作者列表的Pubmed ID+；引用，Python？

我有一个pubmed ID列表，我想用完整的作者列表提取引用。有这样的在线工具：，但作者列表缩写为“et al”

我正在尝试使用Biopython中的Entrez包来完成这项工作，并使用xml.etree.ElementTree来解析xml对象

以下是我所拥有的：

from Bio.Entrez import efetch
import xml.etree.ElementTree as ET

def fetch_abstract(pmid):
    handle = efetch(db='pubmed', id=pmid, retmode='xml')
    xml_data = handle.read()
    print xml_data #this prints the XML data structure correctly

    article = ET.XML(xml_data)

    #problem starts here. I want to create a citation, so I start by trying to
    #get the names of the authors, but I am not sure why this is not working.
    for author_name in article.findall('AuthorValidYN'):
        print author_name

    return 


fetch_abstract(22864638)

XML如下所示：

<?xml version="1.0"?>
<!DOCTYPE PubmedArticleSet PUBLIC "-//NLM//DTD PubMedArticle, 1st January 2014//EN"      "http://www.ncbi.nlm.nih.gov/corehtml/query/DTD/pubmed_140101.dtd">
<PubmedArticleSet>
<PubmedArticle>
    <MedlineCitation Owner="NLM" Status="MEDLINE">
    <PMID Version="1">22864638</PMID>
    <DateCreated>
        <Year>2012</Year>
        <Month>10</Month>
        <Day>31</Day>
    </DateCreated>
    <DateCompleted>
        <Year>2013</Year>
        <Month>04</Month>
        <Day>23</Day>
    </DateCompleted>
    <Article PubModel="Print">
        <Journal>
            <ISSN IssnType="Electronic">1573-7292</ISSN>
            <JournalIssue CitedMedium="Internet">
                <Volume>11</Volume>
                <Issue>4</Issue>
                <PubDate>
                    <Year>2012</Year>
                    <Month>Dec</Month>
                </PubDate>
            </JournalIssue>
            <Title>Familial cancer</Title>
            <ISOAbbreviation>Fam. Cancer</ISOAbbreviation>
        </Journal>
        <ArticleTitle>No evidence for breast cancer susceptibility associated with variants of BRD7, a component of p53 and BRCA1 pathways.</ArticleTitle>
        <Pagination>
            <MedlinePgn>601-6</MedlinePgn>
        </Pagination>
        <ELocationID EIdType="doi" ValidYN="Y">10.1007/s10689-012-9556-0</ELocationID>
        <Abstract>
            <AbstractText>BRD7 (bromodomain 7), a subunit of poly-bromo-associated BRG1-associated factor (PBAF)-specific Swi/Snf chromatin remodeling complexes, has been proposed as a tumour suppressor protein following its identification as an important component of both functional p53 and BRCA1 (breast cancer 1, early onset) pathways. As low BRD7 expression levels have been linked to p53-wild-type breast tumour cells, we hypothesized an implication of BRD7 germline alterations in the pathogenesis of hereditary breast cancer similar to that of TP53 in Li-Fraumeni syndrome. We performed sequence analysis of the BRD7 gene on 61 high-risk individuals with hereditary or very-early-onset breast cancer and 100 healthy controls. Four potentially disease-causing single-nucleotide alterations were detected within the cohort of breast cancer patients (one listed as a rare single-nucleotide polymorphism (SNP) in the NCBI (National Center for Biotechnology Information) SNP database). Two of the detected variants were also each found once within the control collective. Segregation analysis on both families of those carrying the remaining two variants revealed segregation of these BRD7 alterations independent of breast cancer. In conclusion, it seems that the BRD7 variants we detected represent rare polymorphisms and mainly rule out BRD7 as a frequent high-penetrance breast cancer susceptibility gene. However, further analyses in larger cohorts of women with hereditary breast cancer should clarify the role of BRD7 in breast cancer predisposition.</AbstractText>
        </Abstract>
        <AuthorList CompleteYN="Y">
            <Author ValidYN="Y">
                <LastName>Penkert</LastName>
                <ForeName>Judith</ForeName>
                <Initials>J</Initials>
                <Affiliation>Institute of Cell and Molecular Pathology, Hannover Medical School, Carl-Neuberg-Strasse 1, Hannover, Germany.</Affiliation>
            </Author>
            <Author ValidYN="Y">
                <LastName>Schlegelberger</LastName>
                <ForeName>Brigitte</ForeName>
                <Initials>B</Initials>
            </Author>
            <Author ValidYN="Y">
                <LastName>Steinemann</LastName>
                <ForeName>Doris</ForeName>
                <Initials>D</Initials>
            </Author>
            <Author ValidYN="Y">
                <LastName>Gadzicki</LastName>
                <ForeName>Dorothea</ForeName>
                <Initials>D</Initials>
            </Author>
        </AuthorList>
        <Language>eng</Language>
        <PublicationTypeList>
            <PublicationType>Comparative Study</PublicationType>
            <PublicationType>Journal Article</PublicationType>
