diff --git a/src/components/makeSources.tsx b/src/components/makeSources.tsx
index 74565b4036de75ac90f32d599c8978c4e594102c..f95bd3c5d0bdf334a320c119620bac3eef01d025 100644
--- a/src/components/makeSources.tsx
+++ b/src/components/makeSources.tsx
@@ -1,10 +1,10 @@
-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 (
+ <>
+ , <span property="schema:pageBegin">{begin}</span>-<span property="schema:pageEnd">{end}</span>
+ </>
+ );
+ } else if (/^\d+(-\d+)?$/.test(pages)) {
+ // If pages is a single numeric range, return it directly
+ return (
+ <>
+ , <span property="schema:pageBegin">{pages}</span>
+ </>
+ );
+ } else {
+ // Handle non-numeric page info
+ console.warn(`Non-numeric page information detected ('${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 #${index + 1}: `, entry);
+
+ // Use the index as citation number
+ const citationNumber = index + 1;
+ const entryType = entry.entryType.toLowerCase(); // Convert to lowercase for consistent comparison
+ const entryTags = entry.entryTags; // Adjust based on your data structure
+ // console.log("Entry Tags: ", entryTags);
+
+ switch (entryType) {
case "article":
return (
- <li key={index}>
- <span>{renderAuthors(entry.author || "")}</span>
- <span>{entry.title}</span>.
- <i>{entry.journal}</i>,
- <b>{entry.volume}</b>,
- <span>{entry.pages}</span> ({entry.year}).
- {entry.doi && (
- <a href={`https://doi.org/${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 ${citationNumber} --> */}
+ {formatAuthors(entryTags.AUTHOR || entryTags.EDITOR || "")}
+ <span property="schema:name">{entryTags.TITLE.replace(/[?!.]/g, '').replace(/\n/g, ' ').trim()}.</span>
+ <i property="schema:publisher" typeof="schema:Organization">{entryTags.JOURNAL}</i>
+ <b property="issueNumber" typeof="PublicationIssue">{entryTags.VOLUME}</b>
+ {formatPages(entryTags.PAGES) && <span>{formatPages(entryTags.PAGES)}</span>}
+ {entryTags.YEAR && (
+ <span> (<time property="schema:datePublished" datatype="xsd:gYear" dateTime={entryTags.YEAR}>{entryTags.YEAR}</time>).</span>
+ )}
+ {entryTags.DOI && (
+ <span> <a className="doi" href={`https://doi.org/${entryTags.DOI}`}>doi: {entryTags.DOI}</a></span>
)}
</li>
);
-
+
case "book":
return (
- <li key={index}>
- <span>{renderAuthors(entry.author || entry.editor || "")}</span>
- <span>{entry.title}</span>.
- <i>{entry.publisher}</i>, {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"> {entryTags.TITLE.replace(/[?!.]/g, '').replace(/\n/g, ' ').trim()}.</span>
+ ) : entryTags.BOOKTITLE ? (
+ <span property="schema:name"> {entryTags.BOOKTITLE.replace(/[?!.]/g, '').replace(/\n/g, ' ').trim()}.</span>
+ ) : (
+ console.warn(`No title or booktitle found for entry ${citationNumber}`)
+ )}
+ {/* Render publisher */}
+ {entryTags.PUBLISHER && (
+ <i property="schema:publisher" typeof="schema:Organization">
+ {entryTags.PUBLISHER}
+ </i>
+ )}
+ {/* Render year */}
+ {entryTags.YEAR && (
+ <span>
+ (<time property="schema:datePublished" datatype="xsd:gYear" dateTime={entryTags.YEAR}>
+ {entryTags.YEAR}
+ </time>).
+ </span>
+ )}
+ {entryTags.ISBN && (
+ <span property="isbn"> {entryTags.ISBN}</span>
+ )
+ }
</li>
);
-
+
case "misc":
return (
- <li key={index}>
- <span>{entry.author}</span>
- <span>{entry.title}</span>.
