The Haversian Canal

I was studying at Barnes and Noble, and an old man was sitting next to the window. Outside, on the other side of the window was his dog. Amidst the chatter, which is the reason I go to there, I overheard him tell another fellow the dog was 150 pounds. It was huge. And lean. I could see its ribs and muscles, the ridges of the vertebrae protruding under the skin. Not a fat dog, 150 pounds of muscle and bone. Laying in the shade, next to the window, unrestrained. Obedient. From stage right a woman walked the sidewalk toward her gold Lexus SUV, parked in front of the dog. Her hair was nearly the same hue as the car's. Behind her, like a lone duckling, her daughter followed. Her hair was a shade lighter than her mother's and longer, possibly all the hair she had grown in her short life.

Mom needed to put her purchases in the car, so she left her daughter at the curb, opening the driver's door. The door was now between her and her daughter. Nothing was between her daughter and the dog. Daughter saw the doggy. And waved. And smiled. Mom reached into the back seat. Daughter, in her white cotton sundress and white sandels, took a wobbly step toward the dog. The old man looked up. And rapped on the glass. Daughter looked up and saw him. And smiled even more. Two friends! A doggy and a grandpa! Yay! He rapped on the glass repeatedly. She stepped closer, halving the distance between her and the dog. His head came up. The man was pounding the glass and waving his hands. Shaking his head. I was about to run out to the curb. I should have run earlier. The dog cocked his head a bit to one side. Daughter's gaze caught the dog's. Everyone was looking. Daughter leaned her head toward the dog, reaching up to pet him with her left hand. His ears were bigger than her hand. Mom stood up. Still looking in the car. She turned. Stepped. Closed the car door. Smiled. Daughter looked up and back, over her shoulder, at Mom. And smiled. And reaching out her hand, pointed to the dog. She must have felt the dog's breath on her finger. The old man had stopped waving. Daughter and Mom stepped toward each other and away they went, down the sidewalk, toward the framing store.

I found this question in my site statistics. Someone had typed that question into a search engine, and one of my pages came up. It's a tough question to answer, because it's relative. I mean, really, hard compare to what? Compared to qualifying as a tactical action officer in the Navy? Well, not really, but then, that didn't take four years. Harder than labor? My wife assures me med school isn't that bad, but that labor only lasts so long, though I'm sure it must seem like forever.

"Medical school isn't hard, there's just so much of it" is what all the docs told me before I started. I tend to agree there. My rule is there are only two things in life that are really hard, rocks and quantum mechanics. If you can wrap your head around quantum mechanics, the rest of your life will be a little different. Most people can't do it. 5000 people a year graduate with bachelors degrees in Physics from American universities, while the US produces 16000 MDs a year. So I'll agree, in that sense, medical school just isn't that hard. There's not a lot of conceptual 'wows', moments where you get all tingly because you just realized some deep truth that can only be spoken in the language of math.

Physics, however, is a very deep sort of learning. People talk about reaching up to the stars and diving down into the nucleus. Its a foot wide and a thousands of miles deep. I used to think of biology as a mile wide and a foot deep. It's got a limits. Biologists, biochemists, doctors, just don't care much about quarks, and the parking garage doesn't have many enzymes running around. It is, however, more like a 1000 miles wide and 1000 feet deep. Volume, volume, volume. The scope of medicine encompasses air quality in the parking garage and the quantum spin of hydrogen, the decay of which causes the electrons to emit photons that make magnetic resonance imaging possible. And everything in between.

I would caution those approaching medicine from business, the social sciences and humanities. Come on in, plenty of room, but the core skill developed in the training of business people, political analyists, and book critics—defending a position or selling an idea—isn't the ultimate yardstick in medicine. Rhetoric really is the ultimate yardstick in politics, fiction, and sales. It is. That's cool. Nothing wrong with that. But the body is only so amenable to pursuasion. Hey, don't get me wrong, persuasion works. . . . During Hurricane Rita I was at an emergency clinic with 185 patients in a school gymnasium when I was called out at three in the morning to a woman who was hyperventilating. I happened to know from earlier in the day that she was bipolar and asthmatic. Her breathing wasn't the sort of labored, panicked breathing of an asthma attack. Not knowing what else to do, with no doctor around and a dozen people huddled around, staring, in the dark, I put my hand on her shoulder. And she calmed down. Her breathing returned to normal. She stopped sweating. Turned out she just really wanted to go home. Yeah, so mind-body-soul, biopsychosocial, moral-mental-physical, whatever you want to call it, that's true. But everybody spends their lives on the mind and soul. Doctors earn their keep in society by knowing the body, the physical, the bio-. And that part isn't particularly amenable to persuasion. It comes down to actually knowing how the body works.

