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Commit 664268e1 authored by Liliana Sanfilippo's avatar Liliana Sanfilippo
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citations automated

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import React, { useState } from "react";
import React, { useState, useEffect } from "react";
import bibtexParse from 'bibtex-parser-js';
interface BibEntry {
ENTRYTYPE: string;
title?: string;
author?: string;
TITLE?: string;
AUTHOR?: string;
journal?: string;
volume?: string;
pages?: string;
......@@ -17,105 +17,236 @@ interface BibtexParserProps {
bibtexSources: string[]; // Accept an array of BibTeX strings
}
function formatPages(pages: string | undefined): JSX.Element | null {
// Check if pages is provided and is a non-empty string
if (pages && pages.length > 0) {
// Check for common page range separators
const pageRangeRegex = /--|-|–|–/; // RegEx to match various dash types
if (pageRangeRegex.test(pages)) {
const pag = pages.split(pageRangeRegex).map(p => p.trim());
const begin = pag[0];
const end = pag[1];
// Return formatted JSX
return (
<>
,&nbsp;<span property="schema:pageBegin">{begin}</span>-<span property="schema:pageEnd">{end}</span>
</>
);
} else if (/^\d+(-\d+)?$/.test(pages)) {
// If pages is a single numeric range, return it directly
return (
<>
,&nbsp;<span property="schema:pageBegin">{pages}</span>
</>
);
} else {
// Handle non-numeric page info
console.warn(`Non-numeric page information detected ('${pages}'). Treating as missing.`);
return null; // Return null if invalid
}
} else {
console.warn("Sorry, no page information.");
return null; // Return null if no page info
}
}
export const BibtexParser: React.FC<BibtexParserProps> = ({ bibtexSources }) => {
const [parsedEntries, setParsedEntries] = useState<BibEntry[]>([]);
// Parse BibTeX on component mount or when sources change
// Inside the useEffect
React.useEffect(() => {
useEffect(() => {
console.log("Parsing BibTeX sources: ", bibtexSources);
try {
const allEntries: BibEntry[] = [];
bibtexSources.forEach((bibtex) => {
// console.log(`Parsing BibTeX entry #${index + 1}: `, bibtex);
const parsed = bibtexParse.toJSON(bibtex);
// console.log(`Parsed entry: `, parsed);
allEntries.push(...parsed);
});
setParsedEntries(allEntries);
//console.log("All parsed entries: ", allEntries);
} catch (error) {
console.error("Error parsing BibTeX: ", error);
alert("An error occurred while parsing the BibTeX entries.");
// console.error("Error parsing BibTeX: ", error);
alert("An error occurred while parsing the BibTeX entries. Please check the format.");
}
}, [bibtexSources]);
// Helper function to render authors
const renderAuthors = (authors: string) => {
const authorList = authors.split(" and ");
return authorList.map((author, index) => (
<span key={index}>
{author}
{index < authorList.length - 1 ? ", " : ""}
</span>
));
};
// Helper function to render AUTHORS
const formatAuthors = (authors: string): string => {
console.log("Original input:", authors);
// Bereinigen des Eingabestrings und Ersetzen von "and" durch "|"
const cleanedAuthors = authors
.replace(/\s*and\s*/g, "|") // "and" durch "|" ersetzen
.replace(/\{|\}/g, "") // geschweifte Klammern entfernen
.trim();
console.log("Cleaned authors string:", cleanedAuthors);
// Autoren in ein Array aufteilen
const authorList = cleanedAuthors.split("|").map(author => author.trim());
console.log("Split author list:", authorList);
// Maximale Anzahl der anzuzeigenden Autoren
const maxAuthors = 7;
// Formatiere jeden Autor
const formattedAuthors = authorList.map((author, index) => {
console.log(`Processing author #${index + 1}:`, author);
// Nachname und Vornamen aufteilen
const [last, firstNames] = author.includes(",") ?
