Spatial and seasonal variation in leaf temperature within the canopy of a tropical forest

Understanding leaf temperature (Tleaf) variation in the canopy of tropical forests is critical for accurately calculating net primary productivity because plant respiration and net photosynthesis are highly sensitive to temperature. The objectives of this study were to (1) quantify the spatiotemporal variation of Tleaf in a semi-deciduous tropical forest in Panama and (2) create a season-specific empirical model to predict Tleaf in the canopy. To achieve this, we used a 42 m tall construction crane for canopy access and monitored the microenvironment within the canopy of mature, 20-35 m tall trees of 5 tropical tree species during the wet and the dry season. Tleaf was correlated to photosynthetic photon flux density (PPFD) in the wet season but not in the dry season, possibly due to seasonal differences in wind speed, physiology, and canopy phenology. A structural equation model showed that Tleaf is best explained by air temperature (Tair) and PPFD in the wet season, whereas in the dry season, Tair alone predicted most of the variation in Tleaf. These results suggest the utility of an empirical approach to estimate Tleaf variability where simple meteoro logical data are available. This approach can be incorporated in future models of vegetation-atmosphere carbon and water exchange models of mature tropical forests with similar seasonality. © Inter-Research 2016

Azithromycin for the Treatment of Chronic Cough in Idiopathic Pulmonary Fibrosis: A Randomized Controlled Cross-over Trial.

RATIONALE Patients with idiopathic pulmonary fibrosis (IPF) frequently suffer from difficult to treat chronic cough, which substantially affects their quality of life. Azithromycin has been demonstrated to relieve chronic cough in some populations, however this has not been investigated in IPF. OBJECTIVES To determine the safety and efficacy of azithromycin for the treatment of chronic cough in patients with IPF. METHODS In a double-blind randomized controlled cross-over trial, patients with IPF underwent two 12-week intervention periods (azithromycin 500mg or placebo 3 times per week). The primary outcome was change in cough-related quality of life measured by the Leicester cough questionnaire (LCQ). Secondary outcomes included cough severity measured using Visual Analog Scale (VAS), health-related quality of life assessed by the St. George's Respiratory Questionnaire (SGRQ), and objective cough frequency using audiovisual readings from 24h respiratory polygraphy. RESULTS 25 patients were randomized (23 men, 2 women), 20 patients completed the study. Mean (standard deviation, SD) age was 67 (8) years, mean (SD) forced vital capacity (FVC) was 65 (16) %-predicted, and diffusion capacity (DLCO) 43 (16) %-predicted. Mean (SD) baseline LCQ was 11.7 (3.7) and 11.3 (3.3) for the azithromycin and the placebo period, respectively, and the corresponding mean (SD) cough VAS 5.6 (2.3) and 5.8 (2.1). There was no significant change in LCQ and VAS with azithromycin or placebo. Similarly, there was no significant difference in change in polygraphy measured cough frequency between the azithromycin and placebo periods. Gastrointestinal adverse effects were more frequent with azithromycin than with placebo (diarrhea 43% vs 5%, p=0.03). CONCLUSIONS This randomized controlled trial does not support the use of low dose azithromycin for chronic cough in patients with IPF. Clinical trial registered with ClinicalTrials.gov (NCT02173145)

Case report on the spontaneous resolution of a traumatic intracranial acute subdural haematoma: evaluation of the guidelines

Rapid spontaneous resolution of traumatic acute subdural haematomas (ASDH) can occur but is rare. We present an 88-year-old female who presents with a large left acute subdural haematoma (ASDH) measuring 18 mm in thickness with midline shift of 10.7 mm. We managed her conservatively based upon good consciousness level and absent neurological deficits. Repeat computed tomography (CT) the following day demonstrated near complete resolution of the ASDH and midline shift regression; a further CT confirmed resolution. Most patients with large ASDH require surgical evacuation; however, in rare cases, they can resolve spontaneously with extreme rapidity. Conservative management can be a valid option in carefully selected cases

Not Hot, but Sharp: Dissociation of Pinprick and Heat Perception in Snake Eye Appearance Myelopathy

Following a traumatic spinal cord injury, a 53-year-old male developed a central cord syndrome with at-level neuropathic pain. Magnetic resonance imaging revealed a classical “snake eye” appearance myelopathy, with marked hyperintensities at C5-C7. Clinical examination revealed intact pinprick sensation coupled with lost or diminished thermal/heat sensation. This dissociation could be objectively confirmed through multi-modal neurophysiological assessments. Specifically, contact heat evoked potentials were lost at-level, while pinprick evoked potentials were preserved. This pattern corresponds with that seen after surgical commissural myelotomy. To our knowledge, this is the first time such a dissociation has been objectively documented, highlighting the diagnostic potential of multi-modal neurophysiological assessments. In future studies, a comprehensive assessment of different nociceptive modalities may help elucidate the pathophysiology of neuropathic pain

