It's Alive!
Robotics is a field in which I don't have a lot of experience, but I find the results terribly cool. Especially fascinating are those robots which are designed for biofidelic movement, or which mimic the movement capabilities of living creatures. Here is a perfect example: Boston Dynamics' DARPA-funded "BigDog."
Mobile Robots Take Baby Steps (full article >>)"
A robot dog could one day become a soldier's best friend -- if an Army program works out as planned."
New Video: Robot Mule Conquers Ice, Snow (full article & video >>)"
BigDog, the alarming life-like, four-legged robot, is back in action. And this time, it's trudging through snow, marching up hills, and picking itself up after slipping on some ice."
--
Labels: engineering, science
ABO blood types
Here's a (relatively) simple explanation.
The four basic types are A, B, AB, and O. These types are determined by which certain antigens, or protein markers, are found on a person's blood cells. A person can have 'A' antigens only, 'B' antigens only, both 'A' and 'B' antigens, or none.
Which (if any) of these antigens a person has is determined by genetics. In a person's genetic code, the gene pair that determines these antigens can be any combination of 'A', 'B', and 'O', making for six possible genetic sequences: 'AA', 'AO', 'AB', 'BB', 'BO', and 'OO'. The genes for 'A' and 'B' are codominant, and 'O' is recessive. This means that if a person's genes code for 'AA' or 'AO' their blood cells will carry 'A' antigens (this is blood type A), 'BB' or 'BO' will yield 'B' antigens (type B), 'AB' will cause both 'A' and 'B' antigens to be produced (type AB), and 'OO' will produce no antigens (type O).
Now for the important part: anti-A and anti-B antibodies. (Antibodies are one of the human body's defensive mechanisms.)
A person with type AB blood carries both 'A' and 'B' antigens, so neither type of antibody is produced. This is what makes type AB the "universal receiver"; because it has no anti-A or anti-B antibodies, it can accept any blood type.
Type A blood carries only 'A' antigens, so in this case only anti-B antibodies are produced, which will attack only cells with 'B' antigens; vice versa, for type B with 'B' antigens, only anti-A antibodies are produced.
Type O blood carries neither 'A' nor 'B' antigen markers, so both anti-A and anti-B antibodies are produced; if these antibodies encounter any blood cells that carry 'A' or 'B' markers, they will recognize those cells as foreign and attack them. For this reason, a person with type O blood cannot accept any other blood type; each of the other types (A, B, and AB) carries 'A' and/or 'B' antigen markers. However, for this same reason, type O is the "universal donor"; these blood cells, because they carry no 'A' or 'B' antigens, can safely mingle with any other blood type.
Those are the basics of ABO blood types in a nutshell. (Bonfils gave me a complimentary keychain; I might as well know about what goes on with the blood that I've been giving away.)
The good news is that my blood type (AB+) can accept every other known blood type. The less-than-great news is that my blood cells are only acceptable to other people with the same exact type, or only about 3.4 percent of the population.
Anyone, however, can use my blood plasma, because it contains none of the blood cells (with their pesky antigens and Rh factors) that cause the incompatibility.
This warrants some thoughtful consideration.
The process by which they (the nebulous conglomerate of licensed phlebotomists) collect plasma is called plasmapheresis. This involves several iterations of a cycle in which blood is collected and separated into its components in a centrifuge, the plasma is drawn off, and the remaining components are fed back into your bloodstream. The entire process (including paperwork, donation, and prescribed downtime) takes about an hour and a half, and most donation centers offer to "compensate" plasma donors for their time.
Plasma is a fairly versatile blood product. According to several informational websites, a bone marrow or organ transplant surgery requires over a hundred units of plasma. Plasma also contains proteins that are used to treat immunodeficiency and blood coagulation disorders (such as hemophilia); for these same reasons, it is also a sought-after material for biomedical research purposes.
--
Labels: everyday, science
Injury repair in the central nervous system
This is such a promising development. Also, you know, it's really cool science.
Injuries to the central nervous system (CNS) are notoriously difficult to repair, though in many cases the surrounding CNS tissues adapt to work around the resulting scar. This "glial scar" is very inhibitory to the regeneration of damaged axons, which carry outgoing signals from neurons (signal-conducting nerve cells). In order to understand the inhibitory nature of the glial scar and consequent failure of axon regeneration after CNS injury, we should first understand the cells and processes involved in the formation of the glial scar.
