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  • Current Challenges and Opportunities in Treating Glioblastoma
    Pharmacol. Rev. (IF 17.893) Pub Date : 2018-07-01
    Andrea Shergalis,Armand Bankhead,Urarika Luesakul,Nongnuj Muangsin,Nouri Neamati,Eric L. Barker,ASSOCIATE EDITOR,Andrea Shergalis,Armand Bankhead,Urarika Luesakul,Nongnuj Muangsin,Nouri Neamati,Andrea Shergalis,Armand Bankhead,Urarika Luesakul,Nongnuj Muangsin,Nouri Neamati
    更新日期:2018-04-19
  • Interindividual Differences in Caffeine Metabolism and Factors Driving Caffeine Consumption
    Pharmacol. Rev. (IF 17.893) Pub Date : 2018-04-01
    Astrid Nehlig,Stephen P. H. Alexander,ASSOCIATE EDITOR,Astrid Nehlig,Astrid Nehlig

    Most individuals adjust their caffeine intake according to the objective and subjective effects induced by the methylxanthine. However, to reach the desired effects, the quantity of caffeine consumed varies largely among individuals. It has been known for decades that the metabolism, clearance, and pharmacokinetics of caffeine is affected by many factors such as age, sex and hormones, liver disease, obesity, smoking, and diet. Caffeine also interacts with many medications. All these factors will be reviewed in the present document and discussed in light of the most recent data concerning the genetic variability affecting caffeine levels and effects at the pharmacokinetic and pharmacodynamic levels that both critically drive the level of caffeine consumption. The pharmacokinetics of caffeine are highly variable among individuals due to a polymorphism at the level of the CYP1A2 isoform of cytochrome P450, which metabolizes 95% of the caffeine ingested. Moreover there is a polymorphism at the level of another critical enzyme, N-acetyltransferase 2. At the pharmacodynamic level, there are several polymorphisms at the main brain target of caffeine, the adenosine A2A receptor or ADORA2. Genetic studies, including genome-wide association studies, identified several loci critically involved in caffeine consumption and its consequences on sleep, anxiety, and potentially in neurodegenerative and psychiatric diseases. We start reaching a better picture on how a multiplicity of biologic mechanisms seems to drive the levels of caffeine consumption, although much more knowledge is still required to understand caffeine consumption and effects on body functions.

    更新日期:2018-03-08
  • Transcription Factor NRF2 as a Therapeutic Target for Chronic Diseases: A Systems Medicine Approach
    Pharmacol. Rev. (IF 17.893) Pub Date : 2018-04-01
    Antonio Cuadrado,Gina Manda,Ahmed Hassan,María José Alcaraz,Coral Barbas,Andreas Daiber,Pietro Ghezzi,Rafael León,Manuela G. López,Baldo Oliva,Marta Pajares,Ana I. Rojo,Natalia Robledinos-Antón,Angela M. Valverde,Emre Guney,Harald H. H. W. Schmidt,Martin C. Michel,ASSOCIATE EDITOR,Antonio Cuadrado,Gina Manda,Ahmed Hassan,María José Alcaraz,Coral Barbas,Andreas Daiber,Pietro Ghezzi,Rafael León,Manuela G. López,Baldo Oliva,Marta Pajares,Ana I. Rojo,Natalia Robledinos-Antón,Angela M. Valverde,Emre Guney,Harald H. H. W. Schmidt,Antonio Cuadrado,Gina Manda,Ahmed Hassan,María José Alcaraz,Coral Barbas,Andreas Daiber,Pietro Ghezzi,Rafael León,Manuela G. López,Baldo Oliva,Marta Pajares,Ana I. Rojo,Natalia Robledinos-Antón,Angela M. Valverde,Emre Guney,Harald H. H. W. Schmidt
    更新日期:2018-03-06
  • Etiology and Pharmacology of Neuropathic Pain
    Pharmacol. Rev. (IF 17.893) Pub Date : 2018-04-01
    Sascha R. A. Alles,Peter A. Smith,Lori L. Isom,ASSOCIATE EDITOR,Sascha R. A. Alles,Peter A. Smith,Sascha R. A. Alles,Peter A. Smith
    更新日期:2018-03-06
  • Neuroimmune Axes of the Blood–Brain Barriers and Blood–Brain Interfaces: Bases for Physiological Regulation, Disease States, and Pharmacological Interventions
    Pharmacol. Rev. (IF 17.893) Pub Date : 2018-04-01
    Michelle A. Erickson,William A. Banks,Robert Dantzer,ASSOCIATE EDITOR,Michelle A. Erickson,William A. Banks,Michelle A. Erickson,William A. Banks
    更新日期:2018-03-02
  • Drugs for Insomnia beyond Benzodiazepines: Pharmacology, Clinical Applications, and Discovery
    Pharmacol. Rev. (IF 17.893) Pub Date : 2018-04-01
    Tobias Atkin,Stefano Comai,Gabriella Gobbi,Eric L. Barker,ASSOCIATE EDITOR,Tobias Atkin,Stefano Comai,Gabriella Gobbi,Tobias Atkin,Stefano Comai,Gabriella Gobbi

