WEDNESDAY, May 27 (HealthDay News) — As the H1N1 swine flu virus continues to wax and wane in different parts of the country, U.S. health officials said they were working as fast as possible to learn as much as they can about the novel pathogen before the return of the flu season in the fall.
The reason for the urgency: Some past pandemics were preceded by “herald waves” of a flu strain that surfaced at the end of one flu season, only to return with far greater consequences the next flu season.
“We are mindful that pandemics of influenza have sometimes come in waves,” Dr. Anne Schuchat, the U.S. Centers for Disease Control and Prevention’s interim deputy director for science and public health program, said during a Tuesday afternoon news conference. “The very severe 1918 pandemic had a moderate herald wave in the spring and a much more severe second wave in the fall. So that very terrible experience of 1918 is in our minds.”
Some estimates have placed the worldwide death toll from the 1918 outbreak — often referred to as the “Spanish Flu” — as high as 40 million people.
“We are really on a fast track, over the next to eight to 10 weeks, to learn as much as we can as this virus heads to the Southern Hemisphere [where flu season is just beginning] and to strengthen our planning for the surge of illness that we expect to experience here in the fall,” Schuchat added.
Scientists will be looking to see if the H1N1 swine flu virus mutates or becomes resistant to antiviral medications, or is more easily spread among people, she said.
Schuchat said there’s no way to tell now if the H1N1 virus will be more virulent when — and if — it returns to the Northern Hemisphere with the approach of winter. “Whether it will dominate among the seasonal flu viruses or whether it will disappear is not predictable right now,” she said.
To date there have been 7,927 confirmed and probable cases of infection in the United States, the CDC reported Wednesday. Most of the cases have been mild and patients have recovered quickly.
The CDC was reporting 11 deaths linked to the swine flu, and all of the victims had underlying health problems before they were infected.
The World Health Organization said Wednesday that 48 countries have reported 13,398 cases of infection, including 95 deaths, most of them in Mexico, where the outbreak began.
The CDC said last week that progress was being made toward the development of an H1N1 swine flu vaccine, with two promising candidate viruses for use in such a shot. And U.S. Department of Health and Human Services Secretary Kathleen Sebelius said Friday that the federal government was allocating $1 billion to the search for a swine flu vaccine.
In the United States, most cases of the swine flu continue to be no worse than seasonal flu. Testing has found that the swine flu virus remains susceptible to two common antiviral drugs, Tamiflu and Relenza, according to the CDC.
The CDC says some older people may have partial immunity to the H1N1 swine flu virus because of possible exposure to another H1N1 flu strain circulating prior to 1957. So far, 64 percent of cases of swine flu infection in the United States have been among people aged 5 to 24, while only 1 percent involves people over 65, officials said last week.
GoogleNews.com, May 27, 2009, by Mgoozner at GoozNews.com — In an online article in the New England Journal of Medicine , the new leaders at the Food and Drug Administration have laid out their public health orientation in broad strokes, promising a new era where the agency that oversees more than one-seventh of the U.S. economy puts science at the helm and gives safety equal standing with the new product approval process.
But they also pledged a new day for drug developers who worry the agency is failing to keep up with the frontiers of medicine. Indeed, nearly every constituency with a stake in FDA regulation will find something to like in the guideline offered yesterday by newly-installed Commissioner Margaret Hamburg and Deputy Commissioner Joshua Sharfstein.
Drug safety advocates will be heartened by their promise to use the tools created by the 2007 reform law that allow the agency to pay greater attention to the risks of newly approved drugs. At the same time the drug and biotechnology industries can point to their pledge to speed new life-saving drugs to market and develop the new science of personalized medicine.
A pragmatic centrism that has been characteristic of most Obama administration appointees lies at the core of their philosophy. Will the FDA hurdle for new drug and device applications become more or less stringent? Wrong question, the new leaders say.
Some benefits are not worth the risk; some risks are worth taking. Key considerations are the severity of the illness at issue, the availability of alternative treatments or preventive interventions, and the current state of knowledge about individual responses.