- <i>{entry.howpublished}</i>, {entry.year}.
+ <li key={index} typeof="schema:WebPage" role="doc-biblioentry" property="schema:citation" id={`desc-${citationNumber}`}>
+ {/* Render authors */}
+ {formatAuthors(entryTags.AUTHOR || entryTags.EDITOR || "")}
+ {/* Render title */}
+ {entryTags.TITLE && (
+ <span property="schema:name"> {entryTags.TITLE.replace(/[?!.]/g, '').replace(/\n/g, ' ').trim()}.</span>
+ )}
+ {/* Render howpublished */}
+ {entryTags.HOWPUBLISHED && (
+ <i property="schema:publisher" typeof="schema:Organization"> {entryTags.HOWPUBLISHED}</i>
+ )}
+ {/* Render year */}
+ {entryTags.YEAR && (
+ <span> (<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>
- <span>{entry.title}</span>. In <i>{entry.booktitle}</i>,
- <b>{entry.editor}</b>, {entry.year}.
+ <span>{formatAuthors(entryTags.AUTHOR || "")}</span>
+ <span>{entryTags.TITLE}</span>. In <i>{entryTags.BOOKTITLE}</i>,
+ <b>{entryTags.editor}</b>, {entryTags.YEAR}.
</li>
);
-
+
case "phdthesis":
return (
<li key={index}>
- <span>{renderAuthors(entry.author || "")}</span>
- <span>{entry.title}</span>, PhD thesis, {entry.school}, {entry.year}.
+ <span>{formatAuthors(entryTags.AUTHOR || "")}</span>
+ <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>
);
};
diff --git a/src/contents/methods.tsx b/src/contents/methods.tsx
index 031f6bcd841f8e1f5138b15a18f1127f7351f626..4162b856ec90c8ae75b5f8e52e2fbcedfaceebb3 100644
--- a/src/contents/methods.tsx
+++ b/src/contents/methods.tsx
@@ -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"> Die Entwicklung der Patch-Clamp-Technik</span>.
- <i property="schema:publisher" typeof="schema:Organization"> Springer eBooks</i>
- <b property="issueNumber" typeof="PublicationIssue"> </b>
- , <span property="schema:pageBegin"> 1</span>-<span property="schema:pageEnd">14</span>
- (<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"> Patch clamp electrophysiology: methods and protocols.</span>
- <i property="schema:publisher" typeof="schema:Organization"> Humana Press</i>
- (<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">
-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>
- , <span property="schema:pageBegin"> 3893</span>-<span property="schema:pageEnd">3900</span>
- (<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">
-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">
-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>
- , <span property="schema:pageBegin"> 379</span>-<span property="schema:pageEnd">387</span>
- (<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">
-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"> 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>
- (<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">
-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>
- (<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>
- (<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"> Cilia: methods and protocols.</span>
- <i property="schema:publisher" typeof="schema:Organization"> Humana Press</i>
- (<time property="schema:datePublished" datatype="xsd:gYear" dateTime="2024">2024</time>).
-</li>
-
-
- </ol>
+ <MethodSources/>
</Section>
diff --git a/src/soures/methods-sources.tsx b/src/soures/methods-sources.tsx
new file mode 100644
index 0000000000000000000000000000000000000000..dc28b718103533d63b744a2124716f61f50beeef
--- /dev/null
+++ b/src/soures/methods-sources.tsx
@@ -0,0 +1,267 @@
+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 organoidsâ€).}
+}
+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
diff --git a/src/soures/test-sources.tsx b/src/soures/test-sources.tsx
index 77cce4c6405bd821146fc422fc87b1ca67234a8b..6f7d9e455d03d36929ed9b1c4d5d67ea2c07bd03 100644
--- a/src/soures/test-sources.tsx
+++ b/src/soures/test-sources.tsx
@@ -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}
+}
`
];