Lois Lowry's Blog


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Posted by Lois Lowry
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on Thursday, 10 June 2010 in Uncategorized
 Funny little email interchange with my brother, a doctor, yesterday. He sent me an excerpt from an article from  the New England Journal of Medicine---he so hates opacity and pedantry, and this (rightly) seemed an example of that to him:

Inflammation is risky. Leukocytes recruited to fight microbes cause collateral damage that is often more severe than that originally triggered by the pathogen. Moreover, inflammation takes place even in patients with sterile tissue injuries such as trauma and ischemia–reperfusion.

The immune system recognizes mitochondria released from dying tissues as the bacteria they (the mitochondria) once were, and it mobilizes its destructive potential to limit their proliferation and arrest a mistaken invasion. This tragic "misunderstanding" could have a role in several human diseases, leading to inflammation in conditions as clinically diverse as post-traumatic systemic inflammatory response syndrome, myocardial infarction, cerebral ischemia, and systemic and organ autoimmunity.

Mitochondria are membrane-bound organelles that produce energy in virtually all eukaryotic cells. They have evolved from an endosymbiont alpha-proteobacterium (a relative of brucella and rickettsia). Mitochondria have their own DNA, enriched in hypomethylated CpG-containing sequences, which is duplicated when mitochondria divide. The origin of the eukaryotic cell is still controversial, and transitional forms between prokaryotes and eukaryotes have not been persuasively documented.3  The amalgamation of two prokaryotes or the amalgamation of a prokaryote with an eukaryotic precursor cell are possible scenarios. Regardless, the merger would have occurred long before the existence of an immune system, which by definition is a feature that is unique to multicellular organisms.

Zhang et al. detected mitochondrial DNA in the blood of patients with systemic inflammatory response syndrome after major trauma. Intravenous injection of mitochondrial proteins into mice resulted in activation of circulating neutrophils, with random extravasation in peripheral organs such as the liver and lung. Acute lung injury developed in these mice. Mitochondrial constituents also selectively activate an inflammasome, suggesting a possible link with other sterile inflammatory conditions such autoinflammatory diseases

Zhang et al. reason that, by virtue of their evolutionary origin, mitochondria might be recognized by pattern-recognition receptors and thus might initiate inflammation. This event seems unlikely to occur in healthy tissues, in which membrane-bound mitochondria are contained within cells

Mitochondrial structures released by injured cells possibly prompt inflammation during heart, kidney, or brain ischemia–reperfusion injuries, in which local neutrophil activation and further tissue damage occur when the blood flow is restored. Finally, mitochondria are probably released in patients with infectious disease — in whom substantial cell death takes place — possibly contributing to the molecular pathology of sepsis.

I gulped when I read it,  and then replied to him with this:

I feel I owe you an apology
For my molecular pathology.
I thought I might have hypochondria
Turned out it’s just my mitochondria!
I felt so ill, weak and sedated…
But my CPG was hypomethylated!
Wouldn’t a good strong antibiotic
Keep my cells eukaryotic?
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Jude Monday, 29 November 1999

This sounds like a good adventure, especially for a winter trip.
Yesterday, as I was going through 55 years of detritus of my occasionally interesting life (a cleaning which has been influenced by regular reading of 6 blogs on minimalism), I thought about what I've done that might be remembered, and for some reason that made me think of you.
When I was a high school librarian, every year I included The Giver in my banned books display. It was the one book that everyone exclaimed about: "The Giver was banned?" "Well, challenged," I'd explain. "But I love that book!" the student would exclaim, and frequently, they'd check it out to re-read.
That, I thought yesterday, is a good legacy: "But I love that book!"

Miki Monday, 29 November 1999

Have a wonderful time. I have heard from friends that it is a magical and wonderful place.

Jasmine Monday, 29 November 1999

Thank you so much for wisely choosing to not write a story set in some place that you've only visited. I feel that there are too many books like that that end up boiling a culture down to only the parts that the author feels will best serve their story and minimalizes their customs.

anne Monday, 29 November 1999

Bon voyage! If pictures are so awe-inspiring, I can't imagine what it will be like to be there. That should be an experience that adjusts your world
view and sense of place.
Enjoy the adventure!

Annie Monday, 29 November 1999

Bon voyage! One of my favorite under-the-radar novels of recent years was Easter Island by Jennifer Vanderbes. It's about a modern-day botanist (a woman) traveling to Easter Island to research with a parallel story of--of course!--a woman anthropologist traveling there in 1913.
You are already en route but perhaps the miracles of kindle will let you download this to read during your travels...

ojimenez Monday, 29 November 1999

My daughter and I were talking about foreign lands to visit, just the other day. She wants to see Europe, Japan. She asked me where I've been, and went Wow! I told her then that "you don't impress people by telling them where you've been." ( a lesson I learned quickly as a photojournalist ) I explained to her that you don't do things to impress other people, you do them to enrich your life and learn, so that you may become a better person, and use this knowledge to get a clear perspective of the world we share...
Papa, she said, why are you such a killjoy?
"Feliz viaje!"

Caroline Monday, 29 November 1999

But you do know that we'd read and love your book about Polynesia, right? Have a good trip and many more observations! I hope you will be able to blog while there.

sasa diana
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sasa diana Thursday, 05 October 2017
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