author.split(",").map(part => part.trim()) :
['', author]; // Wenn kein Komma vorhanden ist, wird der gesamte Name als Vorname behandelt
console.log(`Last name: "${last}", First names: "${firstNames}"`);
// Initialen für Vornamen erstellen
const initials = firstNames.split(' ').map(n => n[0] + '.').join(' ');
console.log(`Initials for "${firstNames}": "${initials}"`);
const formattedName = `${last}, ${initials}`.trim(); // Rückgabe des formatierten Namens
console.log(`Formatted name: "${formattedName}"`);
return formattedName;
});
console.log("Formatted authors before adding et al.:", formattedAuthors);
// Kombiniere die formatierten Autoren mit korrekter Interpunktion
const output = formattedAuthors.slice(0, maxAuthors).join('; ') +
(formattedAuthors.length > maxAuthors ? ' et al.' : '');
console.log("Final output:", output);
return output;
};
// Helper function to render individual citations based on their type
// Helper function to render individual citations based on their type
const renderCitation = (entry: BibEntry, index: number) => {
switch (entry.ENTRYTYPE) {
const renderCitation = (entry: BibEntry, index: number) => {
// console.log(`Rendering citation for entry #${index + 1}: `, entry);
// Use the index as citation number
const citationNumber = index + 1;
const entryType = entry.entryType.toLowerCase(); // Convert to lowercase for consistent comparison
const entryTags = entry.entryTags; // Adjust based on your data structure
// console.log("Entry Tags: ", entryTags);
switch (entryType) {
case "article":
return (
<li key={index}>
<span>{renderAuthors(entry.author || "")}</span>&nbsp;
<span>{entry.title}</span>.&nbsp;
<i>{entry.journal}</i>,&nbsp;
<b>{entry.volume}</b>,&nbsp;
<span>{entry.pages}</span> ({entry.year}).&nbsp;
{entry.doi && (
<a href={`https://doi.org/${entry.doi}`}>
doi: {entry.doi}
</a>
<li key={index} typeof="schema:ScholarlyArticle" role="doc-biblioentry" property="schema:citation" id={`desc-${citationNumber}`}>
{/* Citation number as comment */}
{/*<!-- Citation num ${citationNumber} --> */}
{formatAuthors(entryTags.AUTHOR || entryTags.EDITOR || "")}
&nbsp;<span property="schema:name">{entryTags.TITLE.replace(/[?!.]/g, '').replace(/\n/g, ' ').trim()}.</span>
&nbsp;<i property="schema:publisher" typeof="schema:Organization">{entryTags.JOURNAL}</i>
&nbsp;<b property="issueNumber" typeof="PublicationIssue">{entryTags.VOLUME}</b>
{formatPages(entryTags.PAGES) && <span>{formatPages(entryTags.PAGES)}</span>}
{entryTags.YEAR && (
<span>&nbsp;(<time property="schema:datePublished" datatype="xsd:gYear" dateTime={entryTags.YEAR}>{entryTags.YEAR}</time>).</span>
)}
{entryTags.DOI && (
<span>&nbsp;<a className="doi" href={`https://doi.org/${entryTags.DOI}`}>doi: {entryTags.DOI}</a></span>
)}
</li>
);
case "book":
return (
<li key={index}>
<span>{renderAuthors(entry.author || entry.editor || "")}</span>&nbsp;
<span>{entry.title}</span>.&nbsp;
<i>{entry.publisher}</i>,&nbsp;{entry.year}.
<li key={index} typeof="schema:Book" role="doc-biblioentry" property="schema:citation" id={`desc-${citationNumber}`}>
{/* Render authors */}
{formatAuthors(entryTags.AUTHOR || entryTags.EDITOR || "")}
{/* Render title or booktitle */}
{entryTags.TITLE ? (
<span property="schema:name">&nbsp;{entryTags.TITLE.replace(/[?!.]/g, '').replace(/\n/g, ' ').trim()}.</span>
) : entryTags.BOOKTITLE ? (
<span property="schema:name">&nbsp;{entryTags.BOOKTITLE.replace(/[?!.]/g, '').replace(/\n/g, ' ').trim()}.</span>
) : (
console.warn(`No title or booktitle found for entry ${citationNumber}`)
)}
{/* Render publisher */}
{entryTags.PUBLISHER && (
<i property="schema:publisher" typeof="schema:Organization">
&nbsp;{entryTags.PUBLISHER}
</i>
)}
{/* Render year */}
{entryTags.YEAR && (
<span>
&nbsp;(<time property="schema:datePublished" datatype="xsd:gYear" dateTime={entryTags.YEAR}>
{entryTags.YEAR}
</time>).
</span>
)}
{entryTags.ISBN && (
<span property="isbn">&nbsp;{entryTags.ISBN}</span>
)
}
</li>
);
case "misc":
return (
<li key={index}>
<span>{entry.author}</span>&nbsp;
<span>{entry.title}</span>.&nbsp;
<i>{entry.howpublished}</i>,&nbsp;{entry.year}.