            <PublicationType>Research Support, Non-U.S. Gov't</PublicationType>
        </PublicationTypeList>
    </Article>
    <MedlineJournalInfo>
        <Country>Netherlands</Country>
        <MedlineTA>Fam Cancer</MedlineTA>
        <NlmUniqueID>100898211</NlmUniqueID>
        <ISSNLinking>1389-9600</ISSNLinking>
    </MedlineJournalInfo>
    <ChemicalList>
        <Chemical>
            <RegistryNumber>0</RegistryNumber>
            <NameOfSubstance>BRCA1 Protein</NameOfSubstance>
        </Chemical>
        <Chemical>
            <RegistryNumber>0</RegistryNumber>
            <NameOfSubstance>BRCA1 protein, human</NameOfSubstance>
        </Chemical>
        <Chemical>
            <RegistryNumber>0</RegistryNumber>
            <NameOfSubstance>BRD7 protein, human</NameOfSubstance>
        </Chemical>
        <Chemical>
            <RegistryNumber>0</RegistryNumber>
            <NameOfSubstance>Chromosomal Proteins, Non-Histone</NameOfSubstance>
        </Chemical>
        <Chemical>
            <RegistryNumber>0</RegistryNumber>
            <NameOfSubstance>TP53 protein, human</NameOfSubstance>
        </Chemical>
        <Chemical>
            <RegistryNumber>0</RegistryNumber>
            <NameOfSubstance>Tumor Suppressor Protein p53</NameOfSubstance>
        </Chemical>
    </ChemicalList>
    <CitationSubset>IM</CitationSubset>
    <MeshHeadingList>
        <MeshHeading>
            <DescriptorName MajorTopicYN="N">Adult</DescriptorName>
        </MeshHeading>
        <MeshHeading>
            <DescriptorName MajorTopicYN="N">Aged</DescriptorName>
        </MeshHeading>
        <MeshHeading>
            <DescriptorName MajorTopicYN="N">BRCA1 Protein</DescriptorName>
            <QualifierName MajorTopicYN="Y">genetics</QualifierName>
        </MeshHeading>
        <MeshHeading>
            <DescriptorName MajorTopicYN="N">Breast Neoplasms</DescriptorName>
            <QualifierName MajorTopicYN="Y">genetics</QualifierName>
        </MeshHeading>
        <MeshHeading>
            <DescriptorName MajorTopicYN="N">Case-Control Studies</DescriptorName>
        </MeshHeading>
        <MeshHeading>
            <DescriptorName MajorTopicYN="N">Chromosomal Proteins, Non-Histone</DescriptorName>
            <QualifierName MajorTopicYN="Y">genetics</QualifierName>
        </MeshHeading>
        <MeshHeading>
            <DescriptorName MajorTopicYN="N">Female</DescriptorName>
        </MeshHeading>
        <MeshHeading>
            <DescriptorName MajorTopicYN="Y">Genetic Predisposition to Disease</DescriptorName>
        </MeshHeading>
        <MeshHeading>
            <DescriptorName MajorTopicYN="N">Humans</DescriptorName>
        </MeshHeading>
        <MeshHeading>
            <DescriptorName MajorTopicYN="N">Male</DescriptorName>
        </MeshHeading>
        <MeshHeading>
            <DescriptorName MajorTopicYN="N">Middle Aged</DescriptorName>
        </MeshHeading>
        <MeshHeading>
            <DescriptorName MajorTopicYN="N">Mutation</DescriptorName>
            <QualifierName MajorTopicYN="Y">genetics</QualifierName>
        </MeshHeading>
        <MeshHeading>
            <DescriptorName MajorTopicYN="N">Pedigree</DescriptorName>
        </MeshHeading>
        <MeshHeading>
            <DescriptorName MajorTopicYN="N">Polymorphism, Single Nucleotide</DescriptorName>
            <QualifierName MajorTopicYN="Y">genetics</QualifierName>
        </MeshHeading>
        <MeshHeading>
            <DescriptorName MajorTopicYN="N">Prognosis</DescriptorName>
        </MeshHeading>
        <MeshHeading>
            <DescriptorName MajorTopicYN="N">Tumor Suppressor Protein p53</DescriptorName>
            <QualifierName MajorTopicYN="Y">genetics</QualifierName>
        </MeshHeading>
        <MeshHeading>
            <DescriptorName MajorTopicYN="N">Young Adult</DescriptorName>
        </MeshHeading>
    </MeshHeadingList>
</MedlineCitation>
<PubmedData>
    <History>
        <PubMedPubDate PubStatus="entrez">
            <Year>2012</Year>
            <Month>8</Month>
            <Day>7</Day>
            <Hour>6</Hour>
            <Minute>0</Minute>
        </PubMedPubDate>
        <PubMedPubDate PubStatus="pubmed">
            <Year>2012</Year>
            <Month>8</Month>
            <Day>7</Day>
            <Hour>6</Hour>
            <Minute>0</Minute>
        </PubMedPubDate>
        <PubMedPubDate PubStatus="medline">
            <Year>2013</Year>
            <Month>4</Month>
            <Day>24</Day>
            <Hour>6</Hour>
            <Minute>0</Minute>
        </PubMedPubDate>
    </History>
    <PublicationStatus>ppublish</PublicationStatus>
    <ArticleIdList>
        <ArticleId IdType="doi">10.1007/s10689-012-9556-0</ArticleId>
        <ArticleId IdType="pubmed">22864638</ArticleId>
    </ArticleIdList>
</PubmedData>

