Malaria is a life-threatening disease transmitted to humans by infected mosquitoes. In 2018 alone there were 228 million cases and 405,000 deaths worldwide, affecting mostly children under five years of age. Scientists have long been looking for an effective vaccine, but haven't yet been able to produce one.
Human malaria is caused by five species of Plasmodium parasites, with Plasmodium falciparum the most deadly of them. But there are other Plasmodium parasites that can infect and cause malaria in other mammals. About ten years years ago, a group of researchers in Portugal, led by Miguel Prudêncio, decided to explore the possibility of using a rodent parasite called Plasmodium berghei in a vaccine against malaria.
They developed a P. berghei parasite genetically modified to look like P. falciparum, meaning that it carried P. falciparium proteins on its surface. Being a rodent parasite makes it non-pathogenic to humans, and as it was covered by proteins from the human parasite they reasoned that it could potentially induce an immune response to the human parasite. They deliberately chose a protein active during the stage where the malaria parasite infects our livers. Acting at this stage blocks the life cycle of the parasite and prevent it from reaching the bloodstream.
A clinical trial for this rodent-inspired vaccine started in 2017. Last month the results of the first stages of this trial were published in Science Translational Medicine. The trial involved 24 healthy adult volunteers in the Netherlands. After the trial showed that the new vaccine was safe at the tested doses, it entered phase two, aimed at testing the efficacy of the immunization. The vaccinated volunteers were actually infected with the human malaria parasite P. falciparum. When compared with the unvaccinated control group, the volunteers had 95% less parasites in their liver and also produced antibodies that recognized P. falciparum.
While the vaccine did not confer full protection to the infection, it looks to be a promising approach and may lead the way to create an effective malaria vaccine.
Carbon dioxide captured and stored in the ocean is called blue carbon. Seagrass meadows, in particular, are important blue carbon sinks, storing massive amounts of carbon in mud and sand for hundreds to thousands of years. Seagrass meadows are large shallow-water areas where the seafloor is covered with seagrass growing in mud or sand. By keeping the carbon out of the atmosphere, they help regulate our climate system. However, a recent study of an Australian estuary found that seagrass meadows are not all equally good at storing carbon.
When the researchers of this study analyzed mud and sand samples from in the seagrass meadow, they found huge variation in its ability to store carbon. Their analysis revealed that carbon storage increases with a higher proportion of mud and carbon inputs from local, non-seagrass sources such as runoff from nearby land. The lead author of this study and a postdoctoral scientist in the research group I work in, Aurora Ricart, said, "this and similar studies will improve quantification of seagrass carbon stocks and tell us more about their capabilities as global carbon sinks."
With better characterization of high carbon storage seagrass meadows, governments can determine which meadows need protection. This will secure their ability to store carbon long into the future, helping mitigate climate change.
On Monday, US Immgration and Customs Enforcement (ICE) announced changes to that require international students to choose between attending in-person classes in the fall or leaving the country. The State Department will not issue visas for students at universities teaching online-only in the fall. This leaves many at universities not offering in-person classes with an impossible choice: transferring schools to fulfill this arbitrary request and risk catching COVID-19, or leave their lives and work behind. Otherwise they face being deported. A researcher I’ll call M reached out to me and described their situation.
“Everyone is telling me to stop being pessimistic but I’m being realistic. I contribute so much to this society and now I have a fear of ICE.”
M is a student and instructor on an F-1 visa at a large, public research university. Leaving the US means going back to their home city, a COVID hotspot where local officials are withholding test results from the public.
Going home and continuing to work from there is an impossibility, because of both an enormous time difference that would make teaching difficult, on top of a lack of consistent internet access. Without consistent internet access their work cannot be done. Documents used for research contain sensitive information and they fear even accessing the documents may result in reprisal or invasions of privacy.
Neither ICE nor M’s university are operating in good faith. ICE’s stipulations for attendance don’t match the university’s, so neither can be satisfied. Minimal face-to-face classes (not enough to satisfy ICE) are being offered, which M sees as just a way to catch COVID-19 and a threat to their life. University administration is preventing students from reaching out to elected officials for assistance.
“I’m way too scared to post anything on social media right now.”
Their university, and by extension the local government, uses international scientists as a source of revenue (counting them as a resident and demanding student fees), without access to many grants offered to other students. Now they are being tossed capriciously out of the country by the federal government after being used as a source of income by the state government.
“I’ve lived in [multiple parts of the US] and I know about ICE and how they deport people and children. I’ve been a scientist and published in all the right journals and it means nothing right now.”
Do I belong here? If you have ever asked this question, you are not alone. This basic need of acceptance reflects on our inherent desire and motivation to form and keep interpersonal relationships, wherever we are, or wherever we want to be.
Low sense of belonging or social exclusion often lead to anxiety, depression, and stress, ultimately influencing our behavior. From a student's perspective, seeing professors that look like us can help us feel like we belong in academia. So, to understand the gender and racial or ethnic underrepresentation at the professoriate level in STEM fields, researchers from the chemistry department at the University of California - Berkeley have investigated graduate students' senses of belonging.