<li key={index} typeof="schema:WebPage" role="doc-biblioentry" property="schema:citation" id={`desc-${citationNumber}`}>
{/* Render authors */}
{formatAuthors(entryTags.AUTHOR || entryTags.EDITOR || "")}
{/* Render title */}
{entryTags.TITLE && (
<span property="schema:name">&nbsp;{entryTags.TITLE.replace(/[?!.]/g, '').replace(/\n/g, ' ').trim()}.</span>
)}
{/* Render howpublished */}
{entryTags.HOWPUBLISHED && (
<i property="schema:publisher" typeof="schema:Organization">&nbsp;{entryTags.HOWPUBLISHED}</i>
)}
{/* Render year */}
{entryTags.YEAR && (
<span>&nbsp;(<time property="schema:datePublished" datatype="xsd:gYear" dateTime={entryTags.YEAR}>{entryTags.YEAR}</time>).</span>
)}
</li>
);
// Handle additional entry types here
case "inproceedings":
return (
<li key={index}>
<span>{renderAuthors(entry.author || "")}</span>&nbsp;
<span>{entry.title}</span>. In <i>{entry.booktitle}</i>,&nbsp;
<b>{entry.editor}</b>, {entry.year}.
<span>{formatAuthors(entryTags.AUTHOR || "")}</span>&nbsp;
<span>{entryTags.TITLE}</span>. In <i>{entryTags.BOOKTITLE}</i>,&nbsp;
<b>{entryTags.editor}</b>, {entryTags.YEAR}.
</li>
);
case "phdthesis":
return (
<li key={index}>
<span>{renderAuthors(entry.author || "")}</span>&nbsp;
<span>{entry.title}</span>, PhD thesis, {entry.school}, {entry.year}.
<span>{formatAuthors(entryTags.AUTHOR || "")}</span>&nbsp;
<span>{entryTags.TITLE}</span>, PhD thesis, {entryTags.SCHOOL}, {entryTags.YEAR}.
</li>
);
default:
return <li key={index}>Unknown entry type: {entry.ENTRYTYPE}</li>;
console.warn(`Unknown entry type: ${entryType}`);
return <li key={index}>Unknown entry type: {entryType}</li>;
}
};
return (
<div>
<h2>Citations</h2>
<ol>
{parsedEntries.map((entry, index) => renderCitation(entry, index))}
</ol>
{parsedEntries.length === 0 ? (
<p>No citations available.</p>
) : (
<ol>
{parsedEntries.map((entry, index) => renderCitation(entry, index))}
</ol>
)}
</div>
);
};
......
......@@ -2,6 +2,7 @@ import { Section, Subesction } from "../components/sections";
import { useTabNavigation } from "../utils/TabNavigation";
import {H5} from "../components/Headings";
import TestSource from "../soures/test-sources";
import MethodSources from "../soures/methods-sources";
export function Methods() {
useTabNavigation();
......@@ -93,179 +94,10 @@ export function Methods() {
<H5 text="Importance of Safety in LNP Development"></H5>
<p>Testing the safety of our LNPs was a critical step in their development. LNPs are increasingly being used in cutting-edge therapies, such as mRNA vaccines and targeted drug delivery systems. For these technologies to be viable, the nanoparticles must not harm the cells they are intended to interact with. The MTT and proliferation assays provided robust data, confirming the biocompatibility of our LNPs and reinforcing their potential for safe use in further research and clinical applications. </p>
</Subesction>
<TestSource/>
</Section>
<Section title="References" id="References">
<ol>
{/*<!-- Citation num 1--> */}
<li typeof="schema:ScolarlyArticle" role="doc-biblioentry" property="schema:citation" id="desc-1">
<span property="schema:author" typeof="schema:Person">
<span property="schema:Name"> Roth, F. C.</span>
<span property="schema:Name"> Draguhn, A.</span>
</span>
<span property="schema:name">&nbsp;Die Entwicklung der Patch-Clamp-Technik</span>.
<i property="schema:publisher" typeof="schema:Organization"> Springer eBooks</i>
<b property="issueNumber" typeof="PublicationIssue"> </b>
,&nbsp;<span property="schema:pageBegin"> 1</span>-<span property="schema:pageEnd">14</span>&nbsp;
(<time property="schema:datePublished" datatype="xsd:gYear" dateTime=" 2023">2023</time>).
<a className="doi" href="https://doi.org/10.1007/978-3-662-66053-9"> doi: 10.1007/978-3-662-66053-9</a>
</li>
{/*<!-- Citation num 2--> */}
<li typeof="schema:Book" role="doc-biblioentry" property="schema:citation" id="desc-2">
<span property="schema:author" typeof="schema:Person">
<span property="schema:Name"> Dallas, M.</span>
<span property="schema:Name"> Bell, D.</span>
</span>
<span property="schema:name">&nbsp;Patch clamp electrophysiology: methods and protocols.</span>
<i property="schema:publisher" typeof="schema:Organization">&nbsp;Humana Press</i>
&nbsp;(<time property="schema:datePublished" datatype="xsd:gYear" dateTime="2021">2021</time>).