    Although the GABAergic benzodiazepines (BZDs) and Z-drugs (zolpidem, zopiclone, and zaleplon) are FDA-approved for insomnia disorders with a strong evidence base, they have many side effects, including cognitive impairment, tolerance, rebound insomnia upon discontinuation, car accidents/falls, abuse, and dependence liability. Consequently, the clinical use of off-label drugs and novel drugs that do not target the GABAergic system is increasing. The purpose of this review is to analyze the neurobiological and clinical evidence of pharmacological treatments of insomnia, excluding the BZDs and Z-drugs. We analyzed the melatonergic agonist drugs, agomelatine, prolonged-release melatonin, ramelteon, and tasimelteon; the dual orexin receptor antagonist suvorexant; the modulators of the α2δ subunit of voltage-sensitive calcium channels, gabapentin and pregabalin; the H1 antagonist, low-dose doxepin; and the histamine and serotonin receptor antagonists, amitriptyline, mirtazapine, trazodone, olanzapine, and quetiapine. The pharmacology and mechanism of action of these treatments and the evidence-base for the use of these drugs in clinical practice is outlined along with novel pipelines. There is evidence to recommend suvorexant and low-dose doxepin for sleep maintenance insomnia; there is also sufficient evidence to recommend ramelteon for sleep onset insomnia. Although there is limited evidence for the use of the quetiapine, trazodone, mirtazapine, amitriptyline, pregabalin, gabapentin, agomelatine, and olanzapine as treatments for insomnia disorder, these drugs may improve sleep while successfully treating comorbid disorders, with a different side effect profile than the BZDs and Z-drugs. The unique mechanism of action of each drug allows for a more personalized and targeted medical management of insomnia.

    更新日期:2018-02-28
  • Biomarkers for In Vivo Assessment of Transporter Function
    Pharmacol. Rev. (IF 17.893) Pub Date : 2018-04-01
    Fabian Müller,Ashish Sharma,Jörg König,Martin F. Fromm,Martin C. Michel,ASSOCIATE EDITOR,Fabian Müller,Ashish Sharma,Jörg König,Martin F. Fromm,Fabian Müller,Ashish Sharma,Jörg König,Martin F. Fromm

    Drug–drug interactions are a major concern not only during clinical practice, but also in drug development. Due to limitations of in vitro–in vivo predictions of transporter-mediated drug–drug interactions, multiple clinical Phase I drug–drug interaction studies may become necessary for a new molecular entity to assess potential drug interaction liabilities. This is a resource-intensive process and exposes study participants, who frequently are healthy volunteers without benefit from study treatment, to the potential risks of a new drug in development. Therefore, there is currently a major interest in new approaches for better prediction of transporter-mediated drug–drug interactions. In particular, researchers in the field attempt to identify endogenous compounds as biomarkers for transporter function, such as hexadecanedioate, tetradecanedioate, coproporphyrins I and III, or glycochenodeoxycholate sulfate for hepatic uptake via organic anion transporting polypeptide 1B or N1-methylnicotinamide for multidrug and toxin extrusion protein–mediated renal secretion. We summarize in this review the currently proposed biomarkers and potential limitations of the substances identified to date. Moreover, we suggest criteria based on current experiences, which may be used to assess the suitability of a biomarker for transporter function. Finally, further alternatives and supplemental approaches to classic drug–drug interaction studies are discussed.