Haptoglobin genotype and outcome after spontaneous intracerebral haemorrhage

OBJECTIVE: Haptoglobin is a haemoglobin-scavenging protein that binds and neutralises free haemoglobin and modulates inflammation and endothelial progenitor cell function. A HP gene copy number variation (CNV) generates HP1 and HP2 alleles, while the single-nucleotide polymorphism rs2000999 influences their levels. The HP1 allele is hypothesised to improve outcome after spontaneous (non-traumatic) intracerebral haemorrhage (ICH). We investigated the associations of the HP CNV genotype and rs2000999 with haematoma volume, perihaematomal oedema (PHO) volume, functional outcome and mortality after ICH. METHODS: We included patients with neuroimaging-proven ICH, available DNA and 6-month follow-up in an observational cohort study (CROMIS-2). We classified patients into three groups according to the HP CNV: 1-1, 2-1 or 2-2 and also dichotomised HP into HP1-containing genotypes (HP1-1 and HP2-1) and HP2-2 to evaluate the HP1 allele. We measured ICH and PHO volume on CT; PHO was measured by oedema extension distance. Functional outcome was assessed by modified Rankin score (unfavourable outcome defined as mRS 3-6). RESULTS: We included 731 patients (mean age 73.4, 43.5% female). Distribution of HP CNV genotype was: HP1-1 n=132 (18.1%); HP2-1 n=342 (46.8%); and HP2-2 n=257 (35.2%). In the multivariable model mortality comparisons between HP groups, HP2-2 as reference, were as follows: OR HP1-1 0.73, 95% CI 0.34 to 1.56 (p value=0.41) and OR HP2-1 0.5, 95% CI 0.28 to 0.89 (p value=0.02) (overall p value=0.06). We found no evidence of association of HP CNV or rs200999 with functional outcome, ICH volume or PHO volume. CONCLUSION: The HP2-1 genotype might be associated with lower 6-month mortality after ICH; this finding merits further study

Urotropin azelate: a rather unwilling co-crystal

Urotropin (U) and azelaic acid (AA) form 1:1 co-crystals (UA) that give rise to a rather complex diffraction pattern, the main features of which are diffuse rods and bands in addition to the Bragg reflections. UA is characterized by solvent inclusions, parasite phases, and high vacancy and dislocation densities. These defects compounded with the pronounced tendency of U to escape from the crystal edifice lead to at least seven exotic phase transitions (many of which barely manifest themselves in a differential scanning calorimetry trace). These involve different incommensurate phases and a peritectoid reaction in the recrystallization regime (T-h >0.6). The system may be understood as an OD (order-disorder) structure based on a layer with layer group P(c)c2 and cell a(o) similar or equal to 4.7, b similar or equal to 26.1 and c similar or equal to 14.4 Angstrom. At 338 K the layer stacking is random, but with decreasing temperature the build-up of an orthorhombic MDO (maximal degree of order) structure with cell a(1) = 2a(o), b(1) = b, c(1) = c and space group Pcc2 is begun (at similar to 301 K). The superposition structure of the OD system at T = 286 (1) K with space group Bmmb and cell (a) over cap = 2a(o), (b) over cap = b and (c) over cap = c/2 owes its cohesion to van der Waals interactions between the AA chains and to three types of hydrogen bonds of varied strength between U-U and U-AA. Before reaching completion, this MDO structure is transformed, at 282 K, into a monoclinic one with cell a(m) = a(o) + c/4, b(m) = b, c(m) = -2(a(o) + c/2), space group P2(1)/c, spontaneous deformation similar to2degrees, and ferroelastic domains. This transformation is achieved in two steps: first a furtive triggering transition, which is not yet fully understood, and second an improper ferroelastic transition. At similar to 233 K, the system reaches its ground state (cell a(M) = a(m), bM = b, c(M) = c(m) and space group P2(1)/c) via an irreversible transition. The phase transitions below 338 K are described by a model based on the interaction of two thermally activated slip systems. The OD structure is described in terms of a three-dimensional Monte Carlo model that involves first- and second-neighbour interactions along the a axis and first-neighbour interactions along the b and c axes. This model includes random shifts of the chains along their axes and satisfactorily accounts for most features that are seen in the observed diffraction pattern

Two new rapid SNP-typing methods for classifying Mycobacterium tuberculosis complex into the main phylogenetic lineages

