마우스, 차강석 씀 | The mouse by Cha, KangSeok

about Mr. Cha

사랑할 수밖에 없는 쥐

2026년 6월 12일

너와 헤어진 내 삶은
물거품처럼 사라질 것이다

너와 함께해야
내 삶은 역동적으로 살아난다

내 삶이 다할 때까지
함께해 주어서 고맙다

내가 살아가기 위해
사랑해야만 하는 마우스!


The Mouse

The love my life cannot do without

Without you,

my life

would vanish

like a bubble.

Only with you

does my life

come alive,

full of motion.

Thank you

for staying with me

for as long

as my life endures.

The Mouse,

the one I must love

to go on living.

[Cook-Korean] Sundubu Jjigae

  🥢Simple mushroom (& seafood) Sundubu Jjigae

Ingredients & Prep

  • Preparing mushrooms: Soak dried shiitake mushrooms in water; wash and slice, or fresh mushrooms.
  • (Option) shrimp, clams or oysters
  • Dried kelp (Dashima)
  • Soft tofu (Silken tofu, Sundubu)
  • 1 teaspoon minced garlic
  • 1 teaspoon soup soy sauce
  • A pinch of pepper
  • 2 tablespoons ground perilla seeds
  • 1 to 2 tablespoons chopped scallions

Cooking Process

  1. Add the mushrooms, dried kelp, (shrimp, clams, or oysters), and water to a pot. 
  2. Bring it to a boil, then reduce the heat to medium. 
  3. Add the soft tofu, minced garlic, soup soy sauce, and pepper, then cook for 5 minutes. 
  4. Stir in the ground perilla seeds (or perilla oil) and cook for another 3 minutes. 
  5. Add the chopped scallions right before turning off the heat
Korean version (한국말 버전)

안 매운 초간단 버섯 (해산물) 순두부

재료 점검

  • 버섯 준비하기 (말린 표고버섯은 물에 담그고, 신선한 버섯들은 씻어서 썰기)
  • 말린 다시마 
  • (이것도 있으면 준비) 새우, 조개 또는 굴
  •  순두부 
  • 다진 마늘 1 작은 술
  • 국간장 1 작은 술
  • 소량의 후추
  • 들께 2 테이블 스푼 또는 들기름
  • 썰은 파 1 ~2 테이블 스푼

조리과정

  1. 버섯, 다시마, (새우, 조개, 또는 굴), 물을 솥에 넣고 끊여 주세요.
  2. 냄비가 끓으면 중불로 좀 끓여요 (새우가 색이 변하고, 조개가 입을 벌리고, 굴도 익어요)
  3. 순두부, 마늘, 국간장, 후추 넣고 좀더 조리 (5분정도)
  4. 들께 (또는 들기름 넣고) 3분 정도 더 조리
  5. 불을 끄기 직전에 파를 넣어 주세요.

그 누군가의 무엇 | Someone’s Something

그 누군가의 무엇

2026. 5. 7.

   곰곰히 생각한다.

    내가 진정
 그 무언가를 위해
 나를
 헌신한 적이 있는지.

곰곰이 되짚어 보지만,

   없다는 생각이 든다.


Someone’s Something


May 7, 2026

I find myself

lost in thought.

Have I ever truly

devoted myself

my very self
to that

something?

The more I think,
the more I realize
I never have.

개미, 차강석 씀 | Ants by Cha, KangSeok

about Mr. Cha

개미

2026년 6월 6일

우리를 작디작고
약하디약한 존재로 아는 인간들

우리는 기중기처럼
우리 몸무게의 20배쯤
들어 올릴 강력한 힘이 있다

우리는 뇌가 몸무게의
6% 정도를 차지하고 활용하여
집단을 가장 성공적으로 이루고 있다

언젠가는 우리가
그들보다 월등히 높은
정신과 신체로 지배할 것이다

그날을 맞이할 생각에
오늘도 기쁘고 성실하게
노동을 하며 살아가고 있다


Ants

June 6, 2026

Humans think we’re nothing more than tiny,

weak little creatures.

