Chapter 2285 - 1478: Uncertainty

Chapter 2285: Chapter 1478: Uncertainty

Yang Ping switched to a new image, showing Manstein’s data on the kidney injury model. The curve for the recovery of kidney function indicators also displayed a steep decline, recovering to seventy percent of normal values within forty-eight hours and ninety percent within seventy-two hours.

"The same antibody activated different repair programs in different organs. In the liver, it activated the liver’s blueprint, while in the kidney, it activated the kidney’s blueprint. This means something important: Receptor X is not an organ-specific molecule; it is a systemic switch. It is not designed for any one organ; it is common to all organs and used by all of them. It’s just that each organ utilizes its own unique development blueprint when using it."

Someone in the audience raised a hand. Yang Ping glanced over and nodded at the editor from "Nature Medicine" in the front row. The person stood up and directly asked a question that many researchers had been pondering, though no one had yet voiced it publicly: "Professor Yang, if Receptor X is a systemic repair switch, why is the repair speed of the liver and kidney noticeably faster than that of the nervous system? Is it because the expression level of Receptor X is higher in the liver and kidney, or because the developmental blueprint of the nervous system is more complex?"

Yang Ping didn’t pause: "Both reasons play a role. First, the expression levels of Receptor X vary among different tissues, and it’s indeed higher in the liver and kidney than in the brain. But that’s not the main reason. The main reason is the complexity of the development blueprint. The liver and kidney have relatively simple structures, whereas the nervous system is extremely complex. Repairing a simple structure is much faster than repairing a complex one."

The editor from "Nature Medicine" sat down. Next to him, a gray-haired professor from Oxford University stood up, speaking with a British accent, each sentence ending with a slight upward inflection: "Professor Yang, earlier you mentioned that repair programs can be trained, so is this training effect universal, or is it specific to certain types of damage? For example, if you train the liver to repair chemical damage, would its response to physical damage also improve?"

"Good question," Yang Ping said. "We haven’t answered this question yet. But we are conducting a validation experiment, training the liver with one type of damage, and then testing its repair speed with another type. If the training effect is universal, it means we’ve found a whole new preventative medical approach, enhancing the body’s overall repair capability by pre-training repair programs."

The Oxford University professor sat down, while several researchers around him began taking notes. Yang Ping continued without pausing: "There’s also a new discovery we made just yesterday. Dr. Chen Xiao resolved the complete three-dimensional structure of Receptor X using cryo-electron microscopy, at a resolution of 2.8 angstroms. In this structure, we found an intracellular tail domain of about forty amino acids that has never been reported before, whose function is unknown. This might be the key structure for Receptor X’s signal transmission or it might be crucial for selectively activating different organ development blueprints. If we can understand the function of this domain, we might understand how repair programs differentially engage with different organs."

The meeting room was momentarily quiet, with only the sound of notes being taken and keyboards being typed.

A young researcher standing in the back row raised a hand. Yang Ping called on him, and he asked a question about the storage location of development blueprints for different organs: "What we’re interested in is, where exactly is this blueprint stored? If the blueprint can be replaced, where does the new blueprint need to be saved?"

"The blueprint is stored in the epigenetic modifications of stem cells," Yang Ping said. "It’s not stored as changes in the DNA sequence, but rather as patterns of chemical marks on DNA, such as methylation, acetylation, and histone modifications. These marks determine which genes can be read and which are turned off. Once Receptor X is activated, stem cells read these marks and perform repairs according to the blueprint indicated. If you want to replace a blueprint, essentially you’re rewriting these marks’ pattern."

The first researcher who asked a question continued with a follow-up, speaking faster as if verifying a hypothesis he had just developed: "So, is the shutdown of repair programs during aging also because these mark patterns have changed?"

"It’s possible," Yang Ping said. "This is exactly a hypothesis that requires extensive experimentation to verify. A unified theory is too grand and requires many scientists to study it over a long time; we’ve only verified a very small part so far."

The report lasted for two hours. Even after the scheduled time ended, the questions continued. Yang Ping didn’t interrupt, and after the last question ended, the audience didn’t immediately disperse. Someone came up to the podium and handed over a business card, identifying themselves as the head of a German research institute, wanting to discuss the possibility of cooperation. Some gathered around Weber, asking about the details of the experiment. Others were sketching on the whiteboard, discussing several possible signaling pathways for Receptor X’s intracellular domain.

After the meeting ended, he stood alone in the empty meeting room. The lights on the podium were still on, the projector hadn’t been turned off, and on the screen was a three-dimensional structure of Receptor X. The yellow intracellular tail stood out against the dark background, like an arrow pointing in an unknown direction.