Monday, July 30, 2012

Crime Fiction Masters: Ian Rankin

Ian Rankin, OBE, DL (born 1960) is a Scottish crime writer. His best known books are the Inspector Rebus novels. He has also written several pieces of literary criticism.

Born 28 April 1960 in Cardenden, Fife, Rankin attended Beath High School, Cowdenbeath. After graduating from the University of Edinburgh, he moved to Tottenham, London for four years and then rural France for six while he developed his career as a novelist. He was a literature tutor at the University of Edinburgh, where he retains an involvement with the James Tait Black Memorial Prize.

Before becoming a full-time novelist he worked as a grape-picker, swineherd, taxman, alcohol researcher, hi-fi journalist, college secretary and punk musician.

Rankin did not set out to be a crime writer. He thought his first novels Knots and Crosses and Hide and Seek were mainstream books, more in keeping with the Scottish traditions of Robert Louis Stevenson and even Muriel Spark (the subject of Rankin's uncompleted Ph.D. thesis).

He was disconcerted by their classification as genre fiction. Scottish novelist Allan Massie, who tutored Rankin while Massie was writer-in-residence at the University of Edinburgh, reassured him by saying, who would want to be a dry academic writer when "they could be John Buchan?"

Rankin's Inspector Rebus novels are set mainly in Edinburgh. They are considered major contributions to the Tartan Noir genre. Ten of the novels were adapted as a television series on ITV, starring John Hannah as Rebus in Series 1 and 2, with Ken Stott taking on the role for Series 3-5.

In 2009, Rankin donated the short story "Fieldwork" to Oxfam's Ox-Tales project, four collections of UK stories written by 38 authors. Rankin's story was published in the Earth collection.

In 2009 Rankin stated on Radio Five Live that he would start work on a five or six-issue run on the comic book Hellblazer, although he may turn the story into a stand-alone graphic novel instead. The Vertigo Comics panel at WonderCon 2009 confirmed that the story would be published as a graphic novel called Dark Entries, the second release from the company's new Vertigo Crime imprint.

He is a regular contributor to the BBC Two arts programme Newsnight Review. His 3-part documentary series on the subject of evil was broadcast on Channel 4 in December 2002. In 2005 he presented a 30-minute documentary on BBC Four called Rankin on the Staircase, in which he investigated the relationship between real-life cases and crime fiction. It was loosely based on the Michael Peterson murder case, as covered in Jean-Xavier Lestrade's documentary series Death on the Staircase. The same year he collaborated with folk musician Jackie Leven on the album Jackie Leven Said.

In 2007, Rankin appeared in programmes for BBC Four exploring the origins of his alter-ego character, John Rebus. Titled "Ian Rankin's Hidden Edinburgh" and "Ian Rankin Investigates Dr Jekyll and Mr Hyde," Rankin looks at the origins of the character and the events that led to his creation.

In the TV show Anthony Bourdain: No Reservations, he takes a trip through Edinburgh with writer/cook Anthony Bourdain.

He lives in Edinburgh with his wife Miranda and their two sons Jack and Kit.

Awards and honours

Elected Hawthornden Fellow
Won the Chandler-Fulbright Award.
Two Crime Writers' Association (CWA) Dagger prizes for short stories
1997 the CWA Macallan Gold Dagger for Fiction for Black and Blue (which was also short-listed for the Mystery Writers of America Edgar Award for best novel).
2002, made an Officer of the Order of the British Empire in the Golden Jubilee Queen's Birthday Honours for services to literature.
2004, Edgar Award for Resurrection Men.
2005, CWA Cartier Diamond Dagger to mark a lifetime's achievement in crime writing.
2008, ITV3 Crime Thriller Award for Author of the Year, for Exit Music.
He has honorary doctorates from the University of Edinburgh, the University of Abertay Dundee, the University of St Andrews and, in 2005, from the University of Hull.

Rankin's novel Exit Music was shortlisted for Theakston’s Old Peculiar Crime Novel of the Year Award 2009.

To date he has written at least 25 novels, two short story collections, one Original Graphic Novel and a non-fiction book. He has also written an entry in Quick Reads 2009.

1986 The Flood 
1987 Knots and Crosses - first Inspector Rebus novel
1988 Watchman 
1990 Westwind 
1991 Hide and Seek second Inspector Rebus novel
1992 Tooth and Nail third Inspector Rebus novel
Strip Jack 4th Inspector Rebus novel
A Good Hanging and Other Stories Short Stories
1993 Witch Hunt (writing as Jack Harvey)
The Black Book 5th Inspector Rebus novel
1994 Bleeding Hearts (writing as Jack Harvey)
Mortal Causes 6th Inspector Rebus novel
1995 Blood Hunt (writing as Jack Harvey)
Let it Bleed 7th Inspector Rebus novel
1997 Black and Blue 8th Inspector Rebus novel
(won Macallan Gold Dagger for Fiction)
1998 The Hanging Garden 9th Inspector Rebus novel
1999 Dead Souls 10th Inspector Rebus novel
2000 Set in Darkness 11th Inspector Rebus novel
2001 The Falls 12th Inspector Rebus novel
2002 Resurrection Men 13th Inspector Rebus novel
(won The Edgar Award )
Beggars Banquet Short Stories
2003 A Question of Blood 14th Inspector Rebus novel
2004 Fleshmarket Close 15th Inspector Rebus novel
2005 Rebus's Scotland: A Personal Journey (Non-Fiction) Awarded CWA Cartier Diamond Dagger
2006 The Naming of the Dead 16th Inspector Rebus novel
2007 Exit Music 17th Inspector Rebus novel
(won ITV3 Crime Thriller Award)

2008 Doors Open 
2009 A Cool Head Quick Reads 2009

The Complaints First Malcolm Fox novel
Dark Entries Vertigo Crime featuring John Constantine (Hellblazer)
2011 The Impossible Dead second Malcolm Fox novel
2012 Standing in Another Man's Grave 18th Inspector Rebus and third Malcolm Fox novel

DVD: The Mentalist

I may have mentioned before that I don't watch broadcat TV or cable. I limit myself to DVDs and Netflix rentals (the two-a-month plan). This is how I end up "behind the curve" on TV series and movies. While in the big box discount store, I spied a show that I'd never seen, and it seemed like something I might enjoy. Since it was listed at such a reasonable retail price, I took a flyer, and bought a season for a trial run. It turns out, I enjoy the series very much, and so I shelled out for two more seasons. The cast is very attractive, and I enjoy the characters as written. I'm sure many of you know about it already, but in case you don't, give it a go.