We can lift around twenty times

our own body weight,

basically we’re living cranes

with six legs.

Our brains account for roughly

six percent of our body weight,

and we’ve built some of the most

successful societies on Earth.

One day, armed with minds and bodies

far superior to theirs,

we shall rise and take control.

Until that glorious day arrives,

we remain cheerful and diligent,

marching to work.

[Wine Bits and Sips] Do You Really Need a Wine Fridge?

a series of Wine Bits and Sips, written by Junghyun.

for the original Korean version

Bottles piling up at home? Wondering whether a wine fridge is worth it?

Wine is, at its core, a bottled beverage with around 13% alcohol. It doesn’t spoil easily. However, that said, if you want it to taste exactly the same a few months from now as it does today, you’ll want to store it somewhere dark and cool, what the French call a cave, essentially a cellar-like environment. Experts give a fairly wide range for ideal storage temperature: anywhere from 45°F to 68°F (7–20°C). In my own experience, a single shelf in a closet, away from direct sunlight and not directly in the path of heating or air conditioning, works perfectly well for up to a year. The key is to lay the bottles on their side, which keeps the cork moist and prevents it from drying out. 

If you’re planning to finish a bottle within a month or two of buying it, there’s really no need to invest in a dedicated wine fridge. And if you just want the look, a stylish wine rack on a sideboard or countertop does the job beautifully and adds a lovely touch to any room.

If you find yourself regularly storing more than 20 to 30 bottles at a time, keeping wines for six months or longer, or aging premium bottles (think $80+) for several years, it’s time to invest in a proper wine fridge. 

Compressor vs. thermoelectric. 

Smaller, quieter thermoelectric (semiconductor) models have become popular, but they’re sensitive to ambient temperature and tend to have shorter lifespans. For long-term storage, a compressor-based unit is the more reliable choice.

Brand matters. 

Look for something with minimal vibration, consistent temperature control, and a solid track record for durability [Top brands worth considering: LG DIOS, Dometic, and Eurocave]. My wine fridge costs more than my main refrigerator 😅.

Dual-zone vs. single-zone.

Some models let you set different temperatures for reds and whites; others don’t. If yours has only one temperature zone, set it to white wine temperature. Reds can be served slightly warmer after taking them out, but whites need that cooler baseline.

A few practical notes:

  • Wine you’re planning to drink soon doesn’t need to go in the fridge, though pulling a perfectly chilled bottle from it does feel rather nice.
  • If you’re moving soon, hold off on buying. The vibration and temperature swings of a move aren’t great for a wine fridge or the wine inside it. Wait until you’re settled.
  • Wine fridges can be noisy; they take up real space. [If you’re short on room, there’s always the sommelier-approved method: clearing out a wardrobe. It works really well 🥰]; they use more electricity than a standard fridge 😭.

From Tylenol to Opium

Korea version | 한국말 버젼
살면서 가끔 이런 생각을 한다.
만약 이 세상에 타이레놀이 없다면, 나는 아이를 어떻게 키웠을까, 끼울까?
열이 나고, 밤새 힘들었던 순간들. 부모라면 누구나 타이레놀의 경이에 의지해 본 경험이 있을 것이다.

우리는 익숙하게 타이레놀을 사용하지만, 타이레놀의 역사는 언제 시작된 것일까?

타이레놀의 긴 역사
많은 사람들이 타이레놀을 현대 의약품이라고 생각하지만, 그 역사는 생각보다 길다.
1955년 미국 McNeil Laboratories는 Tylenol이라는 이름으로 어린이용 해열제를 출시했다. 이후 1959년 Johnson & Johnson이 회사를 인수하면서 타이레놀은 미국 전역으로 보급되었고, 오늘날 가장 널리 사용되는 진통·해열제 중 하나가 되었다. 하지만 아세트아미노펜 자체는 훨씬 오래전인 1878년 미국 화학자 Harmon Northrop Morse에 의해 처음 합성되었다.
1890년대부터 진통과 해열 목적으로 사용되기 시작했지만, 당시에는 이미 의학계를 지배하고 있던 더 강력한 약물이 있었다. 바로 아편(Opium)이다.