They used a visual narrative survey to evaluate how much students related to 15 different situations. They used this technique instead of plain text to convey emotion through the facial expressions, postures, and social interactions of characters in the pictures. These scenarios were chosen to evaluate students' reactions and senses of belonging, as well as previously undefined factors such self-perceived intelligence, value, competence, productivity, and independence.
The researchers found that about 75 percent of students sometimes or rarely felt happy and accepted, like they belonged. Most respondents indicated that students had some form of support from their peers but felt negatively or neutral about whether faculty (meaning, professors) understand the hardships they face. Members of underrepresented racial or ethnic groups were less likely to feel a sense of belonging than members from the majority. Similarly, female-identifying respondents felt less like they belonged than male-identifying respondents
This study is important in that it addresses graduate students, whereas most similar studies have only focused on undergraduate students. To increase diversity in the STEM professoriate, academia clearly needs to change, and one sorely needed fix is to make all people feel like they belong in the ivory tower.
Creativity in the workplace makes an individual an innovator and a company a changemaker. However, cultivating creativity in an office setting can be challenging. Research suggests that moving around while thinking can have positive impacts on our creativity. But having company employees come up with ideas while sprinting on a treadmill isn't exactly ideal, nor is it feasible for everyone.
A group of researchers in France and India has built on this idea by making individuals feel that they were moving, to see if that would provide the same creativity bump as does actually moving. In their study, published in the journal Thinking Skills and Creativity, they used virtual reality to "transport" 32 volunteers to an imaginary empty train car. Half of the volunteers experienced a still car, while the other half saw lights pass them by in the train windows, as if they were in motion and going through a tunnel.
While in the virtual reality environment, the study volunteers participated in tests designed to measure divergent creativity, the ability to come up with many different ideas to solve a problem, and convergent creativity, the ability to drill down to one correct solution based on many ideas. Once each participant’s creativity was scored, the researchers compared the scores of the participants in stationary train cars with those in moving train cars.
The participants who conducted their creativity tests in a virtual moving train showed higher amounts of divergent creativity compared to those in still trains. From this, the researchers concluded that the simple perception of movement can improve our creativity and idea generation, whether or not we are actually moving. So if you are feeling low on ideas, strap on some virtual reality goggles and hop on a train, plane, or boat to recharge!
Pain is a way for our bodies to tell us that we are hurt, and we should take care to protect ourselves from further harm. This signal manifests in the form of inflammation and hypersensitivity to touch, at the site of injury. Once the injury is healed, the associated symptoms also resolve themselves. But in some cases, even after the inflammation subsides, the pain persists for months or years, which can lead to decreased quality of life for people with this long-term (or chronic) pain. While physical therapy and medication can help relieve pain, they are unreliable at best and can sometimes lead to opiod addiction.
To find robust methods of pain relief, we need to understand how our bodies resolve pain naturally and how that process is disrupted in case of chronic pain. In a recent study (currently posted as a pre-print) by scientists based in the Netherlands and the US, researchers unraveled how immune cells, called macrophages, relieve pain caused by damage to sensory cells.
Macrophages are known for their ability to ‘eat’ foreign particles in our body. They also play a substantial role in both the initiation and mitigation of pain. Two types of macrophages are involved in these processes: M1 and M2. The former initially crowd around a wounded area, causing inflammation and pain. As the wound heals they are then replaced by M2 macrophages, which ease these symptoms. The researchers found that an imbalance in the levels of these two types of macrophages can cause chronic pain.
The way that M2 macrophages alleviate pain is fascinating. A wound disrupts the energy-producing cellular machinery, called mitochondria, of surrounding sensory cells. M2 macrophages actually transfer their own mitochondria into the affected cells in small balloon-like structures, easing the pain sensation. This suggests that therapies aimed at increasing the mitochondrial transfer from M2 macrophages into cells around our wounds, giving them a jolt of energy, could help relieve chronic pain.
Some 8.7 million years ago, much of what is now Idaho was torched by clouds of hot volcanic ash, destroying all vegetation and animals in sight. The supervolcano, Yellowstone, was erupting. This was Yellowstone’s largest eruption on record.
Super-eruptions can decimate entire regions, and their cocktail of ash and gases can alter the climate. But, even though they eject huge amounts of material, there are very few documented super-eruptions in the geologic record. So we don’t fully understand why they are so big or how often they occur. Now, details of the Yellowstone supervolcanic eruption are documented in a published in the journal Geology.
Yellowstone’s ancient eruptions scattered volcanic debris across the northwestern US. There are so many deposits — covering an area tens of thousands of square kilometers — that it can be difficult to tell each eruption apart. To get around this, volcanologists collected detailed identifying information, including chemical and chronological data, on each geological deposit.
