For the first time, a team led by Yale University researchers has used nanosensors to measure cancer biomarkers in whole blood. The new device is able to read out biomarker concentrations in a just a few minutes. Extremely small concentrations are being measured, the equivalent of detecting a single grain of salt within a swimming pool size volume of liquid.
"The new device could also be used to test for a wide range of biomarkers at the same time, from ovarian cancer to cardiovascular disease, Reed said. Science Daily.
Authors of the paper, "Label-free biomarker detection from whole blood", include Eric Stern, Aleksandar Vacic, Nitin Rajan, Jason Criscione, Jason Park, Mark Reed and Tarek Fahmy (all of Yale University); Bojan Ilic (Cornell University); David Mooney (Harvard University).
Distinct components within the sensor perform purification and detection. A microfluidic purification chip simultaneously captures multiple biomarkers from blood samples and releases them, after washing, into purified buffer for sensing by a silicon nanoribbon detector. This two-stage approach isolates the detector from the complex environment of whole blood, and reduces its minimum required sensitivity by effectively pre-concentrating the biomarkers. Nature Nanotechnology, Dec 13, 2009
Courtesy kristiewellsLately, there’s been a lot of hoopla in the news about the over-screening of certain cancers, particularly breast and prostrate cancers. Back in October, an opinion piece published in the journal of the American Medical Association (JAMA) by researchers at the University of California, San Francisco and San Antonio’s University of Texas Health Science Center, called for rethinking in the screening guidelines for those two cancers. Although the researchers admit the regular screenings are beneficial, Laura Esserman, MD at UCSF says, “The benefit is not nearly as much as we hoped and comes at the cost of over diagnosis and over treatment.”
In a New York Times story about the report, Dr. Otis Brawley, chief medical officer of the American Cancer Society (ACS) is quoted saying “We don’t want people to panic, but I’m admitting that American medicine has over-promised when it comes to screening. The advantages to screening have been exaggerated.”
The report went on to say the ACS was “quietly working on a message, to put on its Web site early next year, to emphasize that screening for breast and prostate cancer and certain other cancers can come with a real risk of over treating many small cancers while missing cancers that are deadly.”
But the American Cancer Society responded with a claim that, despite the headlines, it wasn’t changing its guideline recommendations regarding screenings, and continued to stress that a mammogram was still “one of the best things a woman can do to protect her health.”
The story resurfaced again in late November when the United States Preventive Services Task Force issued new recommendations regarding breast cancer screenings, calling for postponing initial mammograms for women until the age of 50 rather than 40. The task force, a federal advisory board, made its decision to change the guidelines after reviewing evidence presented to it by a team of oncologists. The American Cancer Society opposes the new guidelines.
This whole story is somewhat confusing. And it’s that confusion that causes some in medical community to worry.
“I am concerned that the complex view of a changing landscape will be distilled by the public into yet another ‘screening does not work’ headline,” said Dr. Colin Begg a biostatistican at New York’s Memorial Sloan-Kettering Cancer Center. “The fact that population screening is no panacea does not mean that it is useless.”
On a recent post on the KevinMD blogsite, Dr. Amy Tuteur tries to unravel some of the confusion explaining why some medical experts think aggressive screening (and severe treatment) for breast and prostate cancer has done little to lower the death rate from these particular cancers. The PSA test, for instance, is utilized much more often in the United States than it is in the United Kingdom to screen for prostate cancer, yet the death rate from the cancer in each country is pretty much the same. It should be noted that for some cancers regular screenings are making a difference. Colon and cervical cancers are often treated successfully with early detection and by removal of cancerous or pre-cancerous tissue.
