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XML 문서를 파싱하는 것이 잘 작동하지만, 내가 알아챈 점은 특정 태그 ("AbstractText") 사이의 텍스트가 무작위로 잘라지고 무엇이 있는지 전혀 모르는 것입니다. 다시 말하지만,이 태그는 여기저기서 만 나타나며 항상이 태그의 경우는 아닙니다. 구문 분석을위한 내 코드는 아래에 있으며 또한 잘린 텍스트의 예입니다.구문 분석 XML - 캡처 된 문자열이 잘립니다. Swift
var abstractBool = false
var abstract = ""
func parser(_ parser: XMLParser, didStartElement elementName: String, namespaceURI: String?, qualifiedName qName: String?, attributes attributeDict: [String : String] = [:]) {
switch elementName {
case "AbstractText":
abstractBool = true
}
}
func parser(_ parser: XMLParser, foundCharacters string: String) {
if abstractBool{
abstract = string
}
}
func parser(_ parser: XMLParser, didEndElement elementName: String,
namespaceURI: String?, qualifiedName qName: String?) {
switch elementName {
case "AbstractText":
abstractBool = false
}
}
원격 서버에서
원시 XML :
내가 추출 할 수있는 무슨<Abstract>
<AbstractText>
Protein kinase C (PKC) has been shown to activate the mammalian target of
rapamycin complex 1 (mTORC1) signaling pathway, a central hub in the
regulation of cell metabolism, growth and proliferation. However, the
mechanisms by which PKCs activate mTORC1 are still ambiguous. Our previous
study revealed that activation of classical PKCs (cPKC) results in the
perinuclear accumulation of cPKC and phospholipase D2 (PLD2) in recycling
endosomes in a PLD2-dependent manner. Here, we report that mTORC1 activation
by phorbol 12,13-myristate acetate (PMA) requires both classic, cPKC, and
novel PKC (nPKC) isoforms, specifically PKCη, acting through distinct
pathways. The translocation of mTOR to perinuclear lysosomes was detected
after treatment of PKC activators, which was not colocalized with PKCα- or
RAB11-positive endosomes and was not inhibited by PLD inhibitors. We found
that PKCη inhibition by siRNA or bisindolylmaleimide I effectively decreased
mTOR accumulation in lysosomes and its activity. Also, we identified that
PKCη plays a role upstream of the v-ATPase/Ragulator/Rag pathway in response
to PMA. These data provides a spatial aspect to the regulation of mTORC1 by
sustained activation of PKC, requiring co-ordinated activation of two
distinct elements, the perinuclear accumulation of cPKC- and PLD-containing
endosomes and the nPKC-dependent translation of of mTOR in the perinuclear
lysosomes. The close proximity of these two distinct compartments shown in
this study suggests the possibility that transcompartment signaling may be a
factor in the regulation of mTORC1 activity and also underscores the
importance of PKCη as a potential therapeutic target of mTORC-related
disorders.
</AbstractText>
</Abstract>
문자열의 다음 프런트 엔드 절단 된 부분이다 :
scompartment signaling may be a factor in the regulation of mTORC1 activity
and also underscores the importance of PKCη as a potential therapeutic target
of mTORC-related disorders.
귀하의 PS는 iOS에는 적용되지 않으며 MacOS에만 적용됩니다. – rmaddy
코멘트 주셔서 감사합니다. 질문에 "iOS"라는 태그가 붙어 있으므로 PS를 삭제했습니다. –