May 23, 2013
Most people consider saving the Amazon rainforest a noble goal, but nothing comes without a cost. Cut down a rainforest, and the planet loses untold biodiversity along with ecosystem services like carbon dioxide absorption. Conserve that tract of forest, however, and risk facilitating malaria outbreaks in local communities, a recent study finds.
Nearly half of malaria deaths in the Americas occur in Brazil, and of those nearly all originate from the Amazon. Yet few conservationists consider the forest’s role in spreading that disease. Those researchers who do take malaria into account disagree on what role forest cover plays in its transmission.
Some think that living near a cleared patch of forest–which may be pockmarked with ditches that mosquitoes love to breed in–increase malaria incidence. Others find the opposite–that living near an intact forest fringe brings the highest risk for malaria. Still more find that close proximity to forests decrease malaria risk because the mosquitoes that carry the disease are kept in check through competition with mosquitoes that don’t carry the disease. Most of the studies conducted in the past only focused on small patches of land, however.
To get to the bottom of how rainforests contribute to malaria risk, two Duke University researchers collected 1.3 million positive malaria tests from a period of four-and-a-half years, and ranging over an area of 4.5 million square kilometers in Brazil. Using satellite imagery, they added information about the local environment where each of the cases occurred and also took rainfall into account, because precipitation affects mosquitoes’ breeding cycles. Using statistical models, they analyzed how malaria incidences, the environment and deforestation interacted.
Their results starkly point towards the rainforest as the main culprit for malaria outbreaks. “We find overwhelming evidence that areas with higher forest cover tend to be associated with higher malaria incidence whereas no clear pattern could be found for deforestation rates,” the authors write in the journal PLoS One. People living near forest cover had a 25-fold greater chance of catching malaria than those living near recently cleared land. Men tended to catch malaria more often the women, implying that forest related jobs and activities–traditionally carried out by men–are to blame by putting people at greater risk for catching the disease. Finally, the authors found that people living next to protected areas suffered the highest malaria incidence of all.
Extrapolating these results, the authors calculated that, if the Brazilian government avoids just 10 percent of projected deforestation in the coming years, citizens living near those spared forests will contend with a 2-fold increase in malaria by 2050. “We note that our finding directly contradicts the growing body of literature that suggests that forest conservation can decrease disease burden,” they write.
The authors of the malaria study do not propose, however, that we should mow down the Amazon in order to obliterate malaria. “One possible interpretation of our findings is that we are promoting deforestation,” they write. “This is not the case.” Instead, they argue that conservation plans should include malaria mitigation strategies. This could include building more malaria detection and treatment facilities, handing out bed nets and spraying for mosquitoes.
This interaction between deforestation and disease outbreakis just one example of the way efforts to protect the environment can cause nature and humans to come into conflict. Around the world, other researchers have discovered that conservation efforts sometimes produce negative effects for local communities. Lyme disease–once all but obliterated–reemerged with a vengeance (pdf) in the northeastern U.S. when abandoned farmland was allowed to turn back into forest. Human-wildlife conflict–including elephants tearing up crops, tigers attacking livestock, and wolves wandering into people’s backyards–often comes to a head when a once-declining or locally extinct species makes a comeback due to conservation efforts.
“We believe there are undoubtedly numerous ecosystem services from pristine environments,” the PLoS One authors conclude. “However, ecosystem disservices also exist and need to be acknowledged.”
February 23, 2013
It seems like science fiction, but researchers have actually grown organs from stem cells, organs that were successfully transplanted into humans. Two years ago, a man received a new trachea to replace his, damaged by cancer—the trachea was made by Swedish researchers who infused a synthetic scaffold with the patient’s own stem cells. Earlier, in 2006, scientists at Wake Forest used stem cells to successfully implant laboratory-grown bladders in young patients with spina bifida, a developmental birth defect.
Now, science has set its sights on even bigger lab-grown organs: hearts. Researchers are currently growing them in labs using scaffolds made of biomaterial which guide stem cells into becoming cardiomyocytes, the contracting cells that are basis of cardiac muscle.
Such stem cell research in humans comes with a host of ethical problems. However, a new study, published yesterday in the Journal of Clinical Investigation, suggests a different type of cell could do the job when it comes to artificially engineering new tissue. It involves a biological process that doesn’t exist in mammals: parthenogenesis
Parthenogenesis is a form of asexual reproduction that occurs naturally in plants, insects, fish, amphibians and reptiles. During this process, unfertilized eggs begin to develop as if they’ve been fertilized. For example, the entire species of marmorkrebs, a type of crayfish, is female, and the offspring produced, without any male contribution, are genetically identical to the mother.
