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Predictors of the placebo response in a nutraceutical randomized controlled trial for depression

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Journal of Integrative Medicine 2024年第1期22卷 46-53页

作者： Rosemary Arnold Jenifer Murphy-Smith Chee H.Ng David Mischoulon Gerard J.Byrne Chad A.Bousman Con Stough Michael Berk Jerome Sarris Professorial Unit the Melbourne ClinicDepartment of PsychiatryUniversity of MelbourneRichmond 3121Australia Depression Clinical and Research Program Department of PsychiatryMassachusetts General HospitalHarvard Medical SchoolBostonMA 02115USA Faculty of Medicine Discipline of PsychiatryCentre for Clinical ResearchRoyal Brisbane&Women’s HospitalHerstonthe University of QueenslandBrisbane 4006Australia departments of medical genetics PsychiatryPhysiology&Pharmacology and Community Health SciencesUniversity of CalgaryCalgaryAB T2N 1N4Canada Department of Psychiatry the University of MelbourneMelbourne 3052Australia Centre for Human Psychopharmacology Swinburne UniversityMelbourne 3122Australia The Institute for Mental and Physical Health and Clinical Translation School of MedicineBarwon HealthDeakin UniversityGeelong 3220Australia The Centre of Excellence in Youth Mental Health the University of MelbourneParkville 3052Australia Florey Institute of Neuroscience and Mental Health the University of MelbourneParkville 3052Australia NICM Health Research Institute Western Sydney UniversityWestmeadNSW 2145Australia

Objective The placebo response in depression studies is the change in symptoms amongst those who receive an inactive *** well-designed randomized controlled trials(RCTs)of depression have a high proportion of placebo responders,with little understanding as to *** present study assesses characteristics associated with the placebo response in a nutraceutical trial with a large proportion of placebo *** This is a secondary analysis of a nutraceutical depression RCT which identified no overall treatment benefit relative to placebo(n=69 in placebo group).We investigated participant characteristics such as socio-demographics,clinical features,and recruitment methods,and their association with the placebo *** genetic polymorphisms were also *** response was measured based on change in Montgomery-Asberg Depression Rating Scale *** association of these hypothesis-driven variables of interest and the placebo response was examined using linear mixed effects *** Greater levels of education,particularly pursuing post-high school education,better self-reported general health,marriage/de facto,greater improvement in the first trial week,and more failed antidepressant therapies in the current depressive episode were associated with greater placebo *** increased placebo response was not found in those recruited via social media nor in those with concomitant antidepressant *** nucleotide polymorphisms from the tryptophan hydroxylase 1(TPH1)gene(A779C and A218C)were weakly associated with greater placebo response,although the evidence was attenuated after accounting for multiple *** This is,to our knowledge,the first study within nutraceutical research for depression to assess the association between participant characteristics and variation in the placebo *** variables appeared to predict the placebo *** findings may encourage future trial design

关键词： Randomized controlled trial Placebo Depression Nutraceutical Psychiatry

Dynamics of Advantageous Mutant Spread in Spatial Death-Birth and Birth-Death Moran Models

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Communications on Applied Mathematics and Computation 2024年第1期6卷 576-604页

作者： Jasmine Foo Einar Bjarki Gunnarsson Kevin Leder David Sivakoff School of Mathematics University of MinnesotaTwin CitiesMN55455USA Department of Industrial and Systems Engineering University of MinnesotaTwin CitiesMN55455USA departments of Statistics and Mathematics The Ohio State UniversityColumbusOH43210USA

The spread of an advantageous mutation through a population is of fundamental interest in population genetics. While the classical Moran model is formulated for a well-mixed population, it has long been recognized that in real-world applications, the population usually has an explicit spatial structure which can significantly influence the dynamics. In the context of cancer initiation in epithelial tissue, several recent works have analyzed the dynamics of advantageous mutant spread on integer lattices, using the biased voter model from particle systems theory. In this spatial version of the Moran model, individuals first reproduce according to their fitness and then replace a neighboring individual. From a biological standpoint, the opposite dynamics, where individuals first die and are then replaced by a neighboring individual according to its fitness, are equally relevant. Here, we investigate this death-birth analogue of the biased voter model. We construct the process mathematically, derive the associated dual process, establish bounds on the survival probability of a single mutant, and prove that the process has an asymptotic shape. We also briefly discuss alternative birth-death and death-birth dynamics, depending on how the mutant fitness advantage affects the dynamics. We show that birth-death and death-birth formulations of the biased voter model are equivalent when fitness affects the former event of each update of the model, whereas the birth-death model is fundamentally different from the death-birth model when fitness affects the latter event.