Which brings us back to medicine being 1000 miles wide and 1000 feet deep. It's an ocean. You don't have to know all of it. But you will be expected to understand how things work. That's the core skill in science: understanding how things work. The basic science professors, they kind of swim around in this big ocean. The molecular biologist will lecture about the neural plaques of Alzheimer's disease and everything they say, I mean, every word, is testable, but they don't have to know if a plaque in a particular location is going to cause a deficit in sensation in the foot or make the patient extremely irritable. The neuroscientist might know that, but isn't going to lecture the next day on the physiology of the gall bladder. Doctors are the ones that know about all the systems and how they all interact. At least, that's what Joe Q. Public is going to assume when he presents with pain in his belly every time he breathes in. As will the retired colonel, the state legislator, even the pharmacologist who teaches night classes.

It's great, it really is. Because you really can know a lot of it. And a lot of people without science backgrounds do better than the science majors. But I would suspect the biology majors, the neuroscience, physiology, and biochemistry majors probably get the best preparation for medical school. If you want a sense of the level of material you should be able to understand by the end of your first year without any look-ups, (well, maybe a couple), this review article on diabetes is representative. The contents of this article were dispatched in about five minutes of lecture, and the students were expected to know all the pathways discussed, all their enzymes, the structures of the substrates and products, and their consequences on the body.

So, how hard is medical school? Well, with all those caveats, you make it as hard as you want it to be. There are really bright folks with good intentions, research backgrounds and years under their belts who struggle. There are folks who are just back from England after finishing their Fulbright scholarships and work really hard and get really good grades but might actually tank their board exams and irritate their classmates. There are slackers who can't avoid As if they try, make friends with every patient, impress every attending, and are liked by everyone. The only thing I can caution you about the last group, is, if you're not one of them, don't take study advice from them. If they don't have to study, what would they know about studying?

Michael Brownlee wrote an excellent review article in Nature in 2001 (414:813-820), Biochemistry and Molecular Cell Biology of Diabetic Complications. It talks about AGEs, sorbitol and the polyol pathway, reactive oxygen species, glutathione and free radicals, the hexosamine pathway, protein kinase C (PKC), and offers that a high mitochondrial membrane potential might play a central role in all of these. The excess glucose raises the mitochondrial membrane potential, but this is converted to heat by thermogenin (uncoupling protein-1), until thermogenin is overwhelmed. Brownlee argues that it is only when thermogenin is overwhelmed that the glucose becomes so great that it starts backing up into these other pathways (polyols, hexosamines, AGEs, and PKC activation). Just gotta get over the British spelling of hyperglycaemia.

What the others do:

Polyol pathway: increases sorbitol, causing damage.
AGEs: inhibit proper protein function, particularly among structural proteins.
Hexosamine pathway: creates glycoproteins
PKCs: activate lots of processes involved with making new vessels and laying down fibrous proteins, but also inhibits nitric oxide synthesis in capillaries and kidney glomeruli, so these vessels don't dialate. Also causes increased vessel permeability via VEGF.

And I really hate it when I make additions to the Wikipedia but forget to sign in before they're recorded.

Is Chomsky finally demonstrated wrong? Is there not a universal syntactic structure? Daniel Everett seems to think Brazil's 310 to 350 Pirahãs, whose language includes no words of time, numeracy, or any subordinate clauses, may in fact demonstrate this. I wonder how this affects Lakhoff's position?

I'm going to preface this whole thing by saying its all highly speculative. Also, here's a quick review of several other factors at play.