The problem is not all cancers behave the same way. Some can start small, grow slowly and if caught in the early stages, be treated (or removed) before they become fatal. And that’s been the classic cancer treatment paradigm for a long time. If all cancers behaved this way, aggressive screenings would be the way to go. But over the past decades doctors and researchers have learned a lot more about cancer biology. They now know certain cancers can erupt suddenly and explosively and become fatal very quickly. Others can appear and remain dormant - sometimes for years - and never become a problem during the lifetime of the patient. But because screening practices have become more agressive, more of the non-fatal tumors are being spotted and treated unnecessarily. At the same time the screenings can sometimes be missing some of the aggressive cancers because they’re detected too late to treat. What’s needed is for doctors to be able to find a way to determine which tumors will become fatal.
“Without the ability to distinguish cancers that pose minimal risk from those posing substantial risk and with highly sensitive screening tests, there is an increased risk that the population will be over-treated.” --Dr. Laura Esserman
This topic is of interest to me, particularly this month, because December is when I get to subject myself to various post-cancer screenings (CT scan, blood and urine tests) and an annual visit to my oncologist. Three years ago I had my first colonoscopy. I was 54 years old at the time, and 4 years beyond the recommended age for a first colonoscopy. Although no cancer or pre-cancerous polyps were found in the colon, during the procedure the gastroenterologist – who, lucky for me, was thorough enough to go beyond the end of the large colon - discovered a tumor at the very beginning of my small intestine. It turned out to be a rare cancer that can usually be cured with surgery if it’s not too advanced. In researching it, I read that it is usually a slow-growing cancer – you can have it for years without experiencing any symptoms - but the surgeon told me it could also be very aggressive. It just depends. Getting it removed was the most prudent thing to do (it’s amazing how quickly you want to rid it from your body when you learn you have cancer), so I had the surgery and fortunately the tumor was still contained and the cancer hadn’t spread elsewhere. No chemotherapy or radiation was necessary (my type of cancer doesn’t respond to it), and I’ll be considered cancer-free if I pass my annual screenings for four years. I just passed my third checkup on Wednesday.
But here’s my point: when I was first diagnosed, one of my friends chastised me for waiting so long to have my first colonoscopy. I admit I dragged my feet, despite my doctor’s recommendation. It’s my nature to avoid dealing with unpleasant things. But who knows? Had I not delayed having the procedure done, maybe the carcinoid tumor in my small intestine would have been too small to be detectable during a colonoscopy, and then much more advanced (or completely gone on its own) by the time I had my next screening. I have no way of knowing if that would be the case. But I’m not saying I’ll continue to buck my doctors’ recommendations for screenings (my oncologist set me up for another colonoscopy next month - so I got that going for me), but I can’t help but think – at least in my case – maybe some of it did come down to luck and timing.
The "flu shot" vaccine side effects are usually the normal common reactions, and usually minor. some reactions are: about one in three people get a sore arm, little redness, or low fever from the shot, and an average of 10-15% of people feel tired or get a headache. The flu itself can cause serious problems, including GBS (Guillain-Barré Syndrome); the body's immune system attacks part of the peripheral nervous system.
A large proportion of the world population will get H1N1 and the vaccine side effect risk is far smaller than the sickness. When vaccines are approved, which includes the H1N1 vaccine, they are guaranteed to be much less risky than the sickness they prevent. "There could be unknown side effects. Something could happen, but it hasn't, but we think that is highly unlikely," infectious disease and vaccine expert Mark Mulligan, MD, executive director of the Hope Clinic of the Emory Vaccine Center in Atlanta.
An interview with the health teacher, Mr. Mcginnis at Central Sr. high school, gave a new direction for this topic. He explained to me that when people encounter the H1N1 flu, teenagers and young adults are not in the high level of complications and death. As to the age range of an elder, or 7 and under, are at the high risk. Students at Central Sr. high have encounter with the H1N1, and at least 1 in 10 people at Central knows who has or had it. Teenagers to get the H1N1 vaccine aren't on the top of the list but, as a matter of fact they really don't need it. Their bodies can fight it off and can get it out of their body systems. There has been little deaths so far relating teens dying from this vaccine. Mr. Mcginnis added that "we should still stay home when we have signs of the flu. It could happen to be something else, and getting the vaccine should be kept a priority to get done for everyone."
