Anyway, we are a homogenous group, all more or less identical, and we meet every Thursday night in a secret fairy dell that lies within a beautiful ferny glade in the old-growth forest - the moral high ground you might say, where we practise preaching and the double standards for which we are famous. We hug trees and skip about celebrating atheism and moral cancer, and indulge in the sublime pleasure of gleefully ignoring the human rights abuses of terrorists and certain fascist regimes. We achieve this state of rapture and denial by drinking chardonnay and losing ourselves in reminiscences about the '60s when we were all promiscuous hippies living on social welfare, smoking dried banana peel and making snide jokes about Vietnam War veterans.
Gene variations contribute to aggression and anger in women
BUDAPEST, HUNGARY, March 9 – Ever wonder why some women seem to be more ill-tempered than others? University of Pittsburgh researchers have found that behaviors such as anger, hostility and aggression may be genetic, rooted in variations in a serotonin receptor gene. Indrani Halder, Ph.D., of the Cardiovascular Behavioral Medicine Program at the University of Pittsburgh, will present the findings today at the American Psychosomatic Society's Annual Meeting, held in Budapest, Hungary.
Previous studies have associated the hormone serotonin with anger and aggression in both humans and animals and have shown that increased serotonin activity is related to a decrease in angry and aggressive behaviors. In the study being presented today, researchers sought to determine if this relationship was genetically determined. The study is the first to look at the relationship between variations in the serotonin receptor 2C gene and anger and hostility."Because the Halder paper looks at only one gene in a relatively small sample, I bet that this report will join the ranks of thousands of other reports that fail to replicate. On the other hand, in dozens of studies of humans and rodents, serotonin has been shown to play a role in emotional responding so it is not unreasonable to consider DNA variations in the serotonin transporter as a source of individual differences in aggression and anger. I would just need a lot more convincing."
A Shock to the SystemThe procedure has been remarkably successful, allowing most patients to resume their normal activities after being held captive by tremors, rigidity, and bradykinesia for years:
To slow the progress of Parkinson’s disease, doctors planted electrodes deep in my brain. Then they turned on the juice.
By Steven Gulie
I'm lying in an operating room at the Stanford University hospital, head shaved, waiting for my brain surgery to begin. Sure, I feel anxious, but mostly I feel crowded. There are 10 people milling about, tinkering with instruments and examining me. It’s an impressive crew, including a neurosurgeon and his fellow, a neurologist and her fellow, an anesthesiologist, an experimental physicist, and a graduate student in electrical engineering. That’s right, a physicist and an electrical engineer. Directly behind me, out of my sight, is the star of the show, chief neurosurgeon Jaimie Henderson: 44 years old, tall, erudite, and handsome. On my right, flexing my hands, is neurologist Helen Bronte-Stewart: brisk, smart, and beautiful. In fact, nearly everyone is not only brilliant but also pretty enough to play themselves in the movie version of this story. I call them Team Hubris.
Today, eight years since the first signs of Parkinson’s and after months of fiddling, my body is almost free of symptoms. With the stimulator turned off, a Parkinson’s test shows 20 significant impairments. With the stimulator on, it drops to two. Add just a touch of L-dopa and it drops to zero.
The last wisps of fog have cleared away. My jokes make people laugh again. I can keep up with conversation. I can ride a bike. I can write. It’s been five months since the surgery, but it has finally all come together: It works. I forget that I even have Parkinson’s most of the time. And last November, I went back to work full-time. It’s a miracle. A second chance at life.
DBS isn't limited to Parkinson's, however. The Neurocritic has previously covered DBS for severe intractable depression and phantom limb pain.
The cause of Tourette syndrome has been controversial ever since Georges Gilles de la Tourette, a neurologist who shared a mentor with Sigmund Freud at the Salpêtrière Hospital in Paris, first described the condition in 1885. Is the syndrome the result of hysteria (Tourette’s hypothesis), repressed sexual conflicts, or oppressive mothers, which were the favored explanations for much of the 20th century? Or is it an organic defect of the brain, as many neuroscientists and physicians now hold? The ability of neuroleptic drugs, beginning with haloperidol in the 1960s, to reduce tics supported the neurologic position.Or maybe it's just because DBS for TS hasn't gotten the publicity that DBS for depression has received...
Furthermore, when controlling for ISPV, the face-specific effect for the N170 went away. The face N170 peaked earlier in time than the car N170, but they did not differ in amplitude. However, a face-dominant effect for an earlier component, the P1, emerged (which was an unexpected finding, since it suggests that category-specificity can manifest itself at 100 msec, 70 msec before the N170 component).On the other hand, the P1, a peak generally regarded as an index of lower level perceptual processing, was surprisingly unaffected by differences in ISPV, but was sensitive to object category in both Experiments 1 and 2. This should not be interpreted as evidence for absolute category selectivity because only three object categories were tested here. Indeed, faces, cars and butterflies differ in terms of overall composition and various perceptual properties such as outline, contrast, subparts and complexity, which were not manipulated here. It is therefore possible that the P1 still reflects perceptual differences between these objects; that is, that apparent category selectivity in this component is an emergent property arising from low perceptual invariants.Thierry G, Martin CD, Downing P, Pegna AJ (2007). Controlling for interstimulus perceptual variance abolishes N170 face selectivity. Nature Neuroscience. Published online: 04 March 2007.
That's why they call it Dope-a-mine
Once again the chicken/egg argument is revisited vis-a-vis addiction. Do drugs make us impulsive or does impulsivity make us do drugs?
A new article in Science shows evidence that a paucity of functional D2/3 receptors in the ventral striatum "high-impulsivity" rats is correlated to a higher tendency to self-administer cocaine when given access to drug.
The implications are positive, in that it is always good to see work that supports a non-moral-depravity line of reasoning behind addiction; on the other hand, some reports in the more mainstream news take a harder nature/nurture line with headers like "Study: Addicts born, not made." and that sort of thing. I always worry about backlash from social scientists whenever I see stuff like that.