After a prolific serial killer named Red John kills his wife and daughter, Patrick Jane (Simon Baker) gives up his prosperous life as a phony psychic and uses his staggering powers of observation to aid the California Bureau of Investigation. Although Jane's eccentric methods annoy skeptical agent Teresa Lisbon (Robin Tunney), they get results, enabling Lisbon's team to apprehend even the most cunning and cold-blooded of criminals.

Simon Baker (in his first Emmy-nominated role) stars as Patrick Jane, a rogue detective and case-cracking consultant for the California Bureau of Investigation -- a far cry from his last gig as a semi-famous "psychic medium" with no paranormal abilities. Despite his bogus past, Patrick's charm and powers of observation endear him to the CBI team -- except for Senior Agent Teresa Lisbon (Robin Tunney), who doesn't care for his antics. Tim Kang and Amanda Righetti also star.

OCD and D-cycloserine: A Promising Medication for OCD Treatment

by Steven J. Seay, Ph.D., August 25, 2011

OCD D-cycloserine 

"OCD, I'd like you to meet my friend, D-cycloserine. D-cycloserine, this is OCD. I think you two should get to know each other a little better. You just might have a future together..."

As someone who has long been enamored with basic science, I find it fascinating when classic medications are re-purposed in surprising ways.  One of the newest examples of this is the use of D-cycloserine (also known as Seromycin) in the treatment of obsessive-compulsive disorder (OCD). What’s interesting about D-cycloserine is not so much what it is…but what it isn’t:
  • D-cycloserine is neither an SRRI nor any other type of antidepressant (e.g., Prozac).
  • It’s not an anti-anxiety medication (e.g., Xanax, Klonopin).
  • It’s not even an atypical antipsychotic (e.g., Abilify, Risperdal).
If it’s not one of the above, then what is it?

The answer might surprise you.  Seromycin is actually an antibiotic that was originally developed to help fight off tuberculosis.  What’s exciting about using an antibiotic to treat OCD is that it’s not subject to the same side effects as other medications (i.e., the SSRIs, anxiolytics, or antipsychotics).  In fact, most clinical studies have found few, if any, significant side effects when using D-cycloserine in OCD treatment.

Before I go further, there’s an important caveat to keep in mind:

Research on D-cycloserine in OCD treatment is still a work-in-progress, so it’s important to maintain some healthy skepticism on this issue.

Research studies looking at using D-cycloserine to treat OCD have been fairly limited, and the results of these studies have been mixed.  Some studies have suggested that the medication has small or non-significant effects, whereas other studies have found the medication to be beneficial.  Several recent, placebo-controlled studies have been quite promising and have indicated that taking seromycin can initially “speed up” the therapeutic response to exposure and response prevention therapy (ERP), a form of cognitive behavioral therapy (CBT) developed to treat OCD.  In essence, you benefit more from initial ERP therapy sessions.  D-cycloserine doesn’t appear to have any effects on OCD when taken on its own (i.e., when not combined with exposure and response prevention).  Read more about how ERP is thought to work.

It’s important to note that D-cycloserine doesn’t appear to offer any long-term benefits above and beyond what you would get from ERP alone.  In the end, you’re likely to achieve the same amount of symptomatic improvement whether or not you take the medication.  However, the research indicates that you’re likely to get more “bang for your buck” if you’re taking Seromycin during early exposure sessions.  This is important, because it reduces early treatment frustration and drop out.

How does D-cycloserine work?  Does the fact that it is an antibiotic mean that OCD is caused by bacteria?

No.  Like most medications, D-cycloserine is a complicated chemical that has many different biological effects.  It is not D-cycloserine’s antibiotic properties that are thought to make it useful in OCD treatment, but rather how this medication works on certain neurotransmitter receptors in the amygdala (a part of your brain that is associated with emotions like fear).

Without getting too technical, D-cycloserine is thought to affect certain amygdala receptors (i.e., NMDA receptors) that are associated with learning and memory.  Researchers theorize that action at these receptors facilitates learning/fear extinction, which is why the medication can apparently augment learning-based treatments like ERP. On a related note, feel free to read my short blog post on whether or not ERP works via learning or unlearning.
Can D-cycloserine be used to treat other anxiety disorders? 

Yes.  Research indicates that behavioral treatment of other anxiety disorders (panic, phobias, and the like) may also be enhanced by the addition of D-cycloserine.  Again, overall symptom reduction may be the same whether or not the medication is used; however, the addition of seromycin may help individuals benefit more from early exposure sessions.

You can also access some of the original research about D-cycloserine at the links below:
Some Effects Found:
  • D-Cycloserine Augmented Exposure Therapy for Obsessive-Compulsive Disorder (abstract only)
  • A Meta-Analysis of D-Cycloserine and the Facilitation of Fear Extinction and Exposure Therapy (full-text)
  • Augmentation of Behavior Therapy With D-Cycloserine for Obsessive-Compulsive Disorder (full-text)
No Effects Found:
  • D-cycloserine does not enhance exposure-response prevention therapy in obsessive-compulsive disorder (abstract only)

Anxiety: Face Your Fears: Extinction through CBT

Some of the best ways to treat anxiety disorders are through the processes of desensitization, exposure response prevention (ERP), and fear extinction. It seems that those with high levels of anxiety may suffer a super-sensitive "fear circuit," that stores and recalls emotionally-charged learned memories much more quickly and strongly than neurotypicals.

Cognitive Behavioral Therapy (or CBT) retrains the arousal system and "overwrites" the phobias or triggers until at last the mind relents, and accepts that the feared situations are not so threatening. The mind is basically sending out a "Chicken Little"-styled false alarm. However, although desensitized, the fearful memories remain encoded in the brain, and under stress and certain conditions, a person may experience a relapse or resurgance. Then it's time to pick yourself up, dust yourself off, and go back to the same technique.

Avoidance is the worst response, because the fears can grow, and become debilitating.

From yee Wiki:

Extinction is the conditioning phenomenon in which a previously learned response to a cue is eliminated when the cue is presented in the absence of the previously paired aversive (unpleasant) or appetitive (pleasant) stimulus.

Fear conditioning

Extinction is typically studied within the Pavlovian fear conditioning framework in which extinction refers to the reduction in a conditioned response (CR; e.g., fear response/freezing) when a conditioned stimulus (CS; e.g., neutral stimulus/light or tone) is repeatedly presented in the absence of the unconditioned stimulus (US; e.g., foot shock/loud noise) with which it has been previously paired.

