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Most of qualitative dietary changes observed one year post-bariatric surgery can be achieved with a preoperative dietary intervention

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Endocrinología, Diabetes y Nutrición (English ed.) 2020年第1期67卷 20-27页

作者： Benaiges, David Parri, Alejandra Subirana, Isaac Pedro-Botet, Juan Villatoro, Montserrat Ramon, Jose M. Climent, Elisenda Flores Le Roux, Juana A. Goday, Alberto Department of Endocrinology and Nutrition Hospital del Mar Barcelona Spain Cardiovascular Risk and Nutrition Research Group (CARIN-ULEC) IMIM-Hospital del Mar Barcelona Spain Departament de Medicina Universitat Autònoma de Barcelona Spain PhD Research Program in Dietetics and Nutrition (EEES 101105 Nutrició i salut) Barcelona University Barcelona Spain Cardiovascular Epidemiology and Genetics Research Group REGICOR Study Group IMIM (Hospital del Mar Medical Research Institute) Barcelona Catalonia Spain CIBER Epidemiology and Public Health (CIBERESP) Barcelona Catalonia Spain Unit of Gastrointestinal Surgery Hospital del Mar Institut de Recerca IMIM-Hospital del Mar Barcelona Spain Centro de Investigaciones Biomédicas en Red de Obesidad y Nutrición CIBERobn Spain

AbstractBackground and objectivesBariatric surgery (BS) leads to several changes in nutritional habits that can be attributed to different mechanisms. Some of these changes could be achievable with a preoperative nutritional intervention. The objective was to evaluate dietary modifications during the preoperative and postoperative periods of BS. MethodsProspective observational study of patients who underwent BS between 2010 and 2014 at the Hospital del Mar; 60 consecutive patients were included. Food consumption was measured by a validated food-frequency questionnaire at inclusion in the bariatric surgery program, after preoperative nutritional intervention, and one year after surgery. Generalized estimating equation models were used to assess differences in food group intake during follow up. ResultsEnergy intake significantly decreased from inclusion to 1 year of surgery ( p= 0.003). After the preoperative intervention and prior to surgery, there was an increase in intake of nuts, vegetables, poultry and rabbit, fruit, fish and skimmed milk products and a decrease in bread, soft drinks and pastry. At one year post-surgery, a continued decrease in the consumption of bread and soft drinks and an increase in nuts was observed (linear non-quadratic trend). Consumption of fruit, pastry, fish and skimmed milk products remained stable showing a linear and quadratic trend. Vegetables and poultry and rabbit increased in the preoperative period and decreased after surgery, showing a quadratic but not linear trend. Conclusionsa preoperative nutritional intervention in morbidly obese patients can associate favorable dietary changes that are mostly maintained one year after bariatric surgery.

关键词： Dietary intake Preoperative Bariatric surgery Food groups Micronutrients Ingesta dietética Cirugía bariátrica Grupos de alimentos Micronutrientes

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GestaltMML: Enhancing Rare Genetic Disease Diagnosis through Multimodal Machine Learning Combining Facial Images and Clinical Texts

arXiv

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arXiv 2023年

作者： Wu, Da Yang, Jingye Liu, Cong Hsieh, Tzung-Chien Marchi, Elaine Blair, Justin Krawitz, Peter Weng, Chunhua Chung, Wendy Lyon, Gholson J. Krantz, Ian D. Kalish, Jennifer M. Wang, Kai Raymond G. Perelman Center for Cellular and Molecular Therapeutics Children's Hospital of Philadelphia PhiladelphiaPA19104 United States Department of Biomedical Informatics Columbia University Irving Medical Center New YorkNY10032 United States Institute for Genomic Statistics and Bioinformatics University Hospital Bonn Rheinische Friedrich-Wilhelms-Universität Bonn Bonn Germany Department of Human Genetics New York State Institute for Basic Research in Developmental Disabilities Staten IslandNY United States Division of Human Genetics Children's Hospital of Philadelphia PhiladelphiaPA19104 United States Department of Pediatrics Boston Children’s Hospital Harvard Medical School BostonMA United States Biology PhD Program The Graduate Center The City University of New York New York United States Department of Genetics Perelman School of Medicine University of Pennsylvania PhiladelphiaPA United States Department of Pediatrics Perelman School of Medicine University of Pennsylvania PhiladelphiaPA United States Department of Pathology and Laboratory Medicine Perelman School of Medicine University of Pennsylvania PhiladelphiaPA19104 United States

