From cb20e7ff6a16b6aa5745a434cffbde23ef996573 Mon Sep 17 00:00:00 2001
From: Isabell Alexandra Guckes <isabell.guckes@uni-bielefeld.de>
Date: Wed, 25 Sep 2024 12:52:33 +0000
Subject: [PATCH] Update file drug-data.tsx
---
src/data/drug-data.tsx | 4 ++--
1 file changed, 2 insertions(+), 2 deletions(-)
diff --git a/src/data/drug-data.tsx b/src/data/drug-data.tsx
index 514742ba..d1a3d6e6 100644
--- a/src/data/drug-data.tsx
+++ b/src/data/drug-data.tsx
@@ -46,11 +46,11 @@ export const drugdata: (Array<DrugDatensatz>) = [
{
name: "Modulators",
picture: "...",
- introduction: "",
+ introduction: "CFTR modulators represent a significant advancement in CF treatment since they are small molecules improving the function of the defective CFTR protein in a mutation-specific way, which helps restore chloride ion transport across cell membranes. Notable pharmaceutical agents include Trikafta®, Symdeko®, Orkambi® and Kalydeco® [1]. These medications have been demonstrated to significantly improve lung function and reduce pulmonary exacerbations. However, they are expensive and may cause side effects such as liver enzyme elevations and cataracts in pediatric patients [2]. Furthermore, they are not suitable for all CF patients since only mutations which produce a CFTR channel can be supported by CFTR modulators, not those mutations which lead to a missing CFTR channel (knock out) [1], e.g. stop-mutations including p.Arg553Ter or p.Gly542Ter [3]. ",
examples: [
{
title: "",
- text: "string"
+ text: "test"
},
{
title: "",
--
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