Regulation of the pre-approval stage of drug development is in for an overhaul. Echoing the rhetoric of the Critical Path Initiative, which has come under fire from some consumer groups as a Trojan horse to undermine drug safety standards, the new leaders pledged to work more closely with scientists funded by the National Institutes of Health and the pharmaceutical and biotechnology industries as they explore potential breakthroughs. “As scientists identify fruitful pathways for research on treatments for debilitating diseases, FDA regulators should discuss with them the level of evidence necessary for the initiation of human trials and the eventual approval of treatments,” they wrote. And in what should be music to innovators’ ears, Hamburg and Sharfstein offered to collaborate with the Centers for Medicare and Medicaid Services “to explore ways of shortening the time from approval to reimbursement.”
Food safety has dominated the headlines in recent months, and food processors — many of which are crying out for more inspections and tighter regulations — are going to see major changes in the months ahead.
The recent salmonella outbreak linked to contaminated peanut butter represented far more than a sanitation problem at one troubled facility. It reflected a failure of the FDA and its regulatory partners to identify risk and to establish and enforce basic preventive controls. And it exposed the failure of scores of food manufacturers to adequately monitor the safety of ingredients purchased from this facility.
The agency is also likely to pay much more attention to nutrition issues under their leadership. Not only are they promising to crack down on false nutritional claims (such as the recent Cheerios claim that it lowers cholesterol), but they want to work with consumer groups and industry “to promote more healthful foods.”
It’s never wise to read too much into broad statements made at the outset of an administration. This is as true for regulatory agencies as it is in politics. But if there is any group that should come away emboldened by this first broadside by the Hamburg and Sharfstein leadership team, it is the career scientists at the FDA.
“We recognize the importance of a management approach that respects the expertise and dedication of the FDA’s career scientists,” they wrote. “Establishing the FDA as a public health agency requires a culture that encourages scientific exchange and respects alternative viewpoints along the path of decision making.”
There will be no winners and losers in that approach. It pragmatically recognizes that when it comes to promoting and protecting public health, the facts on the ground matter most.
Pain is more than a symptom of osteoarthritis, it is an inherent and damaging part
of the disease itself, according to a new study. (Credit: iStockphoto/Sebastian Meckelmann)
University of Rochester Medical Center,. Pain Is Not A Symptom Of Arthritis, Pain Causes Arthritis, Study Shows. ScienceDaily – Pain is more than a symptom of osteoarthritis, it is an inherent and damaging part of the disease itself, according to a study just published in journal Arthritis and Rheumatism. More specifically, the study revealed that pain signals originating in arthritic joints, and the biochemical processing of those signals as they reach the spinal cord, worsen and expand arthritis.
In addition, researchers found that nerve pathways carrying pain signals transfer inflammation from arthritic joints to the spine and back again, causing disease at both ends.
Technically, pain is a patient’s conscious realization of discomfort. Before that can happen, however, information must be carried along nerve cell pathways from say an injured knee to the pain processing centers in dorsal horns of the spinal cord, a process called nociception. The current study provides strong evidence that two-way, nociceptive “crosstalk” may first enable joint arthritis to transmit inflammation into the spinal cord and brain, and then to spread through the central nervous system (CNS) from one joint to another.
Furthermore, if joint arthritis can cause neuro-inflammation, it could have a role in conditions like Alzheimer’s disease, dementia and multiple sclerosis. Armed with the results, researchers have identified likely drug targets that could interfere with key inflammatory receptors on sensory nerve cells as a new way to treat osteoarthritis (OA), which destroys joint cartilage in 21 million Americans. The most common form of arthritis, OA eventually brings deformity and severe pain as patients loose the protective cushion between bones in weight-bearing joints like knees and hips.
“Until relatively recently, osteoarthritis was believed to be due solely to wear and tear, and inevitable part of aging,” said Stephanos Kyrkanides, D.D.S., Ph.D., associate professor of Dentistry at the University of Rochester Medical Center. “Recent studies have revealed, however, that specific biochemical changes contribute to the disease, changes that might be reversed by precision-designed drugs. Our study provides the first solid proof that some of those changes are related to pain processing, and suggests the mechanisms behind the effect,” said Kyrkanides, whose work on genetics in dentistry led to broader applications. The common ground between arthritis and dentistry: the jaw joint is a common site of arthritic pain.
Past studies have shown that specific nerve pathways along which pain signals travel repeatedly become more sensitive to pain signals with each use. This may be a part of ancient survival skill (if that hurt once, don’t do it again). Secondly, pain has long been associated with inflammation (swelling and fever).