Seth Roberts, a psychologist at Berkeley, has posited a rather intriguing diet theory for the citizens of developed countries, and offers explanations of how his theory addresses a host of studies in humans and other mammals (dogs, rats, mice, cats, etc), but he doesn't address the physiological set point that must exist for his theory to work. Surely he has heard of leptin and ghrelin and insulin, but it doesn't appear he has decided they, or any of the other many molecules involved, are worth talking about. Perhaps he believes the theory stands on its own merits, regardless of the ultimate molecular mechanisms. Here's a quick redux:

A Body-Fat Setpoint

Adipocytes secrete leptin, which depresses appetite, when they have a usual-to-high amount of fat on board. If the adipocytes are chronically engorged it has been hypothosized (Friedman, Nature, 1998) that the hypothalamus may reduce its response to leptin. This could be done by invaginating some of the leptin receptors, a well documented mechanism in other membrane proteins, like aquaporons, or the hypothalamus may reduce the response to leptin by some concordant intracellular downregulation.

Ghrelin is secreted by endocrine cells in the stomach epithelium, into the blood, in advance of a meal. This preprandial secretion suggests the vagus nerve, which originates in the brainstem, controls ghrelin secretion, probably via acetylcholine synapses. Why ghrelin is produced in the stomach, I don't know, but ghrelin acts on receptors in neurons of the hypothalamic feeding centers of the brain to increase hunger via neuropeptide Y. Anorexics report being always hungry and have been found to have high ghrelin levels. Gastric bypass patients, who find excess eating painful, have low ghrelin levels, particularly those whose surgery included removal of the fundus, which contains the P/D1 cells that secrete ghrelin. In normal people, there is a sharp rise in ghrelin before a meal, and a sharp drop toward the end, or possibly after a meal.

There is an insulin receptor in the brain, and absence of this receptor in knockout mice causes obesity. The body doesn't detect calories. It can detect bulk (stomach stretch), and it can detect fat (cholecystokinin), and it can detect sugar via pancreatic beta cells, which secrete insulin in response to blood glucose. Insulin is the closest thing we have to a calorie detector. In fact, the insulin receptor and the leptin receptor activate the same intracellular cascade in the hypothalamic cells: insulin receptor substrate 2, PI-3K, and ultimately inhibition of food intake. Even if the knockout mice had high blood glucose, the body's primary signal for high glucose, insulin, never managed to make its report to the hypothalamus. Perhaps even more than insulin, CCK signals when you've had enough to eat. At least, insulin may not be the during-the-meal signal, because insulin levels rise well after the meal. Also, CCK responds more immediately to the consumption of food: fat only has to get to the duodenum to cause CCK release, where as insulin isn't secreted until glucose has been absorbed into the blood.

Other hormones are known to affect hunger and satiety but leptin, CCK, insulin, and ghrelin are current front-runners as long-term and short-term regulators of stored fat and energy consumption. How do you increase leptin and decrease ghrelin? Since this hunger-satiety processing goes through the brain, which controls the ultimate hand-to-mouth feeding motion, there may be opportunities to regulate this without drugs.

What the Body Does With Fat

Where do adipocytes get fat from? The blood. How do we get fat into the blood? Well, there are a lot of ways. I've got charts of biochemical pathways that make the Boston street map look tame, and most of them can produce fat. What fat can't do is become glucose, which, as noted above, is what stimulates the secretion of insulin.

If you consume fat, the digestive system breaks each molecule down to the basic fat building blocks, fatty acids, and then repackages them for blood transport as triglycerides. If you eat fat, you increase your blood triglycerides. Humans can convert triglycerides back to fatty acids, but we cannot convert fatty acids to glucose. We either store them in adipocytes as triglycerides or metabolize them to acetyl-CoA and then to ATP, the energy currency of the cell. Indeed, until the advent of liposuction, you eventually either converted all your fatty acids to ATP or stored them. If you eat pure fat, what you won't do is stimulate insulin because there is no glucose produced and there is no glycemic excursion. Foreshadowing the final section below, if you consume a pure fat, particularly one that stimulates little sensory input to the brain (no flavor, no odor, very little texture), there is little overlap between the conditioned stimulus (seeing, smelling, thinking about food) and the usual unconditioned response (glycemic excursion). There is, however, a satiety response from CCK, but this may limited if dosing is small. Need more research here. Fructose would bypass all of these. Which would really help explain how fructose water could at once be used to decouple existing flavor-calorie associations, and why the rise in food products containing high-fructose corn syrup is correlated with the rise in obesity. Causation is not certain, but fructose may be increasing caloric content as a trojan horse. You taste it, but it offers no satiety signal to the body (via CCK or insulin).