关键词： Spatial death-birth models Spatial birth-death models Spatial evolutionary models Spatial cancer models Evolutionary graph theory Stochastic processes Biased voter model Dual process Fixation probability Shape theorem

Identification of telomere maintenance gene variations related to lung adenocarcinoma risk by genome-wide association and whole genome sequencing analyses

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Cancer Communications 2024年第2期44卷 287-293页

作者： Kouya Shiraishi Atsushi Takahashi Yukihide Momozawa Yataro Daigo Syuzo Kaneko Takahisa Kawaguchi Hideo Kunitoh Shingo Matsumoto Hidehito Horinouchi Akiteru Goto Takayuki Honda Kimihiro Shimizu Masahiro Torasawa Daisuke Takayanagi Motonobu Saito Akira Saito Yuichiro Ohe Shun-ichi Watanabe Koichi Goto Masahiro Tsuboi Katsuya Tsuchihara Sadaaki Takata Tomomi Aoi Atsushi Takano Masashi Kobayashi Yohei Miyagi Kazumi Tanaka Hiroyuki Suzuki Daichi Maeda Takumi Yamaura Maiko Matsuda Yoko Shimada Takaaki Mizuno Hiromi Sakamoto Teruhiko Yoshida Yasushi Goto Tatsuya Yoshida Taiki Yamaji Makoto Sonobe Shinichi Toyooka Kazue Yoneda Katsuhiro Masago Fumihiro Tanaka Megumi Hara Nobuo Fuse Satoshi S.Nishizuka Noriko Motoi Norie Sawada Yuichiro Nishida Kazuki Kumada Kenji Takeuchi Kozo Tanno Yasushi Yatabe Kuniko Sunami Tomoyuki Hishida Yasunari Miyazaki Hidemi Ito Mitsuhiro Amemiya Hirohiko Totsuka Haruhiko Nakayama Tomoyuki Yokose Kazuyoshi Ishigaki Toshiteru Nagashima Yoichi Ohtaki Kazuhiro Imai Ken Takasawa Yoshihiro Minamiya Kazuma Kobayashi Kenichi Okubo Kenji Wakai Atsushi Shimizu Masayuki Yamamoto Motoki Iwasaki Koichi Matsuda Johji Inazawa Yuichi Shiraishi Hiroyoshi Nishikawa Yoshinori Murakami Michiaki Kubo Fumihiko Matsuda Yoichiro Kamatani Ryuji Hamamoto Keitaro Matsuo Takashi Kohno Division of Genome Biology National Cancer Center Research InstituteTokyoJapan Department of Clinical Genomics National Cancer Center Research InstituteTokyoJapan Laboratory for Statistical Analysis Center for Integrative Medical SciencesRIKENYokohamaJapan Department of Genomic Medicine Research InstituteNational Cerebral and Cardiovascular CenterOsakaJapan Laboratory for Genotyping Development Center for Integrative Medical SciencesRIKENYokohamaJapan Center for Antibody and Vaccine Therapy Research HospitalInstitute of Medical ScienceThe University of TokyoTokyoJapan Department of medical Oncology and Cancer Center and Center for Advanced Medicine against CancerShiga University of Medical ScienceOtsuJapan Division of medical AI Research and Development National Cancer Center Research InstituteTokyoJapan Center for Genomic Medicine Graduate School of MedicineKyoto UniversityKyotoJapan Department of medical Oncology Japanese Red Cross Medical CenterTokyoJapan Department of Thoracic Oncology National Cancer Center Hospital EastJapan Department of Thoracic Oncology National Cancer Center HospitalTokyoJapan Department of Cellular and Organ Pathology Graduate School of MedicineAkita UniversityAkitaJapan Department of Respiratory Medicine Tokyo Medical and Dental UniversityBunkyo-kuTokyoJapan Division of General Thoracic Surgery Department of SurgeryShinshu University School of MedicineMatsumotoNaganoJapan Department of General Surgical Science Division of General Thoracic SurgeryGunma University Graduate School of MedicineIntegrative Center of General SurgeryGunma University HospitalGunmaJapan Department of Gastrointestinal Tract Surgery Fukushima Medical University School of MedicineFukushimaJapan StaGen Co. LtdTokyoJapan Division of Thoracic Surgery National Cancer Center HospitalTokyoJapan Department of Thoracic Surgery National Cancer Center Hospital EastChibaJapan Division of Translational Informatics Exploratory Oncology Research and Clinical Trial Center(EPOC

Dear editor,Lung carcinoma is responsible for the highest fatal-ity rate among cancer-related deaths globally,with lung adenocarcinoma(LADC)emerging as the prevailing sub-type.

