Evaluation of pain incidence and pain management in a South African paediatric trauma unit

Objectives. To evaluate pain incidence and pain management in a South African paediatric trauma unit, and to compare the usefulness of 5 different assessment tools. Design. A prospective observational study, using the Numerical Rating Scale for pain (NRS pain), Numerical Rating Scale for anxiety (NRS anxiety), the Alder Hey Triage Pain Score (AHTPS), the COMFORT behaviour scale and the Touch Visual Pain Scale (TVPS). All patients were assessed at admission; those who were hospitalised were again assessed every 3 hours until discharge. Results. A total of 165 patients, with a mean age of 5.3 years (range 0 - 13), were included. NRS scores were indicative of moderate to severe pain in 13.3% of the patients, and no pain in 24% at admission. Two-thirds of the patients received no analgesics; for them, NRS pain, AHTPS and TVP scores were lower than the scores for the other children. Conclusion. Pain and anxiety incidences in this paediatric trauma unit are relatively low. Implementation of a standard pain assessment tool in the emergency department triage system can improve pain management. The AHTPS is the most promising for use in non-Western settings

Artificial intelligence for dementia drug discovery and trials optimization

Drug discovery and clinical trial design for dementia have historically been challenging. In part these challenges have arisen from patient heterogeneity, length of disease course, and the tractability of a target for the brain. Applying big data analytics and machine learning tools for drug discovery and utilizing them to inform successful clinical trial design has the potential to accelerate progress. Opportunities arise at multiple stages in the therapy pipeline and the growing availability of large medical data sets opens possibilities for big data analyses to answer key questions in clinical and therapeutic challenges. However, before this goal is reached, several challenges need to be overcome and only a multi-disciplinary approach can promote data-driven decision-making to its full potential. Herein we review the current state of machine learning applications to clinical trial design and drug discovery, while presenting opportunities and recommendations that can break down the barriers to implementation

Artificial intelligence for dementia drug discovery and trials optimization

Drug discovery and clinical trial design for dementia have historically been challenging. In part these challenges have arisen from patient heterogeneity, length of disease course, and the tractability of a target for the brain. Applying big data analytics and machine learning tools for drug discovery and utilizing them to inform successful clinical trial design has the potential to accelerate progress. Opportunities arise at multiple stages in the therapy pipeline and the growing availability of large medical data sets opens possibilities for big data analyses to answer key questions in clinical and therapeutic challenges. However, before this goal is reached, several challenges need to be overcome and only a multi-disciplinary approach can promote data-driven decision-making to its full potential. Herein we review the current state of machine learning applications to clinical trial design and drug discovery, while presenting opportunities and recommendations that can break down the barriers to implementation

CaZF, a Plant Transcription Factor Functions through and Parallel to HOG and Calcineurin Pathways in Saccharomyces cerevisiae to Provide Osmotolerance

Salt-sensitive yeast mutants were deployed to characterize a gene encoding a C2H2 zinc finger protein (CaZF) that is differentially expressed in a drought-tolerant variety of chickpea (Cicer arietinum) and provides salinity-tolerance in transgenic tobacco. In Saccharomyces cerevisiae most of the cellular responses to hyper-osmotic stress is regulated by two interconnected pathways involving high osmolarity glycerol mitogen-activated protein kinase (Hog1p) and Calcineurin (CAN), a Ca2+/calmodulin-regulated protein phosphatase 2B. In this study, we report that heterologous expression of CaZF provides osmotolerance in S. cerevisiae through Hog1p and Calcineurin dependent as well as independent pathways. CaZF partially suppresses salt-hypersensitive phenotypes of hog1, can and hog1can mutants and in conjunction, stimulates HOG and CAN pathway genes with subsequent accumulation of glycerol in absence of Hog1p and CAN. CaZF directly binds to stress response element (STRE) to activate STRE-containing promoter in yeast. Transactivation and salt tolerance assays of CaZF deletion mutants showed that other than the transactivation domain a C-terminal domain composed of acidic and basic amino acids is also required for its function. Altogether, results from this study suggests that CaZF is a potential plant salt-tolerance determinant and also provide evidence that in budding yeast expression of HOG and CAN pathway genes can be stimulated in absence of their regulatory enzymes to provide osmotolerance