</li>
{/*<!-- Citation num 3--> */}
<li typeof="schema:ScolarlyArticle" role="doc-biblioentry" property="schema:citation" id="desc-3">
<span property="schema:author" typeof="schema:Person">
<span property="schema:Name"> Priel, A.</span>
<span property="schema:Name"> Gil, Z.</span>
<span property="schema:Name"> Moy, V. T.</span>
<span property="schema:Name"> Magleby, K. L.</span>
<span property="schema:Name"> Silberberg, S. D.</span>
</span>
<span property="schema:name">&nbsp;
Ionic Requirements for Membrane-Glass Adhesion and Giga Seal Formation in
Patch-Clamp Recording
</span>.
<i property="schema:publisher" typeof="schema:Organization"> Biophysical Journal</i>
<b property="issueNumber" typeof="PublicationIssue"> 92</b>
,&nbsp;<span property="schema:pageBegin"> 3893</span>-<span property="schema:pageEnd">3900</span>&nbsp;
(<time property="schema:datePublished" datatype="xsd:gYear" dateTime=" 2007">2007</time>).
<a className="doi" href="https://doi.org/10.1529/biophysj.106.099119"> doi: 10.1529/biophysj.106.099119</a>
</li>
{/*<!-- Citation num 4--> */}
<li typeof="schema:ScolarlyArticle" role="doc-biblioentry" property="schema:citation" id="desc-4">
<span property="schema:author" typeof="schema:Person">
<span property="schema:Name"> Billet, A.</span>
<span property="schema:Name"> Froux, L.</span>
<span property="schema:Name"> Hanrahan, J. W.</span>
<span property="schema:Name"> Becq, F.</span>
</span>
<span property="schema:name">&nbsp;
Development of Automated Patch Clamp Technique to Investigate CFTR Chloride
Channel Function
</span>.
<i property="schema:publisher" typeof="schema:Organization"> Frontiers in Pharmacology</i>
<b property="issueNumber" typeof="PublicationIssue"> 8</b>
(<time property="schema:datePublished" datatype="xsd:gYear" dateTime=" 2017">2017</time>).
<a className="doi" href="https://doi.org/10.3389/fphar.2017.00195"> doi: 10.3389/fphar.2017.00195</a>
</li>
{/*<!-- Citation num 5--> */}
<li typeof="schema:ScolarlyArticle" role="doc-biblioentry" property="schema:citation" id="desc-5">
<span property="schema:author" typeof="schema:Person">
<span property="schema:Name"> DuBridge, R. B.</span>
<span property="schema:Name"> Tang, P.</span>
<span property="schema:Name"> Hsia, H. C.</span>
<span property="schema:Name"> Leong, P. M.</span>
<span property="schema:Name"> Miller, J. H.</span>
<span property="schema:Name"> Calos, M. P.</span>
</span>
<span property="schema:name">&nbsp;
Analysis of mutation in human cells by using an Epstein-Barr virus shuttle
system.
</span>.
<i property="schema:publisher" typeof="schema:Organization"> Molecular and Cellular Biology</i>
<b property="issueNumber" typeof="PublicationIssue"> 7</b>
,&nbsp;<span property="schema:pageBegin"> 379</span>-<span property="schema:pageEnd">387</span>&nbsp;
(<time property="schema:datePublished" datatype="xsd:gYear" dateTime=" 1987">1987</time>).
</li>
{/*<!-- Citation num 6--> */}
<li typeof="schema:ScolarlyArticle" role="doc-biblioentry" property="schema:citation" id="desc-6">
<span property="schema:author" typeof="schema:Person">
<span property="schema:Name"> Qin, J. Y.</span>
<span property="schema:Name"> Zhang, L.</span>
<span property="schema:Name"> Clift, K. L.</span>
<span property="schema:Name"> Hulur, I.</span>
<span property="schema:Name"> Xiang, A. P.</span>
<span property="schema:Name"> Ren, B.</span>
<span property="schema:Name"> Lahn, B. T.</span>
</span>
<span property="schema:name">&nbsp;
Systematic Comparison of Constitutive Promoters and the Doxycycline-Inducible
Promoter
</span>.