The simplest explanation of extinction is that as the CS is presented without the aversive US, the animal gradually "unlearns" the CS–US association which is known as the associative loss theory. However, this explanation is complicated by observations where there is some fear restoration, such as reinstatement (restoration of CR in the context where extinction training occurred but not a different context after aversive US is presented again), renewal (restoration of CR in context A but not in B when learning occurred in context A and extinction in context B), and spontaneous recovery (restoration of CR when the retention test occurs after a long but not a short delay after extinction training) and alternative explanations have been offered.

Research on fear extinction in animal models (typically rats) has clinical implications such as exposure-based therapies for the treatment of phobias and anxiety conditions.


The dominant account of extinction involves associative models. However, there is debate over whether extinction involves simply "unlearning" the US–CS association (e.g., the Rescorla–Wagner account) or, alternatively, a "new learning" of an inhibitory association that masks the original excitatory association (e.g., Konorski, Pearce and Hall account). A third account concerns non-associative mechanisms such as habituation, modulation and response fatigue. Myers and Davis laboratory work with fear extinction in rodents has suggested that multiple mechanisms may be at work depending on the timing and circumstances in which the extinction occurs.

Given the ompeting views and difficult observations for the various accounts researchers have turned to investigations at the cellular level (most often in rodents) to tease apart the specific brain mechanisms of extinction, in particular the role of the brain structures (amygdala, hippocampus, the prefontal cortex), and specific neurotransmitter systems (e.g., GABA, NMDA). A recent study in rodents by Amano, Unal and Paré published in Nature Neuroscience found that extinction is correlated with synaptic inhibition in the fear output neurons of the central amygdala that project to the periaqueductal gray that controls freezing behavior. They infer that inhibition derives from the prefrontal cortex and suggest promising targets at the cellular level for new treatments of anxiety.

Operant conditioning

In the operant conditioning paradigm, extinction refers to the decline of an operant response when it is no longer reinforced in the presence of its discriminative stimulus. Extinction is observed after withholding of reinforcement for a previously reinforced behavior which decreases the future probability of that behavior. For example, a child who climbs under his desk, a response which has been reinforced by attention, is subsequently ignored until the attention-seeking behavior no longer occurs. In his autobiography, B.F. Skinner noted how he accidentally discovered the extinction of an operant response due to the malfunction of his laboratory equipment:

My first extinction curve showed up by accident. A rat was pressing the lever in an experiment on satiation when the pellet dispenser jammed. I was not there at the time, and when I returned I found a beautiful curve. The rat had gone on pressing although no pellets were received. ... The change was more orderly than the extinction of a salivary reflex in Pavlov's setting, and I was terribly excited. It was a Friday afternoon and there was no one in the laboratory who I could tell. All that weekend I crossed streets with particular care and avoided all unnecessary risks to protect my discovery from loss through my accidental death.
When the extinction of a response has occurred, the discriminative stimulus is then known as an extinction stimulus (SΔ or S-delta). When an S-delta is present, the reinforcing consequence which characteristically follows a behavior does not occur. This is the opposite of a discriminative stimulus which is a signal that reinforcement will occur. For instance, in an operant chamber, if food pellets are only delivered when a response is emitted in the presence of a green light, the green light is a discriminative stimulus. If when a red light is present food will not be delivered, then the red light is an extinction stimulus (food here is used as an example of a reinforcer).

Successful extinction procedures

In order for extinction to work effectively, it must be done consistently. Extinction is considered successful when responding in the presence of an extinction stimulus (a red light or a teacher not giving a bad student attention, for instance) is zero. When a behavior reappears again after it has gone through extinction, it is called resurgence.

Extinction burst

While extinction, when implemented consistently over time, results in the eventual decrease of the undesired behavior, in the short-term the subject might exhibit what is called an extinction burst. An extinction burst will often occur when the extinction procedure has just begun. This consists of a sudden and temporary increase in the response's frequency, followed by the eventual decline and extinction of the behavior targeted for elimination.

Take, as an example, a pigeon that has been reinforced to peck an electronic button. During its training history, every time the pigeon pecked the button, it will have received a small amount of bird seed as a reinforcer. So, whenever the bird is hungry, it will peck the button to receive food. However, if the button were to be turned off, the hungry pigeon will first try pecking the button just as it has in the past. When no food is forthcoming, the bird will likely try again ... and again, and again. After a period of frantic activity, in which their pecking behavior yields no result, the pigeon's pecking will decrease in frequency.

Although not explained by reinforcement theory, the extinction burst can be understood using control theory. In perceptual control theory, the degree of output involved in any action is proportional to the discrepancy between the reference value (desired rate of reward in the operant paradigm) and the current input. Thus, when reward is removed, the discrepancy increases, and the output is increased. In the long term, 'reorganisation', the learning algorithm of control theory, would adapt the control system such that output is reduced.

The evolutionary advantage of this extinction burst is clear. In a natural environment, an animal that persists in a learned behavior, despite not resulting in immediate reinforcement, might still have a chance of producing reinforcing consequences if the animal tries again. This animal would be at an advantage over another animal that gives up too easily.

Despite the name, however, not every explosive reaction to adverse stimuli subsides to extinction. Indeed a small minority of individuals persist in their reaction indefinitely.

Extinction-induced variability

Extinction-induced variability serves an adaptive role similar to the extinction burst. When extinction begins, subjects can exhibit variations in response topography (the movements involved in the response). Response topography is always somewhat variable due to differences in environment or idiosyncratic causes but normally a subject's history of reinforcement keeps slight variations stable by maintaining successful variations over less successful variations. Extinction can increase these variations significantly as the subject attempts to acquire the reinforcement that previous behaviors produced. If a person attempts to open a door by turning the knob, but is unsuccessful, they may next try jiggling the knob, pushing on the frame, knocking on the door or other behaviors to get the door to open. Extinction-induced variability can be used in shaping to reduce problematic behaviors by reinforcing desirable behaviors produced by extinction-induced variability.


D-Cycloserine (DCS) is being trialed as an adjuvant to conventional exposure-based treatments for anxiety disorders. The psychotropic responses are related to D-Cycloserine's action as a partial agonist of the neuronal NMDA receptor for glutamate and have been examined in implications with sensory-related fear extinction in the amygdala.

Here's a video link on exposure therapy, that Dr. R. shared with me when I started my CBT with him:

Sunday, July 29, 2012

Dave-o says, "Less brains, more bassets."

In case, you're wondering about my basset hound fixation -- we had a basset when I was a kid -- wee Angus. This isn't him though -- this is a "stunt basset" I found on the web. Bassets always bring a smile to my face. So here you go, Dave-o.