The Caenorhabditis elegans Mucin-Like Protein OSM-8 Negatively Regulates Osmosensitive Physiology Via the Transmembrane Protein PTR-23

The molecular mechanisms of animal cell osmoregulation are poorly understood. Genetic studies of osmoregulation in yeast have identified mucin-like proteins as critical regulators of osmosensitive signaling and gene expression. Whether mucins play similar roles in higher organisms is not known. Here, we show that mutations in the Caenorhabditis elegans mucin-like gene osm-8 specifically disrupt osmoregulatory physiological processes. In osm-8 mutants, normal physiological responses to hypertonic stress, such as the accumulation of organic osmolytes and activation of osmoresponsive gene expression, are constitutively activated. As a result, osm-8 mutants exhibit resistance to normally lethal levels of hypertonic stress and have an osmotic stress resistance (Osr) phenotype. To identify genes required for Osm-8 phenotypes, we performed a genome-wide RNAi osm-8 suppressor screen. After screening ∼18,000 gene knockdowns, we identified 27 suppressors that specifically affect the constitutive osmosensitive gene expression and Osr phenotypes of osm-8 mutants. We found that one suppressor, the transmembrane protein PTR-23, is co-expressed with osm-8 in the hypodermis and strongly suppresses several Osm-8 phenotypes, including the transcriptional activation of many osmosensitive mRNAs, constitutive glycerol accumulation, and osmotic stress resistance. Our studies are the first to show that an extracellular mucin-like protein plays an important role in animal osmoregulation in a manner that requires the activity of a novel transmembrane protein. Given that mucins and transmembrane proteins play similar roles in yeast osmoregulation, our findings suggest a possible evolutionarily conserved role for the mucin-plasma membrane interface in eukaryotic osmoregulation

Ask yeast how to burn your fats: lessons learned from the metabolic adaptation to salt stress