<i property="schema:publisher" typeof="schema:Organization"> PLOS ONE</i>
<b property="issueNumber" typeof="PublicationIssue"> 5</b>
(<time property="schema:datePublished" datatype="xsd:gYear" dateTime=" 2010">2010</time>).
<a className="doi" href="https://doi.org/10.1371/journal.pone.0010611"> doi: 10.1371/journal.pone.0010611</a>
</li>
{/*<!-- Citation num 7--> */}
<li typeof="schema:ScolarlyArticle" role="doc-biblioentry" property="schema:citation" id="desc-7">
<span property="schema:author" typeof="schema:Person">
<span property="schema:Name"> Bulcaen, M.</span>
<span property="schema:Name"> Kortleven, P.</span>
<span property="schema:Name"> Liu, R. B.</span>
<span property="schema:Name"> Maule, G.</span>
<span property="schema:Name"> Dreano, E.</span>
<span property="schema:Name"> Kelly, M.</span>
<span property="schema:Name"> Ensinck, M. M.</span>
<span property="schema:Name"> et al.</span>
</span>
<span property="schema:name">&nbsp;Prime editing functionally corrects cystic fibrosis-causing CFTR mutations in human organoids and airway epithelial cells</span>.
<i property="schema:publisher" typeof="schema:Organization"> Cell Reports Medicine</i>
<b property="issueNumber" typeof="PublicationIssue"> 5</b>
<span property="schema:pageBegin">101544</span>&nbsp;
(<time property="schema:datePublished" datatype="xsd:gYear" dateTime=" 2024">2024</time>).
<a className="doi" href="https://doi.org/https://doi.org/10.1016/j.xcrm.2024.101544"> doi: https://doi.org/10.1016/j.xcrm.2024.101544</a>
</li>
{/*<!-- Citation num 8--> */}
<li typeof="schema:ScolarlyArticle" role="doc-biblioentry" property="schema:citation" id="desc-8">
<span property="schema:author" typeof="schema:Person">
<span property="schema:Name"> Ensinck, M.</span>
<span property="schema:Name"> De Keersmaecker, L.</span>
<span property="schema:Name"> Heylen, L.</span>
<span property="schema:Name"> Ramalho, A. S.</span>
<span property="schema:Name"> Gijsbers, R.</span>
<span property="schema:Name"> Farré, R.</span>
<span property="schema:Name"> De Boeck, K.</span>
<span property="schema:Name"> et al.</span>
</span>
<span property="schema:name">&nbsp;
Phenotyping of Rare CFTR Mutations Reveals Distinct Trafficking and
Functional Defects
</span>.
<i property="schema:publisher" typeof="schema:Organization"> Cells</i>
<b property="issueNumber" typeof="PublicationIssue"> 9</b>
<span property="schema:pageBegin">754</span>&nbsp;
(<time property="schema:datePublished" datatype="xsd:gYear" dateTime=" 2020">2020</time>).
<a className="doi" href="https://doi.org/10.3390/cells9030754"> doi: 10.3390/cells9030754</a>
</li>
{/*<!-- Citation num 9--> */}
<li typeof="schema:WebPage" role="doc-biblioentry" property="schema:citation" id="desc-9">
<span property="schema:author" typeof="schema:Organisation">
<span property="schema:Name"> Zoya Ignatova</span>.
</span>
<span property="schema:name">Research Group Ignatova at the Institute of Biochemistry and Molecular Biology.</span>
<i property="schema:publisher" typeof="schema:Organization">Hamburg University</i>
&nbsp;(<time property="schema:datePublished" datatype="xsd:gYear" dateTime="2023">2023</time>).
</li>
{/*<!-- Citation num 10--> */}
<li typeof="schema:Book" role="doc-biblioentry" property="schema:citation" id="desc-10">
<span property="schema:author" typeof="schema:Person">
<span property="schema:Name"> Mennella, V.</span>
</span>
<span property="schema:name">&nbsp;Cilia: methods and protocols.</span>
<i property="schema:publisher" typeof="schema:Organization">&nbsp;Humana Press</i>
&nbsp;(<time property="schema:datePublished" datatype="xsd:gYear" dateTime="2024">2024</time>).
