Archive for the ‘Global Research’ Category

Tigers Bite

Posted by amanda on Wednesday, May 26th, 2010

Asian tiger mosquito, Aedes Albopictus

Asian tiger mosquito, Aedes Albopictus

Noticed anything new in the air lately? A high-pitched buzzing? Perhaps a six-legged, winged creature with a long proboscis out of the corner of your eye? The time of the mosquito is upon us. I received my first mosquito bite of the year the other day while innocently drinking my tea by the garden. I didn’t notice any stripes, but as the Asian tiger mosquito is now a well-established Maryland resident, I expect to see them soon.

Discovered in Maryland in 1987, the Asian tiger mosquito (Aedes albopictus) is an exotic species introduced to North America from Asia. Unlike the native Maryland mosquito, the Asian tiger is an extremely efficient carrier of viral disease. In 2001, tiger mosquitoes collected in Maryland tested positive for West Nile virus, a virus that mainly infects birds but can also infect humans and may result in flu-like symptoms or swelling of the brain. Only female mosquitoes bite, utilizing blood for egg development. Mosquitoes get most of their energy from flower nectar.

The best way to avoid mosquito bites is to eliminate mosquito breeding grounds. Tiger mosquitoes like to lay their eggs in pools of still water, especially in used tires. (Tires imported to Houston, Texas from Japan in 1985 may have brought tiger mosquitoes to the United States.) Here are some ways we can all work to reduce the number of mosquitoes we see this summer and the next:

  • Tip water out of barrels, buckets and wheelbarrows and turn them over so water cannot collect
  • Tip out containers that could hold water such as toys, cans or plant saucers weekly
  • Empty children’s wading pools weekly
  • Change water in birdbaths, pet watering dishes and animal troughs at least once a week
  • Get rid of old used tires
  • Clean debris from ornamental ponds and keep fountains running during the summer
  • Stock ornamental ponds with mosquito-eating fish, such as goldfish or koi
  • Maintain swimming pools and hot tubs
  • Recycle old bottles, buckets, and cans
  • Clean leaf-clogged gutters
  • Drain flat topped roofs
  • Dump water off of tarps and plastic sheeting
  • Drain water from covers on pools, boats and hot tubs
  • Repair leaky outdoor faucets
  • Cover rain barrels with mosquito screens
  • Cover garbage cans with an appropriate lid
  • Repair ripped window and door screens and make sure they fit tight; use a screen door on doors that often are left open
  • Fight the bite!

    Implanted Genome

    Posted by amanda on Friday, May 21st, 2010

    Mycoplasma

    Mycoplasma

    Is a rose still a rose if it doesn’t smell as sweet? Is a Mycoplasma capricolum still a Mycoplasma capricolum if it expresses a different genome? The answer to the first question is definitely “Yes” (especially if you could smell the roses I received on Mother’s Day). A paper published yesterday in Science confirms that the answer to the second question is a big fat “No”. Researchers at Maryland’s own J. Craig Venter Institute (JCVI) in Rockville in collaboration with their sister institute in San Diego are the first to successfully implant a new genome into a bacterial cell to create a new self-replicating bacteria that never existed before. In the most simplistic description, they created a unique new life.

    Using a novel technique in which large DNA sequences were strung together in yeast, a 1.08 Mbp (Mega base pairs, where a base pair is one unit or nucleotide of double-stranded DNA) encoding all the necessary genes to make Mycoplasma mycoides JCVI-syn1.0 was synthesized. After synthesis, the circular chromosome was implanted into the nucleus of a similar species, Mycoplasma capricolum, for gene expression. This was not easy. After the first attempt failed, the researchers found a single mutation limiting proper gene expression. In their paper, the scientists recall several obstacles that had to be overcome: They needed to develop a method to extract large chromosomes from yeast, learn how to transplant these genomes into a recipient cell, and to choose a fast-growing recipient with the required gene expression machinery as a donor.