Individuals with suspected rare genetic disorders often undergo multiple clinical evaluations, imaging studies, laboratory tests and genetic tests, to find a possible answer over a prolonged period of time. Addressing this "diagnostic odyssey" thus has substantial clinical, psychosocial, and economic benefits. Many rare genetic diseases have distinctive facial features, which can be used by artificial intelligence algorithms to facilitate clinical diagnosis, in prioritizing candidate diseases to be further examined by lab tests or genetic assays, or in helping the phenotype-driven reinterpretation of genome/exome sequencing data. Existing methods using frontal facial photos were built on conventional Convolutional Neural Networks (CNNs), rely exclusively on facial images, and cannot capture non-facial phenotypic traits and demographic information essential for guiding accurate diagnoses. Here we introduce GestaltMML, a multimodal machine learning (MML) approach solely based on the Transformer architecture. It integrates facial images, demographic information (age, sex, ethnicity), and clinical notes (optionally, a list of Human Phenotype Ontology terms) to improve prediction accuracy. Furthermore, we also evaluated GestaltMML on a diverse range of datasets, including 528 diseases from the GestaltMatcher Database, several in-house datasets of Beckwith-Wiedemann syndrome (BWS, over-growth syndrome with distinct facial features), Sotos syndrome (overgrowth syndrome with overlapping features with BWS), NAA10-related neurodevelopmental syndrome, Cornelia de Lange syndrome (multiple malformation syndrome), and KBG syndrome (multiple malformation syndrome). Our results suggest that GestaltMML effectively incorporates multiple modalities of data, greatly narrowing candidate genetic diagnoses of rare diseases and may facilitate the reinterpretation of genome/exome sequencing data. © 2023, CC BY.

关键词： Diseases

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Towards decoding the coupled decision-making of metabolism and epithelial-mesenchymal transition in cancer

arXiv

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arXiv 2020年

作者： Jia, Dongya Park, Jun Hyoung Kaur, Harsimran Jung, Kwang Hwa Yang, Sukjin Tripathi, Shubham Galbraith, Madeline Deng, Youyuan Jolly, Mohit Kumar Kaipparettu, Benny Abraham Onuchic, José N. Levine, Herbert Center for Theoretical Biological Physics Rice University HoustonTX77005 United States Department of Molecular and Human Genetics Baylor College of Medicine HoustonTX77030 United States Centre for BioSystems Science and Engineering Indian Institute of Science BangaloreKarnataka560012 India PhD Program in Systems Synthetic and Physical Biology Rice University HoustonTX77005 United States Department of Physics Northeastern University BostonMA02115 United States Department of Physics and Astronomy Rice University HoustonTX77005 United States Applied Physics Graduate Program Rice University HoustonTX77005 United States Dan L. Duncan Comprehensive Cancer Center Baylor College of Medicine HoustonTX77030 United States Department of Chemistry Rice University HoustonTX77005 United States Department of Biosciences Rice University HoustonTX77005 United States Department of Bioengineering Northeastern University BostonMA02115 United States

Cancer cells have the plasticity to adjust their metabolic phenotypes for survival and metastasis. During metastasis, a developmental program known as the epithelial-mesenchymal transition (EMT) plays a critical role. There is extensive cross-talk between metabolism and EMT, but how this leads to coordinated physiological changes is still uncertain. The elusive connection between metabolism and EMT compromises the efficacy of metabolic therapies targeting metastasis. In this review, we aim for clarifying causation between metabolism and EMT based on recent experimental studies and propose integrated theoretical-experimental efforts to better understand the coupled decision-making of metabolism and EMT. © 2020, CC-BY-NC-ND.

