Hello dear readers and friends, I am Luo Sanguan, who recently checked the literature and found that he began to have some M baldness.

It has been predicted before that Tang Min's case is different from all the diseases described in the previous Sanguan, and a separate chapter needs to be written to explain it. Now, here comes the single chapter.

Some are good at looking up [520] literature at the same time (really...... As you may have noticed, unlike all previous cases, AQP4 protein underexpression disorder is in fact a non-existent disease. And this is the main reason why Sanguan decided to write a single chapter to explain.

Tang Min himself does have a prototype in reality. Similar to what is described in the article, she developed the disease before puberty and her first symptom was vision loss. After going to several hospitals and undergoing a white matter biopsy, the diagnosis is still undefinitive. Six months after the first episode, her vision disappeared completely, and her pupils on both sides did not reflect light. MRI findings show multiple intracranial masses and a meandering and thickening of the optic nerve but no abnormalities in the spinal cord. In the auxiliary examination, the optic nerve potential induced the increase of P100 latency, and the antibody test was negative. Moreover, her uncle did experience rapid vision loss before puberty.

Sanguan learned about this situation because one of my medical consultants shared a case. When discussing and searching relevant literature, Sanguan accidentally found that the symptoms of Tang Min's prototype were highly consistent with those specially made for studying the effect of AQP4 protein.

These specially made mice were knocked out of the gene that produces the AQP4 protein. In related studies, these mice showed a high tolerance to cerebral edema and better survival. But at the cost of vision loss and intractable cerebral edema.

This high degree of agreement made Sanguan suddenly come to the spirit, and I also put forward my own views to the medical consultant at the same time. Of course, readers who see this should also know that Sanguan has not received relevant medical education. My opinion is just a "view".

The consultant praised the assumption of Sanguan, but at the same time believed that Tang Min's prototype was more likely to be a tumor than a new genetic disease. According to the data, the control gene of AQP4 protein is located on the autosome, and although the probability of a "newly discovered genetic disease" is slim, it cannot be completely ruled out.

In the process of discussion, I checked too much information, so that Sanguan felt that it was really ...... not to write about this case It's a waste of the time you've already paid. So...... You've just seen this chapter and plot.

I need to point out and remind you here that AQP4 protein underexpression is not a real-life disease. From the mechanism to the symptoms, it is the personal hypothesis and conjecture of the three views.

Although mechanisms such as mannitol rebound do exist, and the expertise written in the book does come from the work of researchers in related fields.

But the disease does not exist.

So, please pay attention to distinguish between relevant content. Although Sanguan has always boasted that the medical content in the book is completely authentic and reliable, in Tang Min's story, I decided to make an exception.

Tang Min's prototype has been confirmed, and the second biopsy and related immunohistochemistry confirmed that it was a high-grade glioma. The biopsy sample was in red, the nucleic acid extraction concentration was 8.0ng/ul, the cell tumor content in the detection area was 20%, and the nucleic acid purity (A260/A280) was 1.8. The BRAF gene detected the V600E mutation. After consultation with relevant experts, it was determined that he was IDH wild-type, which is IDH wild-type primary glioblastoma.

I hope she recovers soon.