When CNS tissue is damaged it undergoes an injury response called reactive gliosis, or glial scarring. This consists of a series of cellular and molecular events that occur and change over a period of several days; the glial scar structure evolves over time as various cells arrive and participate at different times. The main cell types involved are the neurons themselves, as well as the surrounding glial tissue, which consists of astrocytes (general support cells, providing structural stability and helping to regulate the extracellular environment), microglia (immune cells, the "garbagemen" of the CNS), and oligodendrocytes (provide insulation for axons in the form of myelin sheaths).
Immediately following injury, myelin debris (from damaged oligodendrocytes) will be released into the neural environment as oligodendrocytes and other cells in the injured area are damaged and die. In the first few days following injury, the primary entering cells are microglia. The lesion (damaged area) also expands during this time. The mature glial scar consists mainly of a tightly-woven network of astrocyte processes.
Astrocytes around the lesion exhibit abnormal growth and some undergo cell division; the end result of this activity is the dense, predominantly astrocytic composition of the glial scar. It has been found that this tissue can be both inhibitory to and supportive of axonal regeneration, depending on changes in the CNS environment and/or the population of glial scars by an as-yet undetermined sub-type of astrocyte which is inhibitory.
Oligodendrocytes are directly damaged by traumatic injury to the CNS, causing the release of myelin debris and some oligodendrocyte death. Glial scars, therefore, usually contain some oligodendrocytes and myelin debris. It has been shown that mature oligodendrocytes and myelinated areas of the CNS are inhibitory to axon growth. Also, it has been seen that oligodendrocyte precursor cells are recruited en masse to CNS lesion sites; these cells express several proteoglycans (dense molecular complexes of proteins and polysaccharides) that are inhibitory to axon regeneration.
Microglia exhibit activation and division following injury, and migrate to the injury site, becoming more macrophage-like over time ("macrophage" essentially means "great eater," so you can guess what a macrophage does). Collective evidence suggests that microglia may actually support regeneration, as long as nothing happens to make them overtly toxic.
Interestingly, it has been shown that the eradication of all CNS glia from the lesioned area results in an environment in which robust axonal regeneration can occur for a period of about 4 days, until glia re-invade the area.
With this in mind, we turn to the potential use of a self-assembling nanofiber peptide scaffold. This novel scaffold is a hydrogel (content is over 99 percent water, with 1 to 10 milligrams of peptides per milliliter of water) that forms when a self-assembling peptide (SAP) solution is exposed to salt solution similar to that found in the human body. The figure at right (click to enlarge) shows (a) a molecular model of the SAP, (b) a microscopic image of the SAP nanofibers, (c) a microscopic image of the scaffold, and (d) a photograph of the hydrogel. The components of the scaffold are amphiphilic oligopeptides that have repeated alternating ionic hydrophilic & hydrophobic amino acids. These form beta-pleated sheets with distinct polar & non-polar surfaces. Structurally, macroscopic scaffolds have been formed in various shapes and sizes, depending on SAP concentration, total amount of SAP solution, salt concentration, and the geometry of the processing apparatus. These structures consist of individual interwoven fibers of about 10 to 20 nanometers (one-trillionth of a meter) in diameter, with the density of fibers correlating with the concentration of the SAP solution.
Here's the "really cool science" part. In one study, Holmes et al. seeded neural cells on SAP scaffolds. These cells underwent extensive outgrowth along the contours of the scaffolds; further evidence suggested that the scaffolds also supported the formation of functional neuron synapses.
In another study conducted by Ellis-Behnke et al., a tissue gap was created in the hamster midbrain (by deep transection of the optic tract). When treated with SAP solution, this gap was seen to be reduced or completely eliminated by 72 hours post-surgery and in all subsequent examinations, as compared to the saline-treated controls, which remained visible in macroscopic examination at all times post-surgery. The figure at right shows typical examples from 30 days post-surgery of (a) the saline control case and (b) the SAP-treated case. The SAP-treated animals showed axon regeneration through the injury site; the control animals showed no axon regeneration. Here the SAP treatment was generally found to support axon regeneration with a correlating return of functional vision.
Both of the above studies included tests of the body's toleration of the SAP solution; after an injection of the SAP solution into muscle tissue, examinations found no detectable toxic effects and no observable signs of structural abnormalities, muscle necrosis, inflammation, or motor impairment. Where the SAP solution was injected into brain tissue, no apparent inflammatory response was found; in addition, it was discovered that the amino acid degradation products of the scaffold are mostly eliminated from the body within 3-4 weeks post-injection.