인류와 함께한 진통제, 아편
아편은 인류가 수천 년 동안 사용해 온 천연 진통제이자 만병통치약이었다.
양귀비에서 얻어지는 이 물질은 통증을 줄이는 놀라운 효과를 가지고 있다.하지만 문제는 진통 효과만큼이나 강력한 의존성 중독성이다.

19세기 초 독일의 젊은 화학 견습생 Friedrich Sertürner는 아편 속에서 가장 강력한 활성 성분을 분리하는 데 성공한다. 그는 이 물질에 꿈의 신 Morpheus의 이름을 따서 Morphine이라는 이름을 붙였다. 당시 그는 자신에게 직접 약물을 투여하며 실험했고, 훗날 이 물질이 위험할 수 있다는 강력한 경고를 남긴다. 그러나 의학계는 모르핀의 강력한 진통 효과에 매료되었다.
1827년 Merck가 대량생산을 시작하면서 모르핀은 전 세계 의료 현장으로 빠르게 퍼졌다.

더 강한 약을 향한 욕망
1853년 스코틀랜드 의사 Alexander Wood는 주사기를 이용해 모르핀을 직접 체내에 주입하면 더 적은 양으로 효과를 낼 수 있다고 생각했다. 그 결과 모르핀 주사는 빠르게 확산되었다. 그 첫번째 약물과다 복용의 희생량은 Wood의 부인이었다.

당시 의사들은 더 강력하면서도 중독성이 적은 진통제를 찾았다. 그리고 그 과정에서 탄생한 것이 Heroin (acetylated morphine)이었다. 1898년 Bayer는 모르핀을 화학적으로 변형한 약물을 Heroin이라는 이름으로 판매하기 시작했다. 그 당신 관련 연구자들은 이 약물이 모르핀보다 안전하고 중독성이 적을 것이라는 성급한 결론을 내렸다. 하지만 그것은 치명적인 오판이었다. 헤로인은 더 빠르게 뇌에 도달했고, 더 강한 쾌감과 의존성을 만들었다. 20세기 초가 되자 의사들과 연구자들은 헤로인의 위험성을 인식하기 시작했고, 미국은 1924년 Heroin Act를 통해 헤로인의 제조와 판매를 금지한다.

Natural은 Safe를 의미하지 않는다
흥미로운 점은 모르핀, 헤로인, 그리고 현대의 오피오이드 진통제들이 모두 자연에서 시작되었다는 사실이다.
양귀비는 아름다운 꽃이다. 어떤 사람은 꽃이 아름답다고 말하고, 어떤 사람은 향기가 좋다고 말한다. 하지만 그 아름다운 꽃은 동시에 인류 역사상 가장 강력한 진통제와 가장 심각한 약물 의존 문제를 만들어낸 출발점이다.

우리는 종종 "천연 성분"이라는 말을 들으면 안전하다고 생각하고 상업적으로 이용된다. 그러나 역사는 그렇지 않다고 말한다. 독버섯도 천연이고, 아편도 천연이다. Natural과 Safe는 결코 같은 의미가 아니다.

타이레놀에서 다시 시작된 질문
아마 그래서 합성의약품인 타이레놀이 더 흥미로운지도 모른다.
오늘날 수많은 부모들이 아이의 열을 내리기 위해 사용하는 비교적 안전한 약. 이 약은 안전하지만, 시럽을 물처럼 마시면 물론 안 된다. 간에 치명적인 해로움을 끼칠 수 있다.
100년 넘게 사용되어 왔지만 아직도 작용기전이 완전히 밝혀지지 않은 약 (아무래도 열을 낮춘다는 것 자체가 면역작용을 통제하고, 그 결과가 우회적으로 아픔을 통제할 것같다).
그리고 무엇보다 아편이나 모르핀과는 전혀 다른 길을 걸어온 진통제.