In fact, past research has shown that the same chemicals that cause inflammation also cause the sensation of pain and hyper-sensitivity to pain if injected. Kyrkanides’ work centers around one such pro-inflammatory, signaling chemical called Interleukin 1-beta (IL-1β), which helps to ramp up the bodies attack on an infection.
Specifically, Kyrkanides’ team genetically engineered a mouse where they could turn up on command the production of IL-1β in the jaw joint, a common site of arthritis. Experiments showed for the first time that turning up IL-1β in a peripheral joint caused higher levels of IL-1β to be produced in the dorsal horns of the spinal cord as well.
Using a second, even more elaborately engineered mouse model, the team also demonstrated for the first time that creating higher levels of IL-1β in cells called astrocytes in the spinal cord caused more osteoarthritic symptoms in joints. Past studies had shown astrocytes, non-nerve cells (glia) in the central nervous system that provide support for the spinal cord and brain, also serve as the immune cells of CNS organs. Among other things, they release cytokines like IL-1β to fight disease when triggered. The same cytokines released from CNS glia may also be released from neurons in joints, possibly explaining how crosstalk carries pain, inflammation and hyper-sensitivity back and forth.
In both mouse models, experimental techniques that shut down IL-1β signaling reversed the crosstalk effects. Specifically, researchers used a molecule, IL-1RA, known to inhibit the ability of IL-1β to link up with its receptors on nerve cells. Existing drugs (e.g. Kineret® (anakinra), made by Amgen and indicated for rheumatoid arthritis) act like IL-1RA to block the ability IL-1β to send a pain signal through its specific nerve cell receptor, and Kyrkanides’ group is exploring a new use for them as osteoarthritis treatment.
The implications of this process go further, however, because the cells surrounding sensory nerve cell pathways too can be affected by crosstalk. If 10 astrocytes secrete IL-1β in response to a pain impulse, Kyrkanides said, perhaps 1,000 adjacent cells will be affected, greatly expanding the field of inflammation. Spinal cord astrocytes are surrounded by sensory nerve cells that connect to other areas of the periphery, further expanding the effect. According to Kyrkanides’ model, increased inflammation by in the central nervous system can then send signals back down the nerve pathways to the joints, causing the release of inflammatory factors there.
Among the proposed, inflammatory factors is calcitonin gene related peptide (CGRP). The team observed higher levels calcitonin-gene related peptide (CGRP) production in primary sensory fibers in the same regions where IL-1β levels rose, and the release of IL-1β by sensory neurons may cause the release of CGRP in joints. Past studies in Kyrkanides reveal that CGRP can also cause cartilage-producing cells (chondrocytes) to mature too quickly and die, a hallmark of osteoarthritis.
Joining Kyrkanides in the publication from the University of Rochester School of Medicine and Dentistry were co-authors M. Kerry O’Banion, M.D., Ph.D., Ross Tallents, D.D.S., J. Edward Puzas, Ph.D. and Sabine M. Brouxhon, M.D. Paolo Fiorentino was a student contributor and Jennie Miller was involved as Kyrkanides’ technical associate. Maria Piancino, led a collaborative effort at the University of Torino, Italy. This work was supported in part by grants from the National Institutes of Health.
“Our study results confirm that joints can export inflammation in the form of higher IL-1β along sensory nerve pathways to the spinal cord, and that higher IL-1β inflammation in the spinal cord is sufficient in itself to create osteoarthritis in peripheral joints,” Kyrkanides said. “We believe this to be a vitally important process contributing to orthopaedic and neurological diseases in which inflammation is a factor.”
Duke University Medical Center, May 27, 2009 — This photo shows the same airway after a severe chemical injury that wipes out the normally present cells and activates stem cell mediated repair (clonal patches). Credit: Cancer Research UK
Stem cells that respond after a severe injury in the lungs of mice may be a source of rapidly dividing cells that lead to lung cancer, according to a team of American and British researchers.
“There are chemically resistant, local-tissue stem cells in the lung that only activate after severe injury,” said Barry R. Stripp, Ph.D., professor of medicine and cell biology at Duke University Medical Center. “Cigarette smoke contains a host of toxic chemicals, and smoking is one factor that we anticipate would stimulate these stem cells. Our findings demonstrate that, with severe injury, the resulting repair response leads to large numbers of proliferating cells that are derived from these rare stem cells.”
