Surgery Godfather

Chapter 2182: Chapter 1432: Can We Recombine?

The data from the joint experiment encountered an unexpected turning point.

The cause was a "mistake" by Hans. While conducting proteomics analysis, he accidentally mixed a group of control samples into the culture medium of the joint treatment group. According to standard procedures, this group of data should have been discarded. But Hans is a stickler, he insisted on processing the erroneous samples through mass spectrometry, thinking they could at least be used as negative controls.

When the results came out, he stared at the screen for a long time, then rushed out of the cell room and ran into Tang Shun carrying coffee in the corridor.

"Look at this!" Hans thrust the laptop in front of Tang Shun, nearly spilling the coffee.

Tang Shun put down the cup and squinted at the heatmap: the erroneous samples, which had not undergone any treatment, surprisingly detected three types of cell factors that were highly enriched in the joint treatment group—BDNF, GDNF, and a new type of secreted protein they had never seen before.

"Could be too small," Tang Shun said, "The control group didn’t have anything added, how could there be these factors?"

"That’s why I’m showing you!" Hans’s eyes widened, "I repeated three times, the result was the same. There’s something spontaneously secreting these factors in the control group’s culture medium."

They relayed this discovery to Yang Ping. Yang Ping was silent for a long time and then said something that stunned everyone: "Maybe we’ve been searching in the wrong direction. It’s not the exogenous stem cells secreting these factors, it’s the original cells themselves."

"What do you mean?" Manstein asked.

"I mean," Yang Ping walked up to the whiteboard and drew a simple diagram, "Once activated, the original cells can themselves secrete neurotrophic factors. We thought the exogenous stem cells were ’providing’ support, but in fact, they might only be ’triggering’ the original cells to do what they were capable of doing."

Weber called from Germany for a video conference. After listening to Hans’s report, his first words were: "Hans, are you sure the sample was indeed mixed incorrectly?"

"Absolutely! I performed genotyping, and the SNP profile of that sample is completely different from the joint treatment group."

"Good," Weber nodded, "Then this is a discovery beyond synergistic effects. If original cells, once activated, can autonomously secrete neurotrophic factors, many things we’ve done over the past fifty years may have been unnecessary."

"Not completely unnecessary," Yang Ping corrected, "Exogenous stem cells might play a ’kickstart’ role. Like a car’s ignition system, without it the engine wouldn’t start by itself, but once ignited, the engine can run by itself."

"What we need to do," Weber said, "isn’t to refuel the engine, but to find a better ignition system."

This discovery completely changed the research direction.

In the following two months, the team split into two paths: one continued to optimize the joint scheme, verifying the autonomous secretion capability of original cells; the other began searching for the "minimal effective stimulus" that can singly activate the original cells and simultaneously induce them to differentiate into neurons.

Eva’s electrophysiological data provided crucial clues. She found that in the joint treatment group, M7’s motor evoked potentials exhibited a strange time curve, showing almost no change in the first four weeks, suddenly spiking in the fifth week, and then steadily rising. This "spike" in time precisely corresponded to one week after the original cell markers had peaked.

"There’s a delay," Eva said at the group meeting, "A four-week silent period, followed by an outbreak. This indicates the original cells require a certain period to ’mature’ before they can function effectively."

"The four-week silent period," Yang Ping repeated, "What if we could shorten this silent period?"

"How to shorten it?"

"Change the microenvironment, the original cells requiring four weeks could be due to scar tissue around them inhibiting them. If we could simultaneously clear the scar or alter its nature, perhaps the original cells could mature faster."

This idea led to a third exploration direction: scar regulation.

Scar regulation isn’t a new concept. After spinal cord injuries, astrocyte proliferation forms glial scars, long considered an obstacle to regeneration. But recent research has found that scars aren’t entirely harmful; they provide isolation from damage and protection against inflammatory spread in the early stages, only becoming overly dense and hindering axon regeneration in later stages.

"The key issue isn’t the presence of scars," Yang Ping said in a literature review meeting, "It’s the ’texture’ of the scars. Too loose, inflammation spreads; too dense, axons can’t penetrate. What we need is a ’permeable’ scar, allowing axon penetration but blocking inflammation."

Lina compiled all literature on scar regulation from the past decade, building a database that covered 127 papers, 34 candidate molecules, and 12 biomaterials. She conducted a network analysis and found that all effective scar regulation strategies point to the same pathway: TGF-β/Smad.

"TGF-β is the master switch for scar formation," she presented a complex signal pathway diagram during the report, "Upregulate it, scars thicken; downregulate it, scars thin. But the issue is, TGF-β is protective in the early stages of injury, limiting in the late stages. Simply inhibiting it may exacerbate early damage."

"So spatial-temporal regulation is needed," Weber said from the video, "Preserve it early, inhibit it late."

"Yes, but how to achieve spatial-temporal regulation?"

The meeting room was silent for a long time, then Fritz raised his hand, making his first contribution in a formal group meeting.

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