    更新日期:2018-02-28
  • International Union of Basic and Clinical Pharmacology. CII: Pharmacological Modulation of H2S Levels: H2S Donors and H2S Biosynthesis Inhibitors
    Pharmacol. Rev. (IF 17.893) Pub Date : 2017-10-01
    Csaba Szabo,Andreas Papapetropoulos,Eliot H. Ohlstein,ASSOCIATE EDITOR,Csaba Szabo,Andreas Papapetropoulos,Csaba Szabo,Andreas Papapetropoulos
    更新日期:2018-02-02
  • Connexins in Cardiovascular and Neurovascular Health and Disease: Pharmacological Implications
    Pharmacol. Rev. (IF 17.893) Pub Date : 2017-10-01
    Luc Leybaert,Paul D. Lampe,Stefan Dhein,Brenda R. Kwak,Peter Ferdinandy,Eric C. Beyer,Dale W. Laird,Christian C. Naus,Colin R. Green,Rainer Schulz,Finn Olav Levy,ASSOCIATE EDITOR,Luc Leybaert,Paul D. Lampe,Stefan Dhein,Brenda R. Kwak,Peter Ferdinandy,Eric C. Beyer,Dale W. Laird,Christian C. Naus,Colin R. Green,Rainer Schulz,Luc Leybaert,Paul D. Lampe,Stefan Dhein,Brenda R. Kwak,Peter Ferdinandy,Eric C. Beyer,Dale W. Laird,Christian C. Naus,Colin R. Green,Rainer Schulz

    Connexins are ubiquitous channel forming proteins that assemble as plasma membrane hemichannels and as intercellular gap junction channels that directly connect cells. In the heart, gap junction channels electrically connect myocytes and specialized conductive tissues to coordinate the atrial and ventricular contraction/relaxation cycles and pump function. In blood vessels, these channels facilitate long-distance endothelial cell communication, synchronize smooth muscle cell contraction, and support endothelial-smooth muscle cell communication. In the central nervous system they form cellular syncytia and coordinate neural function. Gap junction channels are normally open and hemichannels are normally closed, but pathologic conditions may restrict gap junction communication and promote hemichannel opening, thereby disturbing a delicate cellular communication balance. Until recently, most connexin-targeting agents exhibited little specificity and several off-target effects. Recent work with peptide-based approaches has demonstrated improved specificity and opened avenues for a more rational approach toward independently modulating the function of gap junctions and hemichannels. We here review the role of connexins and their channels in cardiovascular and neurovascular health and disease, focusing on crucial regulatory aspects and identification of potential targets to modify their function. We conclude that peptide-based investigations have raised several new opportunities for interfering with connexins and their channels that may soon allow preservation of gap junction communication, inhibition of hemichannel opening, and mitigation of inflammatory signaling.

    更新日期:2018-02-02
  • Small-Molecule Screens: A Gateway to Cancer Therapeutic Agents with Case Studies of Food and Drug Administration–Approved Drugs
    Pharmacol. Rev. (IF 17.893) Pub Date : 2017-10-01
    Nathan P. Coussens,John C. Braisted,Tyler Peryea,G. Sitta Sittampalam,Anton Simeonov,Matthew D. Hall,Michael M. Gottesman,ASSOCIATE EDITOR,Nathan P. Coussens,John C. Braisted,Tyler Peryea,G. Sitta Sittampalam,Anton Simeonov,Matthew D. Hall,Nathan P. Coussens,John C. Braisted,Tyler Peryea,G. Sitta Sittampalam,Anton Simeonov,Matthew D. Hall

    High-throughput screening (HTS) of small-molecule libraries accelerates the discovery of chemical leads to serve as starting points for probe or therapeutic development. With this approach, thousands of unique small molecules, representing a diverse chemical space, can be rapidly evaluated by biologically and physiologically relevant assays. The origins of numerous United States Food and Drug Administration–approved cancer drugs are linked to HTS, which emphasizes the value in this methodology. The National Institutes of Health Molecular Libraries Program made HTS accessible to the public sector, enabling the development of chemical probes and drug-repurposing initiatives. In this work, the impact of HTS in the field of oncology is considered among both private and public sectors. Examples are given for the discovery and development of approved cancer drugs. The importance of target validation is discussed, and common assay approaches for screening are reviewed. A rigorous examination of the PubChem database demonstrates that public screening centers are contributing to early-stage drug discovery in oncology by focusing on new targets and developing chemical probes. Several case studies highlight the value of different screening strategies and the potential for drug repurposing.