</li>
</ol>
<MethodSources/>
</Section>
......
import BibtexParser from "../components/makeSources";
export default function MethodSources(){
return (
<div>
<h1>BibTeX to HTML in React</h1>
<BibtexParser bibtexSources={bibtexSources} />
</div>
);
}
const bibtexSources = [
`
@article{article,
title = {Die Entwicklung der Patch-Clamp-Technik},
author = {Roth, F. C., Numberger, M., and Draguhn, A.},
year = 2023,
month = {{}},
journal = {Springer eBooks},
volume = {{}},
pages = {1--14},
doi = {10.1007/978-3-662-66053-9}
}`,
`
@book{dallas_patch_2021,
title = {Patch clamp electrophysiology: methods and protocols},
shorttitle = {Patch clamp electrophysiology},
year = 2021,
publisher = {Humana Press},
address = {New York},
series = {Methods in molecular biology},
number = 2188,
isbn = {978-1-07-160818-0},
language = {en},
editor = {Dallas, Mark and Bell, Damian}
}
`,
`
@article{PRIEL20073893,
title = {
Ionic Requirements for Membrane-Glass Adhesion and Giga Seal Formation in
Patch-Clamp Recording
},
author = {
Avi Priel and Ziv Gil and Vincent T. Moy and Karl L. Magleby and Shai D.
Silberberg
},
year = 2007,
journal = {Biophysical Journal},
volume = 92,
number = 11,
pages = {3893--3900},
doi = {10.1529/biophysj.106.099119},
issn = {0006-3495},
url = {https://www.sciencedirect.com/science/article/pii/S000634950771189X},
abstract = {
Patch-clamp recording has revolutionized the study of ion channels,
transporters, and the electrical activity of small cells. Vital to this
method is formation of a tight seal between glass recording pipette and cell
membrane. To better understand seal formation and improve practical
application of this technique, we examine the effects of divalent ions,
protons, ionic strength, and membrane proteins on adhesion of membrane to
glass and on seal resistance using both patch-clamp recording and atomic
force microscopy. We find that H+, Ca2+, and Mg2+ increase adhesion force
between glass and membrane (lipid and cellular), decrease the time required
to form a tight seal, and increase seal resistance. In the absence of H+
(10−10M) and divalent cations (<10−8M), adhesion forces are greatly reduced
and tight seals are not formed. H+ (10−7M) promotes seal formation in the
absence of divalent cations. A positive correlation between adhesion force
and seal formation indicates that high resistance seals are associated with
increased adhesion between membrane and glass. A similar ionic dependence of
the adhesion of lipid membranes and cell membranes to glass indicates that
lipid membranes without proteins are sufficient for the action of ions on
adhesion.
}
}
`,
`
@article{10.3389/fphar.2017.00195,
title = {
Development of Automated Patch Clamp Technique to Investigate CFTR Chloride
Channel Function
},
author = {
Billet, Arnaud and Froux, Lionel and Hanrahan, John W. and Becq, Frederic
},
year = 2017,
journal = {Frontiers in Pharmacology},
volume = 8,
doi = {10.3389/fphar.2017.00195},
issn = {1663-9812},
url = {
https://www.frontiersin.org/journals/pharmacology/articles/10.3389/fphar.2017.00195
}
}
`,
`
@article{DuBridge_Tang_Hsia_Leong_Miller_Calos_1987,
title = {
Analysis of mutation in human cells by using an Epstein-Barr virus shuttle
system.
},
author = {
DuBridge, R B and Tang, P and Hsia, H C and Leong, P M and Miller, J H and
Calos, M P
},
year = 1987,
month = jan,
journal = {Molecular and Cellular Biology},
volume = 7,
number = 1,
pages = {379–387},
issn = {0270-7306},
abstractnote = {
We developed highly sensitive shuttle vector systems for detection of
mutations formed in human cells using autonomously replicating derivatives of
Epstein-Barr virus (EBV). EBV vectors carrying the bacterial lacI gene as the
target for mutation were established in human cells and later returned to
Escherichia coli for rapid detection and analysis of lacI mutations. The
majority of the clonal cell lines created by establishment of the lacI-EBV
vector show spontaneous LacI- frequencies of less than 10(-5) and are
suitable for studies of induced mutation. The ability to isolate clonal lines
represents a major advantage of the EBV vectors over transiently replicating
shuttle vectors (such as those derived from simian virus 40) for the study of
mutation. The DNA sequence changes were determined for 61 lacI mutations
induced by exposure of one of the cell lines to N-nitroso-N-methylurea. A
total of 33 of 34 lacI nonsense mutations and 26 of 27 missense mutations
involve G X C to A X T transitions. These data provide support for the
mutational theory of cancer.