In 2007, researchers induced human egg cells with chemicals mimicking fertilization so they would undergo the process. The result were parthenogenetic cells that share the same properties as embryos, except that they can’t grow further. The cells are akin to pluripotent stem cells derived from embryos, which means they have the ability to develop into different types of cells—including heart cells.
The German researchers in the new study used this knowledge to turn body cells of mice into parthenogenetic stem cells, which were then grown into mature, functional cardiomyocytes. Researchers used these cells to engineer myocardium–heart muscle–with the same structure and function of normal myocardium. The muscle was then grafted onto the hearts of the mice that had contributed the original eggs for parthenogenesis, where it worked the same way as existing muscle.
For humans, building heart muscle from parthenogenetic stem cell-derived cardiomyocytes in this way could overcome several hurdles, according to a new paper examining the implications of the German team’s discovery. A heart attack can destroy up to one billion cardiomyocytes. These cells can be regrown naturally by the body, but not quickly and not in significant quantities, which means tissue-engineered heart repair may become crucial for a full recovery.
Regeneration via stem cells could also mean the difference between life and death for heart transplant candidates. Approximately 3,000 people in the United States are on the waiting list for a new heart on any given day, but only 2,000 donor organs are available each year. But even if a person receives a new heart from a donor, there’s no guarantee the body will accept the new organ. A person’s immune system sees the new organ as a foreign object, which triggers a chain of events that can damage the transplanted organ. To prevent transplant rejection, patients are treated with immunosuppressive drugs, which can increase cancer risk, and most stay on at least one type of the medication for the rest of their lives. Hearts regrown from parthenogenetic stem cells, however, will likely eliminate organ rejection.
Parthenogenetic stem cells, which can be derived from cells readily made in the blood or skin, contain a genome inherited from only one individual—in this study, the mouse, and potentially in the future, a human patient. This means the cells are likely to be more compatible to the patient’s immune system—the body is less likely to reject organs grown from its own cells.
In humans, the process could remove embryonic stem cells from the equation, taking associated ethical questions with them.
January 23, 2013
Next time you’re reading about a scientific finding and feeling a bit skeptical, you may want to take a look at the study’s authors. One simple trick could give you a hint on whether the work is fraudulent or not: check whether those authors are male or female.
According to a study published yesterday in mBio, men are significantly more likely to commit scientific misconduct—whether fabrication, falsification or plagiarism—than women. Using data from the U.S. Office of Research Integrity, this study’s authors (a group that includes two men and one women but we’re still trusting, for now) found that out of 215 life science researchers who’ve been caught misbehaving since 1994, 65 percent were male, a fraction that outweighs their overall presence in the field.
“A variety of biological, social and cultural explanations have been proposed for these differences,” said lead author Ferric Fang of the University of Washington. “But we can’t really say which of these apply to the specific problem of research misconduct.”
Fang first became interested in the topic of misconduct in 2010, when he discovered that a single researcher had published six fraudulent studies in Infection and Immunity, the journal of which he is editor-in-chief. Afterward, he teamed up with Arturo Casadevall of the Albert Einstein College of Medicine to begin systematically studying the issue of fraud. They’ve since found that the majority of retracted papers are due to fraud and have argued that the intensely competitive nature of academic researcher engenders abuses.
For this study, they worked with Joan Bennett of Rutgers to break down fraud in terms of gender, as well as the time in a scientist’s career when fraud is most likely. They found that men are not only more likely to lie about their findings but are disproportionately more likely to lie (as compared to women) as they ascend from student to post-doctoral researcher to senior faculty.
Of the 215 scientists found guilty, 32 percent were in faculty positions, compared to just 16 percent who were students and 25 perecent who were post-doctoral fellows. It’s often assumed that young trainees are most likely to lie, given the difficulty of climbing the academic pyramid, but this idea doesn’t jive with the actual data.
“Those numbers are very lopsided when you look at faculty. You can imagine people would take these risks when people are going up the ladder,” said Casadevall, “but once they’ve made it to the rank of ‘faculty,’ presumably the incentive to get ahead would be outweighed by the risk of losing status and employment.”
Apparently, though, rising to the status of faculty only increases the pressure to produce useful research and the temptation to engage in fraud. Another (unwelcome) possibility is that those who commit fraud are more likely to reach senior faculty positions in the first place, and many of them just get exposed later on in their careers.
Whichever the explanation, it’s clear that men do commit fraud more often than women—a finding that shouldn’t really be so surprising, since men are more likely to indulge in all sorts of wrongdoing. This trend also makes the fact that women face a systemic bias in breaking into science all the more frustrating.