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Now reading: Chapter 1908 - 1317: Uncontrollable Frenzy from Surgery Godfather, a Fantasy novel by Ocean And Summer.

Yang Ping replied to Dr. Chen’s email, truthfully pointing out that his research was outdated and suggested he take so ti to visit the Digital dical Laboratory at Nandu dical University.

Looking back now, under Yang Ping’s leadership, the entire Nandu System’s research level has risen several tiers. For instance, the Digital dical Laboratory is already at the world-class level, leading the way in the application of digital dicine and artificial intelligence in dicine.

It was precisely the foundation built by these studies that allowed Yang Ping to freely put his ideas into practice.

Yang Ping cald down and carefully detailed the entire research process of his regulation theory, inevitably feeling a surge of emotions.

Because the inspiration for the system regulation theory ca completely by accident.

The regulation theory originated from in-depth research into K Therapy, which was based on a chance discovery of the K Factor in Sisi’s tumor cells.

Initially, when Sisi’s tumor cells were extracted for experintal research and cultured outside the body, one day, those tumor cells suddenly experienced massive death.

In general, this kind of death seems aningless to most, as tumor cells cultured outside the body may die if the conditions are slightly improper. Other tumor researchers might overlook such commonplace occurrences, but Yang Ping did not ignore this issue. After scientifically analyzing the cause of the tumor cell death, he discovered that the cause was unrelated to external conditions, but rather, the tumor cells had self-initiated the apoptosis program.

This result deeply surprised Yang Ping, while also intensely arousing his curiosity.

He decided to explore the reason behind this, and upon further research, found a special protein factor both in the culture dium and inside the tumor cells. This protein factor he had never seen before. Upon extracting and studying it, it turned out to be the "agent" responsible for killing the tumor cells.

Consequently, Yang Ping held onto this finding, continued his studies, and finally developed K Therapy.

At that ti, the research into the K Factor seed quite in-depth, already analyzed at the biochemical microscopic level. Then utilizing the adenovirus as a vector, the K Factor was carried to infect tumor cells, and once inside the tumor cells, the K Factor took effect, initiating the apoptosis program to clear out the tumor cells.

It seed that with the conclusion of the research in this area, the matter was finished. Yet, this result did not satisfy Yang Ping’s powerful curiosity. He continued digging deeper: why could the K Factor initiate the tumor cell apoptosis program? Moreover, he attempted to design new K Factors.

Later on, as the research deepened, Yang Ping discovered that the truth was far from simple.

The previous research only scratched the surface; it appeared to answer "what," but in reality, it remained at the "what is" level.

This left Yang Ping very dissatisfied. After circling around, thinking he had reached the summit, he realized he was still at the foot of the mountain.

Thus, he continued his research. With both ti and money, being idle ant doing nothing, and he vowed not to rest until he unraveled this issue. Eventually, he discovered that the K Factor could initiate the apoptosis program because it could restore the human system’s re-recognition of tumor cells.

Since publishing the "system regulation" theory hypothesis, the team under Yang Ping exploded with papers. So core papers were published in their own journal, dical. For exposure, other papers were published in other world-leading journals.

Tang Shun’s team’s paper, titled "TIM Conformational Dynamics as a Core Regulatory Switch for Cellular Identity State: Single-Molecule Real-Ti Imaging Evidence," was published in Nature. Using super-resolution fluorescence lifeti imaging technology, they observed for the first ti in living cells that when the K Factor binds, the TIM protein clusters undergo a conformational change from a loose dynamic to an orderly lock. This transition precisely couples with downstream mitochondrial mbrane potential fluctuations and chromatin accessibility changes over ti. More importantly, they found that the synchronization rate of this conformational change is very high in normal cells with a stable identity state, decreases in precancerous cells, and almost disappears in aggressive cancer cells. This directly validated the function of the TIM system as an identity signal fidelity amplifier and its gradual desynchronization in the carcinogenic process.

A paper co-authored by Song Zimo, Xu Zhiliang, and Professor He from the Nandu University dical Digital dical Laboratory, titled "Inferring System State Attractor Landscape from Single-Cell Multi-Omics Temporal Data: An Example of Lynch Syndro Precancerous Intervention," was published in Cell. Based on high-density data from Alina and five other early participants, they constructed a personalized systemic dynamics model and successfully simulated how regulatory intervention reshapes the system’s potential landscape from multiple shallow and chaotic disease basins into a deep and broad healthy basin. The post-intervention state trajectory predicted by the model closely matched actual observational data. This research provided the first quantitative evidence at the computational level for the hypothesis of regulatory-change system landscape.

The third paper ca from Lu Xiaolu’s team, who found similar noise increases in the expression pattern and conformational stability of TIM homologous proteins in intestinal stem cells of aged mice, resembling precancerous cells. After treating with a mild regulator targeting the aged TIM variant, not only the capacity to maintain intestinal epithelial hoostasis improved, but the mild inflammation levels throughout the mouse body decreased, and exercise endurance increased. The paper cautiously proposed a hypothesis: age-related functional decline might be partly due to signal wear and error-correction ability reduction in the cellular identity maintenance system, and targeted mild regulation could partially revive this intrinsic maintenance capability. This paper was published in the Science journal.

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