}
}
`,
`
@article{Qin_Zhang_Clift_Hulur_Xiang_Ren_Lahn_2010,
title = {
Systematic Comparison of Constitutive Promoters and the Doxycycline-Inducible
Promoter
},
author = {
Qin, Jane Yuxia and Zhang, Li and Clift, Kayla L. and Hulur, Imge and Xiang,
Andy Peng and Ren, Bing-Zhong and Lahn, Bruce T.
},
year = 2010,
month = may,
journal = {PLOS ONE},
publisher = {Public Library of Science},
volume = 5,
number = 5,
pages = {e10611},
doi = {10.1371/journal.pone.0010611},
issn = {1932-6203},
abstractnote = {
Constitutive promoters are used routinely to drive ectopic gene expression.
Here, we carried out a systematic comparison of eight commonly used
constitutive promoters (SV40, CMV, UBC, EF1A, PGK and CAGG for mammalian
systems, and COPIA and ACT5C for Drosophila systems). We also included in the
comparison the TRE promoter, which can be activated by the rtTA
transcriptional activator in a doxycycline-inducible manner. To make our
findings representative, we conducted the comparison in a variety of cell
types derived from several species. We found that these promoters vary
considerably from one another in their strength. Most promoters have fairly
consistent strengths across different cell types, but the CMV promoter can
vary considerably from cell type to cell type. At maximal induction, the TRE
promoter is comparable to a strong constitutive promoter. These results
should facilitate more rational choices of promoters in ectopic gene
expression studies.
},
language = {en}
}
`,
`
@article{BULCAEN2024101544,
title = {Prime editing functionally corrects cystic fibrosis-causing CFTR mutations in human organoids and airway epithelial cells},
journal = {Cell Reports Medicine},
volume = {5},
number = {5},
pages = {101544},
year = {2024},
issn = {2666-3791},
doi = {https://doi.org/10.1016/j.xcrm.2024.101544},
url = {https://www.sciencedirect.com/science/article/pii/S2666379124002349},
author = {Mattijs Bulcaen and Phéline Kortleven and Ronald B. Liu and Giulia Maule and Elise Dreano and Mairead Kelly and Marjolein M. Ensinck and Sam Thierie and Maxime Smits and Matteo Ciciani and Aurelie Hatton and Benoit Chevalier and Anabela S. Ramalho and Xavier {Casadevall i Solvas} and Zeger Debyser and François Vermeulen and Rik Gijsbers and Isabelle Sermet-Gaudelus and Anna Cereseto and Marianne S. Carlon},
keywords = {cystic fibrosis, prime editing, patient-derived organoids, human nasal epithelial cells, gene editing, machine learning, DETEOR, CRISPR},
abstract = {Summary
Prime editing is a recent, CRISPR-derived genome editing technology capable of introducing precise nucleotide substitutions, insertions, and deletions. Here, we present prime editing approaches to correct L227R- and N1303K-CFTR, two mutations that cause cystic fibrosis and are not eligible for current market-approved modulator therapies. We show that, upon DNA correction of the CFTR gene, the complex glycosylation, localization, and, most importantly, function of the CFTR protein are restored in HEK293T and 16HBE cell lines. These findings were subsequently validated in patient-derived rectal organoids and human nasal epithelial cells. Through analysis of predicted and experimentally identified candidate off-target sites in primary stem cells, we confirm previous reports on the high prime editor (PE) specificity and its potential for a curative CF gene editing therapy. To facilitate future screening of genetic strategies in a translational CF model, a machine learning algorithm was developed for dynamic quantification of CFTR function in organoids (DETECTOR: “detection of targeted editing of CFTR in organoids”).}
}
new8.
@article{Ensinck_Deeersmaecker_Heylen_Ramalho_Gijsbers_Far,
title = {
Phenotyping of Rare CFTR Mutations Reveals Distinct Trafficking and
Functional Defects
},
author = {
Ensinck, Marjolein and De Keersmaecker, Liesbeth and Heylen, Lise and
Ramalho, Anabela S. and Gijsbers, Rik and Farré, Ricard and De Boeck, Kris
and Christ, Frauke and Debyser, Zeger and Carlon, Marianne S.
},
year = 2020,
month = mar,
journal = {Cells},
volume = 9,
number = 3,
pages = 754,
doi = {10.3390/cells9030754},
issn = {2073-4409},
abstractnote = {
Background. The most common CFTR mutation, F508del, presents with multiple
cellular defects. However, the possible multiple defects caused by many rarer
CFTR mutations are not well studied. We investigated four rare CFTR mutations
E60K, G85E, E92K and A455E against well-characterized mutations, F508del and
G551D, and their responses to corrector VX-809 and/or potentiator VX-770.