[EN] Here, we review and update the recent advances in the metabolic control during the adaptive response of budding yeast to hyperosmotic and salt stress, which is one of the best understood signaling events at the molecular level. This environmental stress can be easily applied and hence has been exploited in the past to generate an impressively detailed and comprehensive model of cellular adaptation. It is clear now that this stress modulates a great number of different physiological functions of the cell, which altogether contribute to cellular survival and adaptation. Primary defense mechanisms are the massive induction of stress tolerance genes in the nucleus, the activation of cation transport at the plasma membrane, or the production and intracellular accumulation of osmolytes. At the same time and in a coordinated manner, the cell shuts down the expression of housekeeping genes, delays the progression of the cell cycle, inhibits genomic replication, and modulates translation efficiency to optimize the response and to avoid cellular damage. To this fascinating interplay of cellular functions directly regulated by the stress, we have to add yet another layer of control, which is physiologically relevant for stress tolerance. Salt stress induces an immediate metabolic readjustment, which includes the up-regulation of peroxisomal biomass and activity in a coordinated manner with the reinforcement of mitochondrial respiratory metabolism. Our recent findings are consistent with a model, where salt stress triggers a metabolic shift from fermentation to respiration fueled by the enhanced peroxisomal oxidation of fatty acids. We discuss here the regulatory details of this stress-induced metabolic shift and its possible roles in the context of the previously known adaptive functions.The work of the authors was supported by grants from Ministerio de Economía y Competitividad (BFU2011- 23326 and BFU2016-75792-R).Pascual-Ahuir Giner, MD.; Manzanares-Estreder, S.; Timón Gómez, A.; Proft ., MH. (2017). Ask yeast how to burn your fats: lessons learned from the metabolic adaptation to salt stress. Current Genetics. 64(1):63-69. https://doi.org/10.1007/s00294-017-0724-5S6369641Aguilera J, Prieto JA (2001) The Saccharomyces cerevisiae aldose reductase is implied in the metabolism of methylglyoxal in response to stress conditions. Curr Genet 39:273–283Albertyn J, Hohmann S, Thevelein JM, Prior BA (1994) GPD1, which encodes glycerol-3-phosphate dehydrogenase, is essential for growth under osmotic stress in Saccharomyces cerevisiae, and its expression is regulated by the high-osmolarity glycerol response pathway. Mol Cell Biol 14:4135–4144Alepuz PM, Jovanovic A, Reiser V, Ammerer G (2001) Stress-induced map kinase Hog1 is part of transcription activation complexes. Mol Cell 7:767–777Alepuz PM, de Nadal E, Zapater M, Ammerer G, Posas F (2003) Osmostress-induced transcription by Hot1 depends on a Hog1-mediated recruitment of the RNA Pol II. EMBO J 22:2433–2442Ansell R, Granath K, Hohmann S, Thevelein JM, Adler L (1997) The two isoenzymes for yeast NAD+-dependent glycerol 3-phosphate dehydrogenase encoded by GPD1 and GPD2 have distinct roles in osmoadaptation and redox regulation. EMBO J 16:2179–2187Babazadeh R, Lahtvee PJ, Adiels CB, Goksor M, Nielsen JB, Hohmann S (2017) The yeast osmostress response is carbon source dependent. Sci Rep 7:990Bender T, Pena G, Martinou JC (2015) Regulation of mitochondrial pyruvate uptake by alternative pyruvate carrier complexes. EMBO J 34:911–924Berry DB, Gasch AP (2008) Stress-activated genomic expression changes serve a preparative role for impending stress in yeast. Mol Biol Cell 19:4580–4587Bilsland-Marchesan E, Arino J, Saito H, Sunnerhagen P, Posas F (2000) Rck2 kinase is a substrate for the osmotic stress-activated mitogen-activated protein kinase Hog1. Mol Cell Biol 20:3887–3895Brewster JL, Gustin MC (2014) Hog 1: 20 years of discovery and impact. Sci Signal 7:re7Clotet J, Posas F (2007) Control of cell cycle in response to osmostress: lessons from yeast. Methods Enzymol 428:63–76Clotet J, Escote X, Adrover MA, Yaakov G, Gari E, Aldea M, de Nadal E, Posas F (2006) Phosphorylation of Hsl1 by Hog1 leads to a G2 arrest essential for cell survival at high osmolarity. EMBO J 25:2338–2346Cook KE, O’Shea EK (2012) Hog1 controls global reallocation of RNA Pol II upon osmotic shock in Saccharomyces cerevisiae. 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Nature 493:116–119Escote X, Zapater M, Clotet J, Posas F (2004) Hog1 mediates cell-cycle arrest in G1 phase by the dual targeting of Sic1. Nat Cell Biol 6:997–1002Ferreira C, van Voorst F, Martins A, Neves L, Oliveira R, Kielland-Brandt MC, Lucas C, Brandt A (2005) A member of the sugar transporter family, Stl1p is the glycerol/H+ symporter in Saccharomyces cerevisiae. Mol Biol Cell 16:2068–2076Gonzalez R, Morales P, Tronchoni J, Cordero-Bueso G, Vaudano E, Quiros M, Novo M, Torres-Perez R, Valero E (2016) New genes involved in osmotic stress tolerance in Saccharomyces cerevisiae. Front Microbiol 7:1545Ho YH, Gasch AP (2015) Exploiting the yeast stress-activated signaling network to inform on stress biology and disease signaling. Curr Genet 61:503–511Hohmann S (2015) An integrated view on a eukaryotic osmoregulation system. Curr Genet 61:373–382Hohmann S, Krantz M, Nordlander B (2007) Yeast osmoregulation. Methods Enzymol 428:29–45Hong SP, Carlson M (2007) Regulation of snf1 protein kinase in response to environmental stress. J Biol Chem 282:16838–16845Li SC, Diakov TT, Rizzo JM, Kane PM (2012) Vacuolar H+-ATPase works in parallel with the HOG pathway to adapt Saccharomyces cerevisiae cells to osmotic stress. Eukaryot Cell 11:282–291Maeta K, Izawa S, Inoue Y (2005) Methylglyoxal, a metabolite derived from glycolysis, functions as a signal initiator of the high osmolarity glycerol-mitogen-activated protein kinase cascade and calcineurin/Crz1-mediated pathway in Saccharomyces cerevisiae. J Biol Chem 280:253–260Manzanares-Estreder S, Espi-Bardisa J, Alarcon B, Pascual-Ahuir A, Proft M (2017) Multilayered control of peroxisomal activity upon salt stress in Saccharomyces cerevisiae. Mol Microbiol 104:851–868Mao K, Wang K, Zhao M, Xu T, Klionsky DJ (2011) Two MAPK-signaling pathways are required for mitophagy in Saccharomyces cerevisiae. J Cell Biol 193:755–767Martinez-Montanes F, Pascual-Ahuir A, Proft M (2010) Toward a genomic view of the gene expression program regulated by osmostress in yeast. OMICS 14:619–627Martinez-Pastor M, Proft M, Pascual-Ahuir A (2010) Adaptive changes of the yeast mitochondrial proteome in response to salt stress. OMICS 14:541–552Mas G, de Nadal E, Dechant R, Rodriguez de la Concepcion ML, Logie C, Jimeno-Gonzalez S, Chavez S, Ammerer G, Posas F (2009) Recruitment of a chromatin remodelling complex by the Hog1 MAP kinase to stress genes. EMBO J 28:326–336Mettetal JT, Muzzey D, Gomez-Uribe C, van Oudenaarden A (2008) The frequency dependence of osmo-adaptation in Saccharomyces cerevisiae. Science 319:482–484Molin C, Jauhiainen A, Warringer J, Nerman O, Sunnerhagen P (2009) mRNA stability changes precede changes in steady-state mRNA amounts during hyperosmotic stress. RNA 15:600–614Nadal-Ribelles M, Conde N, Flores O, Gonzalez-Vallinas J, Eyras E, Orozco M, de Nadal E, Posas F (2012) Hog1 bypasses stress-mediated down-regulation of transcription by RNA polymerase II redistribution and chromatin remodeling. Genome Biol 13:R106Pastor MM, Proft M, Pascual-Ahuir A (2009) Mitochondrial function is an inducible determinant of osmotic stress adaptation in yeast. J Biol Chem 284:30307–30317Petelenz-Kurdziel E, Kuehn C, Nordlander B, Klein D, Hong KK, Jacobson T, Dahl P, Schaber J, Nielsen J, Hohmann S, Klipp E (2013) Quantitative analysis of glycerol accumulation, glycolysis and growth under hyper osmotic stress. PLoS Comput Biol 9:e1003084Posas F, Chambers JR, Heyman JA, Hoeffler JP, de Nadal E, Arino J (2000) The transcriptional response of yeast to saline stress. J Biol Chem 275:17249–17255Proft M, Struhl K (2002) Hog1 kinase converts the Sko1-Cyc8-Tup1 repressor complex into an activator that recruits SAGA and SWI/SNF in response to osmotic stress. Mol Cell 9:1307–1317Proft M, Struhl K (2004) MAP kinase-mediated stress relief that precedes and regulates the timing of transcriptional induction. Cell 118:351–361Proft M, Pascual-Ahuir A, de Nadal E, Arino J, Serrano R, Posas F (2001) Regulation of the Sko1 transcriptional repressor by the Hog1 MAP kinase in response to osmotic stress. EMBO J 20:1123–1133Proft M, Mas G, de Nadal E, Vendrell A, Noriega N, Struhl K, Posas F (2006) The stress-activated Hog1 kinase is a selective transcriptional elongation factor for genes responding to osmotic stress. Mol Cell 23:241–250Ratnakumar S, Young ET (2010) Snf1 dependence of peroxisomal gene expression is mediated by Adr1. J Biol Chem 285:10703–10714Regot S, de Nadal E, Rodriguez-Navarro S, Gonzalez-Novo A, Perez-Fernandez J, Gadal O, Seisenbacher G, Ammerer G, Posas F (2013) The Hog1 stress-activated protein kinase targets nucleoporins to control mRNA export upon stress. 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Characterization of Leishmania donovani Aquaporins Shows Presence of Subcellular Aquaporins Similar to Tonoplast Intrinsic Proteins of Plants