    By synthesizing the DNA themselves, the researchers were able to include “markers” within the sequence. For example, if the genes were successfully expressed, the bacteria would be blue in color. Furthermore, they were able to leave a lasting mark on the DNA sequence by including strings of nucleotides (that when expressed into protein) spelled out an email address, the names of the scientists involved in the project, and a few famous quotations. [It isn't clear whether or not these proteins would actually be expressed. If only you could make an enzyme composed of a Shakespeare quote.]

    This paper has raised some ethical and therefore political issues. President Obama has already asked the White House bioethics commission for a review of the issues to be provided to him in a report within 6 months, stating that the creation of a new genome raised “genuine concerns”. The application of this method for the synthesis of novel compounds using bacteria, such as biofuels, make this an important industrial topic as well. Can you patent an organism that you created? Would the laws that apply to genetically engineered crops where patents are in place apply to this as well?

    In the last paragraph of the paper, the researchers write:

    “We have been driving the ethical discussion concerning
    synthetic life from the earliest stages of this work (25, 26). As
    synthetic genomic applications expand, we anticipate that this
    work will continue to raise philosophical issues that have
    broad societal and ethical implications. We encourage the
    continued discourse.”

    Let the discourse begin.

    Hubble Hubbub

    Posted by amanda on Wednesday, May 5th, 2010

    Hubble movie

    2D talk before the 3D movie

    When you see a star-filled picture of space, chances are it was taken by the Hubble Space Telescope (HST). Last night, my daughter and I were treated to a screening of the Hubble 3D IMAX movie at the Maryland Science Center celebrating 20 years of the HST orbiting the earth.

    Before the show, Dr. Jennifer Wiseman, NASA Goddard Chief of the Laboratory for Exoplanets and Stellar Astrophysics, gave a brief history of HST’s adventures in space. In 20 years, HST has orbited the earth over 110,000 times, viewing the universe in a way we never could with ground telescopes. Although it was launched on April 24, 1990, the pristine images that Hubble is known for weren’t possible until December of 1993, when a repair crew carried by the Space Shuttle Endeavor replaced faulty parts and updated others. Whether or not the astronaut crew would be able to complete the difficult repairs was unknown, and the repair was an anxious time for scientists at NASA Goddard who could only watch and hope from the ground. Due to the astronauts’ success at that and other maintenance visits to the telescope, we have garnered immense insights into the birth and death of stars, the distance of far-off galaxies, and the origins of the universe. Servicing Mission 4 in May of 2009 is expected to extend the life of the HST to at least 2013.

    The IMAX movie itself centers around the first astronaut visit, and the joy of astronauts and researchers when the HST finally reaches its full operational potential. The repair portion of the movie is flanked by beautiful in-depth images of nebulae where you enter a star nursery and view what may be the origin of a new galaxy. Besides the drama of space and science, there is also humor, due mostly to astronaut Drew Feustel.

    If you have any interest in space or just an interest in looking at beautiful pictures, see this movie. Viewing the achievements of scientists, astronauts, and the NASA program will inspire you. During the movie, my daughter kept reaching her hands out to catch the stars, certain that the universe was within her grasp.

    Antiwho?

    Posted by amanda on Monday, April 12th, 2010

    TARDIS

    I spent the past two weeks in the well-known parental hell of daycare illness, swapping germs with my beloved sticky-handed, snotty-nosed daughter. As every working parent can attest, missing work first to nurse your child and then to nurse yourself is one of biggest downsides of parenting with career ambition. Watching Doctor Who reruns while in a medicine-induced haze kept me entertained, and now all I think about is traveling carefree through time and space. And this is why you, dear reader, get to hear about quarks and quantum theory.

    In the early 20th century, there was a great revolution in physics with the birth of quantum mechanics, replacing classical mechanics as the description of motion on an atomic scale. Max Planck, the founder of quantum theory (and father of four…although I doubt they attended daycare), showed that electromagnetic radiation in a cavity can only be emitted in quantized form (the energy could only be in a multiple of a certain unit). Modern chemistry now relies on quantum mechanics for the description of most atomic and molecular phenomena.