진통제의 역사를 돌아보면, 그것은 단순한 의학의 발전사가 아니다.

인간의 고통을 줄이려는 노력과 과학적 호기심, 때로는 성급한 결론, 그리고 상업적 이해관계가 끊임없이 교차하고 있는 역사이다.

타이레놀에서 시작된 오늘의 글은… 야산의 양귀비 꽃 (지금 이시대에는 야산에 양귀비 꽃은 없겠지만..)으로 이어졌다. 난 실재로 양귀비 꽃에 대해 초등학교 수업 때 들은 적은 있어도 본 적은 없다.

Sometimes I find myself wondering: if Tylenol had never existed, how would I have raised my children?

The fevers, the countless nights spent comforting a restless child who couldn’t sleep. Almost every parent has probably relied on Tylenol at some point.

We use Tylenol so routinely today that we rarely stop to think about it. But when did the history of pain relief actually begin?

The Long History of Tylenol

Many people think of Tylenol as a modern medicine, but its history is much longer than most realize.

In 1955, McNeil Laboratories introduced a children’s fever reducer under the brand name Tylenol. After Johnson & Johnson acquired the company in 1959, Tylenol became widely available across the United States and eventually grew into one of the most commonly used pain relievers and fever reducers in the world.

Acetaminophen itself, however, dates back much further. It was first synthesized in 1878 by the American🇺🇸 chemist Harmon Northrop Morse. By the 1890s, it was already being used to relieve pain and reduce fever. Yet at the time, medicine was dominated by a much more powerful substance. That substance was opium.

Opium: The Painkiller That Accompanied Human History

Opium is a natural pain reliever that humans have used for thousands of years.

Derived from the opium poppy, it possesses remarkable pain-relieving properties. The problem, however, is that its power to relieve pain is matched by its ability to create dependence.

In the early nineteenth century, a young German🇩🇪 chemical apprentice named Friedrich Sertürner succeeded in isolating the most potent active ingredient found in opium. He named the substance Morphine after Morpheus, the Greek god of dreams.

Like many early scientists, Sertürner experimented on himself. He administered the substance to his own body and later warned that it could be dangerous. Nevertheless, the medical community was captivated by morphine’s extraordinary ability to relieve pain.

When Merck began mass-producing morphine in 1827, it rapidly spread throughout medical practice around the world.

The Desire for a Stronger Drug

In 1853, the Scottish🏴󠁧󠁢󠁳󠁣󠁴󠁿 physician Alexander Wood believed that injecting morphine directly into the body would allow doctors to achieve the same effects with smaller doses. As a result, injectable morphine quickly gained popularity and The first victim of the injected morphine was Wood’s wife.

At the same time, physicians continued searching for a painkiller that was even more effective while being less addictive.

Out of that research came heroin, acetylated morphine.

In 1898, Bayer began marketing a chemically modified form of morphine under the name Heroin.

Early researchers hoped that this new drug would be safer and less addictive than morphine. It was a devastating miscalculation.

Heroin reached the brain more rapidly, produced stronger feelings of euphoria, and ultimately proved even more addictive. By the early twentieth century, doctors and researchers had begun recognizing its dangers. In 1924, the United States passed the Heroin Act, effectively banning the manufacture and sale of heroin.

Natural Does Not Mean Safe

One of the most interesting aspects of this story is that morphine, heroin, and modern opioid painkillers all originated from nature.

The poppy is a beautiful flower. Some people admire its appearance. Others appreciate its fragrance. Yet this beautiful flower also became the starting point for some of the most powerful pain-relieving drugs and some of the most devastating addiction problems in human history.

We often assume that something described as “natural” must also be safe. History tells a different story.