Dr Roberts' Theory

First, a brief overview of Pavlov. Despite all the psychologists who refer to Pavlov, Ivan Pavlov was actually a gastrointestinal physiologist studying salivary enzymes. He found that if a dog hears a bell and is then given food, time after time, eventually the dog will salivate when the bell is rung, whether or not food is presented. the food is an unconditioned stimulus, salivation is a conditioned response, and the bell is a conditioned stimulus. If you're studying salivary enzymes, not feeding the dogs every time saves money.

Seth Roberts's Shangri-La diet advocates a Pavlovian approach to unlearning eating. In moderation. He argues that our modern, grocery-store, prepackaged, consistently flavored foods create very strong flavor-calorie associations in a Pavlovian manner, and that these associations, and commensurate consumption, influence the body-fat setpoint. I submit the 'calorie' in flavor-calorie association should be replaced with 'blood-glucose', because, as discussed above, insulin is the closest thing we have to an internal calorie counter. I also submit that ghrelin is a likely mediator of the conditioned stimulus. Dr Roberts further claims that it may be possible to control body fat by decoupling the association between modern supercharged flavor stimuli and calories, either by eating things that cause neither stimulus, or by eating widely ranging flavors that can't be absolutely replicated (every big mac tastes like the last one, but every apple tastes a little different). This, again, may be testable by testing preprandial ghrelin levels.

This is where I bring in the molecular stuff from above. If you eat varied foods or foods that the brain doesn't closely associate with the various satiety responses, like insulin, Dr Roberts offers quite a bit of evidence that you won't eat as much because the conditioned stimulus, intense, consistent taste and appearance, has been separated from the unconditioned response, elevated blood glucose and the ensuing insulin secretion. He offers one very interesting self-experimentation that really rings a bell. His first self-experimentation in the subject was to drink fructose-water. Relatively tasteless, odorless, and textureless, it bypasses the insulin response and the regulatory steps of glycolysis. It instead increases blood triglycerides. Similarly, eating a couple hundred calories of rather tasteless extra-light olive oil (about two tablespoons) between meals will increase blood triglycerides. They both stimulate a longer term leptin response, which decreases appetite over the long term. This increase in leptin represents the long term lowering of the setpoint.

I recommend olive oil (canola oil, corn oil, whatever bland oil you want) over fructose. Remember how we can't turn fats into glucose? Well, not only can fructose be turned into glucose, fructose can hop onto glucose's metabolic pathway, glycolysis, downstream of the regulatory checkpoints, PFK1 and fructose-1,6-bisphosphatase. There is evidence this glycolytic dysregulation leads to supercharged mitochondria and perhaps a high mitochondrial matrix electrical potiential. Michael Brownlee argued this mitochondrial supercharging may be a cornerstone of diabetic complications (Nature, 2001) . This next sentence is the title of an article by Teff, et al from the Journal of Clinical Endocrinology and Metabolism, and I want to point out I composed the rest of this post before I read the title of this article, which our course director, Dr David Hurley, mentioned in Biochemistry today: Dietary Fructose Reduces Circulating Insulin and Leptin, Attenuates Postprandial Suppression of Ghrelin, and Increases Triglycerides in Women. (Relax all you Y chromosome bashers, it almost certainly works in men too. They only tested women.)

Olive oil on the other hand, doesn't appear to be associated with nasty things like diabetic retinopathy and leg amputations. I'd be very curious to know what happens to leptin levels on the olive oil diet. Do adipocytes take up the olive oil and then secrete more leptin? One could speculate then that mobilized fat stores and additional olive oil would create a new, higher, steady state production of leptin until a new, lower steady state weight was achieved. Roberts claims that leptin levels go down on his diet, indeed, that leptin levels go down on any diet, but I'm not convinced of this. If leptin is being recruited as part of the reduction in eating, it could explain the success of the diet.

