King of Organs (4)
I gazed at the seminar room. It was packed with professors wearing stern expressions. I cleared my throat and continued.
"A male patient in his fifties, undergoing radiation and chemotherapy for small cell lung cancer, suddenly developed neuropsychiatric symptoms, prompting the start of treatment."
The dean nodded, as if urging me to go on. I pressed forward with the presentation.
"Here are the results of the neurological examination. Initially, anxiety and hallucinations appeared. A few days later, the symptoms worsened to seizures and altered consciousness."
Neatly summarized, of course. In one sentence: the classic symptoms and progression of anti-NMDA receptor encephalitis.
"Additionally, lesions in both upper and lower motor neurons were observed. Based on this, we diagnosed autoimmune encephalitis and administered high-dose steroids."
One professor furrowed his brow.
"What's autoimmune encephalitis? Is that even a real diagnosis?"
I nodded.
"It's when the immune system attacks brain tissue. Similar to other autoimmune diseases."
The questioning professor scratched his head, still looking skeptical.
"Sounds pretty experimental to me."
It was a doubt even Professor Kaplan had shared.
"It is, a bit... Anyway, after the steroids, the patient's condition improved."
I kept going, while Alice, sitting in the back, watched me with an encouraging gaze.
"The intriguing part is the specific mechanism behind this patient's neuropsychiatric symptoms."
The seminar room grew a little quieter.
"Think about it. Autoantibodies targeting proteins that mediate neural function—couldn't they cause these psychiatric symptoms?"
This case could unravel the fundamental principles of the brain and nerves.
The neurology chief, Professor Aird, who had been listening silently, now raised his hand with a serious expression.
"That's overly speculative."
I nodded.
"If this truly is autoimmune encephalitis, and if autoantibodies mediating neural function are indeed causing the psychiatric symptoms..."
"Yes."
"Then, shouldn't we find autoantibodies specific to neural surface proteins in the patient's blood? We should start there. The most crucial step first."
He'd nailed the core of it. Professor Aird's point was spot on—more than even he realized.
Specific autoantibodies to neural receptors.
"Sharp observation. Alice, the microscope."
Alice placed the optical microscope she'd brought from the lab in the center of the seminar room. With a thud.
"What..."
Everyone knew what lay under the lens without me saying it.
Anti-NMDA receptor encephalitis. That was the final diagnosis I'd settled on for this patient.
What's NMDA? A receptor in brain neurons responsible for learning, memory, emotion regulation, and more. Tricky stuff, sure. Even in modern times, not everything about the brain is known—far from it.
Professor Aird was right. If there were autoantibodies specifically destroying neural receptors, we could see them experimentally.
The professor had thought that far. But he probably hadn't anticipated I'd prepared the experiment in just a few days.
Professor Aird peered into the microscope. Exactly as he'd predicted.
In the slide under the microscope, fluorescently labeled antibodies clung concentrated to the neural tissue—specifically, the synapses of the neurons.
Under the lens, the fluorescent antibodies glimmered along the shape of the neurons, like stars in the night sky.
Professor Aird looked at me.
"What is this... It's real."
Why was he surprised when he'd guessed it himself?
"Look closely, and you'll see they're not just on the neuron surfaces but concentrated at the connections between neurons."
"When did you even do this?"
Simpler than it sounded. Centrifuged the patient's serum to isolate antibodies, stained them with fluorescent dye. Then applied the fluorescent antibodies to neural tissue on a plate.
The whole process took about a day. I'd deliberately avoided anything that might drag on.
I looked at Professor Aird.
"Took about a day."
"Impossible."
Several professors crowded around the microscope, murmuring.
In medical history, neural receptor functions were elucidated through studies of autoimmune encephalitis patients like this. I'd returned to the podium and continued.
"After World War I, neuroscience advanced dramatically. Because we could find people missing specific cortical areas."
Professor Aird looked at me again.
For example, shrapnel in the left posterior frontal lobe leaves the right arm and leg paralyzed. So that's where the motor cortex controlling one side of the body is.
Apply the same logic: deducing function from absence.
"This patient lacked one brain receptor while ill. Meaning we can reverse-engineer its function from that."
How neural receptors link to clinical symptoms. What autoimmune encephalitis is—all concepts I could package neatly.
A chance to redefine research targets and methods.
I scanned the seminar room again. The professors who'd seen the autoantibody slide were buzzing for a good while about what it meant.
Even Professor Aird had to concede.
He'd been skeptical at first. But this... It was a puzzle that had stumped people for decades.
The specific functions of neural receptors. And how to discover them.
Truth be told, Professor Aird had never considered that receptor types might manifest as clinical symptoms.
That there could be a concrete clinical method to study receptor functions.
It just didn't add up. His head throbbed.
Autoimmune encephalitis as a disease. That the patient's autoantibodies destroyed neural receptors. That it visibly caused specific symptoms.
What the hell? He was dumbfounded.
Professor Aird squinted. But microscopes don't lie.
The specimen was clear: autoantibodies specifically targeting a protein at neural junctions—likely a receptor.
Was it real? Had this resident truly discovered the neuropsychiatric functions of neural receptors?
The link between proteins and mental states.
In context, it might not be undeserving of a Nobel Prize.
Utterly insane.
The presentation ended successfully. I was packing up the microscope and slides when Professor Aird approached.
"Great job on the presentation."
"Thank you."
"I was surprised when you said you'd use steroids on that patient, but connecting it to receptor function methodology... Well..."
No room for debate. I'd experimentally proven the existence of autoantibodies paralyzing neural function.
Autoimmune encephalitis itself was confirmed real today.
The professor stared into space.
"Hearing that, your presentation had parts I never imagined. Especially the clinical traceability..."
He'd grilled me like he wanted to devour me earlier.
But the experimental proof left even Professor Aird no choice but to acknowledge it.
As he explained something about neurology, he turned back to me.
"You should write a paper on this case. If Stanford elucidates neural mechanisms and macro functions..."
I nodded. I recalled someone winning a Nobel in the 2000s for similar work on neural receptors.
Time to write one on this.
"Yes, I'll give it a try."
"Just to check... Do you really have that... insight beyond conventional methods, Mr. Parks?"
Was he serious? Or a bit of racial joking?
I looked at Professor Aird.
"Pardon?"
"My son wants to convert to Buddhism, you see."
I just smiled. A joke, probably?
Orientalism was trendy in California's 1970s hippie culture.
Anyway, Professor Aird was quick on the uptake.
He'd noticed the fluorescent slides and the insight transcending common sense.
"Ah... Not really."
"Alright, keep up the good work."
Stanford was the world's most advanced medical research institution. I'd gone to the trouble of fluorescently labeling antibodies and preparing slides.
And he treats me like a shaman? Ridiculous.
Speaking of which, now that the presentation's done, time for an ice cream sandwich. Where'd Alice go?