deltrittennovels Chapter 1425 New Discovery
Chapter 1425 New Discovery
Chapter 1425 New Discovery
Fortieth week after surgery, Chen Jianguo's recovery entered a relatively stable phase. He could stand for three minutes while holding onto a parallel bar, his right leg muscle strength reached level two, and his left leg level one and a half. He felt stable about five fingers below his navel. This change doesn't conform to traditional theories, nor to the patterns summarized from M7's case.
These figures were meticulously recorded by Mainstein in his experimental notebook, with notes next to them indicating the date, time, and specific conditions under which the evaluation was conducted—indoor temperature, humidity, Chen Jianguo's sleep duration that day, and the time of his last meal. Mainstein's style of recording data mirrored his personality: every piece of data had to be contextualized, and every observation had to be repeatable.
But what truly kept Mannstein up all night was not the numbers themselves, but the biological question behind them.
The phone rang in Yang Ping's office. He answered it, and Mainstein's voice came through the receiver, with that slightly trembling tone that he only used at the most crucial moments.
"professor?"
"Say!"
"Please come over here for a moment, to the lab. I have something to show you."
When Yang Ping arrived at the lab, Mainstein was sitting in front of a microscope, with a dozen or so stained spinal cord slides piled up beside him. Seeing Yang Ping enter, he didn't exchange pleasantries, but pointed directly to the microscope's eyepiece. "Professor, look at this."
Yang Ping leaned closer and adjusted the focus. His field of vision revealed a patch of neural tissue; axons were stained red, cell nuclei blue, and glial cells green.
“This is Chen Jianguo’s spinal cord tissue? How is that possible? He was only 40 weeks post-surgery, how could tissue be taken? I wouldn’t dare to take it either.”
“It’s not Chen Jianguo’s, it’s M8’s, our old spinal cord injury animal model. I re-stained the spinal cord sections of M8 using a new marker. You can see the morphology of the red axons.”
Yang Ping carefully examined the red fibers in his field of vision. Normal axons are thin, smooth, and like a straight line. But the axons in his field of vision were completely different—thicker, with an irregular nodular structure on the surface, as if they were wrapped in something, or as if they were splitting.
"What is this?" Yang Ping straightened up.
“Progenitor cells!” Einstein’s voice trembled slightly. “Professor, these aren’t regenerating axons, they are precursor cells. Your theory has once again proven its power. Our method doesn’t involve letting the remaining nerve fibers grow over; it involves having the damaged area repaired by precursor cells. Wherever the damage occurs, the precursor cells repair it. Only if it’s truly a complete loss will it regenerate and grow back. You see, these repair cells have been reprogrammed into neural progenitor cells with multi-directional differentiation potential, differentiating in situ into new neurons and glial cells, forming functional neural connections.”
Yang Ping didn't speak. He looked at Mainstein, and Mainstein looked at him. The two of them stared at each other for a long time in the laboratory, across the microscope.
Progenitor cell repair and neurogenesis are two completely different biological processes. Neural regeneration involves the regrowth of damaged axons, growing downwards from the broken stump, like reconnecting a broken wire. Progenitor cell repair, on the other hand, activates stem cells or precursor cells already present at the site of injury, allowing them to differentiate into entirely new neurons and glial cells, establishing a completely new relay station at the site of injury—not repairing old wires, but building a new signal tower. Traditional neurogenesis research has been ongoing for decades, with countless laboratories investing enormous resources in this direction, yet no breakthrough has been achieved. The reason is simple: the axonal regeneration capacity of the central nervous system in adult mammals is extremely poor. The glial scars formed after injury are not only physical barriers but also release various molecules that inhibit regeneration. Making the axon grow back is like trying to run in a swamp—every step is fraught with difficulty.
But protocellular repair completely bypasses this problem. It doesn't require long axons or traversing dense scar tissue; it simply activates the protocellular cells already present at the site of injury, allowing them to differentiate into new neurons in situ. Repair occurs wherever the damage occurs. Signal is restored wherever the relay station is built. This is a completely new approach, one that even Yang Ping himself hadn't considered.