Interview with a staff member Edward Cullen*, was a first hand look at the H1N1 virus. He had recently encounter the H1N1 late October in 2009. He first came down with the symptoms after the school homecoming game. The next morning he had a very high fever of 104 degrees, and all the symptoms of a regular cold. After about four days he scheduled an appointment with his doctor, and after about a few questions it was confirmed that he has had the H1N1 for about the last 4 days. He was given Tylenol, Advil, and Delsym to treat the virus. Looking back now he says "it was horrible and hope to never experience it ever again." Adding on he missed a whole week of school, and the teachers compromised for him to catch up on assignments. As to his plans to get the H1N1 shot, he doesn't need it. The virus is already immune to his system. Edward Cullen's* advice to everyone is to " GET THE H1N1 VACCINE!".
All vaccines aren't safe, but we've been using them for years so adding the H1N1 vaccine doesn't make a difference. The vaccines we have used and still using has side effects but people still get the shots for it. The H1N1 has not shown any real side effects other then the usual side effects of the other vaccines. It should be fine and be used to stop the spread of the H1N1. Have you gotten the shot? Do you know someone who has the H1N1? What are your plans to not get the H1N1?
* Name has been changed.
Courtesy sirgabeThere’s something I want to get out of the way straight off the bat: the original title for this post was “Monday Nutrition Extravaganza: Chemicals in your food, playing with your manhood!” And while that has a certain whimsical charm, a re-read revealed hidden, disturbing meaning in those words. And I didn’t want to subject you Buzzketeers to that. I just thought you should know.
So, moving on, what’s this stuff playing with our manhood, now?
Chemicalz in our foodz! And stuff.
Earlier today, I came across this study about how there seems to be a correlation between high levels of chemicals call phthalates in pregnant mothers’ urine, and a lowered incidence of “masculine play” in their male children. (“Girls’ play behavior” didn’t seem to be affected.)
Phthalates are a group of chemicals added to plastics to make them softer and more pliable. We all like soft plastic—no one is arguing that!—but phthalates are all over the place, and increased exposure to them (all sorts of products and packaging use phthalates) is raising concerns about how those chemicals affect us, particularly during childhood development. See, phthalates are antiandrogens, meaning that they mess with the way your body works with hormones like testosterone. Testosterone plays an important role in how we physically develop, and perhaps in how we act. The boys whose mothers had higher levels of a couple kinds of phthalates demonstrated less “male-typical” behavior. The study looked a preferred toy types (trucks versus dolls), activities (“rough-and-tumble play”), and “child characteristics.”
Now, these are slightly sticky things to go judging kids on. Some folks might argue that these characteristics aren’t linked to biology so much as social conditioning. And it feels a little weird quantifying characteristics in children (and, let’s be honest here, characteristics which may not have a solidly identified “norm,” but nonetheless have all sorts of social and sexual baggage that we are uncomfortable with and often deal with in the worst ways). However, there does seem to be some statistical association here, whatever the causal relationship is. One hypothesis is that phthalates alter fetal production of testosterone at an important period of development, affecting “brain sexual differentiation.” It’s not so hard to imagine—a year ago I did a post on how certain common chemicals in pregnant mothers seemed to be causing penis deformities in their male children. The culprit there? Phthalates. The women in that story, however, had had exceptionally high exposure to phthalates (their jobs had them in constant contact with phthalate-containing hairspray), so it’s probably not something to lose sleep over, but it’s worth knowing.
And while phthalates aren’t supposed to be in food packaging, the next article I came across (this is an extravaganza, after all) deals with another plastic additive, BPA, that is found in food packaging, and which may also cause some hormone-related havoc.
BPA has come up on Science Buzz before. It’s in all sorts of packaging and bottles (it’s the reason your over protective mother doesn’t want you to use nalgene bottles) and it may affect tissue development, potentially increasing cancer risks.