Leishmania donovani, a protozoan parasite, resides in the macrophages of the mammalian host. The aquaporin family of proteins form important components of the parasite-host interface. The parasite-host interface could be a potential target for chemotherapy. Analysis of L. major and L. infantum genomes showed the presence of five aquaporins (AQPs) annotated as AQP9 (230aa), AQP putative (294aa), AQP-like protein (279aa), AQP1 (314aa) and AQP-like protein (596aa). We report here the structural modeling, localization and functional characterization of the AQPs from L. donovani. LdAQP1, LdAQP9, LdAQP2860 and LdAQP2870 have the canonical NPA-NPA motifs, whereas LdAQP putative has a non-canonical NPM-NPA motif. In the carboxyl terminal to the second NPA box of all AQPs except AQP1, a valine/alanine residue was found instead of the arginine. In that respect these four AQPs are similar to tonoplast intrinsic proteins in plants, which are localized to intracellular organelles. Confocal microscopy of L. donovani expressing GFP-tagged AQPs showed an intracellular localization of LdAQP9 and LdAQP2870. Real-time PCR assays showed expression of all aquaporins except LdAQP2860, whose level was undetectable. Three-dimensional homology modeling of the AQPs showed that LdAQP1 structure bears greater topological similarity to the aquaglyceroporin than to aquaporin of E. coli. The pore of LdAQP1 was very different from the rest in shape and size. The cavity of LdAQP2860 was highly irregular and undefined in geometry. For functional characterization, four AQP proteins were heterologously expressed in yeast. In the fps1Δ yeast cells, which lacked the key aquaglyceroporin, LdAQP1 alone displayed an osmosensitive phenotype indicating glycerol transport activity. However, expression of LdAQP1 and LdAQP putative in a yeast gpd1Δ strain, deleted for glycerol production, conferred osmosensitive phenotype indicating water transport activity or aquaporin function. Our analysis for the first time shows the presence of subcellular aquaporins and provides structural and functional characterization of aquaporins in Leishmania donovani