Stripp said this finding could be related to the increased incidence of lung cancer in people with chronic disease states, in particular among cigarette smokers.
The findings were published in the advance online edition of the Proceedings of the National Academy of Sciences during the week of May 25.
“On the positive side, I think that it might be possible to improve lung function in the context of disease if we could understand which pathways regulate lung stem cell activation and then target these pharmacologically,” said lead author Adam Giangreco, Ph.D., from Cancer Research UK’s Cambridge Research Institute. “In terms of lung cancer susceptibility, however, our observation that stem cell activation leads to clonal expansion after injury could, in the context of additional mutations, promote the development of cancerous or precancerous lesions from activated stem cells.”
This section of a normal chimeric airway shows a patch distribution of mixed green fluorescent protein positive (green) and negative cells. Credit: Cancer Research UK
The scientists used a chimeric mouse model, part wild-type and part with green fluorescent protein-tagged cells (GFP), so that the behavior of different populations of duplicating lung cells could be evaluated with high-resolution imaging methods. By understanding the extent to which GFP-positive and GFP-negative cells were mixed, the investigators were able to show that the abundant population of progenitor cells that normally maintain the epithelial layer in the lung could be rapidly wiped out with a strong chemical, naphthalene. Then the rare proliferative cells became active and grew into large patches.
The researchers at Duke and Cancer Research UK used a unique whole-lung imaging method to examine and identify the location of stem cells in the lung tissue of mice, and determine the role they play in both healthy and damaged mouse lungs.
They found that, while the stem cells don’t appear to be involved in the normal maintenance of healthy or moderately injured lungs, they do play a vital role in repairing severely damaged lungs.
Even though this repair mechanism is important for restoring lung function, it can come at a price. An acquired mutation in that rare cell or its descendants leads to clonal patches of many identical cells. Secondary mutations in any one of these cells may provide the signals needed for unregulated cell growth and tumor progression.
“This work provides a plausible mechanism to account for this type of event that we previously didn’t have,” Stripp said.
Researchers are reporting progress toward a stronger material for
dental cavities using ingredients from the human body. Arrow points
to a filling made of “composite.” (Credit: NIST)
American Chemical Society (2009, May 27). Stronger Material For Filling Dental Cavities Has Ingredients From Human Body. ScienceDaily – Scientists in Canada and China are reporting development of a new dental filling material that substitutes natural ingredients from the human body for controversial ingredients in existing “composite,” or plastic, fillings. The new material appears stronger and longer lasting as well, with the potential for reducing painful filling cracks and emergency visits to the dentist, the scientists say.
Julian X.X. Zhu and colleagues point out that dentists increasingly are using white fillings made from plastic, rather than “silver” dental fillings. Those traditional fillings contain mercury, which has raised health concerns among some consumers and environmental issues in its production. However, many plastic fillings contain controversial ingredients (such as BisGMA) linked to premature cracking of fillings and slowly release bisphenol A, a substance considered as potentially toxic to humans and to the environment.
The scientists developed a dental composite that does not contain these ingredients. Instead, it uses “bile acids,” natural substances produced by the liver and stored in the gallbladder that help digest fats. The researchers showed in laboratory studies that the bile acid-derived resins form a hard, durable plastic that resists cracking better than existing composites.
Oral Biologists Use Chemistry To Formulate Cavity Fighting Mints
American Institute of Physics – Oral biologists formulated a mint that fights cavities with an ingredient called Cavistat. Cavistat contains two main components that protect the teeth. First, the amino acid arginine metabolizes certain bacteria, which neutralizes the acid generated by sugars. This raises the pH to help prevent damage to teeth. Cavistat also introduces other chemical compounds that protect against the dissolving of the minerals of the teeth.
Sodas, candy and processed foods are packed with tooth-decaying, cavity-causing sugar. For the past 40 years, experts have seen a decrease in the amount of tooth decay in children; but according to Centers for Disease Control statistics, the trend is reversing. To tackle the problem, one dental scientist has found a way to use candy to help prevent cavities.
Tooth decay in kids has increased 28 percent in the past eight years. Experts believe too many sugary, processed foods and not enough brushing are to blame. A key factor in fighting cavities is found in your mouth.