We don’t care about that, though, right? Sure, cancer is out there, but in the future, not right now, you know? I know. But BPA’s latest appearance in the news may bring some immediacy to the concern over its use. Concern for some people. For men, I mean.
Chemical BPA in workers related to sex problems, says the Washington Post. “Sex problems”? We don’t want those! Chinese men working in a factory that uses BPA were found to have high rates of sexual problems. (I won’t be defining what “sexual problems” are because whatever you just imagined was probably correct.) Now, these guys have BPA levels about 50 times higher than the average American. But, still, something like 90% of Americans have detectable levels of BPA in their urine. Again, probably nothing to lose a lot of sleep over, but something worth knowing about. This professor is of the opinion that BPAs should be banned, even though most of us will probably never be exposed to dangerous levels of it, because a) it’s not a natural part of our diet; b) it’s not actually necessary in plastics processing; c) it accumulates in the body, and we still don’t know what level at which it begins to become harmful (ask those Chinese guys); and d) it’d be relatively easy to get it out of the food and water supply, unlike some other potentially harmful chemicals.
Accepting that scientific studies are necessarily very focused to eliminate variables, both of these stories still left me wondering what affect phthalates and BPAs have on women and girls. On one hand, one tries to avoid the mindset that average human physiology=male physiology, but on the other hand it’s usually just males that have penises, making their medical problems a little more hilarious.
There are so many… things out there, and they’re all doing… stuff! Interesting to know.
Courtesy Jiju Kurian Punnoose
In the embryo, the pancreas and liver tissue develop from the same family of cells. Crucial for the creation of the pancreas in the embryo, is the Pdx-1 gene.
By infecting adult human liver cells with a harmless virus engineered to carry Pdx-1, the liver cells began produced Pdx-1 protein.
Sarah Ferber and her colleagues at the Sheba Medical Center in Tel Hashomer, Israel, showed that the gene deactivates a range of genes relevant to the cell's function in the liver, as well as activating unexpressed genes vital for beta cell function (beta cells produce insulin).
The ultimate plan is to take liver cells from people with diabetes, reprogram the cells and reinject them. Because they are the patient's own, the cells should escape rejection by the immune system, sparing the individual a lifetime of daily insulin injections. "Potentially, patients can be donors of their own therapeutic tissue," says Ferber. New Scientist
Ferber is presenting the work on July 9 at an International Society for Stem Cell Research (ISSCR) meeting in Barcelona, Spain.
Courtesy USDALets say you are walking in the woods and you see a 12 point deer ahead of you. You sneek up quietly but not quietly enough. The deer hears you looks right at you and begins to charge. Before you know it its right antler has sheered off your arm! What do you do? Well if you were a salamander you would simple re-grow it.
For centuries scientist have wondered how salamanders regenerate limbs. In recent history they believed the tissue around the injury regressed into pluripotent stem cells (the kind we have all heard about that can morph into many different types of cells) and they reform into each cell type needed to create the limb.
This research was conducted to help understand how the salamander was able to do this amazing feat so that we could apply it to humans. Unfortunately, stem cells are not the easiest thing to work with but, that is old news now.
New research has shown that the salamander's cells do not regress but have memory that allows them to grow into what they once were. The memory is so good that the cartilage from the lower limb re-grows in the lower limb again.
The way scientist were able to do this was by engineering a florescent protein in a group of salamanders and transplanted only a select cells (skin, bone, muscle, etc) into embryos. After the embryos had grown, a limb was amputated. When it re-grew scientists observed that the glowing cells were not spread out amongst all the different cell types, as it would be if the cells had regressed into blank slates, but the florescent protein was only found in the original transplanted cell type.
Good new for us humans. This new finding may, although most likely not in our life time, make it easier to regenerate human organs.
