当博客发布之后

当前博客的最新架构

目前把这个博客的源代码存放在GitHub上，通过cloudflare和edgeone双平台部署了静态网站。平时主要使用ESA对edgeone的源站套cdn，用于加速。
这套架构暂时在阿里云的平台上部署不成功，也就不想折腾了。

中途遇到的困难

在markdown的格式设置上还不熟悉，不知道怎么换行和分段。

还有就是把首页的格式调整了好几遍，最后发现还是ai生成的第一版最简洁。

这个网站是纯粹由ai生成的，自己一个代码都看不懂。

测试一下页面最大显示宽度

https://www.nature.com/articles/d41586-026-00222-7

For decades, researchers have noted that cancer and Alzheimer’s disease are rarely found in the same person, fuelling speculation that one condition might offer some degree of protection from the other.

Now, a study in mice provides a possible molecular solution to the medical mystery: a protein produced by cancer cells seems to infiltrate the brain, where it helps to break apart clumps of misfolded proteins that are often associated with Alzheimer’s disease. The study, which was 15 years in the making, was published on 22 January in Cell1 and could help researchers to design drugs to treat Alzheimer’s disease.

“They have a piece of the puzzle,” says Donald Weaver, a neurologist and chemist at the Krembil Research Institute at the University of Toronto in Canada, who was not involved in the study. “It’s not the full picture by any stretch of the imagination. But it’s an interesting piece.”

Alzheimer’s mystery Weaver has been interested in that puzzle ever since he began his medical training, when a senior pathologist made an offhand comment: “If you see someone with Alzheimer’s disease, they’ve never had cancer.” The remark stuck with Weaver over the years as he diagnosed thousands of people with Alzheimer’s disease. “I can’t remember a single one that has had cancer,” he says.

How common is Alzheimer’s? Blood-test study holds surprises

Epidemiological data do not draw such a clear divide, but a 2020 meta-analysis of data from more than 9.6 million people found that cancer diagnosis was associated with an 11% decreased incidence of Alzheimer’s disease2. It has been a difficult relationship to unpick: researchers must control for a variety of external factors. For example, people might die of cancer before they are old enough to develop symptoms of Alzheimer’s disease, and some cancer treatments can cause cognitive difficulties, which could obscure an Alzheimer’s diagnosis.

Over the years, however, the data converged enough to convince Youming Lu, a neurologist at Huazhong University of Science and Technology in Wuhan, China, to take a closer look at the biology underlying this trend.

Long search Researchers in Lu’s laboratory spent the next six years searching for the best way to model the two conditions in mice. Eventually, the team decided to transplant three different types of human tumour — lung, prostate and colon — into mouse models of Alzheimer’s disease. The mice with cancer did not develop the brain plaques characteristic of Alzheimer’s disease, says Lu. “So then we asked, ‘why’?”

The researchers sifted through the proteins that were secreted by these cancer cells, searching for those that can cross the protective boundary known as the blood–brain barrier to infiltrate the brain. This search, which took more than six years, narrowed the list to one: a protein called cystatin C.

How cancer hijacks the nervous system to grow and spread

Further experiments in mice showed that cystatin C binds to the molecules that make up the hallmark brain plaques of Alzheimer’s disease. This interaction activates a signalling protein, called TREM2, that is found on certain immune cells that patrol the brain.

Those immune cells then degrade the plaques. In Lu’s mice, this plaque degradation was linked to an improved performance on cognitive tests.

If confirmed and replicated in humans, the findings could suggest a path to finding new therapies, says Jeanne Mandelblatt, a cancer researcher at Georgetown University in Washington DC.

后记

今天搭建这个博客主要是为了公开自己战胜拖延症的决心，所以在这方面就尽量少折腾了。