“Saliva is the great protector against cavities,” said Israel Kleinberg, D.D.S., Ph.D., an oral biologist at Stony Brook University in Stony Brook, N.Y.
Dr. Kleinberg says 40 years of research and more than $1 billion has been spent trying to figure out what saliva has that fights tooth decay.
“I’m one of the pioneers in that as a whole new science,” Dr. Kleinberg said. “It’s where one mixes dentistry and biochemistry.”
Dr. Kleinberg discovered how saliva’s chemistry helps teeth neutralize the acidity created from eating food by balancing the pH levels in the mouth.
“[It’s] like if you’ve got a swimming pool,” Dr. Kleinberg said. “You have got to get the pH right. If you’ve got a neutral pH, you’ve got the ideal condition.”
He developed a candy to fight cavities. The candy is fluoride-free and protects teeth in two ways. First, it raises pH levels to neutralize more acid than saliva alone. Second, it protects the minerals in tooth enamel. Arginine, an amino acid, combines with calcium in Cavistat, the candy’s main ingredient, and sticks to teeth — leaving behind a layer of protection.
Kids who ate two mints twice a day for one year had 68 percent fewer cavities in their molars than children who didn’t chew the mints.
“The number of cavities, we think that ultimately is going to get to almost zero,” Dr. Kleinberg said. That would bring a smile to just about everyone’s face.
All the ingredients in the mints are natural and considered foods, so the product doesn’t need FDA approval.
WHAT DOES IT DO? BasicMints contain Cavistat, a cavity-fighting agent that includes two major components. Cavistat disrupts oral chemistry and biology in two ways. First, it introduces an amino acid called arginine to the mouth. When bacteria in the mouth break the arginine down, it neutralizes the acid generated by sugars in food, which reduces the amount of acid in the mouth and helps prevent damage to teeth. Additionally the Cavistat adds other chemical compounds that protect the minerals that make up teeth from dissolving.
ANATOMY OF A TOOTH: We think of teeth as being the part visible above the gum, but this is only the tip, or crown, of a tooth. There is also a neck that lies at the gum line, and a root, located below the gum. The crown of each tooth has an enamel coating to protect the underlying dentine. Enamel is even harder than bone, thanks to rows of tightly packed calcium and phosphorus crystals. The underlying dentine is slightly softer, and contains tiny tubules that connect with the central nerve of the tooth within the pulp. The pulp forms the central chamber of the tooth, and is made of soft tissue containing blood vessels that carry nutrients to the tooth. It also contains nerves so teeth can sense hot and cold, as well as lymph vessels to carry white blood cells to fight bacteria.
University of Minnesota (2009, May 27). New Therapy Substitutes Missing Protein In Those With Muscular Dystrophy. ScienceDaily – Researchers at the University of Minnesota Medical School have discovered a new therapy that shows potential to treat people with Duchenne muscular dystrophy, a fatal disease and the most common form of muscular dystrophy in children.
In the mouse model, researchers were able to substitute for the missing protein – dystrophin, which forms a key part of the framework that holds muscle tissue together – that results in the disease, effectively repairing weakened muscle tissue.
Researchers injected dystrophic mice with a protein called utrophin – a very close relative of dystrophin – that was modified with a cell-penetrating tag, called TAT.
The study is the first to establish the efficacy and feasibility of the TAT-utrophin-based protein as a viable therapy for the treatment of muscular dystrophy as well as cardiac muscle diseases caused by loss of dystrophin.
The research is published in the May 26, 2009 issue of PLoS Medicine.
“This unique approach can replace the missing protein without the complexities of gene replacement or stem cell approaches,” said James Ervasti, Ph.D., principal investigator of the study and a professor in the Department of Biochemistry, Molecular Biology & Biophysics.
Muscular dystrophy causes the muscles in the body to progressively weaken. Duchenne is the most common and severe form of childhood muscular dystrophy. About one of 3,500 boys are born with the crippling disease. Symptoms usually begin in children who are 2 to 3 years-old, most are in a wheelchair by age 12, and many who have the disease pass away by their late teens to early 20s. Current treatment, limited to corticosteroids, are minimally effective and can cause serious side effects.
