Chapter 2166: Chapter 1425: New Discovery
By the fortieth week post-operation, Chen Jianguo’s recovery process had entered a relatively stable stage. He could stand for three minutes holding onto parallel bars, with muscle strength in his right leg reaching level two, and his left leg at one and a half. His sensory plane stabilized at five fingers below the navel. This change does not conform to traditional theories, nor to the patterns summarized on M7.
These numbers were meticulously recorded by Manstein in the laboratory notebook, annotated with the date, time, and specific conditions during evaluation—indoor temperature, humidity, Chen Jianguo’s sleep duration that day, and the time of his last meal. Manstein’s style of recording was just like him; every piece of data must have context, and every observation must be repeatable.
But what truly kept Manstein awake all night was not the numbers themselves but the biological problem behind them.
The phone in Yang Ping’s office rang. He picked it up, and Manstein’s voice came through the receiver, carrying that barely trembling tone he only used at critical moments.
"Professor?"
"Speak!"
"Please come over to the laboratory. I have something to show you."
When Yang Ping arrived at the laboratory, Manstein was seated at the microscope, surrounded by over a dozen stained spinal cord tissue sections. Upon seeing Yang Ping enter, he skipped the formalities and pointed directly at the microscope’s eyepiece. "Professor, look at this."
Yang Ping leaned closer and adjusted the focus. In the field of view was a piece of nerve tissue, with axons stained red, cell nuclei stained blue, and glial cells stained green.
"Is this Chen Jianguo’s spinal cord tissue? How is that possible? It’s only been forty weeks post-operation; how could any tissue be taken? I wouldn’t dare either."
"It’s not Chen Jianguo’s, it’s M8’s, our old spinal cord injury animal model. I re-stained M8’s spinal cord tissue sections using a new marker. Look at the morphology of the red axons."
Yang Ping scrutinized the red fibers in the view. Normal axons are slender, smooth, like a straightened thread. However, these axons in the view had a completely different morphology—thicker, with irregular nodular structures on the surface, as if wrapped in something or undergoing division.
"What is this?" Yang Ping straightened up.
"Original cells!" Manstein’s voice trembled slightly, "Professor, these are not regenerated axons; they are original cells. Your theory has once again proven its prowess. Our method does not involve having residual nerve fibers grow across; instead, the damage site is repaired by original cells. Wherever the damage is, original cells will repair it. If there is truly a complete loss, only then will it regenerate and grow anew. Look, these repair cells have been reprogrammed into neural precursor cells with multidirectional differentiation potential, differentiating in situ into new neurons and glial cells, forming functional neural connections."
Yang Ping did not speak. He looked at Manstein, and Manstein looked at him. The two of them, separated by that microscope, gazed at each other for a long time in the laboratory.
Original cell repair and nerve regeneration are two completely different biological processes. Nerve regeneration involves the damaged axons regrowing, extending downward from the broken remnants, like a severed electrical wire being reconnected. Original cell repair activates the already present stem cells or precursor cells at the damage site, allowing them to differentiate into entirely new neurons and glial cells, establishing a new relay station at the damage site—not repairing old wires, but building a new signal tower. Traditional nerve regeneration research has been ongoing for decades, with countless laboratories investing significant resources in this direction, yet no breakthrough progress has been made. The reason is simple: the central nervous system axon regeneration capability in adult mammals is extremely poor, and glial scars formed after injury are not only physical barriers but also release several molecules inhibiting regeneration. Having axons grow across is akin to running in a swamp, challenging every step of the way.
But original cell repair completely bypasses this issue. There is no need for axons to grow long or traverse dense scars; it merely requires activating the original cells inherently present at the damage site, allowing them to differentiate into new neurons in situ. Wherever the damage is, the repair happens. Wherever the relay station is built, the signal is restored. This is a completely new approach, an approach that Yang Ping himself had not thought of.
"This indicates that the 3D-guided gene technology can still be used in chronic injuries." Yang Ping said.
"Yes, the evidence on the tissue sections is very strong. Look at this—"
Manstein swapped the tissue section, adjusted the focus, and indicated to Yang Ping. The view revealed a group of brightly red-stained cells distributed around the center of the damage, with very irregular shapes—round, oval, and with protrusions. Their cell nuclei were large, with prominent nucleoli, indicating high metabolic activity.
"These cells did not exist in the normal control group’s tissue section within M8’s spinal cord. They appeared post-operation. Moreover, their location is quite unusual, not in the damage center but surrounding it, distributed along the blood vessels. This is precisely the typical distribution pattern of neural precursor cells migrating to the damage site from around blood vessels. Blood-borne precursor cells enter the spinal cord tissue through the vessel walls and are then attracted by chemical signals released from the damage site, migrating toward the damage center. Meanwhile, they continuously proliferate and differentiate during migration, eventually becoming new neurons."
Yang Ping leaned against the lab bench, crossing his arms over his chest, looking at these tissue sections, his mind racing. If Manstein’s observation was correct, if this method indeed activated endogenous original cells, allowing them to differentiate into new neurons in situ, then the entire theory’s value needs to be reassessed; it is greater than imagined.