Do I advocate every American running to Piggly Wiggly and driving up the price of olive oil? Well, no, but between strong candidates for the mechanisms of a metabolic set-point, an extraordinarily cheap Pavlovian means to control the set point, and America's growing middle and concomitant growing demands on the planet, this hypothesis seems like it might merit some research dollars.

Additional reading

People to Look for
Andrew V Schally
Akira Arimura
Cyril Y. Bowers
Giovanni Mantovani
Akio Inui
Akihiro Asakawa
Alessandro Laviano
Michael M Meguid
Mineko Fujimiya

Stimulation of Appetite by Ghrelin Is Regulated by Leptin Restraint
Brain regulation of food intake and appetite: molecules and networks
Adiponectin and Adiponectin Receptors
Adipocyte-Derived Hormones, Cytokines, and Mediators
Ghrelin, appetite, and gastric motility: the emerging role of the stomach as an endocrine organ
Mice fed corn oil secrete more leptin than mice of similar body composition fed fat-free diet
Lipogenic enzymes in rat liver are suppressed by a diet of monounsaturated fats and increased in a fat-free, high-carbohydrate diet
Regulation of Leptin in Humans. Not clear if fatty acids affect leptin secretion. 2000
Eicosapentaenoic fatty acid increases leptin secretion from primary cultured rat adipocytes
In humans, insulin stimulates leptin secretion and epinephrine inhibits leptin secretion. Also, cold stimulates the sympathetic system, indirectly inhibiting leptin, thus securing insulation
Some amount of leptin is stored in human adipocytes, perhaps in vesicles (2001)
Lehninger, Biochemistry, 4th Edition, Chapter 23, especially figures 23-33, 35, 39.

Wikipedia articles
Adiponectin, Wikipedia
Plasminogen activator inhibitor 1
TNFα
Adipokine
Resistin
Amylin
Orexin (A & B)
Oxyntomodulin
The oft-cited Pima Indians
Interleukin-1
Obestatin
Cortisol, ACTH (aka corticotropin), and Corticotropin Releasion Hormone
Neuropeptide Y
Melanocyte-simulating hormone α
Serotonin
Phosphoinositide 3-kinase (PI-3K)
PYY 3-36
Somatostatin
Incretins GLP-1 & GIP
C-peptide, proinsulin less insulin
Glucagon
Bombesin
Motilin
Gastrin
Secretin
Pancreatic Polypeptide
P/D1 cell
Urocortin

Other keywords (need Wikipedia articles written)
lipotoxicity
glucotoxicity
L celll
β cell exhaustion
CART (cocaine- and amphetamine-regulated transcript)
Urocortin
Galanin
Peptide YY
IRS-2 (insulin receptor substrate 2)

It is not likely that I will come up with the classic rules for any subject, not like Strunk and White, Maxwell (of Maxwell's equations), Edward Tufte, or Major Roberts (of Robert's Rules of Parliamentary Procedure). I am, however, interested in the rules. Dr Robert Johnson told me yesterday about Bach Theory, which intrigues me. What is it? Here are some links:

Wikipedia's entry on the Well-Tempered Clavier
Yo Tomita, a internationally known scholar who has posted MIDI files of the Well-Tempered Clavier.
Tim Smith and David Korevaar's site

A message from Dr Gary Field and Lori Koonce of the American Diabetes Association:

Dear Colleagues,

As you may well know Camp Victory (formerly known as ADA Louisiana Lions Camp) is a very unique program to the children with diabetes in Louisiana. Over the past 30+ years the American Diabetes Association has been able to offer this great camping opportunity to Louisiana children FREE of charge. Camp Victory is located in Leesville, LA at the Louisiana Lions Camp and consists to two one-week sessions from July 16-22 (ages 6-10 & CITs age 15) and July 23-29 (ages 11-14). The American Diabetes Association takes great pride in this camp and hopes that we can fill the camp to capacity which is 220 kids.

This year we are faced with a challenge of enormous proportions. Due to the relocation of many of our previous medical staff personnel, we may experience a shortage of medical staff which could severely limit the number of children we can accept to attend Camp Victory.