Research underway to battle muscular dystrophy with gene therapy and stem cell treatment shows promise, but major hurdles must be overcome before these approaches are viable in human patients, Ervasti said.
Delivering treatment to every muscle cell via gene therapy or stem cells is difficult because muscle tissue makes up such a large portion of the human body. Furthermore, the immune system may reject the cell or gene treatment because patients would treat the newly introduced cells or genes as a foreign substance.
Ervasti’s method may conquer both of those problems. Upon injection, the TAT-utrophin combination spreads around the entire body efficiently and is able to penetrate the muscle cell wall to substitute for missing dystrophin. Because every cell in the body makes utrophin naturally, TAT-utrophin circumvents immunity issues associated with other therapeutic approaches.
“Our protein replacement approach most directly and simply addresses the cause of Duchenne muscular dystrophy,” Ervasti said.
This new method is not a cure for muscular dystrophy. Rather, it would be a therapy most likely administered on a regular basis. If the treatment works in larger animal models and humans, it’s most likely researchers would develop a drug for patients. Ervasti is hopeful the therapy can move into human clinical trials within 3 years.
The research was funded by the Muscular Dystrophy Association, the Nash Avery Foundation, Charley’s Fund and the Foundation to Eradicate Duchenne.
Sea Urchins Reveal Medical Mysteries
ScienceDaily.com, Spring 2009 – Researchers are using the sea urchins to study and understand diseases like cancer, Alzheimer’s disease, Parkinson’s disease and muscular dystrophy. Although they are invertebrates, the creatures share a common ancestor with humans and have more than 7,000 of the same genes. With a complete map of their DNA, scientists can learn how to treat and prevent diseases in humans better.
They’re small, spiky and spineless. But what do prehistoric sea urchins have in common with humans? Uncovering their mysteries may help solve some of science’s most difficult and deadly problems.
“At a genetic level, ah, they’re actually related to us. So sea urchins and humans share a common ancestor,” Cristina Calestani, a developmental geneticist at University of Central Florida in Orlando, tells DBIS….Even though they don’t look like us.
Sea urchins and humans share more than 7,000 genes, and biologists are now using these sea creatures to unlock the mysteries of human diseases. In fact, there are several genes in the sea urchin involving Alzheimer’s, Parkinson’s disease, muscular dystrophy and many other cancer-related genes. And infertility may be another problem the sea urchin helps solve. No wonder — each urchin can produce 20 million eggs.
When you compare the human and sea urchin genes, quite a few of the amino acid sequences are a perfect match.
“You really need a relatively simple system in order to study … but still, also you want it to be complex enough and closer enough to vertebrate in order to use this information,” Calestani says.
Sea urchins are one of the few invertebrates on our branch of the evolutionary tree, sharing more genes with humans than fruit flies and worms — and can be reproduced for research faster than other animals. Calestani says that means researchers can produce large amount, practically unlimited amount of material. And with a complete map of the urchin’s DNA, they can better understand how genes work, so when diseases like cancer strike, maybe someday doctors will know exactly how to treat and even prevent them.
Another fascinating fact is sea urchins don’t have eyes, ears or a nose, but they have the genes humans have for vision, hearing and smelling.
BACKGROUND: Sea urchins might not seem to have much in common with human beings, since they are small and spiny, have no eyes, and eat only kelp and algae. But scientists with the Sea Urchin Genome Sequencing Project, funded by the National Institutes of Health, recently completed sequencing of the genome. They found that the sea urchin genome is very similar to that of humans, and may hold the key to preventing and curing several human diseases.
ABOUT SEA URCHINS: Sea urchins are echinoderms, marine animals that originated more than 540 million years ago. Sea urchin “roe” (actually the gonads that produce the creature’s roe) are popular in Korean and Japanese cuisine, and is also a traditional food in Chile. Beyond their culinary attractions, sea urchins are known for strong immune systems and long life spans; some can live up to 100 years The project scientists are especially interested in how the sea urchin’s immune system works. Humans are born with innate immunity and also acquire additional immunities over time, as the body produces antibodies in response to infections. Sea urchins only have innate immunity, with 10 to 20 times as many such genes than humans. The hope is that studying sea urchins will provide a new set of antibiotic and antiviral compounds to fight various infectious diseases.