关键词： Metabolism

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MEDU-39. HIGHLY RECURRENT U1 SMALL NUCLEAR RNA HOTSPOT MUTATIONS DRIVE ALTERNATIVE SPLICING IN SONIC HEDGEHOG MEDULLOBLASTOMA

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Neuro-Oncology 2019年第SUPPLEMENT_2期21卷 ii111–ii111页

作者： Kumar, Sachin Suzuki, Hiromichi Shuai, Shimin Stein, Lincoln Taylor, Michael Department of Laboratory Medicine and Pathobiology - University of Toronto Toronto ON Canada MD/PhD Program - University of Toronto Toronto ON Canada The Arthur and Sonia Labatt Brain Tumour Research Centre - Hospital for Sick Children Toronto ON Canada Developmental & Stem Cell Biology - Hospital for Sick Children Toronto ON Canada Department of Molecular Genetics - University of Toronto Toronto ON Canada Informatics and Biocomputing - Ontario Institute for Cancer Research Toronto ON Canada

Recurrent somatic single nucleotide variants (SNVs) in cancer are largely confined to protein-coding genes, and are rare in pediatric cancers. Similar to many pediatric cancers, medulloblastomas harbor few recurrent somatic SNVs except forTERTpromoter mutations. To investigate non-coding mutations, we analyzed whole-genome sequencing from 341 medulloblastoma cases. We identified hotspot mutations of the U1-snRNAs in ~50% of Shh-medulloblastomas, which were not present across other medulloblastoma subgroups. U1 spliceosomal small nuclear RNA (snRNA) mutations were further analyzed in an additional 179 sonic hedgehog (Shh) medulloblastoma cases using allele-specific PCR. Mutations were largely absent from infant Shh-medulloblastoma, but were prevalent in 97% of adults (Shhδ), and 25% of adolescents (Shhα). The U1-snRNA mutation was found in most adolescents withTP53mutations, and represents a higher risk thanTP53mutation. The mutation was assessed in 2,442 cases across 36 tumour types from the ICGC, and hotspot mutations were highly specific to Shh-medulloblastomas. The U1-snRNA mutation occurs in the 5’ splice site binding region (r.3a>g), and snRNA mutant tumors have significantly disrupted RNA splicing with an excess of 5’ cryptic splicing events. Shh pathway genesPTCH1andGLI2were aberrantly spliced, generating stop codons induced by novel cassette exons. Consequently, both alternative isoforms translate incomplete mRNAs, which reduce Ptch1 function and increase Gli2 function. U1-snRNA mutations also affected several oncogenes and tumor suppressor genes such asCCND2andPAX5. Our results provide the first evidence of a hotspot mutation in U1-snRNA, revealing a novel mechanism of aberrant splicing in cancer and implicating splice site targeting mutations in medulloblastoma pathogenesis. As U1 mutations are present in medulloblastoma patients with the highest mortality, it represents an exciting target for novel therapy.

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Autonomic Dysfunction in REM Sleep Disorder: The Role of Respiration in HRV Analysis*

Autonomic Dysfunction in REM Sleep Disorder: The Role of Res...

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Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC)

作者： Parisa Sattar Nicla Mandas Giulia Baldazzi Elisa Facchini Elisa Casaglia Michela Figorilli Laura Giorgetti Pietro Mattioli Francesco Calizzano Francesco Fama Dario Arnaldi Monica Puligheddu Danilo Pani Pablo Laguna Raquel Bailon Department of Biomedical Sciences Neuroscience PhD Program University of Cagliari Cagliari Italy Department of Electrical and Electronic Engineering MeDSP Lab University of Cagliari Cagliari Italy The Hadron Academy Istituto Universitario di Studi Superiori IUSS Pavia Italy Interdepartmental Sleep Disorder Research Center University of Cagliari Cagliari Italy SC Neurology AziendaOspedaliero-Universitaria Cagliari Italy Department of Neuroscience Rehabilitation Ophthalmology Genetics Maternal and Child Health (DINOGMI) Clinical Neurology University of Genoa Genoa Italy Neurophysiopathology Unit IRCCS Ospedale Policlinico San Martino Genoa Italy Biomedical Signal Interpretation and Computational Simulation (BSICoS) Aragón Institute for Engineering Research (I3A) IIS Aragón University of Zaragoza Spain Zaragoza Spain Centro de Investigacion Biomedica en Red en Bioingeniería Biomateriales y Nanomedicina (CIBER-BBN) Madrid Spain

