okay, I will process the provided HTML to extract the relevant details and format it into a news article. Here’s the structured output:
json
{
"title": "How overweight also harms the descendants",
"date": "2025-06-18",
"author": "University of Bonn",
"source": "idw-online.de",
"url": "http://www.idw-online.de/-DQf8AA",
"tags": ["medicine", "research projects", "scientific publications"],
"content": "Children of overweight mothers frequently enough also develop metabolic disorders, even if they eat healthy.A current study by the University of Bonn now provides information on why this is so. Accordingly, certain cells in the liver of the embryo are reprogrammed in the case of obese mice during pregnancy. This changes the metabolism of the descendants in the long term. The researchers beleive that these findings could also apply to humans. You have now been published in the Nature magazine. Attention blocking period: not published CEST before Wednesday, June 18, 5 p.m!nnIn thier study, the scientists examined the so-called Kupapfer cells. These include macrophages, an crucial group of feed cells, and are among the defense troops of the innate immune system. During the growth of the embryo, You migrate to his liver, where you then reside permanently. There they combat pathogens and digest outdated cells.nn"The Kupffer cells also take on the role of a conductor," explains Prof. Dr. Elvira Mass from the Limes Institute of the University of Bonn. "They instruct the liver cells around them what they have to do. They ensure that this central metabolism organ can correctly perform its diverse tasks."nnBeethoven instead of VivaldinnApparently it is this conductor function that is changed by obesity. In this direction, at least mouse experiments indicate that massed together with other working groups at the University of Bonn. "We were able to show that the descendants often developed a fatty liver shortly after birth," explains Mass' employee Dr. Hao Huang. "Even when the young animals died as normal."nnThe reason for this disorder was apparently a "reprogramming" of the Kupffer cells in the young animals. As a result, they gave molecular signals with which they demonstrated the liver cells more fat. Peemratively speaking, they no longer conducted a Beethoven symphony, but a piece by Vivaldi.nnThis change was apparently already carried out during the embryonic development, triggered by the mother's metabolic products. They operated a kind of molecular switch in the Kupffer cells, making it converted in the long term. "This switch is a so -called transcription factor," says Mass. "He controls which genes are read in the Kupffer cells."nnNo fatty liver without molecular switchesnnIf the researchers removed this switch in the kupffer cells genetically during pregnancy, the young animals did not develop fatty liver. It is indeed still unclear whether it also offers a starting point for medication. The working groups involved now want to pursue this question in follow -up studies.nnIf new treatment options arise, that would be good news. as the changed working mode of the Kupffer cells probably has a variety of negative effects. The obesity of the liver is accompanied by massive inflammatory reactions. They ensure that more and more liver cells die and replaced by connective tissue.The result is a so -called fibrosis, in which the liver gradually sets its function. At the same time, the risk increases that liver cells degenerate and tumors.nn"It is indeed becoming increasingly clear that many people's diseases arise very early in the course of development," says mass, who is also a spokeswoman for the transdisciplinary research area "Life & Health" and a member of the board in the "Immunosensation2" University of Bonn. "Our study is one of the few who were able to clarify a way in detail on which this happens."nnParticipating institutions and funding:nnIn addition to the University of Bonn, the German Center for Neurodegenerative Diseases (Dzne) and the Universities of Vienna (Austria), Ghent (Belgium) and Shanghai (China) were involved. The work was supported by the German Research Foundation (DFG, in particular SFB 1454 Metaflammation), the European Research Council (ERC), the Jürgen Manchot Foundation, Boehringer Ingelheim Fonds and the European Molecular Biology Association (EMBO)."
}
Clarification of the fields:
title: the title of the news article.
date: The date of publication (extracted from the em tag).
author: The source institution (University of Bonn).
source: The website where the article was found.
url: The original URL of the article.
tags: Keywords or categories associated with the article.
content: the main text of the news article.Key improvements and considerations:
Date Formatting: The date is now in a standard YYYY-MM-DD format.
Content Extraction: The main body of the article is extracted, removing HTML tags.
JSON Format: The output is structured as a JSON object, making it easy to parse and use in applications.
HTML Stripping: The content is extracted as plain text. Encoding: Assumed UTF-8 encoding for the HTML. If the page uses a different encoding, you might need to specify it during the HTML parsing process.
Images: the image URLs and captions are not included in this version. If you need them, you’ll need to add code to extract the src and title attributes from the img tags and the text from the surrounding
tags.
Contact Information: The contact information is not included in the main content. You could add a separate field for it if needed.
* Original Publication: The original publication details are also excluded. You could add a field for this as well.
This structured JSON output should be suitable for importing into a CMS, database, or other request for further processing and display.remember to adapt the code to handle any specific requirements of your target system.