I would like to encourage each of you to consider this noble and rewarding experience not only for your patients and the other children with diabetes in Louisiana, but also as a physician. Please remember that it is not required that you attend the entire week, however it is recommended and appreciated that you attend as many days as your schedule will allow. There are a few who have committed to volunteer this year but the need is still great. RNs, LPNs, PAs, NPs, and MAs are also welcome.

As an added bonus, this year we are offering 11.7 CEUs to all nursing staff who attend the pre-camp orientation as well as the professional development periods during camp time. With this in mind, we encourage you to share this gratifying opportunity with the members of your nursing staff.

See you at camp!!

Gary Field, MD, Committee Chair

Lori Koonce, Camp Coordinator
Associate Manager, Programs
American Diabetes Association
2644 S. Sherwood Forest Blvd., Suite 122
Baton Rouge, LA 70816
225-216-3980 x6079

Wading Toward Home - New York Times, by Michael Lewis. 9 October 2005.

Going into the last couple of tests, here's my latest thoughts on how to study with notecards in medical school:

There's to much to learn in medical school to memorize. When writing notecard questions, you've got to make connections between facts rather than learning the same piece of information in multiple different contexts. In fact, you're wasting time if you ask your hippocampus to build a bridge too far. So put lots of information in the question. Make it so you damn near trip over the answer. Write things out, be as conversational as possible. Abbreviations require interpretation when reviewing notecards before a test. Consider:

In an action potential, sodium channels open before potassium channels.

— vs —

In an AP, Na+ channels open before K+ channels.

Did you say "N - A - plus"? "K - plus"? Reading the spelled-out words actually takes fewer bits of thinking and far less interpretation. Be as conversational as possible while being specific. Consider these questions about inhibitory post-synaptic potentials:

What's an IPSP?

What's IPSP mean?

What's IPSP stand for?

The following are some rough stats about my cards. The numbers are median(range).

Number of sentences per question: 1 (1-4)
Number of sentences per answer: 1 (1-4)
Number of questions in a question: 1 (exact)
Nouns per question: 3 (1-15)
Adverbs and adjectives per question: 4 (0-20)
Nouns per answer: 2 (0-15)
Adverbs and adjectives per answer: 4 (0-20)
Questions per card: 4(1-9)
Drawings per lecture: 0 (0-2)
Cards per lecture: 7 (1-20)
Mix of active and passive voice: 50-50
Most common word starting a question: What or what's. Probably 5 occurances for every occurance of any other word.
Others, roughly in order of frequency: How, why, does, if, where, when, are, during, in, membrane, delayed, is, express, for
Time spent per lecture
-- if written once at end of week: 75 minutes (15-180)
-- if notecarding in class then erasing and rewriting every card: 120 minutes (90-180)
-- if notecard in class then rewriting on new cards with minimal erasing: 75 minutes (40-100)

You need to learn what you don't know. Who's teaching you? You. As you study, you need to know what you know and what you don't know, so you can repeat the information you don't know to your future self. So you need to record what you don't know. You need to make a record. You need to produce a record. Making a product, in my case, notecards, is, in essence, you asking questions of your future self, and preparing answers in case your future self doesn't know the answer.

As you go through your notecards, if you know the answer, you can think it faster than you can read it or even say it, but it is still reinforced in your memory. The connection becomes stronger, more permanent. If you don't know, you need to hear the answer again to help the growing axonal processes weave their way through the jungle of connections to the other axonal process, dendritic process it needs to contact.

But that won't be learning for comprehension. Well, maybe, but I think it will, for two reasons. First, medicine is too complex to not be organized, and, secondly, the material is presented gradually, since well before you start medical school. The central piece of pedagogy that students need teachers for is the sequencing of information: general frames first, and proceeding to finer and finer details.