Poisonous mushrooms are natural. Opium is natural. Natural and safe are not the same thing.

A Question That Returns to Tylenol

Perhaps that is one reason why Tylenol, a synthetic drug, remains so fascinating.

It is the medicine countless parents use to bring down a child’s fever. Of course, while this medication is safe, you certainly must not drink the syrup as if it were water. Doing so could cause fatal harm to your liver.

It has been used for well over a century, yet its precise mechanism of action is still not completely understood. (It seems that lowering a fever essentially regulates the immune response, and that this, in turn, indirectly helps control the pain.)

Most importantly, it followed a path very different from that of opium or morphine🪜.

When we look back at the history of painkillers, we are looking at more than the history of medicine.

It is also the story of humanity’s effort to reduce suffering, a story shaped by scientific curiosity, occasional premature conclusions, and powerful commercial interests 🤑.

Today’s reflections began with Tylenol, but somehow led me all the way to the poppy flower 🌺.

Growing up, I heard about poppies in elementary school, but I have never actually seen one in person. Perhaps wild opium poppies once existed in fields and hillsides somewhere in Korea, but certainly not today.

AAV Serotypes for Intravenous Gene Therapy (1)

Today, I wrote a bit about AAV serotypes and doses, and target organs, inspired after reading Reporter’s notebook 

CAP-002 case

clinical fatalities and the limits of IV-delivery

A child died in Capsida’s CAP-002 trial in September 2025,  the first patient treated with an engineered, IV-administered, BBB-crossing AAV for STXBP1 encephalopathy. 

Capsida Biotherapeutics voluntarily halted the SYNRGY trial (NCT06983158) after the first treated paediatric patient with developmental and epileptic encephalopathy (DEE) caused by STXBP1 mutations, died. The cause of death remains under investigation. CAP-002 is notable because its capsid was specifically engineered to cross the blood-brain barrier (BBB) via IV infusion, without intracranial injection. Regulators did not enforce the hold. However, Capsida self-imposed it while searching for the root cause.👍


Now, we should check some adverse events linked to IV AAVs. 

Reported patient deaths linked to IV AAV by serotype
SerotypeDrug / companyIndicationCause of deathStatus
AAV9Zolgensma (Novartis)Spinal muscular atrophy (SMA)Acute liver failure (ALF)2 deaths, 2022 (Zhang et al.)
AAV9Multiple high-dose trialsVarious CNS / neuromuscularThrombotic microangiopathy (TMA)Multiple cases (Zhang et al.)
AAV9 (NGN-40)NeurogeneRett syndromeRare hyperinflammatory syndrome1 deathPhase I/II (Joshua Silverwood)
AAV9-based (RP-A501)Rocket PharmaceuticalsDanon diseaseFatal acute systemic infection1 death, Phase II (Annabel Kartal Allen)
AAV8ASPIRO trial (AT132)X-linked myotubular myopathy (XLMM)Cholestatic liver failure4 deathsPhase I/II (Shieh et al.)
AAVrh74Elevidys (Sarepta)Duchenne muscular dystrophyAcute liver failure3 deaths (Annabel Kartal Allen)
Engineered AAV (CAP-002)Capsida BiotherapeuticsSTXBP1 encephalopathyUnknown — under investigation1 death, Sept 2025 (Annabel Kartal Allen)

What the AAV5 story teaches us

Now, we have to think about AAV5’s successful story. A decade of relative safety, why?

In August 2022, Europe approved the world’s first AAV5-based gene therapy for severe hemophilia A – Roctavian (valoctocogene roxaparvovec), developed by BioMarin. The FDA followed in June 2023. Since Phase 1/2 trials began in the mid-2010s, hundreds of patients have received a single IV infusion of AAV5, and to date, no patient deaths have been directly attributed to the therapy. In a field where other AAV programs have seen multiple fatalities, this is a notable record.