    更新日期:2018-02-02
  • The Hyperpolarization-Activated Cyclic Nucleotide–Gated Channels: from Biophysics to Pharmacology of a Unique Family of Ion Channels
    Pharmacol. Rev. (IF 17.893) Pub Date : 2017-10-01
    Laura Sartiani,Guido Mannaioni,Alessio Masi,Maria Novella Romanelli,Elisabetta Cerbai,Christopher J. Garland,ASSOCIATE EDITOR,Laura Sartiani,Guido Mannaioni,Alessio Masi,Maria Novella Romanelli,Elisabetta Cerbai,Laura Sartiani,Guido Mannaioni,Alessio Masi,Maria Novella Romanelli,Elisabetta Cerbai

    Hyperpolarization-activated, cyclic nucleotide–gated (HCN) channels are important members of the voltage-gated pore loop channels family. They show unique features: they open at hyperpolarizing potential, carry a mixed Na/K current, and are regulated by cyclic nucleotides. Four different isoforms have been cloned (HCN1–4) that can assemble to form homo- or heterotetramers, characterized by different biophysical properties. These proteins are widely distributed throughout the body and involved in different physiologic processes, the most important being the generation of spontaneous electrical activity in the heart and the regulation of synaptic transmission in the brain. Their role in heart rate, neuronal pacemaking, dendritic integration, learning and memory, and visual and pain perceptions has been extensively studied; these channels have been found also in some peripheral tissues, where their functions still need to be fully elucidated. Genetic defects and altered expression of HCN channels are linked to several pathologies, which makes these proteins attractive targets for translational research; at the moment only one drug (ivabradine), which specifically blocks the hyperpolarization-activated current, is clinically available. This review discusses current knowledge about HCN channels, starting from their biophysical properties, origin, and developmental features, to (patho)physiologic role in different tissues and pharmacological modulation, ending with their present and future relevance as drug targets.

    更新日期:2018-02-02
  • International Union of Basic and Clinical Pharmacology CIII: Chemerin Receptors CMKLR1 (Chemerin1) and GPR1 (Chemerin2) Nomenclature, Pharmacology, and Function
    Pharmacol. Rev. (IF 17.893) Pub Date : 2018-01-01
    Amanda J. Kennedy,Anthony P. Davenport,Eliot H. Ohlstein,ASSOCIATE EDITOR,Amanda J. Kennedy,Anthony P. Davenport,Amanda J. Kennedy,Anthony P. Davenport
    更新日期:2017-12-27
  • Ion Channels in Genetic Epilepsy: From Genes and Mechanisms to Disease-Targeted Therapies
    Pharmacol. Rev. (IF 17.893) Pub Date : 2018-01-01
    Julia Oyrer,Snezana Maljevic,Ingrid E. Scheffer,Samuel F. Berkovic,Steven Petrou,Christopher A. Reid,Patrick M. Sexton,ASSOCIATE EDITOR,Julia Oyrer,Snezana Maljevic,Ingrid E. Scheffer,Samuel F. Berkovic,Steven Petrou,Christopher A. Reid,Julia Oyrer,Snezana Maljevic,Ingrid E. Scheffer,Samuel F. Berkovic,Steven Petrou,Christopher A. Reid

    Epilepsy is a common and serious neurologic disease with a strong genetic component. Genetic studies have identified an increasing collection of disease-causing genes. The impact of these genetic discoveries is wide reaching—from precise diagnosis and classification of syndromes to the discovery and validation of new drug targets and the development of disease-targeted therapeutic strategies. About 25% of genes identified in epilepsy encode ion channels. Much of our understanding of disease mechanisms comes from work focused on this class of protein. In this study, we review the genetic, molecular, and physiologic evidence supporting the pathogenic role of a number of different voltage- and ligand-activated ion channels in genetic epilepsy. We also review proposed disease mechanisms for each ion channel and highlight targeted therapeutic strategies.