Notecards, in particular, are a conversation between you and your future self. Diagrams aren't particularly useful here, unless you need to see a picture to reinforce an idea for which you otherwise lack experience. The modern linguists seem to think that we simply have a very hard time talking about what we don't understand. That's why the leading edge folks are working in graphs and numbers and DNA sequences. They don't have all the information yet, so they're using the most basic tools to construct an accurate mental picture. Those more accurate mental pictures are what they pass on to the rest of us to learn. As science becomes more specialized, 'the rest of us' includes most of 'them', so don't worry to much about that. In any case, the idea is, you are having a conversation with your future self when you write notecards. Seeing a drawing made on a napkin can be revealing, as it happens, but the syntax, the order, of how that drawing came together is lost if it's completely written out. In fact, I think there may be a visuotemporographic syntax and grammar to drawing diagrams in conversation, but I'll have to look into that. One place a diagram is helpful, is in the question. Draw a diagram, of say, a sarcomere, label some proteins with letters, and then ask your future self to name those proteins. The answer, on the back, would have the letters with the associated protein names: A - Titin, B - Actin, C - tropomyosin, D - dystrophin, E - Z disk, etc.

Bottom line, write the clearest questions you can, leave no room for anything but the exact answer you're looking for, and then write that answer on the other side. Isn't that what you'd want a professor to do?

I think I'm going to teach myself XML by learning how to contribute to the Google Co-op this summer.

I've been writing about my thoughts on education from a student's perspective, and my thought for you is that the fundamental thing students need from teachers is through the levels of organization in the material, from the huge, grand thoughts, to the minute details, the schema. I came to this while considering what frame of mind a student should be in while studying outside of class. As I look back on my first year of medical education, it is fairly clear to me that some of our lecturers, though brilliant researchers and generally great people, were not good teachers, not because they didn't know the material, but because they did a terrible job of organizing their material and then putting their material in proper order. There are other ways to do a bad job of teaching, like interrupting natural trains of thought with 'clinical' pictures of terribly deformed children, or wasting the first ten minutes of lecture wrestling with the projector, but I want to focus on this large, conceptual, and it's-gotta-be-right-or-just-go-home issue of organization and sequencing.

Organization is somewhat at odds with sequencing. Time is a one-way arrow. Only one word can come out of one's mouth at a time. So how big a deal could organization be? Organization of a course is relatively straight forward: collect all the issues about the arm, break them up in reasonable bits, like, the superficial back, the shoulder, the brachial plexus, the arm, the forearm, the hand, et cetera, lecture for an hour on each of them, and then have a test. It's within a lecture where a lecturer's stock rises or falls. Most lecturers follow something along the lines of the classic "temple" model, where there's an introduction (the roof) three or four or five arguments or issues (the pillars), and a conclusion (the foundation, steps, whatever), and this is a good model. However, there is a challenge when the lecturer lecturer gets to those pillars and the logical organization no longer matches the sequential organization. This is where a lot of lecturers drop their students. Some get dropped as the lecturer dives into the first issue, but the real tragedy is when lecturers go to the second issue without transitioning. Another model for this is the GPG model - general - particular - general. You've got to come up out of the first particular and introduce the second, and when you're finished with the second, introduce the third. And the students need to know that you're doing this, because it's not obvious, particularly in the more abstract issues, like which cell types use which ion channels. If you talk about cell A using transporter A, then cell B using transporter A, then cell A using transporter C, where was the break? What exactly did you shift from and to? This is why I encourage profs to put as much information on one piece of paper as possible for each handout, so the students can anchor themselves in the lecture.

Ed (24 September 2006): There is a ready-made schema for the basic sciences years of medical education: First Aid for USMLE Step 1.

Grand Rounds here on June 13th! Send your submissions to haversian [dot]canal {at}gmail /dot/com.

Grand Rounds, and its audience, continues to grow, and there have been several conversations about the conflict between linking to all who submit the products of their labor and providing readers with a relatively clean, concise introduction to the medical blogosphere. Some Rounds have pushed 100 submissions and the average is over 50. Maybe we should link to everybody. Maybe we should link to five. I don't know. As most hosts link to everyone, I am going to take the road less travelled, and I hope you will join me.