There is increasing evidence that strain variation in Mycobacterium tuberculosis complex (MTBC) might influence the outcome of tuberculosis infection and disease. To assess genotype-phenotype associations, phylogenetically robust molecular markers and appropriate genotyping tools are required. Most current genotyping methods for MTBC are based on mobile or repetitive DNA elements. Because these elements are prone to convergent evolution, the corresponding genotyping techniques are suboptimal for phylogenetic studies and strain classification. By contrast, single nucleotide polymorphisms (SNP) are ideal markers for classifying MTBC into phylogenetic lineages, as they exhibit very low degrees of homoplasy. In this study, we developed two complementary SNP-based genotyping methods to classify strains into the six main human-associated lineages of MTBC, the 'Beijing' sublineage, and the clade comprising Mycobacterium bovis and Mycobacterium caprae. Phylogenetically informative SNPs were obtained from 22 MTBC whole-genome sequences. The first assay, referred to as MOL-PCR, is a ligation-dependent PCR with signal detection by fluorescent microspheres and a Luminex flow cytometer, which simultaneously interrogates eight SNPs. The second assay is based on six individual TaqMan real-time PCR assays for singleplex SNP-typing. We compared MOL-PCR and TaqMan results in two panels of clinical MTBC isolates. Both methods agreed fully when assigning 36 well-characterized strains into the main phylogenetic lineages. The sensitivity in allele-calling was 98.6% and 98.8% for MOL-PCR and TaqMan, respectively. Typing of an additional panel of 78 unknown clinical isolates revealed 99.2% and 100% sensitivity in allele-calling, respectively, and 100% agreement in lineage assignment between both methods. While MOL-PCR and TaqMan are both highly sensitive and specific, MOL-PCR is ideal for classification of isolates with no previous information, whereas TaqMan is faster for confirmation. Furthermore, both methods are rapid, flexible and comparably inexpensive

Genome-Wide Association Study of Clinical Outcome After Aneurysmal Subarachnoid Haemorrhage: Protocol

Aneurysmal subarachnoid haemorrhage (aSAH) results in persistent clinical deficits which prevent survivors from returning to normal daily functioning. Only a small fraction of the variation in clinical outcome following aSAH is explained by known clinical, demographic and imaging variables; meaning additional unknown factors must play a key role in clinical outcome. There is a growing body of evidence that genetic variation is important in determining outcome following aSAH. Understanding genetic determinants of outcome will help to improve prognostic modelling, stratify patients in clinical trials and target novel strategies to treat this devastating disease. This protocol details a two-stage genome-wide association study to identify susceptibility loci for clinical outcome after aSAH using individual patient-level data from multiple international cohorts. Clinical outcome will be assessed using the modified Rankin Scale or Glasgow Outcome Scale at 1-24 months. The stage 1 discovery will involve meta-analysis of individual-level genotypes from different cohorts, controlling for key covariates. Based on statistical significance, supplemented by biological relevance, top single nucleotide polymorphisms will be selected for replication at stage 2. The study has national and local ethical approval. The results of this study will be rapidly communicated to clinicians, researchers and patients through open-access publication(s), presentation(s) at international conferences and via our patient and public network

Genome-Wide Association Study Identifies Risk Loci for Cluster Headache

OBJECTIVE: To identify susceptibility loci for cluster headache and obtain insights into relevant disease pathways. METHODS: We carried out a genome-wide association study, where 852 UK and 591 Swedish cluster headache cases were compared with 5,614 and 1,134 controls, respectively. Following quality control and imputation, single variant association testing was conducted using a logistic mixed model, for each cohort. The two cohorts were subsequently combined in a merged analysis. Downstream analyses, such as gene-set enrichment, functional variant annotation, prediction and pathway analyses, were performed. RESULTS: Initial independent analysis identified two replicable cluster headache susceptibility loci on chromosome 2. A merged analysis identified an additional locus on chromosome 1 and confirmed a locus significant in the UK analysis on chromosome 6, which overlaps with a previously known migraine locus. The lead single nucleotide polymorphisms were rs113658130 (p = 1.92 x 10-17 , OR [95%CI] = 1.51 [1.37-1.66]) and rs4519530 (p = 6.98 x 10-17 , OR = 1.47 [1.34-1.61]) on chromosome 2, rs12121134 on chromosome 1 (p = 1.66 x 10-8 , OR = 1.36 [1.22-1.52]) and rs11153082 (p = 1.85 x 10-8 , OR = 1.30 [1.19-1.42]) on chromosome 6. Downstream analyses implicated immunological processes in the pathogenesis of cluster headache. INTERPRETATION: We identified and replicated several genome-wide-significant associations supporting a genetic predisposition in cluster headache in a genome-wide association study involving 1,443 cases. Replication in larger independent cohorts combined with comprehensive phenotyping, in relation to e.g. treatment response and cluster headache subtypes, could provide unprecedented insights into genotype-phenotype correlations and the pathophysiological pathways underlying cluster headache