Insecticidal activity of essential oil of Cinnamomum cassia and its main constituent, trans-Cinnamaldehyde, against the booklice, Liposcelis bostrychophila

Purpose: To investigate the insecticidal activity of the essential oil of Cinnamomum cassis and its main constituent compound, trans-cinnamaldehyde, against the booklice, Liposcelis bostrychophila．Methods: Steam distillation of C. cassis twigs was carried out using a Clavenger apparatus in order to obtain the volatile oils. Gas chromatography/mass spectrometric (GC/MS) analyses (HP-5MS column) of the essential oil were performed and its contact (using impregnated filter paper method) and fumigant toxicity (sealed space) determined. The bioactive constituent compound, trans-cinnamaldehyde was isolated and identified from the oil based on bioactivity-directed fractionation.Results: A total of 35 components, accounting for 97.44 % of the essential oil of C. cassis, were identified. The principal compounds in the essential oil were trans-cinnamaldehyde (49.33 %), acetophenone (6.94 %), trans-cinnamic acid (5.45 %) and cis-cinnamaldehyde (4.44 %) followed by omethoxycinnamaldehyde (3.48 %), coumarin (3.42 %) and (E)-cinnamyl alcohol (3.21 %). The essential oil displayed contact toxicity against adult L. bostrychophila with a median lethal concentration (LC50) of 55.68 μg/cm2 as well as fumigant toxicity (LC50, 1.33 mg/l air). Trans-cinnamaldehyde exhibited strong contact and fumigant toxicity with LC50 and 1.29 mg/l air, respectively.Conclusion: The findings suggest that the essential oil of C. cassis and its constituent compound, trans-cinnamaldehyde, possess potentials for development into natural fumigants/insecticides for the control of booklice.Keywords: Liposcelis bostrychophila, Cinnamomum cassis, Contact toxicity, Fumigant, trans- Cinnamaldehyde, Essential oi

Identification of masses in digital mammogram using gray level co-occurrence matrices

Digital mammogram has become the most effective technique for early breast cancer detection modality. Digital mammogram takes an electronic image of the breast and stores it directly in a computer. The aim of this study is to develop an automated system for assisting the analysis of digital mammograms. Computer image processing techniques will be applied to enhance images and this is followed by segmentation of the region of interest (ROI). Subsequently, the textural features will be extracted from the ROI. The texture features will be used to classify the ROIs as either masses or non-masses. In this study normal breast images and breast image with masses used as the standard input to the proposed system are taken from Mammographic Image Analysis Society (MIAS) digital mammogram database. In MIAS database, masses are grouped into either spiculated, circumscribed or ill-defined. Additional information includes location of masses centres and radius of masses. The extraction of the textural features of ROIs is done by using gray level co-occurrence matrices (GLCM) which is constructed at four different directions for each ROI. The results show that the GLCM at 0º, 45º, 90º and 135º with a block size of 8X8 give significant texture information to identify between masses and non-masses tissues. Analysis of GLCM properties i.e. contrast, energy and homogeneity resulted in receiver operating characteristics (ROC) curve area of Az = 0.84 for Otsu’s method, 0.82 for thresholding method and Az = 0.7 for K-mean clustering. ROC curve area of 0.8-0.9 is rated as good results. The authors’ proposed method contains no complicated algorithm. The detection is based on a decision tree with five criterions to be analysed. This simplicity leads to less computational time. Thus, this approach is suitable for automated real-time breast cancer diagnosis system