    更新日期:2017-12-21
  • WNT Signaling in Cardiac and Vascular Disease
    Pharmacol. Rev. (IF 17.893) Pub Date : 2018-01-01
    Sébastien Foulquier,Evangelos P. Daskalopoulos,Gentian Lluri,Kevin C. M. Hermans,Arjun Deb,W. Matthijs Blankesteijn,Martin C. Michel,ASSOCIATE EDITOR,Sébastien Foulquier,Evangelos P. Daskalopoulos,Gentian Lluri,Kevin C. M. Hermans,Arjun Deb,W. Matthijs Blankesteijn,Sébastien Foulquier,Evangelos P. Daskalopoulos,Gentian Lluri,Kevin C. M. Hermans,Arjun Deb,W. Matthijs Blankesteijn
    更新日期:2017-12-16
  • G Protein–Coupled Receptors Targeting Insulin Resistance, Obesity, and Type 2 Diabetes Mellitus
    Pharmacol. Rev. (IF 17.893) Pub Date : 2018-01-01
    Darren M. Riddy,Philippe Delerive,Roger J. Summers,Patrick M. Sexton,Christopher J. Langmead,Eric L. Barker,ASSOCIATE EDITOR,Darren M. Riddy,Philippe Delerive,Roger J. Summers,Patrick M. Sexton,Christopher J. Langmead,Darren M. Riddy,Philippe Delerive,Roger J. Summers,Patrick M. Sexton,Christopher J. Langmead

    G protein–coupled receptors (GPCRs) continue to be important discovery targets for the treatment of type 2 diabetes mellitus (T2DM). Many GPCRs are directly involved in the development of insulin resistance and β-cell dysfunction, and in the etiology of inflammation that can lead to obesity-induced T2DM. This review summarizes the current literature describing a number of well-validated GPCR targets, but also outlines several new and promising targets for drug discovery. We highlight the importance of understanding the role of these receptors in the disease pathology, and their basic pharmacology, which will pave the way to the development of novel pharmacological probes that will enable these targets to fulfill their promise for the treatment of these metabolic disorders.

    更新日期:2017-12-13
  • Anti-Inflammatory Effects of Omega-3 Fatty Acids in the Brain: Physiological Mechanisms and Relevance to Pharmacology
    Pharmacol. Rev. (IF 17.893) Pub Date : 2018-01-01
    Sophie Layé,Agnès Nadjar,Corinne Joffre,Richard P. Bazinet,Robert Dantzer,ASSOCIATE EDITOR,Sophie Layé,Agnès Nadjar,Corinne Joffre,Richard P. Bazinet,Sophie Layé,Agnès Nadjar,Corinne Joffre,Richard P. Bazinet

    Classically, polyunsaturated fatty acids (PUFA) were largely thought to be relatively inert structural components of brain, largely important for the formation of cellular membranes. Over the past 10 years, a host of bioactive lipid mediators that are enzymatically derived from arachidonic acid, the main n-6 PUFA, and docosahexaenoic acid, the main n-3 PUFA in the brain, known to regulate peripheral immune function, have been detected in the brain and shown to regulate microglia activation. Recent advances have focused on how PUFA regulate the molecular signaling of microglia, especially in the context of neuroinflammation and behavior. Several active drugs regulate brain lipid signaling and provide proof of concept for targeting the brain. Because brain lipid metabolism relies on a complex integration of diet, peripheral metabolism, including the liver and blood, which supply the brain with PUFAs that can be altered by genetics, sex, and aging, there are many pathways that can be disrupted, leading to altered brain lipid homeostasis. Brain lipid signaling pathways are altered in neurologic disorders and may be viable targets for the development of novel therapeutics. In this study, we discuss in particular how n-3 PUFAs and their metabolites regulate microglia phenotype and function to exert their anti-inflammatory and proresolving activities in the brain.

    更新日期:2017-12-10
  • RAL GTPases: Biology and Potential as Therapeutic Targets in Cancer
    Pharmacol. Rev. (IF 17.893) Pub Date : 2018-01-01
    Chao Yan,Dan Theodorescu,Richard Dequan Ye,ASSOCIATE EDITOR,Chao Yan,Dan Theodorescu,Chao Yan,Dan Theodorescu

    More than a hundred proteins comprise the RAS superfamily of small GTPases. This family can be divided into RAS, RHO, RAB, RAN, ARF, and RAD subfamilies, with each shown to play distinct roles in human cells in both health and disease. The RAS subfamily has a well-established role in human cancer with the three genes, HRAS, KRAS, and NRAS being the commonly mutated in tumors. These RAS mutations, most often functionally activating, are especially common in pancreatic, lung, and colorectal cancers. Efforts to inhibit RAS and related GTPases have produced inhibitors targeting the downstream effectors of RAS signaling, including inhibitors of the RAF-mitogen-activated protein kinase/extracellular signal-related kinase (ERK)-ERK kinase pathway and the phosphoinositide-3-kinase-AKT-mTOR kinase pathway. A third effector arm of RAS signaling, mediated by RAL (RAS like) has emerged in recent years as a critical driver of RAS oncogenic signaling and has not been targeted until recently. RAL belongs to the RAS branch of the RAS superfamily and shares a high structural similarity with RAS. In human cells, there are two genes, RALA and RALB, both of which have been shown to play roles in the proliferation, survival, and metastasis of a variety of human cancers, including lung, colon, pancreatic, prostate, skin, and bladder cancers. In this review, we summarize the latest knowledge of RAL in the context of human cancer and the recent advancements in the development of cancer therapeutics targeting RAL small GTPases.