"This shows that three-dimensional guided gene technology can still be used in old injuries," Yang Ping said.
"Yes, the evidence from the slide is very strong. Look at this—"
Mainstein switched to a different slide, adjusted the focus, and pointed it out to Yang Ping. In the field of view, a group of bright red cells were distributed around the center of the damage, with irregular shapes—some round, some oval, and some with protrusions. Their nuclei were large, and their nucleoli were clearly visible, indicating high metabolic activity.
“These cells were not present in the normal control group sections of the spinal cord in M8. They appeared newly after surgery. Moreover, their location was unique; they were not in the center of the injury, but rather in the periphery of the injury center, distributed along blood vessels. This is a typical distribution pattern of neural progenitor cells migrating from the perivascular area to the injury site. Hematogenous progenitor cells enter the spinal cord tissue through the blood vessel walls and are then attracted by chemical signals released at the injury site, migrating towards the injury center. During their migration, they continuously proliferate and differentiate, eventually becoming new neurons.”
Yang Ping leaned against the lab bench, arms crossed over his chest, staring at the slides, his mind racing. If Mainstein's observations were correct, if this method did indeed activate endogenous progenitor cells, causing them to differentiate into new neurons in situ, then the entire theory needed to be re-examined; it was far greater than imagined.
“More evidence is needed,” Yang Ping said. “Immunohistochemistry, in situ hybridization, single-cell sequencing. We need to see what type of cells these newly emerging cells are. Are they neurons or glial cells? Are they excitatory or inhibitory? Are the synaptic connections they form functional or randomly formed? These questions all need to be answered.”
"I know."
How long will it take you?
"If all the technology platforms are in place, it will take two months."
"You do it."
Mannstein looked up at Yang Ping: "Okay."
For the next two months, Mannstein practically lived in the laboratory.
He cut the spinal cord tissue from M8 into thousands of slices, each stained with a different antibody. He scanned each slice one by one using a confocal microscope, stacking the images into a three-dimensional reconstructed model. He extracted tissue from the damaged area and performed single-cell sequencing, finding hundreds of cells with transcriptomic characteristics completely different from normal tissue among tens of thousands of cells.
Data accumulates little by little, and each new piece of the puzzle points in the same direction.
The first piece of the puzzle came from immunohistochemistry. The newly emerging cells expressed a protein called dicortin, a specific marker of migrating neural progenitor cells. These cells were not present in the M8 spinal cord before the injury, nor in the untreated control group, but only in the treated experimental group, and only in the peripheral region of the injury site. This means these cells were not pre-existing, but appeared after the intervention. The second piece of the puzzle came from in situ hybridization. These cells not only expressed dicortin but also a transcription factor called NeuroD, an early marker of neural differentiation. They were differentiating from a stem cell state to a neuronal state—not overnight, but over the past few months. This is a dynamic process, not a one-off burst, but a continuous, organized, and directional differentiation process.
The third piece of the puzzle came from electron microscopy. Mainstein stayed up all night taking hundreds of electron microscope images. In those images, newly generated neurons extended axons, forming clear synaptic connections with downstream target cells. These weren't chaotic, random connections, but rather organized, functional, and correctly oriented connections. The synaptic cleft was approximately 20 nanometers, the presynaptic membrane showed clear vesicle aggregation, and the postsynaptic membrane had a dense region—all the structural features of a typical, functional chemical synapse were present.
The fourth piece of the puzzle came from single-cell sequencing. Those hundreds of cells with transcriptomic anomalies could be clearly divided into three groups: one in a stem cell state, one in the early stages of neuronal differentiation, and one already differentiated into mature neurons. They constitute a complete lineage—from the original cell to the new neuron, every step is captured in the data. This isn't a static slice; it's a movie in progress, every frame captured by Mainstein.