Tor1/Sch9-Regulated Carbon Source Substitution Is as Effective as Calorie Restriction in Life Span Extension

The effect of calorie restriction (CR) on life span extension, demonstrated in organisms ranging from yeast to mice, may involve the down-regulation of pathways, including Tor, Akt, and Ras. Here, we present data suggesting that yeast Tor1 and Sch9 (a homolog of the mammalian kinases Akt and S6K) is a central component of a network that controls a common set of genes implicated in a metabolic switch from the TCA cycle and respiration to glycolysis and glycerol biosynthesis. During chronological survival, mutants lacking SCH9 depleted extracellular ethanol and reduced stored lipids, but synthesized and released glycerol. Deletion of the glycerol biosynthesis genes GPD1, GPD2, or RHR2, among the most up-regulated in long-lived sch9Δ, tor1Δ, and ras2Δ mutants, was sufficient to reverse chronological life span extension in sch9Δ mutants, suggesting that glycerol production, in addition to the regulation of stress resistance systems, optimizes life span extension. Glycerol, unlike glucose or ethanol, did not adversely affect the life span extension induced by calorie restriction or starvation, suggesting that carbon source substitution may represent an alternative to calorie restriction as a strategy to delay aging

Beak and feather disease virus in wild and captive parrots: an analysis of geographic and taxonomic distribution and methodological trends

Psittacine beak and feather disease (PBFD) has emerged in recent years as a major threat to wild parrot populations and is an increasing concern to aviculturists and managers of captive populations. Pathological and serological tests for screening for the presence of beak and feather disease virus (BFDV) are a critical component of efforts to manage the disease and of epidemiological studies. Since the disease was first reported in the mid-1970s, screening for BFDV has been conducted in numerous wild and captive populations. However, at present, there is no current and readily accessible synthesis of screening efforts and their results. Here, we consolidate information collected from 83 PBFD- and BFDV-based publications on the primary screening methods being used and identify important knowledge gaps regarding potential global disease hotspots. We present trends in research intensity in this field and critically discuss advances in screening techniques and their applications to both aviculture and to the management of threatened wild populations. Finally, we provide an overview of estimates of BFDV prevalence in captive and wild flocks alongside a complete list of all psittacine species in which the virus has been confirmed. Our evaluation highlights the need for standardised diagnostic tests and more emphasis on studies of wild populations, particularly in view of the intrinsic connection between global trade in companion birds and the spread of novel BFDV strains into wild populations. Increased emphasis should be placed on the screening of captive and wild parrot populations within their countries of origin across the Americas, Africa and Asia