WHAT IS A GENOME? A genome is all of the DNA found in an organism, including its genes and DNA that does not contribute to genes. Every animal and plant has its own unique genome. Genetic DNA carries information for making the proteins required to sustain a living organism. The genome of the purple sea urchin is comprised of 814 million “letters” that code for 23,300 genes. Of those, it has 7,000 genes in common with humans, including genes associated with Parkinson’s, Alzheimer’s, and Huntington’s diseases, as well as muscular dystrophy. Despite having no eyes, nose, or ears, the creature has genes involved in vision, hearing and smell in humans.
By Jim Lemire, May 27, 2009 — Sea urchins are spiny marine invertebrates that comprise, along with sand dollars, sea biscuits, and heart uchins the Class Echnoidea within the Phylum Echinodermata. Sea urchins differ from the other echinoids by having a more-or-less spherical body-plan and are thus referred to as “regular” or “globose” echinoids. Like other echinoderms, sea urchins utilize a hydraulic system of tube feet for locomotion and display pentameral or five-rayed symmetry – most clearly delineated in their test (a.k.a. shell). Although relatively small (generally less than 15 cm in diameter), some species can have spines over 20 cm long. With somewhere around 800 extant species, sea urchin are a cosmopolitan critter – found from the Arctic to the Antactic and from the intertidal zone to the deep-sea.
Sea urchin tests are are comprised of calcium/magnesium carbonate plates, specifically, five alternating pairs of columns of ambulacral and interambulacral plates. The ambulacral plates contain pores through which the tube feet protrude. Both kinds of plates have tubercles – ball-and-socket type spine attachments (urchin spines are capable of moving somewhat like your index finger around the first knuckle). The test and spines are all covered in a thin epidermis.
The oral surface of an urchin is on the bottom where its five teeth can be found (contained within “Aristotle’s lantern“, one of nature’s most impressive feeding structures – more on this in a later post). The aboral surface is on top and contains the anus, surrounded by aptly-named anal plates, which are in turn surrounded by genital plates, each of which contains a gonadopore, through which gametes are released. One of the gonadal plates (known as the sieve plate) contains the madreporite – the structure through which water is drawn to power the water vascular system, the hydraulic system used by echinoderms for locomotion.
Sea urchins are epifaunal, using their Aristotle’s lantern to graze upon algae and sessile organisms. Their spines are used for protection against predators (otters, fish, sea birds). Some urchin species have specialized spines that are capable of injecting venom that causes intense pain. Urchins can be voracious eaters and, if their numbers are unchecked, a population of urchins can completely strip an area of vegetation, resulting in a seriously-altered ecosystem generally termed an “urchin barren”. Likewise if urchin numbers crash, the resulting algal growth can severely alter the local ecosystem.
Cranium. A) Anterior view demonstrates bilateral erosive lesions at the supraorbital region and glabella, erosion/remodeling of the margin of the nasal aperture, including the anterior nasal spine, bilateral necrosis of the infraorbital region of the maxilla, and resorption of the alveolar region of the maxilla with associated antemortem tooth loss. B) Inferior view of the maxilla demonstrates pathological changes to the palatine process including pitting near the midline and in the alveolar region. (Credit: Robbins et al., DOI: 10.1371/journal.pone.0005669)
Public Library of Science (2009, May 27). Oldest Evidence Of Leprosy Found In India. ScienceDaily – A biological anthropologist from Appalachian State University working with an undergraduate student from Appalachian, an evolutionary biologist from UNC Greensboro, and a team of archaeologists from Deccan College (Pune, India) recently reported analysis of a 4000-year-old skeleton from India bearing evidence of leprosy. This skeleton represents both the earliest archaeological evidence for human infection with Mycobacterium leprae in the world and the first evidence for the disease in prehistoric India.
The study, published in the journal PLoS One, demonstrates that leprosy was present in human populations in India by the end of the mature phase of the Indus Civilization (2000 B.C.) and provides support for one hypothesis about prehistoric transmission routes for the disease. This finding also supports the hypothesis that the Sanskrit Atharva Veda, composed before the first millennium B.C., is the earliest written reference to the disease and that burial traditions in the second millennium B.C. in one northwestern Indian village bear some resemblance to practices in Hindu tradition today.