ISBN: (数字)9798350371499

ISBN: (纸本)9798350371505

Autonomic nervous system (ANS) has been suggested often associated with the isolated rapid eye movement (REM) sleep behavior disorder (iRBD), with iRBD, and heart rate variability (HRV) is a commonly used tool to assess it. However, the accuracy of HRV is heavily influenced by respiratory rate (RespR), potentially causing misinterpretation of frequency domain HRV indices. This study compares sleep-related ANS function between iRBD patients and a control group (CG) using respiratory-adjusted HRV spectral analysis. It involves 20 iRBD and 20 CG participants in each group, from which five-minute ECG signal epochs during N2, N3, and REM sleep phases are analyzed. RespR were estimated from ECG-derived respiratory signals. Both low and high frequency bands definition for HRV analysis were redefined using the RespR. The results indicate significant differences in HRV parameters between iRBD and CG subjects during REM sleep, highlighting disrupted autonomic regulation in iRBD. This finding is also evident in non-REM phases, thus emphasizing the need to incorporate RespR in HRV analysis, especially in sleep-related studies, for a comprehensive understanding of autonomic dysfunction.

关键词： Phase modulation Frequency-domain analysis Electrocardiography Regulation Rapid eye movement sleep High frequency Heart rate variability Engineering in medicine and biology Spectral analysis Parasympathetic nervous system

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Integration of Protein Interactome Networks with Congenital Heart Disease Variants Reveals Candidate Disease Genes

SSRN

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SSRN 2020年

作者： Gonzalez-Teran, Barbara Pittman, Maureen Felix, Franco Richmond-Buccola, Desmond Thomas, Reuben Choudhary, Krishna Moroni, Elisabetta Colombo, Giorgio Alexanian, Michael Cole, Bonnie Samse-Knapp, Kaitlen McGregor, Michael Gifford, Casey A. Huttenhain, Ruth Gelb, Bruce D. Conklin, Bruce R. Black, Brian L. Bruneau, Benoit G. Krogan, Nevan J. Pollard, Katherine S. Srivastava, Deepak Gladstone Institutes San FranciscoCA United States SCITEC-CNR Milano Italy University of Pavia Department of Chemistry Pavia Italy Developmental and Stem Cell Biology PhD Program University of California San FranciscoCA United States Department of Cellular and Molecular Pharmacology University of California San Francisco San FranciscoCA United States Department of Genetics and Genomic Sciences Icahn School of Medicine at Mount Sinai New YorkNY United States Mindich Child Health and Development Institute Icahn School of Medicine at Mount Sinai New YorkNY United States Department of Pediatrics Icahn School of Medicine at Mount Sinai New YorkNY United States Cardiovascular Research Institute University of California San FranciscoCA United States Department of Pediatrics UCSF School of Medicine San FranciscoCA United States Roddenberry Center for Stem Cell Biology and Medicine at Gladstone San FranciscoCA United States University of California San Francisco San FranciscoCA United States Chan Zuckerberg Biohub San FranciscoCA United States Department of Epidemiology & Biostatistics Institute for Computational Health Sciences Institute for Human Genetics University of California San FranciscoCA United States Department of Biochemistry and Biophysics University of California San FranciscoCA United States Gladstone Institutes 1650 Owens St San FranciscoCA94158 United States

Congenital heart disease (CHD) is present in 1% of live births, yet identification of causal mutations remains a challenge despite large-scale genomic sequencing efforts. We hypothesized that genetic determinants for CHDs may lie in protein interactomes of GATA4 and TBX5, two transcription factors that cause CHDs. Defining their interactomes in human cardiac progenitors via affinity purification-mass spectrometry and integrating results with genetic data from the Pediatric Cardiac Genomic Consortium revealed an enrichment of de novo variants among proteins that interact with GATA4 or TBX5. A consolidative score that prioritized interactome members based on variant, gene, and proband features identified likely CHD-causing genes, including the epigenetic reader GLYR1. GLYR1 and GATA4 widely co-occupied cardiac developmental genes, resulting in co-activation, and the GLYR1 missense variant associated with CHD disrupted interaction with GATA4. This integrative proteomic and genetic approach provides a framework for prioritizing and interrogating the contribution of genetic variants in disease. © 2020, The Authors. All rights reserved.