I will link to thirty articles from thirty authors. My goal is not to select the most popular bloggers or those I think are the best. I want the thirty best articles written. I don't care when they were written, how many times they've been edited, or what your credentials are. I like Henci Goer's opinion on this:

You may be wondering about my credentials to write this book since I am not a doctor—either M.D. or Ph.D. I respond with a story. Penny Simkin, well known educator, writer, speaker, and editor, was called on the carpet by an anesthesiologist, irate that she had written a handout listing the potential trade-offs of epidural anesthesia when she was not a doctor (although he did not dispute her accuracy). "What are your credentials?" he demanded. "I can read," was her reply. So can I. For that matter, you can too.

I will place emphasis, and you can see it the categories below, on references. Those articles not included will either be posted in an 'extended post' in the order they are received or I'll pass them on to the next host. Here are the categories and what I'm looking for in each:

Case Studies - pictures and studies highly desired. Presentation, evaluation (history and physical, labs, differential diagnosis, etc), treatment, follow-up. These most often come from docs and nurses (Clinical Cases and Pulmonary Roundtable come to mind), but anybody can write one. They may be from your own experience, or that of a relative or friend. Do, however, make sure you protect the privacy of others. Some statement of consent or anonymization should be made "Some names have been changed..."

Articles in Brief - Summary of one original article from a journal cataloged by PubMed. Only that article must be cited, but supporting background and evidence is encouraged. Author should take a position on the article's quality and suggest how their position could be applied by patients, providers, or both. Statements presented as fact should be supported with a citation or link unless it is common knowledge. Article should be from the past six months. Extra consideration to write-ups that include abundant links to Wikipedia.

Interviews - Gotta favorite doc? Nurse? Physical therapist? Are you a medical student and your attending 'wrote the book'? Do you have a patient who learned the trumpet from Louis Armstrong? Was a coworker an Olympic competitor? Ask them for an hour, ask some questions, and write up what you learn. In our age of burning helicopter props and storyboard civilizations, this may be the only way we will find out about the great people who walk amongst us. You're notes and recording of your interviews constitute primary historical sources.

Ethics - Must address a topic of bioethics or general ethics in health care, take a position, and address how at least two cases have been resolved in the past. Cases may be personal, drawn from the legal literature, or anything in between.

Encounters - Patients, nurses, physicians, therapists, techs, administrators, business people, researchers, their encounters with each other, their selves, and the world. No need for references here. Quality of writing, from punctuation to poignancy, will play heavily.

Complementary and Alternative Medicine - Brief reviews of over-the-counter supplements, devices, off-label uses currently making the rounds, diets, etc, somewhat like Medline Plus or The Medical Letter. Author must take a position, not necessarily the consensus position, and address and rebut one or more alternate viewpoints. Must link to current FDA findings (example), specialty guidelines, primary sources via PubMed, or some equivalent authorities. Again, abundant links to Wikipedia are encouraged.

Announcements - DVT Awareness month? Donations sought? Position to fill? The anesthesiologists are going on strike? If it's happening on or after June 13th, let me know. I'm not going to count these as part of the thirty.

Other topics I'll consider but may pass on to the next host:

Book Reviews - Must address the nature of the work — collected essays, position piece, memoir, biography, fiction, et cetera. Should introduce a few to several vignettes or issues raised in the work, then evaluate the quality of writing and consider alternate viewpoints for each.

Business and Politics - Any issue, from a personal experience with billing, novel IT solutions, to national or international concerns are welcome. At least two pertinent cases should be described, including how they were resolved. Cases may range from the personal to major historical outcomes, but should describe them, including resolution.

Original works of poetry, music, spoken word, film, video, photography, litho, electron micrograph, painting, or other visual art. Seriously, I would love to lead the issue with some original art.

Anything I haven't thought of...

Admin

• submissions are due by 6 PM EST Monday night 6/12.

• Grand Rounds will posted on Tuesday 6/13 at 7 AM.

• Send the link to your post and tell me, if I don't put your post in the main event, would you rather have it forwarded to the next week's host or have me put it in an 'extended' entry on a first-come, first-serve basis?

• No word limit: War and Peace, haiku, or anything in between.

• Posts should be written for a general audience. I firmly believe the average newspaper reader can grasp lipid solubility in the duodenal unstirred water layer, but I will be checking for Latin, Greek, and passive voice.

If my method creates a certain degree of tension, well, perhaps that's not so bad.