development Fund (ERDF) (2016-2019). QTIM: We thank the twins and singleton siblings who gave generously of their time to participate in the QTIM study. We also thank the many research assistants, radiographers, and IT support staff for data acquisition and DNA sample preparation. This study was funded by White matter disturbances in major depressive disorder: a coordinated analysis across 20 international. . . 1521 the National Institute of Child Health & Human Development (RO1 HD050735); National Institute of Biomedical Imaging and Bioengineering (Award 1U54EB020403-01, Subaward 56929223); National Health and Medical Research Council, Australia (Project Grants 496682, 1009064). NIH ENIGMA-BD2K U54 EB020403 (Thompson); R01 MH117601 (Jahanshad/Schmaal). Magdeburg: M.L. and M.W. are funded by SFB 779. Bipolar Family Study: This study has received funding from the European Community's Seventh Framework Programme (FP7/2007-2013). This paper reflects only the author's views and the European Union is not liable for any use that may be made of the information contained therein. This work was also supported by a Wellcome Trust Strategic Award (104036/Z/14/Z). Minnesota Adolescent Depression Study: The study was funded by the National Institute of Mental Health (K23MH090421), the National Alliance for Research on Schizophrenia and Depression, the University of Minnesota Graduate School, the Minnesota Medical Foundation, and the Biotechnology Research Center (P41 RR008079 to the Center for Magnetic Resonance Research), University of Minnesota, and the Deborah E. Powell Center for Women's Health Seed Grant, University of Minnesota. Dublin: This study was supported by Science Foundation Ireland through a Stokes Professorhip grant to TF. MPIP: The MPIP Sample comprises patients included in the Recurrent Unipolar Depression (RUD) Case-Control study at the clinic of the Max Planck Institute of Psychiatry, Munich, German. The RUD study was supported by GlaxoSmithKline.Alterations in white matter (WM) microstructure have been implicated in the pathophysiology of major depressive disorder (MDD). However, previous findings have been inconsistent, partially due to low statistical power and the heterogeneity of depression. In the largest multi-site study to date, we examined WM anisotropy and diffusivity in 1305 MDD patients and 1602 healthy controls (age range 12-88 years) from 20 samples worldwide, which included both adults and adolescents, within the MDD Working Group of the Enhancing Neuroimaging Genetics through Meta-Analysis (ENIGMA) consortium. Processing of diffusion tensor imaging (DTI) data and statistical analyses were harmonized across sites and effects were meta-analyzed across studies. We observed subtle, but widespread, lower fractional anisotropy (FA) in adult MDD patients compared with controls in 16 out of 25 WM tracts of interest (Cohen's d between 0.12 and 0.26). The largest differences were observed in the corpus callosum and corona radiata. Widespread higher radial diffusivity (RD) was also observed (all Cohen's d between 0.12 and 0.18). Findings appeared to be driven by patients with recurrent MDD and an adult age of onset of depression. White matter microstructural differences in a smaller sample of adolescent MDD patients and controls did not survive correction for multiple testing. In this coordinated and harmonized multisite DTI study, we showed subtle, but widespread differences in WM microstructure in adult MDD, which may suggest structural disconnectivity in MDD

Assessing impacts and responses to global-mean sea-level rise

One of the more certain impacts of human-induced climate change is a rise in global-mean sea level (Nicholls and Lowe, 2004). While the impacts of this sea-level rise are confined to coastal areas, these include the most densely populated land areas on Earth and they support important and productive ecosystems that are sensitive to sea-level change. Further, coasts are also experiencing significant human-induced modification, so sea-level rise and climate change are an additional stress, which amplifies their impacts (Bijlsma, 1996; Kremer et al., 2005). During the twenty-first century, global-mean sea-level rise will likely be less than 1 metre (Church and Gregory, 2001), but still potentially directly affecting at least 200 million people based on 1990 population (Hoozemans et al., 1993; Mimura, 2000). Over the longer term (many centuries), a much larger sea-level rise exceeding 10 m is possible under some emission pathways owing to ablation of the Greenland Ice Sheet and collapse of the West Antarctic Ice Sheet, among other changes (Oppenheimer and Alley, 2004; Nicholls and Lowe, 2005). Further, the high human exposure to sea-level rise is increasing rapidly because of global population growth and coastward migration. Therefore, any global assessment of the climate change issue must include the coastal implications. A fundamental result that has long been recognized by climate scientists, but less considered by policy, is that irrespective of future greenhouse gas emissions, there is a “commitment to sea-level rise” (Nicholls and Lowe, 2004; 2005)