Hemophilia A is caused by a missing clotting protein (Factor VIII) that is normally made in the liver. So the therapeutic goal of Roctavian is simply to deliver a working gene to liver cells  and the liver happens to be exactly where AAV naturally travels after an IV injection. The vector does not need to fight its way past any biological barriers. It goes where it was always going to go.

So what makes AAV5 different? The answer is not the stereotype itself [I think, and some others would agree with me although it is some part of stories].  


The dose matters. 

Because the liver is the natural destination for IV-delivered AAV5-based gene therapies, a relatively modest dose is enough to achieve a therapeutic effect in hemophilia. Roctavian is given at 4–6 × 10¹³ vg/kg, roughly half to a third of the doses used in CNS or muscle-targeting programs. That difference in dose is, in large part, the difference between a therapy with an acceptable safety profile and one that has killed patients.

Why does the target organ change everything?

Think of it this way. When you give AAV through an IV, the vector enters the bloodstream and travels throughout the body. The liver acts like a sponge as always. It absorbs a large fraction of whatever AAV is circulating, regardless of where the doctor wants it to go. This is simply how our body works.

For hemophilia, this is actually favorable: you want the gene delivered to liver cells, and the liver is already soaking it up. A dose of 4–6 × 10¹³ vg/kg is enough to transduce enough liver cells to restore Factor VIII production. The liver handles this dose without triggering a dangerous immune response in most patients.

But for diseases of the brain or muscle, the liver is an obstacle, not a destination. To get enough AAV past the blood-brain barrier or into muscle tissue, you have to flood the entire system with a much larger dose, often 2 to 10 times higher. The liver still absorbs most of it, now overwhelmed by vectors it was never meant to receive in such quantities. The result, in the worst cases, is acute liver failure, immune storms, or vascular damage.

The safety record of AAV5 in hemophilia is genuinely encouraging, but it would be a mistake to conclude that AAV5 is simply a “safe” serotype. The real lesson is more specific and more important: IV gene therapy works best and most safely when the target organ is the liver. AAV5 has never been tested at the doses that CNS or muscle delivery would require, so we simply do not know how it would perform in that context.

What the full clinical picture tells us is that the moment gene therapy asks AAV to travel beyond the liver via IV, the dose requirements climb into a range where serious toxicity and death become real risks regardless of which serotype is used. AAV8, AAV9, and AAVrh74 have all produced fatal outcomes in this higher dose regime. Engineered capsids designed to cross the blood-brain barrier represent the field’s attempt to break this trade-off, but as the September 2025 death in Capsida’s trial shows, even the most advanced designed next-generation vectors carry unknowns that only human trials can reveal [The dose not disclosed yet]

A lower dose of IV gene therapy targeting other organs might be successful, which underscores the need for more efficient AAV engineering or local injection to resolve these matters.


Reference

Annabel Kartal Allen. “Child Dies in Phase I Capsida Gene Therapy Trial.” Child Dies in Phase I Capsida Gene Therapy Trial, Clinicaltrialsarena, 12 Sept. 2025″

Joshua Silverwood. “Patient Dies in Neurogene’s Phase I/II Rett Syndrome Trial.” Patient Dies in Neurogene’s Phase I/II Rett Syndrome Trial, Clinicaltrialsarena, 22 Nov. 2024″

Shieh, Perry B., et al. “Safety and Efficacy of Gene Replacement Therapy for X-Linked Myotubular Myopathy (ASPIRO): A Multinational, Open-Label, Dose-Escalation Trial.” The Lancet Neurology, vol. 22, no. 12, Dec. 2023, pp. 1125–39. DOI.org (Crossref)

Zhang, Wenwen, et al. “Comprehensive Analysis of Adverse Events Associated with Onasemnogene Abeparvovec (Zolgensma) in Spinal Muscular Atrophy Patients: Insights from FAERS Database.” Frontiers in Pharmacology, vol. 15, Jan. 2025, p. 1475884.

Design a site like this with WordPress.com
Get started