Mannstein compiled all the data into a report, and this time only printed two copies. One was given to Yang Ping, and the other was kept by himself.
After reading the report, Yang Ping put the document on the table, took off his glasses, and rubbed the bridge of his nose.
“Mannstein, do you know what this means?”
"I know! The three-dimensional guidance gene is smarter than we thought. The human body is truly amazing."
"We're not fixing the nerves, we're fixing the method itself. Neural regeneration is a decades-old concept; everyone's been trying to make axons grow faster, longer, and more accurately. We've bypassed that problem. We don't need the axons to grow very long because we've built a new relay station at the site of injury. Signals travel from the higher neurons to the relay station, and from the relay station to the lower neurons, bypassing the injury area. We originally thought our new method only worked with fresh injuries, but now it seems it can even work with old injuries. Most amazingly, we can even see the disintegration of some scar tissue, with the original cells replacing these scar cells. This means our method is not only adding new neurons, but also subtracting them, clearing away the glial scars that hinder regeneration. With this addition and subtraction, the effect is naturally magnified many times over."
Einstein leaned back in his chair, staring at the ceiling. He recalled the first time he read Yang Ping's paper in his German laboratory. At that time, he had only one thought: if what this Chinese man said was true, it would change everything. Now, sitting in his Chinese laboratory, looking at Yang Ping's face, he was thinking a different thing: what this Chinese man said was indeed true, not only true, but also more profound than he had initially understood.
"Professor, we need to publish a new paper, either in Nature or Science, to announce this discovery. But I haven't figured out exactly what I've discovered yet; I need to organize my thoughts."
Yang Ping thought for a moment and then shook his head.
"No, don't rush. Let's complete the human trials on Chen Jianguo first. If the discovery is verified on him, it means that the M8 result is not unique to primates and can be replicated in humans. Then we can publish the paper with more complete data and stronger persuasiveness."
Mannstein remained silent for a long time.
“I need to reanalyze Chen Jianguo’s data. Once the data is available, we’ll write the paper.”
"it is good."
For the next week, Mainstein's mind was constantly filled with those red cells on the slides, those protocells dividing, differentiating, and connecting. He thought about them while walking, eating, and showering. One night, he suddenly sat up in bed, startling August.
"what happened?"
"I've been thinking about a question. If protocellular repair can be done at such a high level, then how did the monkey in our previous animal experiment, the non-targeted intervention group, recover? We didn't perform precise gene regulation, we just made a broad adjustment to the microenvironment, but it still stood up."
Mannstein turned on the bedside lamp, picked up his notebook, and began to record his thoughts.
After finishing writing, he closed his notebook and turned off the light. He lay in the darkness, thinking about the monkey named "Surprise." How was it now? Was it also reconnecting its spinal cord through protocellular repair? They had no idea what a momentous discovery had occurred within them. They had simply stood up, and continued to stand.
The first thing Mainstein did upon arriving at the lab the next morning was to go see Fritz.
"Fritz, M21—"
“Surprise?” Fritz looked up at him.
"Yes! Is its spinal cord still there?"
Fritz thought for a moment, and the monkey was euthanized after the experiment, and the tissue samples were preserved according to regulations.
"In the low-temperature freezer, the slicing was not finished, and there were still some wax blocks."
“Take them all out. I want to redo the staining with a new marker. What about M8?”
“You sliced its spinal cord, and now it’s paralyzed and needs care.”
Fritz didn't ask why. He put down his notebook and turned to go to the cryogenic freezer room. Mainstein stood in the animal room, looking at M7's cage. M7 was lying in its cage sunbathing, its eyes half-closed. He squatted down and gently stroked M7's head through the cage.
"M7, do you know what? Right now, you're the only one walking. Don't worry, M8 will be like you one day."
M7 opened its eyes, glanced at him, then stretched out a hand, slipped it through the gap in the cage, and placed it on Mainstein's wrist. Its fingers were cool, its grip not strong, but precise. Mainstein didn't move, letting the hand rest on his wrist.