Hey!! Kids Comics: From Trash to Treasure

X-Men #1 Pacific Coast pedigree (Marvel, 1963) CGC NM/MT 9.8 White pages - $492,937.50

Heritage Auctions shattered its own comic art auction records again this Thursday-Saturday. There were 2,633 lots in the mamoth three-day auction, and they sold for a grand total of $10.463,000. All but two of the lots sold, a near-100% sell through with an average price realized of $3,876.81 per lot.

When I started collecting comics in 1962 at the age of eight (we lived outside of the USA before that), comics cost 12 cents. I missed out on the 10-cent years. I started reading the Walt Disney character based titles from Gold Key, then began collecting superheroes with The Justice League of America (starting with issue #25, 2/64), Batman (coincidentally, the first "New Look" issue, with issue #164, 6/64), Green Lantern (issue #30, 7/64), and The Flash (issue #151, 3/65).

My Marvel comics collection began with Avengers issue #6 (7/64), Daredevil issue #6 (2/65), and X-Men issue #4 (3/64). the Marvels, with their offbeat brand of heroic monsters, flawed heroes, and charismatic villains, were different that the other companies' stories. Even stranger were the oddball Charlton comics, which had a wonky appeal for me.

I grew up collecting in Anchorage, Alaska, from 1962-74, in school grades 1-12. Back then in Anchorage, there was no organized fandom, no used book stores with old comics, and no comic stores -- the only comic retailers were the spinner racks at the grocery stores and drug stores.

You basically had a one-two week window to acquire the lastest issues, and they hit the racks every Thursday. I usually had to haunt three or four stores in order to make sure I found every issue I needed to keep my "runs" intact. I mainly shopped at the Rexall drugstores, F. W. Woolwoth's and Carr's grocery stores (a local Alaskan chain).

I was a well-heeled collector, because my dad paid me (and Alf) an unheard of weekly allowance of $5.00. All we had to do to "earn" it was take out the garbage, shovel snow from the driveway and walks in the winters, and water/mow the grass in the summers. With such an magnificent endowment I could buy virtually every current comic or magazine I wanted, and still have money left over for candy and movies.

My brother collected stamps and built model kits, and he used to chide me about "wasting" my money on comics, which were mostly seen as disposable entertainment back then. You were supposed to read them and threw them away. Only a few kids saved them. "Yeah," I'd reply in justification, "but you can't read a stamp." I was way, way, way into the art and stories. Today as we can see, the comics from that era are quite valuable, while my brother's stamps, sadly, are virtually worthless. Only a few (ahem) visionaries saw it turning out this way.

As the weeks and months went by comic collection grew and grew. At first, I stored my prized Avengers issues in a large wooden cirgar box, then with the rest of the comics in the bottom shelf of my chest of drawers, and finally as a lopsided stacks in the closet. There were no comic bags, backing boards, or special boxes back then.

In later years, I stored them in large banker's document boxes or better yet, in a metal file cabinet. Back then those who read comics were regarded as dolts by the public at large, because "funnybooks" relied heavily on the visuals rather than text. Once again the comics defied popular perception. The comic fans would go on to become the scientific and financial nerds, geeks, and downright brainy folks of our time, much as the science fiction and pulp magazine fans had done in earlier years. In these early years comics were often lumped in as a lower order of s-f fandom, as the somewhat abused "red-headed stepchild."

One summer in the early sixties, mom finally laid down the law and commanded me to give my comic stash away, except for 100 issues. Naturally, I was torn about which ones to keep, and was haunted by loss. I felt I had made many ill-advised decisions, and so, her scheme backfired, inciting an even more unrelenting obsession to reacquire the "lost issues," and more. When comic books started to climb in value throughout the seventies (thanks in part to an offical price guide), I would constantly remind mom that I had owned many of those valuable treasures ($2-$35 each). She had long ago relented on the quota and let me amass a huge collection. Dad hated the "clutter", and would often make a snide comment or two. Still, I was allowed to keep them all.

Collecting comics was very uncool in those years, and as boys aged, they often "outgrew" their comics. Once alerted, I could swoop in and buy their entire cache for $10-$20. I'd rush home with paper grocery bags filled to the top, overjoyed, and would fill in missing issues in my runs thanks to thes "super-scores."

I didn't attend my first comic convention until I was 18, when mom and I traveled to New York City just so I could attend the 1974 Comic Art Convention put on by Phil Seuling. I had a blast, and bought a marred copy of Daredevil #1 at the show for $6.

The most I've ever paid for any single comic book issue was $75.00 (I actually paid that much for three different issues -- an Incredible Hulk #1, a Tales of Suspense #39, and a Fantastic Four #2 from the personal collection of Jack Kirby). My "magic number" for pulling the trigger on a purcahse was $6, though I would sometimes pay as much as $20-$50 for certain prized issues (like Batman #4, #5, and #10).

Original comic book art was scarce in the market place in these early years. I moved to Dallas in 1974 to attend SMU, but even in the much bigger fan mecca of Dallas, I seldom saw art for sale. My first art purchase was consumated at my first San Diego Comic Con in 1991. I bought a complete six-page Alex Toth Standard Comics romance yarn for $500. Toth was my favorite artist back then. After I bought that art I was hooked. To use a metaphor, if comics were as enjoyable and addictive as cocaine, then original art was a crack-cocaine'like rush (only not as cheap).

I started collecting comic art via phone calls to other collectors, Buyer's Guide ads, and San Diego conventions. In the early days of eBay, I started selling some of my art and comics to get the cash for new acquisitions, and being local lad, I landed my job as an art/expert cataloger at Heritage Auctions. Jim Halperin liked the writing of my eBay ads and contacted me personally via email.

As much as I have always loved and treasured comics, the prices now being realized for many of these lots blow me away. A copy of the X-Men #1 comic book from 1963 (said to be in the best condition known) sold for $492,000 and change. Todd McFarlane's 1990 original cover art for The Amazing Spider-Man #328 sold for $657,250. That was the year I started collecting art. These are relatively recent collectibles, not even hailing from the truly scarce Golden Age era. It seems that the world has been turned on its ear, and all those years and quarters I "wasted" honing my expertise in comic art have paid off big time.

An old school "spinner rack."

Saturday, July 28, 2012

The Clash: Tommy Gun, 1978

Joe Strummer (1952-2002).

Allostatic load

Bruce McEwen.
From Wiki:

The term allostatic load, coined by McEwen and Stellar in 1993, is defined as the physiological consequences of chronic exposure to fluctuating or heightened neural or neuroendocrine response that results from repeated or chronic stress.