    Quantum field theory is used in particle physics and combines quantum mechanics with special relativity (theory on the structure of spacetime, ala Doctor Who). In the simplest of descriptions, quantum field theory tells us that all types of particles have antiparticles of the same mass but the opposite electric charge. Or that for all matter for any physical system describable in quantum field theory, there exists an antimatter analog. If we could describe you with quantum field theory, we would need to account for the existence of an antiyou. But not all is based on charge. For neutral atoms, an antiatom can also exist. Whereas a neutron is made up of quarks, an antineutron is made of antiquarks.

    Yet we see very little antimatter. Look around and you see a lot of plain old matter, but where is the antimatter? We can see some examples, such as positively charged electrons (positrons in some radioactive decay) and antiprotons (present in cosmic rays) which can be used to form an antihydrogen atom. This lack of antimatter in our matter-filled universe is not completely understood but has been hypothesized to be caused by a temporary difference in physical laws for matter and antimatter occurring after the Big Bang (explained by a theory known as the CP violation). If there were complete symmetry, our universe would simply be an empty sea of radiation consisting of no matter at all.

    Published recently in Science, researchers from something called the STAR Collaboration (made up of researchers from 54 separate institutions) describe how they formed and detected an antihypertriton, a variant of the heavy isotope of hydrogen called tritium. By using the Relativistic Heavy-Ion Collider (RHIC) at Brookhaven National Laboratory (BNL), they were able to briefly produce hot and dense matter (a quark gluon plasma) with an energy density similar to that of the universe a few microseconds after the Big Bang. In this process of extremely energetic heavy-ion collisions, they were able to create and observe the antihypertriton containing nine antiquarks (if you must know: four up, four down, and one “strange”). This is the first observation of an antimatter hypernucleus, an antinucleus with net strangeness. This research confirms our understanding of the existence of antimatter and helps scientists explore the dynamics of heavy ion collisions.

    I’m secretly hoping that someday this research will help in creating the TARDIS.

    Heat-sensing Vipers

    Posted by amanda on Thursday, March 18th, 2010

    pit viper

    Timber rattlesnake; Taken by Tad Arensmeier from St. Louis, MO, USA

    Hikers in Maryland are repeatedly warned at trailheads about the presence of venomous snakes. According to the Maryland DNR, there are over 27 species and subspecies of snakes in Maryland, including two venomous pit vipers, the copperhead and timber rattlesnake. Pit vipers are named for their large specialized pit organs located between the nostril and eye on each side of their face. These organs allow pit vipers to sense infrared radiation, detecting warm-blooded prey at temperatures above ~30°C and distances of up to one meter.

    The pit organ is composed of a thin membrane suspended in a hollow chamber. This membrane, serving as an infrared antenna, is packed with mitochondria (cellular power plants) and linked to many nerve fibers. These fibers send signals from the pit organs to the brain. The sensitivity of detection is dependent on the anatomical and molecular characteristics of the pit organ.

    This week in a Nature advance online publication, scientists reveal the identity of the molecular sensor used by pit vipers and describe how these sensors convey information to the snake brain. Rather than “seeing” in infrared, the pit organ actually heats up due to the ion channel TRPA1. Researchers found TRPA1 in nerve endings leading to the pit organ at levels 400x that in other nerve endings. Humans and other mammals also have TRPA1 (63% similar to pit viper) which is activated by the pungent agent from wasabi and mustard plants. Unlike our TRPA1, the pit viper receptor is not only activated by the mustard agent but also by heat above 28°C. The heat activation of these channels provides an infrared map to the snake brain.

    Interestingly, the researchers found no activation of TRPA1 channels in cooler temperatures, although it is known that snakes can respond to temperatures well below 28°C, perhaps to locate cooler areas in which to rest. Is there another receptor that can detect cooler climes? Or maybe the anatomy of the pit organ tunes TRPA1 in a way we haven’t yet explored.