Courtesy Apollo13Ma (background photo), public domain and Mark RyanA study out of New Zealand says a warmer climate speeds up molecular evolution in mammals. The concept isn’t exactly a new one. Scientists have known that a warmer environment increases the pace of microevolution for other types of life, such as some plants and marine animals, but evidence that it affects mammals – which are warm-blooded (meaning their temperature is regulated internally) – has not been observed before.
Lead researcher, Len Gillman from Auckland University of Technology, said the result of the study was “unexpected”.
""We have previously found a similar result for plant species and other groups have seen it in marine animals. But since these are 'ectotherms' - their body temperature is controlled directly by the environment - everyone assumed that the effect was caused by climate altering their metabolic rate.""
Since DNA can potentially mutate each time a cell divides into two copies of itself, the faster (and more often) these divisions take place, the more chances advantageous mutations will be passed onto subsequent generations, and the faster microevolution takes place.
Gillman and his crew traced and compared small genetic changes in 130 pairs of related species that lived in different latitudes, focusing on a single gene in each pair. They then compared the gene against that of a common ancestor, and were able to determine which of the two mammals’ DNA had mutated (microevolved) more rapidly. The changes were small-scale, but the species living in the more tropical environment showed a faster pace in its level of molecular evolution.
The results of the study appear in Proceedings of the Royal Society B.
Wait, you say, fractionally raising your heads from your overstuffed couches and baths full of tepid water. Didn’t John Snow actually die in June? And, like, didn’t he die on June 16, not on the 17th?
Well, yes, June 16, 1858, was in fact the day John Snow died. But I only just made up Snow day, and I wasn’t paying attention yesterday. Plus, do y’all even know who John Snow was?
Oh, John Snow was the most marvelous man! He drugged queen Victoria! He deprived thirsty communities of pump handles! He saved London from tiny invisible monsters! Oh, what a man!
John Snow was the sort of guy that posthumously gets the Cleverboots Award for Correct Thinking. Sort of like how I will surely be recognized with a Cleverboots Award years after I die, for how strikingly accurate my public ranting on the subjects of invisible lasers, lizard people, and “stay away from me, wizards!” will prove to be.
Snow was one of the first people to study the used of ether and chloroform as anesthetics. Which is to say, people had used those compounds as anesthesia before, but Snow calculated doses that would leave you somewhere between horrible pain and drugged to death. That was important. Everybody’s favorite queen of England (Victoria, duh) had Snow personally administer her anesthesia during the births of her eighth and ninth children. Once people saw Victoria doing it, everybody wanted in on anesthesia.
Snow’s greatest achievement, perhaps, came in an episode I like to call “Johnny Snow vs. Cholera.”
See, in the middle of 19th century in London, people were sort of split into three groups. There was the “Cholera is caused by poisonous gases” group. Most everybody thought that theory was the best, and it was called the “miasma theory.” There was also the “Cholera is caused by something tiny or invisible in water” group. This was pretty much what we call “germ theory,” and most everybody was all, “Germs? That’s stupid. Check your head!” And, finally, there was the “Hey, we’re actually dying of cholera over here” group, and most everybody thought they were gross.
But not John Snow! Instead of arguing and making up theories based on what seemed reasonable, he actually went out and looked at stuff. Gasp!
Without knowing for certain exactly how cholera was being transmitted (germs or miasma, or whatever), Snow began to record who in London was getting the disease, and he plotted cases on city street maps. He saw clusters of the disease in certain areas of the map, and so he looked for common elements. In the case of one outbreak, Snow realized that the majority of infected people were getting their water from one of two water companies, both of which were pulling water from a dirty (read: full of sewage) section of the Thames river. In another outbreak, Snow found that most of the victims of the disease were getting their water from a particular public pump. When John Snow had the handle of the pump removed, so that nobody could get water from anymore, the outbreak ended.