关键词： adenocarcinoma lung Lung

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基因组结构变异研究的前瞻性及临床应用

Science Bulletin 2024年第6期69卷 705-708页

作者：陈仲中 Richard H.Finnell 雷云平王红艳 Obstetrics and Gynecology Hospital State Key Laboratory of Genetic EngineeringInstitute of Reproduction and DevelopmentFudan UniversityShanghai 200011China Shanghai Children’s Hospital School of MedicineShanghai Jiao Tong UniversityShanghai 200062China Center for Precision Environmental Health Department of Molecular and Cellular BiologyBaylor College of MedicineHouston 77030USA departments of Molecular and Human genetics and Medicine Baylor College of MedicineOne Baylor PlazaHouston 77030USA Shanghai Key Laboratory of Metabolic Remodelling and Health Institute of Metabolism and Integrative BiologyFudan UniversityShanghai 200438China Children’s Hospital of Fudan University Shanghai 201102China

The challenges and breakthroughs in human genetics can largely depend on the depth of exploring the missing heritability[1]and understanding of genetic variants,which enabled scientists to better elucidate the underlying causes of diseases and apply this knowledge in clinical *** genomes differ from one individual to another in the form of single nucleotide variants(SNVs),small insertions and deletions(indels)(<50 base pairs(bp)),and structural variants(SVs)[2].

关键词： diseases breakthrough insertion

The next generation of cancer management

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Cancer Biology & Medicine 2016年第1期13卷 1-2页

作者： Wayne W.Grody Divisions of medical genetics and Molecular Diagnostics Departments of Pathology & Laboratory Medicine Pediatrics and Human Genetics UCLA School of Medicine UCLA Institute for Society and Genetics Molecular Diagnostic Laboratories and Clinical Genomics Center UCLA Medical Center

As readers of Cancer Biology and Medicine well know,there has been a seismic shift in human molecular biology over the past few years,as momentous in its own way as the discovery of the double-helical structure of DNA by Watson and Crick 60 years ago,the elucidation of the genetic code shortly thereafter,the advent of recombinant DNA and gene

关键词： DNA重组管理癌症聚合酶链反应基因编码肿瘤生物学分子生物学双螺旋结构

Biallelic mutations in UGDH cause congenital microcephaly

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Genes & Diseases 2023年第5期10卷 1816-1819页

作者： Li Shu Guangyao Xie Daoqi Mei Rui Xu Shixian Liu Bo Xiao Xing Li Yuanyuan Xie Xiao Mao Hua Wang National Health Commission Key Laboratory for Birth Defect Research and Prevention Hunan Provincial Maternal and Child Health Care HospitalChangshaHunan 410005China departments of Biochemistry Molecular Biology and Medical GeneticsCumming School of MedicineUniversity of CalgaryCalgary T2N 4N1Canada Alberta Children's Hospital Research Institute University of CalgaryCalgary T2N 4N1Canada Department of Neurology Children's Hospital Affiliated to Zhengzhou UniversityZhengzhouHenan 450018China Department of Cell Biology and genetics School of Basic Medical ScienceXinjiang Medical UniversityUrumqiXinjiang 830054China Department of Pediatric Neurological and Rehabilitation Ganzhou Women and Children's Health Care HospitalGanzhouJiangxi 341000China Department of Neurology Xiangya HospitalChangshaHunan 410005China Department of Pediatrics The First Affiliated Hospital of Guangxi Medical UniversityNanningGuangxi 530021China Department of medical genetics Hunan Provincial Maternal and Child Health Care HospitalChangshaHunan 410005China Clinical Research Center for Placental Medicine in Hunan Province Hunan Provincial Maternal and Child Health Care HospitalChangshaHunan 410005China Department of medical genetics Hunan Children's HospitalChangshaHunan 410007China

Hengel et al recently reported that bi-allelic loss-of-function mutations in UDP-Glucose 6-Dehydrogenase(UGDH)caused a severe epileptic encephalopathy syndrome-Jamuar syndrome(OMIM#618792).1 The functional studies partially recapitulated the clinical phenotypes in the patient-derived cerebral organoid.A reduced number of proliferating neuronal progenitors in cerebral organoids was shown,which is a critical mechanism in congenital microcephaly(CM)whose patients were born with an occipitofrontal circumference(OCF)more than 2 standard deviations below average for age and ***,none of the reported patients in the article presented the phenotype as CM.