关键词： Proteins

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Autosomal recessive nonsyndromic hearing loss

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American Journal of Medical genetics Part A 2002年第3期89卷

作者： Rachel A. Sundstrom Lut van Laer Guy Van Camp Richard J.H. Smith Rachel Sundstrom is a graduate student in the Interdepartmental Genetics PhD Program at the University of Iowa. She is doing her thesis work on recessive non-syndromic hearing loss in the Molecular Otolaryngology Research Laboratories. Dr. Lut van Laer (PhD) is a post-doctoral student working in Dr. Van Camp's laboratory. She had identified the DFNA5 gene in 1998 and her current focus is determining the function of the DFNA5 gene product. Dr. Guy Van Camp (PhD) is an investigator and docent working at the Department of Medical Genetics of the University of Antwerp. Dr. Van Camp is Head of the Hereditary Hearing Loss Research Unit in the Department. Department of Otolaryngology–Head and Heck Surgery University of Iowa Iowa City IA 52242 Dr. Richard Smith is the Sterba Hearing Research Professor and Director of the Molecular Otolaryngology Research Laboratories in the Department of Otolaryngology—Head and Neck Surgery. Both groups have extensively collaborated since 1994 and are as a collaborative unit responsible for several gene localizations and identifications for hearing loss over the past 6 years.

Nearly all genes for autosomal recessive nonsyndromal inherited hearing loss (ARNSHL) localized thus far cause prelingual severe to profound or profound hearing impairment. Of the 25 reported loci, most have been identified using single consanguineous families. Six of these genes have been cloned and encode a variety of proteins, including ion channels, extracellular matrix components, cytoskeletal components, and proteins essential for synaptic vesicular trafficking. One of these genes appears to be responsible for approximately 50% of all congenital severe to profound or profound hearing loss in many world populations, and mutations in two other genes can lead to either syndromic or nonsyndromic forms of deafness. The identification of additional genes that cause ARNSHL and elucidation of their function will refine our understanding of auditory physiology at the molecular level. Am. J. Med. Genet. (Semin. Med. Genet.) 89:123–129, 1999. © 2000 Wiley-Liss, Inc.

关键词： GJB2 MYO7A MYO15 PDS OTOF TECTA

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Manifestations of human atherosclerosis across vascular beds

JVS-vascular insights

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JVS-vascular insights 2024年 2卷 100089页

作者： Daniel G Jovin Bauer E Sumpio Daniel M Greif Yale Cardiovascular Research Center Section of Cardiovascular Medicine Department of Internal Medicine Yale University. Yale Cardiovascular Research Center Section of Cardiovascular Medicine Department of Genetics Yale University. Yale Cardiovascular Research Center Section of Cardiovascular Medicine Stem Cell Center Yale University. Yale Cardiovascular Research Center Section of Cardiovascular Medicine MD-PhD Program Yale University. Yale Cardiovascular Research Center Section of Cardiovascular Medicine Division of Vascular and Endovascular Surgery Department of Surgery Yale University.

Objective:Atherosclerosis underlies the most common etiologies of mortality worldwide, resulting in nearly 10 million deaths annually. In atherosclerosis, inflammation, metabolic factors, and hemodynamics cause the accumulation of extracellular lipids and the formation of plaques in the tunica intima of specific arteries. Atherosclerotic plaques primarily form in the coronary and carotid arteries, the aorta, and the peripheral arteries of the lower extremities. Although a common conceptual model of atherogenesis across these arteries has evolved over decades, there is a limited understanding of the important differences in regional atherosclerotic disease. Methods:This review summarizes clinical studies, meta-analyses, and case reports to compare and contrast the impact, risk, plaque features, and clinical management of carotid, coronary, and femoral atherosclerosis in humans. Results:Common risk factors, such as smoking and diabetes, influence disease risk differently across vascular beds. In addition, biological variables demonstrate a region-specific relationship with disease as peripheral atherosclerosis is most heritable, and male sex increases the risk of coronary and carotid, but not peripheral artery disease. The pathology of atherosclerotic lesions also varies between vascular territories. Specifically, carotid plaques are primarily lipid rich, whereas coronary plaques more commonly include fibrotic components with lipid-rich features, and femoral plaques are predominantly fibrocalcific. Clinically, interventional outcomes are worst in the carotid arteries and response to medical therapies, particularly statins, is not consistent across diseased regions, even within individual patients. Conclusions:Atherosclerosis manifests in site-specific ways with regional differences in susceptibility and treatment response. Despite advances in the scientific understanding and clinical management of atherosclerosis, little is known about the mechanisms determining vesse