    更新日期:2017-12-02
  • Chemical Tools for Studying Lipid-Binding Class A G Protein–Coupled Receptors
    Pharmacol. Rev. (IF 17.893) Pub Date : 2017-07-01
    Anna Cooper,Sameek Singh,Sarah Hook,Joel D. A. Tyndall,Andrea J. Vernall,Stephen P. H. Alexander,ASSOCIATE EDITOR,Anna Cooper,Sameek Singh,Sarah Hook,Joel D. A. Tyndall,Andrea J. Vernall,Anna Cooper,Sameek Singh,Sarah Hook,Joel D. A. Tyndall,Andrea J. Vernall

    Cannabinoid, free fatty acid, lysophosphatidic acid, sphingosine 1-phosphate, prostanoid, leukotriene, bile acid, and platelet-activating factor receptor families are class A G protein–coupled receptors with endogenous lipid ligands. Pharmacological tools are crucial for studying these receptors and addressing the many unanswered questions surrounding expression of these receptors in normal and diseased tissues. An inherent challenge for developing tools for these lipid receptors is balancing the often lipophilic requirements of the receptor-binding pharmacophore with favorable physicochemical properties to optimize highly specific binding. In this study, we review the radioligands, fluorescent ligands, covalent ligands, and antibodies that have been used to study these lipid-binding receptors. For each tool type, the characteristics and design rationale along with in vitro and in vivo applications are detailed.

    更新日期:2017-08-24
  • Botulinum Neurotoxins: Biology, Pharmacology, and Toxicology
    Pharmacol. Rev. (IF 17.893) Pub Date : 2017-04-01
    Marco Pirazzini,Ornella Rossetto,Roberto Eleopra,Cesare Montecucco,Jeffrey M. Witkin,ASSOCIATE EDITOR,Marco Pirazzini,Ornella Rossetto,Roberto Eleopra,Cesare Montecucco,Marco Pirazzini,Ornella Rossetto,Roberto Eleopra,Cesare Montecucco
    更新日期:2017-08-24
  • Systems Chronotherapeutics
    Pharmacol. Rev. (IF 17.893) Pub Date : 2017-04-01
    Annabelle Ballesta,Pasquale F. Innominato,Robert Dallmann,David A. Rand,Francis A. Lévi,Stephanie W. Watts,ASSOCIATE EDITOR,Annabelle Ballesta,Pasquale F. Innominato,Robert Dallmann,David A. Rand,Francis A. Lévi,Annabelle Ballesta,Pasquale F. Innominato,Robert Dallmann,David A. Rand,Francis A. Lévi
    更新日期:2017-08-24
  • International Union of Basic and Clinical Pharmacology. CI. Structures and Small Molecule Modulators of Mammalian Adenylyl Cyclases
    Pharmacol. Rev. (IF 17.893) Pub Date : 2017-04-01
    Carmen W. Dessauer,Val J. Watts,Rennolds S. Ostrom,Marco Conti,Stefan Dove,Roland Seifert,Eliot H. Ohlstein,ASSOCIATE EDITOR,Carmen W. Dessauer,Val J. Watts,Rennolds S. Ostrom,Marco Conti,Stefan Dove,Roland Seifert,Carmen W. Dessauer,Val J. Watts,Rennolds S. Ostrom,Marco Conti,Stefan Dove,Roland Seifert
    更新日期:2017-08-24
Some contents have been Reproduced with permission of the American Chemical Society.
Some contents have been Reproduced by permission of The Royal Society of Chemistry.
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华中师范大学化学生物学研究中心诚聘质谱实验员
深圳大学张晗特聘教授团队高薪招聘博士后 年薪30万左右
南方科技大学“青千”团队诚聘“有机合成或材料”方向博士后与研究助理
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