    According to the Maryland DNR, only 2-5 people get bitten by a venomous snake in the state each year. If you happen to be one of the unlucky ones, just remember:
    - Don’t apply ice.
    - Do keep the bite immobilized and below your heart.
    - Don’t apply a tourniquet.
    - Do wash it with soap and water.
    - Don’t make an incision.
    - Do get help immediately.

    Carol Greider

    Posted by amanda on Sunday, March 14th, 2010

    Carol Greider

    Recipient of the 2009 Nobel Prize for Physiology or Medicine, Carol Greider is the first woman at a Maryland institution to win the award. Along with the work of co-winners Elizabeth Blackburn (her graduate advisor at U.C. Berkeley) and Jack Szostak, Greider’s research at Johns Hopkins has contributed immensely to the understanding of telomeres and their shortening.

    Telomeres are sequences of repetitive DNA at the ends of chromosomes that protect the chromosome from unintentional annealing and degradation. In each replication of a chromosome, telomeres shorten due to the way they are added on to chromosome ends by the enzyme telomerase, which was discovered by Greider and Blackburn in 1985. Intriguingly, most of what we know about telomeres comes from the study of a protozoan with 40,000 chromosomes per cell (compared to our 46), Tetrahymena. More on Greider’s research can be read at her lab’s website.

    In a talk she gave last week at Johns Hopkins School of Medicine, Greider made a list of what you need to become a successful scientist:

  • Show up.
  • Pay close attention.
  • Work on something you love.
  • Read, read, read…
  • Read critically.
  • Don’t believe everything you read.
  • Make bold hypotheses.
  • Don’t believe the status quo.
  • Critically test your hypotheses.
  • Disprove your own models.
  • Be nice to people.
  • Stand up for yourself.
  • Ignore (perceived) obstacles.
  • Rely on friends and family.
  • Talk to people about your ideas.
  • Have fun (most of the time).
  • Although her talk was mainly on her research with telomeres, this list is the part that I really took to heart. It can now be found above my lab bench.

    Henrietta Lacks

    Posted by amanda on Tuesday, March 2nd, 2010

    March is National Women’s History Month. In celebration, I plan to make one post a week featuring women that contributed significantly to science in Baltimore.

    Immortal Life of Henrietta Lacks

    I want to start with Henrietta Lacks, a woman from Turner Station whose cancerous cells were taken and turned into one of the most powerful scientific tools we have today. The tumorous cells that were removed from Henrietta’s cervix at Johns Hopkins Hospital during her treatment in 1951 were the first immortal human tissue cells to be cultured. First grown in the lab of George and Margaret Gey, Henrietta’s cells can be maintained indefinitely and have been used for countless experiments to study everything from cancer to the effects of atomic radiation on human tissue. Named HeLa, these cells led to advances in human genetics, such as the numbering of chromosomes, as well as to the cell culture, cloning, and in vitro fertilization methods we use today.

    The Immortal Life of Henrietta Lacks by Rebecca Skloot is an excellent read on the history of Henrietta and HeLa cells and highlights the moral and legal dilemmas of tissue collection. In her book, Skloot discusses how the Lacks family (who still reside in Baltimore) did not know about the use of HeLa cells until decades after their spread into laboratories around the world, and that while biotechnology companies that produce and sell HeLa continue to profit, the Lacks family has struggled with affording health insurance.

    According to Skloot, there has never been an official effort by Johns Hopkins to honor Henrietta Lacks and her biological contribution to science. With the amazing press Skloot’s book has generated, I have a feeling this may change soon.

    What’s in YOUR Water?

    Posted by amanda on Sunday, February 28th, 2010

    water drop

    http://www.flickr.com/photos/hypergurl/ / CC BY-NC 2.0

    In an article published last week in Current Opinion in Pediatrics, a well-respected professor at Mount Sinai School of Medicine in New York, Philip Landrigan, talks about the environmental chemicals implicated in neurodevelopmental disabilities. He discusses the possibility that environmental toxins may be contributing to autism, alerting the scientific community to the need for more research on the effects of common chemicals on brain biology. In his article, he states that synthetic chemicals that are ubiquitous at hazardous waste sites are commonly found in our air, food, and drinking water. And fewer than 20% of these have been tested for brain developmental toxicity.