关键词： Atherosclerosis Carotid stenosis Coronary artery disease Peripheral arterial disease Plaque

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Exposure to fine particulate matter 2.5 from wood combustion smoke causes vascular changes in placenta and reduces fetal size

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Placenta 2024年 153卷 e30-e30页

作者： Francisca Villarroel Nikol Ponce Fernando A. Gómez Cristián Muñoz Eder Ramírez Francisco Nualart Paulo Salinas Laboratory of Animal & Experimental Morphology Institute of Biology Faculty of Sciences Pontificia Universidad Católica de Valparaíso Valparaíso Chile MSc. Program in Biological Sciences Pontificia Universidad Católica de Valparaíso Valparaíso Chile PhD Program in Morphological Sciences Universidad de La Frontera Temuco Chile Center of Excellence in Surgical and Morphological Studies (CEMyQ) Universidad de La Frontera Temuco Chile Laboratory of Genetics and Molecular Immunology Institute of Biology Faculty of Sciences Pontificia Universidad Católica de Valparaíso Valparaíso Chile Laboratory of Neurobiology and Stem Cells NeuroCellT Department of Cellular Biology Faculty of Biological Sciences Universidad de Concepcion Concepcion Chile Center for Advanced Microscopy CMA BIO-BIO Universidad de Concepcion Concepcion Chile

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Author Correction: L1CAM defines the regenerative origin of metastasis-initiating cells in colorectal cancer

Nature cancer

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Nature cancer 2020年第11期1卷 1128页

作者： Karuna Ganesh Harihar Basnet Yasemin Kaygusuz Ashley M Laughney Lan He Roshan Sharma Kevin P O'Rourke Vincent P Reuter Yun-Han Huang Mesruh Turkekul Ekrem Emrah Er Ignas Masilionis Katia Manova-Todorova Martin R Weiser Leonard B Saltz Julio Garcia-Aguilar Richard Koche Scott W Lowe Dana Pe'er Jinru Shia Joan Massagué Cancer Biology and Genetics Program Sloan Kettering Institute Memorial Sloan Kettering Cancer Center New York NY USA. Department of Medicine Memorial Sloan Kettering Cancer Center New York NY USA. Molecular Pharmacology Program Sloan Kettering Institute Memorial Sloan Kettering Cancer Center New York NY USA. Louis V. Gerstner Jr. Graduate School of Biomedical Sciences Memorial Sloan Kettering Cancer Center New York NY USA. Institute for Computational Biomedicine Department of Physiology and Biophysics Weill Cornell Medicine New York NY USA. Computational and Systems Biology Program Sloan Kettering Institute Memorial Sloan Kettering Cancer Center New York NY USA. Department of Applied Physics and Applied Math Columbia University New York NY USA. New York Genome Center New York NY USA. Weill Cornell/Rockefeller/Sloan Kettering Tri-Institutional MD-PhD Program New York NY USA. Center for Epigenetics Research Memorial Sloan Kettering Cancer Center New York NY USA. Molecular Cytology Core Facility Memorial Sloan Kettering Cancer Center New York NY USA. Department of Physiology and Biophysics University of Illinois at Chicago Chicago IL USA. Department of Surgery Memorial Sloan Kettering Cancer Center New York NY USA. Department of Pathology Memorial Sloan Kettering Cancer Center New York NY USA. Cancer Biology and Genetics Program Sloan Kettering Institute Memorial Sloan Kettering Cancer Center New York NY USA. j-massague@***.

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