22864638
2012
10
31
2013
04
23
1573-7292
11
4.
2012
12月
家族性癌症
法姆。巨蟹座
没有证据表明BRD7变异与乳腺癌易感性相关，BRD7是p53和BRCA1通路的一个组成部分。
601-6
10.1007/s10689-012-9556-0
BRD7（bromodomain 7）是多溴相关BRG1相关因子（PBAF）特异性Swi/Snf染色质重塑复合物的一个亚单位，经鉴定是功能性p53和BRCA1（乳腺癌1，早发）通路的重要组成部分，被认为是一种肿瘤抑制蛋白。由于BRD7低表达水平与p53野生型乳腺肿瘤细胞有关，我们假设BRD7种系改变在遗传性乳腺癌发病机制中的意义与Li-Fraumeni综合征中的TP53相似。我们对61名遗传性或极早发性乳腺癌高危人群和100名健康对照进行了BRD7基因序列分析。在乳腺癌患者队列中检测到四种可能导致疾病的单核苷酸改变（其中一种在NCBI（国家生物技术信息中心）单核苷酸多态性数据库中被列为罕见单核苷酸多态性（SNP））。检测到的两种变体也在对照组中各发现一次。对携带其余两种变体的两个家族进行的分离分析显示，这些BRD7改变的分离独立于乳腺癌。总之，我们检测到的BRD7变体似乎代表了罕见的多态性，并且主要排除了BRD7作为一种常见的高外显率乳腺癌易感基因的可能性。然而，在更大的遗传性乳腺癌妇女队列中进行进一步分析，应该澄清BRD7在乳腺癌易感性中的作用。
彭克特
朱迪思
J
汉诺威医学院细胞和分子病理学研究所，卡尔·纽伯格大街1号，汉诺威，德国。
施勒格贝格尔
布里吉特
B
史泰曼
多丽丝
D
加兹基
多萝西娅
D
英格
比较研究
期刊文章
研究支持，非美国政府
荷兰
家族癌
100898211
1389-9600
0
BRCA1蛋白
0
BRCA1蛋白，人
0
BRD7蛋白，人
0
染色体蛋白质类，非组蛋白
0
TP53蛋白，人
0
肿瘤抑制蛋白p53
感应电动机
成人
…岁
BRCA1蛋白
遗传学
乳腺肿瘤
遗传学
病例对照研究
染色体蛋白质类，非组蛋白
遗传学
女性
易感性
人类
男性
中年人
突变
遗传学
纯种
单核苷酸多态性
遗传学
预后
肿瘤抑制蛋白p53
遗传学
年轻人
2012
8.
7.
6.
0
2012
8.
7.
6.
0
2013
4.
24
6.
0
发表
10.1007/s10689-012-9556-0
22864638

---

我认为您在寻找错误的XML节点。ValidYN是节点作者的属性。因此，您应该使用：

for author_name in article.findall('Author')

“Element.findall（）只查找带有标记的元素，这些元素是当前元素的直接子元素。”我认为需要将当前元素设置为AuthorList。像这样的

article.find('AuthorList').findall('Author')

---

我认为您正在寻找错误的XML节点。ValidYN是节点作者的属性。因此，您应该使用：

for author_name in article.findall('Author')

“Element.findall（）只查找带有标记的元素，这些元素是当前元素的直接子元素。”我认为需要将当前元素设置为AuthorList。像这样的

article.find('AuthorList').findall('Author')

---

我认为您正在寻找错误的XML节点。ValidYN是节点作者的属性。因此，您应该使用：

for author_name in article.findall('Author')

“Element.findall（）只查找带有标记的元素，这些元素是当前元素的直接子元素。”我认为需要将当前元素设置为AuthorList。像这样的

article.find('AuthorList').findall('Author')

---

我认为您正在寻找错误的XML节点。ValidYN是