Warped Riemannian metrics for location-scale models

The present paper shows that warped Riemannian metrics, a class of Riemannian metrics which play a prominent role in Riemannian geometry, are also of fundamental importance in information geometry. Precisely, the paper features a new theorem, which states that the Rao-Fisher information metric of any location-scale model, defined on a Riemannian manifold, is a warped Riemannian metric, whenever this model is invariant under the action of some Lie group. This theorem is a valuable tool in finding the expression of the Rao-Fisher information metric of location-scale models defined on high-dimensional Riemannian manifolds. Indeed, a warped Riemannian metric is fully determined by only two functions of a single variable, irrespective of the dimension of the underlying Riemannian manifold. Starting from this theorem, several original contributions are made. The expression of the Rao-Fisher information metric of the Riemannian Gaussian model is provided, for the first time in the literature. A generalised definition of the Mahalanobis distance is introduced, which is applicable to any location-scale model defined on a Riemannian manifold. The solution of the geodesic equation is obtained, for any Rao-Fisher information metric defined in terms of warped Riemannian metrics. Finally, using a mixture of analytical and numerical computations, it is shown that the parameter space of the von Mises-Fisher model of $n$-dimensional directional data, when equipped with its Rao-Fisher information metric, becomes a Hadamard manifold, a simply-connected complete Riemannian manifold of negative sectional curvature, for $n = 2,\ldots,8$. Hopefully, in upcoming work, this will be proved for any value of $n$.Comment: first version, before submissio

Microbial ligand costimulation drives neutrophilic steroid-refractory asthma

Funding: The authors thank the Wellcome Trust (102705) and the Universities of Aberdeen and Cape Town for funding. This research was also supported, in part, by National Institutes of Health GM53522 and GM083016 to DLW. KF and BNL are funded by the Fonds Wetenschappelijk Onderzoek, BNL is the recipient of an European Research Commission consolidator grant and participates in the European Union FP7 programs EUBIOPRED and MedALL. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Peer reviewedPublisher PD

Safety of Artemether-Lumefantrine Exposure in First Trimester of Pregnancy: An Observational Cohort.

There is limited data available regarding safety profile of artemisinins in early pregnancy. They are, therefore, not recommended by WHO as a first-line treatment for malaria in first trimester due to associated embryo-foetal toxicity in animal studies. The study assessed birth outcome among pregnant women inadvertently exposed to artemether-lumefantrine (AL) during first trimester in comparison to those of women exposed to other anti-malarial drugs or no drug at all during the same period of pregnancy. Pregnant women with gestational age <20 weeks were recruited from Maternal Health clinics or from monthly house visits (demographic surveillance), and followed prospectively until delivery. 2167 pregnant women were recruited and 1783 (82.3%) completed the study until delivery. 319 (17.9%) used anti-malarials in first trimester, of whom 172 (53.9%) used (AL), 78 (24.4%) quinine, 66 (20.7%) sulphadoxine-pyrimethamine (SP) and 11 (3.4%) amodiaquine. Quinine exposure in first trimester was associated with an increased risk of miscarriage/stillbirth (OR 2.5; 1.3-5.1) and premature birth (OR 2.6; 1.3-5.3) as opposed to AL with (OR 1.4; 0.8-2.5) for miscarriage/stillbirth and (OR 0.9; 0.5-1.8) for preterm birth. Congenital anomalies were identified in 4 exposure groups namely AL only (1/164[0.6%]), quinine only (1/70[1.4%]), SP (2/66[3.0%]), and non-anti-malarial exposure group (19/1464[1.3%]). Exposure to AL in first trimester was more common than to any other anti-malarial drugs. Quinine exposure was associated with adverse pregnancy outcomes which was not the case following other anti-malarial intake. Since AL and quinine were used according to their availability rather than to disease severity, it is likely that the effect observed was related to the drug and not to the disease itself. Even with this caveat, a change of policy from quinine to AL for the treatment of uncomplicated malaria during the whole pregnancy period could be already envisaged.\u

Hypoxia increases neutrophil-driven matrix destruction after exposure to Mycobacterium tuberculosis.

The importance of neutrophils in the pathology of tuberculosis (TB) has been recently established. We demonstrated that TB lesions in man are hypoxic, but how neutrophils in hypoxia influence lung tissue damage is unknown. We investigated the effect of hypoxia on neutrophil-derived enzymes and tissue destruction in TB. Human neutrophils were stimulated with M. tuberculosis (M.tb) or conditioned media from M.tb-infected monocytes (CoMTB). Neutrophil matrix metalloproteinase-8/-9 and elastase secretion were analysed by luminex array and gelatin zymography, gene expression by qPCR and cell viability by flow cytometry. Matrix destruction was investigated by confocal microscopy and functional assays and neutrophil extracellular traps (NETs) by fluorescence assay. In hypoxia, neutrophil MMP-8 secretion and gene expression were up-regulated by CoMTB. MMP-9 activity and neutrophil elastase (NE) secretion were also increased in hypoxia. Hypoxia inhibited NET formation and both neutrophil apoptosis and necrosis after direct stimulation by M.tb. Hypoxia increased TB-dependent neutrophil-mediated matrix destruction of Type I collagen, gelatin and elastin, the main structural proteins of the human lung. Dimethyloxalylglycin (DMOG), which stabilizes hypoxia-inducible factor-1α, increased neutrophil MMP-8 and -9 secretion. Hypoxia in our cellular model of TB up-regulated pathways that increase neutrophil secretion of MMPs that are implicated in matrix destruction