As infectious diseases go, leprosy is still one of the least well-understood, in part because the Mycobacterium is difficult to culture for research and it has only one other animal host, the nine banded armadillo. An Indian or African origin for the disease has often been assumed based on historical sources that support an initial spread of the disease from Asia to Europe with Alexander the Great’s army after 400 B.C. Skeletal evidence for the disease was previously limited to 300-400 B.C. in Egypt and Thailand.
A report on genomics of Mycobacterium published in the magazine Science by Monot and colleagues in 2005, indicated the disease may have originated in Africa during the Late Pleistocene and that M. leprae spread out of Africa sometime after 40,000 years ago, when human population densities were small. A counter hypothesis was proposed in the same volume of Science by Pinhasi and colleagues suggesting that the same data could be interpreted as evidence for a Late Holocene migration of the disease out of India after the development of large urban centers.
Dr. Robbins and colleagues report on a case of leprosy in a skeleton buried around 2000 B.C. in Rajasthan, India, at the site of Balathal. From 3700-1800 B.C., Balathal was a large agrarian settlement at the margins of the Indus (or Harappan) Civilization. The mature phase of the Indus Civilization during the latter half of the third millennium B.C., was a period of social complexity characterized by urbanization, a system of writing, standardized weights and measures, monumental architecture, and trade networks that stretched to Mesopotamia and beyond.
The presence of leprosy in India toward the end of this period indicates that M. leprae existed in South Asia at least 4000 years ago. This suggests that there may be some validity to Pinhasi and colleagues hypothesis that the disease spread between Africa and Asia during a period of incipient urbanization, increasing population density, and regular inter-continental trade networks. Dr. Robbins is currently attempting to recover ancient DNA from the skeleton to determine if the strain of M. leprae infecting the individual from Balathal is similar to strains common in Africa, Asia and Europe today. If it is successful, this work could shed additional light on the origin and transmission routes of this disease.
Understanding more about the disease can help clear up some of the many popular misconceptions about leprosy. It is generally associated with outcast and neglected people suffering their contagion on the margins of urban centers in late Biblical or Medieval times. In reality, leprosy is transmitted only through prolonged close contact with nasal droplets or infected regions of the body. It is not highly contagious and the infection can remain latent for decades. In fact, most people infected with Mycobacterium leprae have few or very mild symptoms. Because leprosy is not highly contagious and its survival is likely dependent upon dense populations, the association with urban environments is possibly the only accurate part of the popular perception.
The presence of leprosy at Balathal 4000 years ago also supports translations of the Eber’s papyrus in Egypt and a Sanskrit text in India (the Atharva Veda) that refer to the disease as early as 1550 B.C. The Atharva Veda is a set of Sanskrit hymns devoted to describing health problems, their causes and treatments available in ancient India. Translations of leprosy have been questioned because it is difficult to perform a differential diagnosis on descriptions in such ancient texts particularly since diagnosis was not why the conditions were being described. The evidence from Balathal indicates that it is possible that the authors were describing leprosy as the disease was present in the subcontinent in prehistoric times.
Furthermore, in contemporary Hindu tradition burial is uncommon unless an individual is a highly respected member of the community (like an ascetic) or is an individual seen as unfit to be sacrificed through cremation. These latter individuals are buried, including outcastes, pregnant women, children under 5, victims of magic or curses, and lepers. During the second millennium B.C., when there was disintegration of Indus settlements and new, smaller settlements sprang up all over the western half of peninsular India, adult burial becomes rare, children under 5 begin to predominate in the skeletal assemblages, and this early leper was one of only five individuals buried at the site of Balathal (the others were middle-aged women, an ascetic from the Early Historic period, and a fragmentary clavicle found with the leprous skeleton). Thus there is a similarity in terms of the demography of the burial populations from the second millennium and Vedic tradition.
In addition, another feature of this burial that resembles Vedic symbolism is the burial site itself. The leper’s skeleton was interred within a large stone enclosure that had been filled with vitrified ash from burned cow dung, the most sacred and purifying of substances in Vedic tradition. The presence of this skeleton at Balathal, the manner in which it was interred, and the preponderance of children in burial assemblages from this time period throughout western India suggest deep time for the origin of these practices still common in Vedic tradition today.
The skeleton is currently housed at Deccan College Post-Graduate Research Institute in Pune, India.