It is used to explain how frequent activation of the body's stress response, essential for managing acute threats, can in fact damage the body in the long run. Allostatic load is generally measured through a composite index of indicators of cumulative strain on several organs and tissues, but especially on the cardiovascular system.

The hormones and other physiological agents that mediate the effects of stress on the body have protective and adaptive benefits in the short run and yet can accelerate pathophysiology when they are over-produced or mismanaged; this kind of stress can cause hypertension and lead to heart disease. Constant or even irregular exposure to these hormones can eventually induce illnesses and weaken the body's immune system.

Adaptation in the face of stressful situations and stimuli involves activation of neural, neuroendocrine and neuroendocrine-immune mechanisms. This adaptation has been called "allostasis" or "maintaining stability through change", which is an essential component of maintaining homeostasis. The main hormonal mediators of the stress response, cortisol and epinephrine (adrenaline), have both protective and damaging effects on the body.

In the short run, they are essential for adaptation, maintenance of homeostasis, and survival “allostasis”. Yet, over longer time intervals, when called upon frequently, the resulting “allostatic load” exacts a cost that can accelerate disease processes. Allostatic load can be measured in physiological systems as chemical imbalances in autonomic nervous system, central nervous system, neuroendocrine, and immune system activity as well as perturbations in the diurnal rhythms, and, in some cases, plasticity changes to brain structures.

Four conditions that lead to allostatic load are:

Repeated frequency of stress responses to multiple novel stressors;
Failure to habituate to repeated stressors of the same kind;
Failure to turn off each stress response in a timely manner due to delayed shut down; and
Inadequate response that leads to compensatory hyperactivity of other mediators.
The effects of these forms of dysfunctional allostasis cause allostatic load and this, over time, leads to diseases. Allostatic load effects can be measured in the body. When tabulated in the form of allostatic load indices using sophisticated analytical methods, it gives an indication of cumulative lifetime effects of all types of stress on the body.

Brain Rules has the most succinct, clear-cut description of the harmful effects of chronic stress that I've read. I've decided that chronic stress will be the next focal point of my research. I'm particulary interesting in moderating/reducing the cortisol levels in my own system.

To start with, I found a book which I'll rush to the top of the to-read pile. It a great overview at a browse, even though the title is almost certainly pure hype -- unless by that, they simply mean that McEwen has redefined toxic chronic stress as allostatic load.

From Amazon: The End of Stress As We Know It by Bruce McEwen

"There's a whole new way to think about stress. Sure, some stress is inevitable, but being 'stressed out' isn't. In fact, we can learn to rechannel the powerful stress activators in our lives to make us even more effective. "Hamlet" spoke of 'suffering the slings and arrows of outrageous fortune.' These days we simply use the word 'stress' to describe that feeling. And if you ask ten random people if they feel stressed, chances are that at least nine will reply with a resounding, 'Yes!'

Indeed, the very way we use the word implies that we are its victims - as in, 'I'm under so much stress' or 'I'm completely stressed out.' There's now a better way to look at this picture, a way to move from victim to victor.

The first step is to look to the science behind it all because in the science lies a whole new message about stress. Science allows us to understand what the stress response is and why our bodies react the way they do. Like all living creatures, we're mapped to respond instinctually in certain ways, and generally for good reasons. We know, for example, that in times of emergency, we effortlessly shift into a different biological mode. Based on our perception of the crisis, our brains initiate the 'stress response' or the 'flight-or-fight reaction. ' Our attention becomes keenly focused. Our heart and lungs accelerate to ready us for action. Our glands mobilize extra energy resources and summon the immune system to battle stations. This whole process is Nature's way of empowering us to respond swiftly, sometimes dramatically, to sudden events, while remaining mentally alert and physically prepared to meet a challenge. 

But what if the crisis situation does not present us with a foe to be fought? Or if fleeing is not the answer? Too often in modern times, the situations that bring on the stress response require neither the fight nor flight response for which our bodies are genetically programmed. The stress response is nevertheless likely to kick in - just as it's programmed to do - even though it cannot help speed us toward a resolution. Deprived of its natural successful result, the very system that's designed to protect us begins to cause wear and tear on our bodies - actually bringing on illnesses as diverse and severe as asthma, diabetes, heart disease, ulcers, and increased susceptibility to colds and infections.

The good news is that there are definite things that we can do to prevent this process from ultimately taking this wrong turn. New research in brain functioning allows us to understand the reactions our bodies have to various stressful circumstances.That knowledge is power - the power to harness the energy stored within us and to channel it in positive ways. "The End of Stress as We Know It" leads us to a new appreciation of the mind - body connection so that we learn how to reduce stress and increase our overall sense of health and well-being-and even turn aside the slings and arrows of life."

Thursday, July 26, 2012

Todd McFarlane The Amazing Spider-Man #328 Cover (1990)

New world record for a comic book cover -- $657,250.00

Dell Map Back Bookshelf

Mr. Door Tree's Dell Map Back bookshelf

Thrilling Detective Web Site Link

For all things Private Eye:

An Interview with Stafford Lightman, Endocrinologist, Bristol University, England

Q:  What are the origins of the stress response?

A:  Stress is an extremely important protective mechanism for human beings, and in fact for all animals, because if you're being chased by a lion it's important to get away. In order to get away you need to give as much oxygen and as much sugar to your muscles to make them work as fast as they can, so your blood flow needs to go faster. When you're being frightened, your brain detects the danger, it sends signals down your spinal cord to your adrenal medulla to release adrenaline. The adrenaline increases the amount of sugar in your blood and increases your heart rate, and this helps your efficiency of getting away from the lion. Your brain also sends signals down to the pituitary gland, which releases another hormone which acts on the outside of the adrenal, the adrenal cortex, and that releases cortisol. Cortisol is also very important in keeping your blood sugar up, keeping your blood pressure up, and helping allow the body to have maximal exertion to get away from danger.

Q:  What happens to the body as a result of the stress response in the brain?

A:  One of the fascinating things that happens is [that] the body is being prepared only to use its really essential functions, so the muscles work well, the liver releases more sugar, for energy, but things are actually being turned off as well. Although the heart rate is going up and more blood is going round the body, parts of the body which aren't needed urgently are being turned off. The blood supply to the gut and areas like this is actually decreased, so your digestion diminishes—you don't need digestion when you're running away from a lion—obviously your sexual function is turned off, and a lot of the non-essential activities of the body just decrease so that you preserve the really essential ones to get away from the dangerous situation.

In a modern situation we don't have these same sorts of dangerous problems, but what we have are other very stressful situations. And the interesting thing, of course, is that your blood sugar goes up, your heart rate goes up and your blood pressure goes up, but you're not utilizing all of this, you're not running away, you're not having energy, so all of these hormonal responses are happening, but they're actually not being used.