    As I sat reading the article, drinking my cup of tap water tea, I asked myself: What’s in your water?

    According to the Environmental Working Group, a watchdog organization that compiles data from water utility companies and state departments, Baltimore ranks 69 out of 100 cities for quality of water with 1 being the best and 100 the worst. The list of chemicals found in the Baltimore City Department of Public Works water is astounding. In the past five years, two contaminants were found to be above legal limits with eleven others above health guidelines. A total of 22 pollutants were identified in Baltimore City water, 14 more than the national average. 22!

    Let’s do a rundown on some of them:

    • Lead: Even my 2-year old daughter knows this one is bad. The EPA has a restriction of 15 ppb for drinking water, and levels above that value (at 19.3 ppb) were detected in Baltimore City water in the past 5 years with an average of 5.16 ppb overall. Lead is known to cause brain damage.
    • Total haloacetic acids (HAAs), Total trihalomethanes (TTHMs), Chloroform, Bromoform, and Trichloroacetic acid: Disinfectants that cause DNA damage and cell death. Carcinogens aplenty. Both HAAs and TTHMs were found above legal limits during the past 5 years. In fact, Baltimore City water ranks among the top 10 cities with the highest levels of TTHMs (at an average of 44.5 ppb).
    • Alpha Particle Activity and Radium-226: Radioactive. Any chemical with a number after it is generally bad. Luckily, the data is from only one test and is at very low levels that we probably don’t need to worry about.
    • Di(2-ethylhexyl) phthalate: Phthalates, found in soft plastics, have been in the news for awhile now, so you probably have heard their name. They are beginning to be phased out of products in both the United States and Europe due to their toxicity.  Phthalates can cause both reproductive and developmental problems. The level in Baltimore City water is at an average of 0.85 ppb. The danger lies in a build-up of phthalates within the body over time.

    In his article, Landrigan stresses that in the examples of known chemicals that are relevant to autism (where women were taking certain medications that lead to a higher incidence of autism in their children, such as thalidomide, misoprostol, and valproic acid), exposure occurs prenatally, very early in the first trimester of pregnancy. Therefore, this may be the most important time to avoid harmful chemicals that can affect fetal brain development. Whether or not other chemicals or known neurotoxins, such as phthalates, organophosphate pesticides, and BPA, cause an increase in autism or other specific brain development disorders is not known, and Landrigan encourages future toxicological studies to answer these questions.

    But I know one thing for sure: I’m off to get a water filter.

    How do we taste?

    Posted by amanda on Monday, February 22nd, 2010

    What tastes good to you right now? A sweet carrot? A bitter beer? Or maybe some salty pretzels? Whatever it is, how it tastes to you is determined by your cells. So how do we taste?

    boy eating cookies

    We separate tastes for humans (and probably most mammals) into five categories: bitter, sour, sweet, salty, and umami (the taste generated when you consume certain amino acids, such as MSG). Our taste preferences when we are born are genetically encoded. We prefer sweet tastes as babies, because “sweet” is associated with healthy foods that contain proteins and energy. We avoid bitter and sour things, because these are associated with toxins and acidic foods, like spoiled fruits or harmful plants. Humans (and mice) generally prefer salty foods when our bodies are low in sodium with our tastes fitting our physiological need. As we mature (or most of us anyway), we acquire tastes for more bitter and sour things, such as coffee and lemons, and may prefer salty and sweet foods even though we really don’t need to build up our salt or sugar supply.

    From studies in mice, it is thought that the five tastes are determined by separate taste-receptor cells (TRCs) in the mouth each tuned to a specific taste. TRCs are organized into taste buds, composed of 50-100 cells, and these taste buds are housed within papillae (the bumps on your tongue). Taste buds from all regions of the mouth contain cells that respond to the five tastes and are connected to nerves that carry taste information to your brain stem and into the primary gustatory cortex (where your response to a food and your perception of flavor is dictated). Contrary to popular belief, there is no “taste map” on the tongue.