Also, one important feature of the SAP scaffold is its ability to fill irregular voids (because it is a hydrogel) such as injury sites in damaged tissue. This allows close contact between the scaffold nanofibers and surrounding tissues.
References:
> J.W. Fawcett et al.:
"The glial scar and central nervous system repair" [PDF, 183 KB],
Brain Research Bulletin, 1999.
> T.C. Holmes et al.:
"Extensive neurite outgrowth and active synapse formation on self-assembling peptide scaffolds" [PDF, 522 KB],
Proceedings of the National Academy of Sciences, 2000.
> R.G. Ellis-Behnke et al.:
"Nano neuro knitting: Peptide nanofiber scaffold for brain repair and axon regeneration with functional return of vision" [PDF, 1.7 MB],
Proceedings of the National Academy of Sciences, 2003.
--
Labels: engineering, science
Wanderlust
I've got it bad. I have always romanticized the adventure of traveling: cruising down the open highway, rolling across the country over railroad tracks, making a brand new journey. Perhaps this is part of the reason that I prefer not to travel by jetliner; on the road or on a train, you get a real sense that you're actually traveling. I love looking out the window and discovering a new panorama at every moment. I want to freeze every one of those moments and remember it, treasure it, because who knows when I might pass this way again; for each moment I have experienced, every place I've ever been, one thing remains true: I came, I saw, I moved on. And while it's nice to slow down, maybe even stop for a while and really experience a place, I want to keep moving, because there's something new another mile down the road, around the next bend.
Every single time I cross a set of railroad tracks, see a train, hear a train engine's horn, I want to follow those tracks, I want to catch that train and see where it takes me. Interstate highways are a perpetual temptation; I usually manage to curb the impulse, and I pull off at my planned exit and go wherever it was that I meant to go, but I always think,
What if I just kept going? San Francisco, here I come. Or Cheyenne, or Chicago, or Albuquerque, or whatever else may lie ahead.
The open road: the steady hum of the engine, the rhythmic rumble of pavement under the wheels, milemarkers ticking away the distance, an endless stream of asphalt stretching ahead and behind, land spread out wide all around. Every now and then I find that I have come unexpectedly into a moment that is almost a kind of nirvana; in those moments of near-perfection, I could just keep following that road, going onward forever.
--
Labels: everyday, imagine yourself here, ponderings, travel
"Whiplash" injuries: a car safety lecture
Today we're going to learn about one of our friendly vehicle safety features, the "head restraint" (apparently, it is not properly referred to as a "head rest"), how it can save us from nasty "whiplash"-type neck injuries, and how to properly adjust it so that it will be more effective in the event of a crash.
In a rear-impact car crash, as the vehicle is effectively given a shove forward, a poorly protected occupant will undergo three primary phases of movement, as illustrated in the three-part diagram above [IIHS, 1997]. Initially, the torso is forced against the seatback and is pushed forward; the head, prior to contacting the head restraint, initially remains level and lags behind the torso. This results in a characteristic "S"-shape of the neck, where the upper portion of the neck is in flexion while the lower part is in extension (above, left). Following the "S-phase" is the extension phase, in which poor head support will allow the neck to transition into full extension (above, center). Here the torso may "ramp" up the seatback, causing the head restraint to provide even less head support. The forces on the head then accelerate it to catch up with and pass the torso, giving rise to the full flexion or "rebound" phase (above, right). So-called "whiplash" injuries may occur in one or more of these phases. In general, it is thought that the risk of whiplash injuries may be reduced or even completely eliminated if we can minimize relative motion between the head and torso. Controlling this relative motion involves various safety features, but head restraint geometry is especially important to reducing the risk of whiplash injuries in rear-impact crashes.
The two common measurements of head restraint geometry are vertical offset and horizontal backset. Vertical offset is commonly measured as the distance of the head’s center of gravity above the top of the head restraint; in U.S. federal safety regulations, this measurement is replaced by that of height above the so-called "seating reference point" (SRP). Horizontal backset is measured as the horizontal distance between the back of the head and the head restraint. The Insurance Institute for Highway Safety (IIHS) and the Research Council for Automobile Repair (RCAR) commonly define these as shown in the diagrams above [RCAR, 2001]. Studies over the last four decades have generally agreed that whiplash will be reduced if the head restraint is positioned sufficiently high and close behind the head. Independently from federal regulation, IIHS evaluates head restraints according to guidelines set by RCAR. IIHS recommended that head restraints have a vertical offset of less than 90 mm (3.5 inches), so as to make the top of the head restraint at least level with the head’s center of gravity, and a backset of less than 100 mm (4 inches) [IIHS, 1997].