Q:  When does the stress response become dangerous?

A:  The important thing about the stress response is it's adapted for short-term responses. It becomes dangerous when you get multiple stress responses, one after the other, or experience chronic stress that goes on for weeks or years. When that happens your levels of cortisol can be raised for very prolonged periods of time, and it can have lots of nasty effects on the body. It can damp down your immune system, for instance, so that you can't respond to diseases as well as you should. It can also have effects on the brain, actually decreasing the number of brain cells in certain parts of the brain and decreasing your memory. It also can affect your blood pressure, and it can affect the fats in the blood and make it more likely for you to have heart attacks and strokes. So when you have chronic stress, that's when stress becomes dangerous.

Q:  Can caring for people with chronic illnesses actually lead to illnesses in caregivers?

A:  There's been quite a lot of interest recently about what chronic stress can do to cause disease. We did a study on caregivers of patients with Alzheimer's disease…We've looked at their hormones and we find that their cortisol is indeed raised, so they have a hormonal stress response which is prolonged for a very long period of time. We've also looked at their immune function by giving them influenza vaccination, which is routinely given to elderly people, and we've found that their antibody response to the influenza vaccination is much poorer than equivalent people of the same age who aren't caring for a loved one with Alzheimer's or some other disease.

So it's clear that chronic stress does damp down the immune system. And other people have also shown that chronic stress can decrease your ability to heal wounds, so that if you've got small wounds they just don't heal as well. The body just doesn't function quite as well when you have large, high levels of cortisol circulating through it for long periods of time.

Q:  Has stress been linked to depression and other mental illnesses?

A:  It's quite clear that chronic stress is related with depression. Depression is a very major common disease in our society, and it is undoubtedly related to the chronic stress that we have in our society.

The ability of stress to cause depression as well as other problems like heart disease and high blood pressure are connected in an interesting way. [Patients who are depressed after a] heart attack are much more likely to die within the next few years than people who've had heart attacks and who aren't depressed. So again this depression, which is related to chronic stress, actually has a major effect on life expectancy.

Q:  Might there someday be a pill to reduce the effects of stress?

A:  We are involved in an intensive program to develop an anti-stress pill, and the only way we can do this really is to try and block the beginning of the pathway in the brain that causes the response to stress. And this happens at the hypothalamus, which makes a hormone called CRH. We're making a pill that blocks the effect of CRH, and therefore blocks all of the effects of stress on the body, including the effects of stress in causing an increase in cortisol. We're not designing a drug to give to everybody who's stressed. But this can be very important and hopefully should actually be an extremely useful treatment for … depression that's associated with severe stress.

The Lifetime Effects of Stress: Cortisol Pulses

Professor Stafford Lightman and his team in the Laboratories for Integrative Neuroscience and Endocrinology are interested in how stress impacts upon human health throughout the lifespan – just how does it affect your body and the way it responds to disease?

Stress-related disease is a rapidly increasing feature of our society, but the mechanisms through which stress causes disease are poorly understood. It is an area of research that fascinates Stafford Lightman, who has been working on finding answers to some of these questions for many years. Recently he has been able to demonstrate that events that happen to you around the time of your birth, or even before you are born, can have epigenetic effects on your later life.

What that means is that while such events do not actually affect the genes themselves they can affect the way your genes function. So if you had a very stressful childhood, this can have long-lasting influences throughout the whole of your life.

Lightman has looked at these effects in rodents and has seen that if rats are stressed early on in their lives, this can change the way they produce their stress hormones throughout the rest of their lives. For example, if a mother rat neglects her pups, when those pups become adults and are examined to see how they respond to stress they have a much stronger response than pups that had caring mothers. In adult rats the levels of the stress hormone corticosterone in those stressed as pups goes much higher during a stressful event and lasts much longer than in rats that were well looked after as pups.

In humans the situation is much the same. If adult stress is superimposed on a stressful childhood, that combination not only means that are you more susceptible to stress in later life, but also that when you encounter a stressful situation your stress hormones – called cortisol in humans – dramatically increase. If these hormone levels are raised chronically for a long period of time, they can cause problems with the whole range of biochemical processes that occur within us and we become more susceptible to diseases such as depression, diabetes and hypertension, and also to memory loss. High levels of cortisol cause shrinkage of the hippocampus which can lead to poor memory function.

If stress hormone levels are raised for long periods we become more susceptible to diseases such as depression, diabetes and hypertension

Having established that stress hormones can have such effects, Lightman naturally asked the question – how does it happen? What he found was extremely interesting. It seems that cortisol is secreted in a circadian rhythm, which means that it has a peak level early in the morning and then decreases throughout the rest of the day. In humans, this peak occurs just before we wake up; cortisol is thus labelled as an ‘anticipatory hormone’ because it goes up in anticipation of what our body will need during the day. Since cortisol and corticosterone act on the liver to release glucose, this morning peak ensures that we have enough sugar in our blood to provide sufficient energy for us to function properly during the day. One fascinating outcome from Lightman’s studies is the fact that the circadian rhythm of cortisol and corticosterone is made up of multiple pulses that occur roughly every hour, so in fact hormone levels are going up and down all the time, especially in the morning in humans when cortisol levels are really high and the pulses are very big.

The relevance of these pulses is that they allow the body’s tissues to respond not just to the level of the hormones, but also to the frequency with which the hormone pulses occur. In fact, it is the basis of a digital signalling system. In arthritis, for example, the frequency of these pulses is doubled, allowing our natural hormones to moderate the disease process. Also, in patients with obstructive sleep apnea – an unpleasant condition in which people stop breathing for periods of a few seconds several times every night whilst they are asleep – the size of each individual cortisol pulse is markedly increased. This may well be one of the reasons why these patients develop high blood pressure, heart disease, diabetes and other stress-related disorders. Indeed, it is clear that in different physiological or pathological conditions not only do levels of hormones change but the frequency and pattern of their pulses change as well.

The next step for Lightman and his team was to look at the molecular biology of these pulses to try to understand what was going on at the cellular level. What they revealed is that every single pulse of corticosterone in rats is associated with a pulse of corticosterone receptors charging into the nucleus of the cell, binding on to DNA and making messenger RNA. Almost all cells in the body have these receptors which can be thought of as the ‘lock’ in a cell that is activated by the hormonal ‘key’ of corticosterone.  The messenger RNA that is made in response to these pulses is the signal for the production of new proteins by the cell and thus is vital for normal cellular function.