    Recently published online in Nature, Jayaram Chandrashekar and colleagues (including scientists from the National Institute of Health in Bethesda) illustrate how salty taste occurs in sodium sensing in mice. Each TRC that determines a salty taste contains a sodium channel (or sodium transporter). This channel is present in many cells within your body, including your kidneys, lungs, and sweat glands, and is important in salt transport. Its role is so important that if this channel is made completely nonfunctional in mice, death occurs soon after birth. In order to study the importance of this channel in taste, scientists used a clever technique (attaching the channel mutation-causing agent to a known TRC-specific gene) to generate mice that were missing the sodium channel only in their taste buds. Unlike their ‘normal’ peers, these mice displayed a complete loss of salt attraction and sodium taste response while responding normally to the other four tastes. And most importantly, all of the TRC cells that carried the mutated salt channel did not carry any markers for the other four taste sensors, showing again that individual TRC cells are only able to determine one taste.

    Whether or not this specific sodium channel is as important to salty tastes in humans as it is in mice is unknown. Due to our molecular similarities, the authors note that it is likely. But unlike mice, our innate responses to salty taste may be overridden by our high-salt diets.

    Now, pass me those fries. All this talk of salt has made me hungry.

    The Genetics of Stuttering

    Posted by amanda on Thursday, February 18th, 2010

    When we think of genetically affected characteristics, we often think of hair and eye color, height, and the size of our nose. But what about speech? This week, Changsoo Kang and Dennis Drayna, from the National Institute on Deafness and Other Communication Disorders in Bethesda, and colleagues report on the genetics of stuttering in the New England Journal of Medicine.

    Stuttering is found in all cultures and languages, affecting 5% of children in twice as many boys as girls. Nearly 80% of childhood stuttering resolves itself, mostly in girls, leaving male stutterers outnumbering female stutterers 4:1. 60 million people in the world are stutterers, and Winston Churchill, John Updike, King George VI and James Earl Jones join their ranks. The history of stuttering is fraught with erroneous theories and damaging medical practices. The ancient Greeks thought that stuttering resulted from tongue dryness and recommended enlargement of the veins by surgical or chemical means. In the 1800s, stuttering was thought to be an anatomical defect, and surgical treatments were popular. By the 1900s, stuttering was ruled a psychological disorder and treated with conditioning and psychoanalysis that were eventually proven ineffective. The modern theory is that stutterers have a neurophysical problem that disrupts the precise timing in speech.

    human chromosomes

    Human chromosomes; NIH

    The evidence for a genetic component to stuttering is apparent, such as the existence of identical twin stutterers and a high incidence of stuttering in first degree relatives. Approximately half of stutterers have a family history of the disorder. By examining genetic linkage in families of stutterers, geneticists have honed in on several chromosomes that may be involved in stuttering.

    recycling

    In Kang and Drayna’s most recent study, they’ve focused on chromosome 12 to examine the genes involved in stuttering in the largest well-studied group of stutterers, a Pakastani family simply known as PKST72. By comparing the DNA of stutterers in the family to non-stuttering control subjects, the researchers were able to pinpoint the genetic sequences affected in stuttering individuals. Interestingly, the genes they identified affect the cell’s recycling center, the lysosome. The lysosome takes unwanted material in the cell, such as old proteins, and breaks them down into something more usable. In this family of stutterers, the genes that direct proteins to the lysosome for recycling are mutated, most likely resulting in a build-up of this cell litter in other compartments of the cell. Somehow this accumulation of trash in cells leads to speech disturbance. The way this occurs is unknown, and the implication of these results for both treatment of stuttering and future studies is profound.

    One other thing of note is that all but two of the stutterers with these mutations were heterozygous, meaning that the mutations were only found on one of the two strands of chromosome 12. If the mutations were found on both strands of DNA, the affected persons may have had a severe lysosomal storage disease called mucolipidosis.

    DNA is amazing.