As of January 1, 1969, Federal Motor Vehicle Safety Standard (FMVSS) No. 202 required that all passenger cars manufactured for U.S. sale must have a head restraint in the front outboard seating positions that could achieve a specified height above the SRP, providing adequate protection for a 50th-percentile male [Kahane, 1982]. This standard has not changed since then. According to IIHS, the standard is weak; two major deficiencies are the lack of a minimum height requirement for head restraints in the down position, and the lack of a backset requirement. FMVSS 202 states only that head restraints must achieve a certain minimum height above the SRP when in the fully-extended position; when adjustable head restraints meeting this requirement are left in the down position, the occupant will be inadequately protected. In addition, the required height is only minimally protective. An IIHS evaluation of 1997 model year cars rated over 50% as having poor head restraint geometry, and less than 3% were rated "good" [IIHS, 1997].
To address the deficiencies, the National Highway Traffic Safety Administration (NHTSA) has revised FMVSS 202 in recent years [NHTSA, 2000]. Effective Sept. 1, 2009, head restraints must achieve a new, greater height above the SRP and lock in this position, with a specified minimum lowest height; the head restraint's backset must also fall within a specified range in any adjustment position. According to NHTSA, the new front outboard standards will provide adequate protection for 99.7% of the male population and all females, where "adequate protection" is defined as the head restraint reaching at least as high as the head’s center of gravity.
IIHS and RCAR support these revisions, but nonetheless there is still concern that the revised standards are not what they should be [IIHS, 2001]. RCAR recommended, and IIHS has adopted, stricter testing standards consisting of both geometric and dynamic tests [RCAR, 2006]. By these standards, an IIHS evaluation of 2004 model year cars rated 80% as having "good" or "acceptable" head restraint geometry; however, once seats passing this static geometry test were subjected to RCAR dynamic tests, ratings dropped significantly. By the combined static and dynamic testing standards, only about 33% (24 out of 73) passed with a rating of "good" or "acceptable." Including the 24 car seats that did not pass the static test, a total of about 56% (54 out of 97) were rated "poor" [IIHS, 2004].
With the average level of current technology, it's important to promote education among vehicle drivers and occupants alike. Most occupants don't properly position their adjustable head restraints; in many cases this may be due to mere ignorance and/or indifference, but it is likely that many other people leave their head restraints down for reasons of comfort. Ford Motor Company, for example, reported a recent increase in customer complaints pertaining to head restraint comfort; it is believed that these complaints correlate with reduced backsets in head restraints [NHTSA, 2004].
Next time you hop in the car, check your head restraint. The first time I did so, I was dismayed to realize that mine was positioned far too low to provide any real protection against rear-impact whiplash injuries. Now, however, it's adjusted as it should be. Remember: horizontal backset within 4 inches, and vertical offset within 3.5 inches, or such that the top of the head restraint is at least level with your head’s center of gravity. If you fail to comply with these recommendations, I will feel free to call you stupid.
References and further reading:
>> IIHS (1997):
"Special Issue: Head Restraints" [PDF, 575 KB],
Status Report Vol.32, No.4.
>> RCAR (2001):
"A Procedure for Evaluating Motor Vehicle Head Restraints" [PDF, 471 KB].
>> C.J. Kahane, NHTSA (1982):
"An Evaluation of Head Restraints.">> NHTSA (2000):
FMVSS 202: Head Restraints, Code of Federal Regulations, Title 49, Part 571.202.
>> NHTSA (2004):
"Final Regulatory Impact Analysis, FMVSS No. 202 Head Restraints for Passenger Vehicles" [PDF, 4.3 MB].
>> IIHS (2001):
"New head restraint rule would prevent many whiplash injuries, but proposed dynamic tests could compromise safety" [PDF, 230 KB],
Status Report Vol.36, No.4.
>> RCAR (2006):
"RCAR-IIWPG Seat/Head Restraint Evaluation Protocol" [PDF, 3.2 MB].
>> IIHS (2004):
"Special issue: protection against neck injury in rear crashes" [PDF, 504 KB],
Status Report Vol.39, No.10.
--
Labels: engineering, everyday, travel