关键词： congenital cerebral patients

HER3-targeted therapeutic antibodies and antibody-drug conjugates in non-small cell lung cancer refractory to EGFR-tyrosine kinase inhibitors

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Chinese medical Journal Pulmonary and Critical Care Medicine 2023年第1期1卷 11-17页

作者： Margaret E.Larsen Hui Lyu Bolin Liu departments of Interdisciplinary Oncology and genetics Stanley S.Scott Cancer CenterSchool of MedicineLouisiana State University(LSU)Health Sciences CenterNew OrleansLA 70112USA

Human epidermal growth factor receptor 3(HER3)is a unique member of the human epidermal growth factor receptor(HER/EGFR)family,since it has negligible kinase ***,HER3 must interact with a kinase-proficient receptor to form a heterodimer,leading to the activation of signaling *** of HER3 is observed in various human cancers,including non-small cell lung cancer(NSCLC),and correlates with poor clinical outcomes in *** on the underlying mechanism demonstrate that HER3-initiated signaling promotes tumor metastasis and causes treatment failure in human *** of HER3 is frequently observed in EGFR-mutant NSCLC treated with EGFR-tyrosine kinase inhibitors(TKIs).Increased expression of HER3 triggers the so-called EGFR-independent mechanism via interactions with other receptors to activate“by-pass signaling pathways”,thereby resulting in resistance to *** date,no HER3-targeted therapy has been approved for cancer *** both preclinical and clinical studies,targeting HER3 with a blocking an-tibody(Ab)is the only strategy being *** evaluations of an anti-HER3 Ab-drug conjugate(ADC)show promising results in patients with EGFR-TKI-resistant ***,we summarize our understanding of the unique biology of HER3 in NSCLC refractory to EGFR-TKIs,with a focus on its dimerization partners and subsequent activation of signaling *** also discuss the latest development of the therapeutic Abs and ADCs targeting HER3 to abrogate EGFR-TKI resistance in NSCLC.

关键词： Human epidermal growth factor receptor 3(HER3) Epidermal growth factor receptor-tyrosine kinase inhibitors(EGFR-TKI) Resistance Antibody Antibody-drug conjugate(ADC) Non-small cell lung cancer(NSCLC)

CETP as a Target in HDL-raising Therapy:lessons from APOE*3-Leiden. CETP Transgenic Mice

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中国动脉硬化杂志 2009年第7期17卷 574-575页

作者： Willeke de Haan Jitske de Vries-van der Weij Caroline C. van der Hoogt José W.A. van der Hoorn Johannes A. Romijn J. Wouter Jukema Louis M. Havekes Hans M.G. Princen Patrick C.N. Rensen departments of General Internal Medicine Endocrinologyand Metabolic Diseases departments of Human genetics TNO-Biosciences Gaubius Laboratory departments of Cardiology Leiden University Medical Center

Background Cardiovascular disease (CVD) is mainly caused by atherosclerosis,for which dyslipidemia (i.e. high (V)LDL-cholesterol (C),high triglycerides and low HDLC is a major risk factor. To reduce the risk to develo... 详细信息

关键词：心血管疾病动脉粥样硬化血脂胆固醇临床分析

Proteolytic processing of SDF-1α by matrix metalloproteinase-2 impairs CXCR4 signaling and reduces neural progenitor cell migration

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Protein & Cell 2012年第11期3卷 875-882页

作者： Hui Peng Yumei Wu Zhiyuan Duan Pawel Ciborowski Jialin C.Zheng Laboratory of Neuroimmunology and Regenerative Therapy University of Nebraska Medical CenterOmahaNE 68198USA departments of Pharmacology and Experimental Neuroscience University of Nebraska Medical CenterOmahaNE 68198USA departments of Pathology and Microbiology University of Nebraska Medical CenterOmahaNE 68198USA Institute of genetics and Developmental Biology Chinese Academy of SciencesBeijing 100101China

Neural stem cells and neural progenitor cells(NPCs)exist throughout life and are mobilized to replace neurons,astrocytes and oligodendrocytes after ***-omal cell-derived factor 1(SDF-1,now named CXCL12)and its receptor CXCR4,an α-chemokine receptor,are critical for NPC migration into damaged areas of the *** previous studies demonstrated that immune activated and/or HIV-1-infected human monocyte-derived-macrophages(MDMs)induced a substantial increase of SDF-1 production by human ***,matrix metalloproteinase(MMP)-2,a protein up-regulated in HIV-1-infected macrophages,is able to cleave four amino acids from the N-terminus of SDF-1,resulting in a truncated SDF-1(5-67).In this study,we investigate the diverse signaling and function induced by SDF-1α and SDF-1(5-67)in human cortical ***-1(5-67)was generated by incubating human recombinant SDF-1α with MMP-2 followed by protein determination via mass spectrometry,Western blotting and ***-1α induced time-dependent phosphorylation of extracellular signal-regulated kinases(ERK)1/2,Akt-1,and diminished cyclic adenosine monophosphate(cAMP).In contrast,SDF-1(5-67)failed to induce these ***-1α activation of CXCR4 induced migration of NPCs,an effect that is dependent on ERK1/2 and Akt-1 pathways;whereas SDF-1(5-67)failed to induce NPC *** observation provides evidence that MMP-2 may affect NPC migration through post-translational processing of SDF-1α.

关键词： proteolysis chemokine neurogenesis and migration