The circadian rhythm of cortisol and corticosterone is made up of multiple pulses that occur roughly every hour

The other important discovery was that different tissues in the body experience these pulses in different ways. The liver, for example, is extremely sensitive to pulses and so immediately responds to every individual pulse. Some parts of the brain, however, need two or three pulses before a response is generated. This is useful, as in a stressful situation you need your blood sugar levels to rise very quickly, while the brain may need more time for preparation before it wakes up. This research area is still in its infancy and its implications are not yet fully understood. However, what Lightman’s group does know is that these fluctuations or oscillations of hormones, which are going on all the time, allow us to have a system that reacts extremely fast in stressful situations. When confronted with a lion, for example, you want to have a really massive hormone response so that your brain focuses on how to escape and your blood sugar goes up so you have the energy to run away very fast.

But what does all this mean in today’s society where we are not often confronted by lions? “Now that we understand how these stress mechanisms work,” says Lightman, “we can begin to work out why some people appear to be at greater risk than others of getting diseases that are associated with stress. Furthermore, we will be much better positioned to design therapeutic ways of dealing with it. In the longer term we hope to be able to identify people who have had a particularly stressful childhood, for example, and provide them with advice that will protect them from developing the diseases to which they will be susceptible.” In the future, Lightman hopes to better understand what is called the epigenome – the way that past experiences have modified our cells, making us more vulnerable to certain diseases. “We will be able to look at people who, perhaps because of their childhood experiences, have had a change in their epigenome, which means that their genes respond more readily to stress, thereby putting them at more risk of getting certain diseases. Whether or not it’s a good or a bad thing, of course, one can argue about, but I think it will happen in the not-too-distant future. So personalised medicine won’t only be related to the genes you have – your genome – it will also be related to your epigenome.” Despite these fascinating results, there is still a great deal of work to be done investigating whether or not stress is a risk factor for all kinds of diseases. While we know, for instance, that there is a good correlation between being depressed and having a heart attack, we don’t know what mediates that. “Is it because the individual has a cortisol abnormality?” asks Lightman. “We know that people who are depressed have abnormal cortisol secretion. Is that the link?” Clearly the answer to these questions with regard to specific individuals would be extremely valuable.

To help further this work, Lightman and his team were thrilled to discover recently they had won a grant of £1.7 million from the Wellcome Trust. They will use these funds to look at how different patterns of stress hormones can affect genes in the brain and the liver, as well as how these patterns affect memory and the development of diseases such as diabetes. Undoubtedly they will have more answers in a few years’ time.

Smirk-Free Living

 "Hello all you happy people ... you know what? I'm the hero." -- Droopy Dog, Dumb-Hounded, 1943

Jimmy Smith Trio Organ Grinder's Swing 1969

Hammond B3 innovator Jimmy Smith.

Lonnie Mack and Stevie Ray Vaughan Live 1986


John Medina's Brain Rules #8: Stress -Video

... And here's some information on Learned Helplessness cribbed from the You Are Not So Smart website:

The Misconception: If you are in a bad situation, you will do whatever you can do to escape it.

The Truth: If you feel like you aren’t in control of your destiny, you will give up and accept whatever situation you are in.

In 1965, a scientist named Martin Seligman started shocking dogs.

He was trying to expand on the research of Pavlov – the guy who could make dogs salivate when they heard a bell ring. Seligman wanted to head in the other direction, and when he rang his bell instead of providing food he zapped them with electricity. To keep them still, he restrained them in a harness during the experiment.

After they were conditioned, he put these dogs in a big box with a little fence dividing it into two halves. They figured if they rang the bell, the dog would hop over the fence to escape, but it didn’t. It just sat there and braced itself. They decided to try shocking them after the bell. The dog still just sat there and took it. When they put a dog in the box which had never been shocked before and tried to zap it – it jumped the fence.

You are just like these dogs.
If, over the course of your life, you have experienced crushing defeat or pummeling abuse or loss of control, you learn over time there is no escape, and if escape is offered, you will not act – you become a nihilist who trusts futility above optimism.

Studies of the clinically depressed show that when they fail they often just give in to defeat and stop trying. The average person will look for external forces to blame when they fail the mid-term. They will say the professor is an asshole, or they didn’t get enough sleep. Depressed people will blame themselves and assume they are stupid.

Do you vote? If not, is it because you think it doesn’t matter because things never change, or politicians are evil on both sides, or one vote in several million doesn’t count? Yeah, that’s learned helplessness.

When battered women, or hostages, or abused children, or long-time prisoners refuse to escape, they do so because they have accepted the futility of the attempt. What does it matter? If those people do get out of their situation, they often have a hard time committing to anything which may lead to failure.

Any extended period of negative emotions can lead to you giving in to despair and accepting your fate. If you remain alone for a long time, you will decide loneliness is a fact of life and pass up opportunities to hang out with people. The loss of control in any situation will lead to this state. A study in 1976 by Langer and Rodin showed in nursing homes where conformity and passivity is encouraged and every whim is attended to, the health and well-being of the patients declines rapidly. If, instead, the people in these homes are given responsibilities and choices, they remain healthy and active. This research was repeated in prisons. Sure enough, just letting prisoners move furniture and control the television kept them from developing health problems and staging revolts. In homeless shelters where people can’t pick out their own beds or choose what to eat, the residents are less likely to try and get a job or find an apartment.

When you are able to succeed at easy tasks, hard tasks feel possible to accomplish. When you are unable to succeed at small tasks, everything seems harder.

Rats given the opportunity to escape electric shocks are half as likely to develop tumors than those who are forced to bear them. Rats already suffering from cancer will die faster if placed into the inescapable shock experiment.

Every day – your job, the government, your addiction, your depression, your money – you feel like you can’t control the forces affecting your fate. So, you stage microrevolts. You customize your ringtone, you paint your room, you collect stamps. You choose.

Choices, even small ones, can hold back the crushing weight of helplessness, but you can’t stop there. You must fight back your behavior and learn to fail with pride. Failing often is the only way to ever get the things you want out of life. Besides death, your destiny is not inescapable.

You are not so smart, but you are smarter than dogs and rats. Don’t give in yet.

The book that started the study of learned helplessness. I have a copy, but it's a bit of a technical read. You can learn about the concept in other books.

Wednesday, July 25, 2012

Noise -- I Can't Stand Noise!

I find I'm relating to this bear more and more as I age. So, just for laughs, here's Tex Avery's classic Rock-A-Bye Bear, MGM, 1952. Click the link below:

Noise -- I can't stand noise!