Methods. Using complementary assays in HEK293T stable cell lines, we
determined maturation by Western blotting, trafficking by flow cytometry
using extracellular 3HA-tagged CFTR, and function by halide-sensitive YFP
quenching. In the forskolin-induced swelling assay in intestinal organoids,
we validated the effect of tagged versus endogenous CFTR. Results. Treatment
with VX-809 significantly restored maturation, PM localization and function
of both E60K and E92K. Mechanistically, VX-809 not only raised the total
amount of CFTR, but significantly increased the traffic efficiency, which was
not the case for A455E. G85E was refractory to VX-809 and VX-770 treatment.
Conclusions. Since no single model or assay allows deciphering all defects at
once, we propose a combination of phenotypic assays to collect rapid and
early insights into the multiple defects of CFTR variants.
},
language = {eng}
}
`,
`
@misc{ignatova2023,
author = {Zoya Ignatova},
title = {Research Group Ignatova at the Institute of Biochemistry and Molecular Biology},
year = {2023},
howpublished = {Hamburg University},
note = {Accessed: 28 September 2024},
institution = {University of Hamburg},
}
`,
`
@book{Mennella_2024,
title = {Cilia: methods and protocols},
year = 2024,
author = {Mennella, Vito},
publisher = {Humana Press},
address = {New York, NY},
isbn = {978-1-07-163507-0},
abstractnote = {
This volume covers the latest advancements in the study of ciliary
complexity. Protocols cover genomic, proteomic, imaging, and functional
analysis of different ciliated tissues and their wide applicability in cilia
biology. Chapters in this book primarily focus on methods to study
multiciliated cells, and discuss topics such as SARS-CoV-2 infections of
human primary nasal multiciliated epithelial cells; expansion microscopy of
ciliary proteins; live-imaging centriole amplification in mouse brain
multiciliated cells; biophysical properties of cilia motility; and
mucociliary transport device construction. Written in the highly successful
Methods in Molecular Biology series format, chapters include introductions to
their respective topics, lists of the necessary materials and reagents,
step-by-step, readily reproducible laboratory protocols, and tips on
troubleshooting and avoiding known pitfalls. Cutting-edge and thorough,
Cilia: Methods and Protocols is a valuable resource for researchers who are
interested in learning more about this developing field.
},
language = {eng}
}
`
]
\ No newline at end of file
......@@ -3,15 +3,45 @@ import BibtexParser from "../components/makeSources";
export function TestSource(){
const bibtexSources = [
`
@article{doe2023,
author = {John Doe and Jane Smith},
title = {A Great Paper},
journal = {Important Journal},
volume = {12},
pages = {123-456},
year = {2023},
doi = {10.1000/journal-doi}
}
@article{Ensinck_Deeersmaecker_Heylen_Ramalho_Gijsbers_Far,
title = {
Phenotyping of Rare CFTR Mutations Reveals Distinct Trafficking and
Functional Defects
},
author = {
Ensinck, Marjolein and De Keersmaecker, Liesbeth and Heylen, Lise and
Ramalho, Anabela S. and Gijsbers, Rik and Farré, Ricard and De Boeck, Kris
and Christ, Frauke and Debyser, Zeger and Carlon, Marianne S.
},
year = 2020,
month = mar,
journal = {Cells},
volume = 9,
number = 3,
pages = 754,
doi = {10.3390/cells9030754},
issn = {2073-4409},
abstractnote = {
Background. The most common CFTR mutation, F508del, presents with multiple
cellular defects. However, the possible multiple defects caused by many rarer
CFTR mutations are not well studied. We investigated four rare CFTR mutations
E60K, G85E, E92K and A455E against well-characterized mutations, F508del and
G551D, and their responses to corrector VX-809 and/or potentiator VX-770.
Methods. Using complementary assays in HEK293T stable cell lines, we
determined maturation by Western blotting, trafficking by flow cytometry
using extracellular 3HA-tagged CFTR, and function by halide-sensitive YFP
quenching. In the forskolin-induced swelling assay in intestinal organoids,
we validated the effect of tagged versus endogenous CFTR. Results. Treatment
with VX-809 significantly restored maturation, PM localization and function
of both E60K and E92K. Mechanistically, VX-809 not only raised the total
amount of CFTR, but significantly increased the traffic efficiency, which was
not the case for A455E. G85E was refractory to VX-809 and VX-770 treatment.
Conclusions. Since no single model or assay allows deciphering all defects at
once, we propose a combination of phenotypic assays to collect rapid and
early insights into the multiple defects of CFTR variants.
},
language = {eng}
}
`
];
......
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