Theorems for asymptotic safety of gauge theories

We classify the weakly interacting fixed points of general gauge theories coupled to matter and explain how the competition between gauge and matter fluctuations gives rise to a rich spectrum of high- and low-energy fixed points. The pivotal role played by Yukawa couplings is emphasised. Necessary and sufficient conditions for asymptotic safety of gauge theories are also derived, in conjunction with strict no go theorems. Implications for phase diagrams of gauge theories and physics beyond the Standard Model are indicated

Glial cell type-specific changes in spinal dipeptidyl peptidase 4 expression and effects of its inhibitors in inflammatory and neuropatic pain

Altered pain sensations such as hyperalgesia and allodynia are characteristic features of various pain states, and remain difficult to treat. We have shown previously that spinal application of dipeptidyl peptidase 4 (DPP4) inhibitors induces strong antihyperalgesic effect during inflammatory pain. In this study we observed low level of DPP4 mRNA in the rat spinal dorsal horn in physiological conditions, which did not change significantly either in carrageenan-induced inflammatory or partial nerve ligation-generated neuropathic states. In naive animals, microglia and astrocytes expressed DPP4 protein with one and two orders of magnitude higher than neurons, respectively. DPP4 significantly increased in astrocytes during inflammation and in microglia in neuropathy. Intrathecal application of two DPP4 inhibitors tripeptide isoleucin-prolin-isoleucin (IPI) and the antidiabetic drug vildagliptin resulted in robust opioid-dependent antihyperalgesic effect during inflammation, and milder but significant opioid-independent antihyperalgesic action in the neuropathic model. The opioid-mediated antihyperalgesic effect of IPI was exclusively related to mu-opioid receptors, while vildagliptin affected mainly delta-receptor activity, although mu- and kappa-receptors were also involved. None of the inhibitors influenced allodynia. Our results suggest pathology and glia-type specific changes of DPP4 activity in the spinal cord, which contribute to the development and maintenance of hyperalgesia and interact with endogenous opioid systems

Essential versus accessory aspects of cell death: recommendations of the NCCD 2015

Cells exposed to extreme physicochemical or mechanical stimuli die in an uncontrollable manner, as a result of their immediate structural breakdown. Such an unavoidable variant of cellular demise is generally referred to as ‘accidental cell death’ (ACD). In most settings, however, cell death is initiated by a genetically encoded apparatus, correlating with the fact that its course can be altered by pharmacologic or genetic interventions. ‘Regulated cell death’ (RCD) can occur as part of physiologic programs or can be activated once adaptive responses to perturbations of the extracellular or intracellular microenvironment fail. The biochemical phenomena that accompany RCD may be harnessed to classify it into a few subtypes, which often (but not always) exhibit stereotyped morphologic features. Nonetheless, efficiently inhibiting the processes that are commonly thought to cause RCD, such as the activation of executioner caspases in the course of apoptosis, does not exert true cytoprotective effects in the mammalian system, but simply alters the kinetics of cellular demise as it shifts its morphologic and biochemical correlates. Conversely, bona fide cytoprotection can be achieved by inhibiting the transduction of lethal signals in the early phases of the process, when adaptive responses are still operational. Thus, the mechanisms that truly execute RCD may be less understood, less inhibitable and perhaps more homogeneous than previously thought. Here, the Nomenclature Committee on Cell Death formulates a set of recommendations to help scientists and researchers to discriminate between essential and accessory aspects of cell death