Bad Ads #3: Jazz Wad Is ALWAYS Fun

Double entendre has its charms for any demented cartoonist, I suppose. It's a tip of the hat to my Silly Putty years.

Map Mind Review of Schulz and Peanuts

A mind map book review of David Michaelis' Schulz and Peanuts: A Biography, drawn by Austin Kleon.

The Five Factor Model of Personality

The old left-brain/right-brain model.

In psychology, the Big Five factors of personality are five broad domains or dimensions of personality that are used to describe human personality. The theory based on the Big Five factors is called the Five Factor Model (FFM).

The Big Five framework of personality traits from Costa & McCrae, 1992 has emerged as a robust model for understanding the relationship between personality and various academic behaviors. The Big Five factors are:

Openness to experience – (inventive/curious vs. consistent/cautious). Appreciation for art, emotion, adventure, unusual ideas, curiosity, and variety of experience. Openness reflects the degree of intellectual curiosity, creativity and a preference for novelty and variety. Some disagreement remains about how to interpret the openness factor, which is sometimes called "intellect" rather than openness to experience.

Conscientiousness – (efficient/organized vs. easy-going/careless). A tendency to show self-discipline, act dutifully, and aim for achievement; planned rather than spontaneous behavior; organized, and dependable.

Extraversion (outgoing/energetic vs. solitary/reserved). Energy, positive emotions, surgency, assertiveness, sociability and the tendency to seek stimulation in the company of others, and talkativeness.

Agreeableness – (friendly/compassionate vs. cold/unkind). A tendency to be compassionate and cooperative rather than suspicious and antagonistic towards others.

Neuroticism – (sensitive/nervous vs. secure/confident). The tendency to experience unpleasant emotions easily, such as anger, anxiety, depression, or vulnerability. Neuroticism also refers to the degree of emotional stability and impulse control, and is sometimes referred by its low pole – "emotional stability

Acronyms commonly used to refer to the five traits collectively are OCEAN, NEOAC, or

Beneath each factor, a cluster of correlated specific traits are found; for example, extraversion includes such related qualities as gregariousness, assertiveness, excitement seeking, warmth, activity and positive emotions.

Here's a link to the full Wiki entry:

And here's a link if you want to take the personality test:

Tuesday, July 24, 2012

Jan and Dean Live in Color c. 1964-65

Norman Doidge on the Brain and Neuroplasticity Videos

The Brain That Chances Itself youtube video:

Lecture excerpt:

Full Version:

Brain Book Bonanza: A Recommended Reading List



Giuseppe Arcimboldo (1527-1593) Librarian.

Recommended Brain Books

RSAnimate Steve Johnson Where Good Ideas Come From

As a cartoonist, I love these RSAnimate shorts. Here's one's on Steve Johnson's Where Good Ideas Come From.

RSAnimate Drive: The Surprising Truth About What Motivates Us

Watch the RSAnimate video below and you won't have to read the book! What a fun technique.

Bankruptcy Bonuses: Another Way Execs Cheat Workers (and Taxpayers)

By Bruce Watson Posted 07/24/12

Ever since 2008, when sordid tales of big bonuses at bailed-out Wall Street banks flooded the news media, the huge checks that top executives often write themselves have been reliable class warfare bait. Little wonder: That year, amid failing banks, mass foreclosures, skyrocketing unemployment and frenzied bailouts, New York financial companies paid their workers an estimated $18.4 billion in bonuses.

Since then, Wall Street has gotten a bit more careful about its bonus structure. Many companies reduced their bonuses, some capped the amount that employees could receive, and still others found creative ways to conceal their biggest paychecks. Even so, banker bonuses remain a tough sell to the general public, especially when it appears that they are coming at the expense of average workers -- and taxpayers.

The New Bonus Math

Recently, Hawker Beechcraft (HBC), a Wichita-based aircraft company, landed at the cutting edge of the bonus battle. Earlier this year, it entered bankruptcy and is now in the process of being sold to a Chinese firm, Superior Aviation Beijing Co. Ltd. In return for negotiating the sale of the company, HBC's nine top executives are hoping to get more than $5.3 million in bonuses -- 200% of their base salaries. Meanwhile, another 31 members of management will presumably split $1.9 million.

And what of HBC's workers? In preparation for the sale, the company is trying to shed its pension fund, which is currently $751 million in the hole. To put it mildly, the company's new Chinese owners don't want responsibility for its pensions; one plan is to dump responsibility for the fund onto taxpayers through the Pension Benefit Guaranty Corporation, an agency of the federal government.

The Outsourcing Business Plan

This isn't the first time that Hawker Beechcraft has hung its workers out to dry. The company was formed in March 2007, when Goldman Sachs and Onex Partners, a Canadian investment firm bought the division from Raytheon. Seven months later, HBC opened a huge new factory in Chihuahua, Mexico.

Between October 2008 and mid-August 2009, the company laid off 2,800 employees -- 25% of its workforce. They got rid of another 300 in late August 2009, 240 in September 2009, 350 in October 2010, and 906 in 2012.

Even apart from the costs of providing for the company's laid-off workers, much of the bill for HBC's downfall has landed on taxpayers. In 2010, the company struck a deal with the state of Kansas, promising to keep 4,000 jobs in Wichita until 2020, in exchange for which it received $45 million in tax benefits.

Currently, the company has 4,100 workers in Wichita, but it's unclear if those jobs will survive the company's sale to China. According to the International Association of Machinists and Aerospace Workers, a union that represents 3,500 HBC workers, "there is no reason to believe that Superior, an entity owned and financed by the Chinese government and the Beijing municipal development corporations, would preserve jobs in the United States rather than eventually transporting the work to China."

Emptying the Coffers

For that matter, Hawker Beechcraft's slow-motion march to bankruptcy seems to have gone hand-in-hand with the deflation of its pension fund. Recently, The Atlantic's James Fallows quoted a former employee of the company who claimed that "The pension plan was fully funded at the time of the sale in 2007 and was 98% in 2009."

So, to recap: In 2007, a pair of investment funds bought HBC. They proceeded to fire over 4,000 workers, looted the company's pensions, and are now hoping to leave U.S. taxpayers holding the bag on their responsibilities while top execs sell the company to China and pocket $7.2 million in bonuses in the bargain.

As horrifying as the HBC story is, it's not uncommon. Recently, Kodak, MF Global, Lear Corp, Lee Enterprises, and dozens of other bankrupt companies have asked for permission to give their execs huge bonuses -- often while carrying billions in government bailout funds.

In context, it's not hard to see why many critics are arguing that Wall Street is playing by a skewed set of rules, and the middle class is paying the price.