Snow’s discoveries from studying the cholera outbreaks added to the evidence for germ theory, and, perhaps more importantly, constituted a huge stride forward in the science of epidemiology. Snow wasn’t just figuring out how to cure diseases, he was tracking down where they start, and learning about how they move through populations. These are the same basic principles behind the actions health organizations still take today when dealing with outbreaks in the much larger population pools (or pool) of the 21st century.
It’s pretty interesting stuff. Check out this Snow-stravaganza: UCLA’s comprehensive page on John Snow and the cholera outbreaks.
Now enjoy what’s left of your Snow day.
Stem cells are the body's master cells, able to morph into any type of tissue, organ, or blood. Patient specific stem cells hold the promise of reversing cancer, diabetes, Alzheimer's and other diseases and also allow researchers to grow patient-specific organ and tissue transplants which will not require harmful anti-rejection drugs.
Up until now, the stem cells produced from a patients own skin had within them remnants which made them unsafe (linked to health problems such as genetic disorders and cancer).
Robert Lanza and a team led by Kwang Soo Kim of Harvard University succeeded in delivering the genes by fusing them with a cell penetrating peptide which does not pose the risk of genetic mutation. Their findings are published in the journal Cell Stem Cell.
This system eliminates the potential risks associated with the use of viruses, DNA transfection, and potentially harmful chemicals and in the future could potentially provide a safe source of patient-specific cells for regenerative medicine. Cell Stem Cell
Their technique involves soaking cells in human proteins that turn back the clock biologically, making the cells behave like powerful embryonic stem cells. They plan to seek Food and Drug Administration permission to test the cells in people by next year.
"This method eliminates the risks associated with genetic and chemical manipulation, and provides for the first time a potentially safe source of iPS cells for translation into the clinic," Lanza said.
"This is the ultimate stem cell solution -- you just add some proteins to a few skin cells and voila! Patient-specific stem cells!" Reuters
Only a tiny percentage of skin cells in the study transformed into iPS cells over two months (0.001%).
"How readily or quickly this technology is applied, and whether the efficiency is improved, are things that we will have to wait and see. said Dr. Arnold Kriegstein, director of the Institute for Regeneration Medicine at the University of California" Time
So, let’s see… if we’re arranging the list in terms of the order in which I’ve realized each one, then this new development falls at the end, right after “better resistance to sunburn” and “less likely to get testicular cancer.”
If the list is alphabetical (how nice and neat!), it goes between “more powerful backstroke” and “more powerful interpersonal skills.”
Despite my rabbit-killing-strength grip and my powerful stammer (each unlikely to be beaten by women as a whole), the bite of each item on the list burns like jalapeño scorpion stings.
It’s nice, then, that this new fact isn’t quite so painful to accept. See, I like getting sick. I want to get sick. In particular, I want to get the swine flu. My great-grandfather was beaten (i.e. killed) by the swine flu back in 1920 or so, and I’ve been aching for a rematch. Swine Flu vs. JGordon Round II: The Final Showdown: This Time it’s Personal: A Century-Old Family Feud Comes to Blows: To the Death!
Sure, I don’t actually want to die at all, but this disease needs to at least get a foothold in my system if we’re finally going to see who’s the bigger man. (Me, duh.)
If I were what we often call a “lady,” my powerful immune system would make the flu showdown less likely. So thank goodness that that’s not the case. My female body would be producing estrogen left and right, and that estrogen would be blocking the production of an enzyme called Caspase-12. Caspase-12, precious Caspase-12, is needed in my body, because it blocks my inflammatory processes. Inflammation is one of the body’s primary defenses against infection. Blood flow increases at the site of an injury or infection during inflammation, beginning the healing process and delivering structures that kill and absorb pathogens. And I don’t want that. I mean, if every time Evander Holyfield approached Mike Tyson’s boxing ring a flood of blood and plasma crushed Holyfield and washed him away, how would The Dynamite Kid ever have gotten the chance to prove who’s tougher? I want to let the swine flu into my ring, and then I want to bite its ear off and threaten to eat its children.
I’m leaving it up to my frail male body to arrange this fight.