When they looked at the data, they found that much of the volcanic debris, which was thought previously to come from repeated smaller eruptions, had the same chemical makeup and age. In fact, these deposits were produced by two previously unrecognized super-eruptions. Both eruptions were searingly hot, and would have baked the landscape in a thick coating of molten volcanic glass. The youngest of the two, known as the Grey’s Landing super-eruption, is dated to roughly 8.7 million years ago, and, according to the volume of debris released, is 30% larger than all other eruptions recorded from Yellowstone.
Recognition of these events brings Yellowstone's total number of eruptions during the late Miocene to six. That makes for one eruption about every 520,000 years. Since then, however, the pace of eruptions has slowed to once every 1.5 million years.
The evidence seems to suggest that Yellowstone is slowing down. And if this trend continues, the next super-eruption won't happen for another 900,000 years. Predicting eruptions is however a risky business, and the United States Geological Survey still maintain a permanent monitoring network on Yellowstone — just in case.
If you’re a female black widow spider, it can be tough to know who to mate with. If you’re not picky at all, you may mate with the first male that comes along, missing out on other, better males that come by later. On the other hand, if you’re too picky and wait a long time, you might run out of available males and miss the opportunity to mate altogether.
Scientists from the University of Toronto thought that early life social context might play a role in mate choosiness. The researchers set up their experiment at Island View Beach on Vancouver Island, which is known to have an especially dense population of black widow spiders.
Researchers placed cages with immature female spiders either close to (within 1 meter) or far from (more than 10 meters) another wild female spider. Once the spiders had matured, researchers took them back to the lab and introduced them to potential mates.
Females that had grown up far from other spiders jumped quickly at the chance to mate. But females raised near other spiders were more picky. These spiders were more likely to reject the males — sometimes even eating the potential mates. Their findings shows that female black widows can adjust their mate choosiness in response to population density.
The novel coronavirus SARS-CoV-2 was first identified in December 2019 and is now responsible for over (correct as of 24 June 2020). But currently, the long-term immune response, and whether exposure protects against future infection, is unknown.
highlighted which reported that non-hospitalized patients who have recovered from a mild COVID-19 infection carry T cells that target SARS-CoV-2. T cell responses may provide better routes for immunity and vaccine development than the other ‘arm’ of the immune system — the B cell response — even though the latter response has received far more attention to date than T cells.
B cells produce antibodies which are important in immune system recognition and memory of features of pathogens called antigens. Antibody testing is increasing, enabling identification of individuals who have been infected with SARS-CoV-2.
A key question remains: are people with antibodies immune from reinfection? has addressed the antibody response of asymptomatic patients. The researchers reported that their antibody levels begin to decrease 2-3 months after infection, and that they exhibited a weaker immune response to infection compared to symptomatic patients. Therefore, we certainly shouldn’t depend on the idea that having antibodies for SARS-CoV-2 means that a person is immune. Allowing recovered patients to resume their normal lives without masks and social distancing is not as simple as first thought.
Our knowledge about the novel coronavirus is rapidly expanding. It remains unknown whether the T cell or B cell response actually provides long-lasting, or any, immunity to reinfection with SARS-CoV-2. But, studies such as these are fundamental in our continued understanding of this disease and will certainly be important knowledge for vaccine development and continued social distancing strategies.
A parasite prominent in sub-saharan African rivers called Onchocerca volvulus (pictured above) is one of the 17 neglected tropical diseases selected by WHO in 2003 for directed control or elimination. Transmitted by bites of Simulium blackflies that breed in rivers, the parasite causes 'river blindness'. Approximately 500,000 people are visually impaired by the disease, and many more have other symptoms of the disease. The WHO estimates that 205 million people in sub-Saharan Africa are at risk of infection.
The biggest barrier to treatment of the parasite is lack of proper diagnostic tools. Currently, an ELISA-based test that determines presence of an immune response specific for the parasite is used. However, this test does not discriminate between active and past infections, nor does it cover all potential markers for the parasite. As a result, it too-commonly returns false-negative readings.
A study led by scientists at the National Institutes of Health identified other biomarkers that can be used for more accurate detection of the parasite. Their test was able to determine whether the infection was old and recovered or active, and had more accurate results compared to the previous method.
The biomarkers they identified, along with others, could also be used in the future for more sensitive platforms for surveillance. The testing procedure found by this group has a sensitivity rate of 94% (meaning, it correctly identifies positive cases 94% of the time), and the researchers describe a way by which the test could even reach the WHO-recommended rate of 99%.
As people age, both and decrease, playing a role in the development of many chronic diseases. has been shown to attenuate the development of these declines; however, it is not recommended for the aging population due to its other . Are there other interventions that keep some benefits obtained from calorie restriction to promote healthy aging without the drawbacks?
is a dietary intervention that alters the timing of eating without changing the types of foods a person eats. It requires eating daily within a limited window, usually 8 to 12 hours per day, that often begins in the morning and ends in the afternoon. in both animals and humans have demonstrated that time-restricted eating can mimic some of the benefits of longer duration fasting and calorie restriction.
Earlier this year, tested a time-restricted eating regimen in healthy older adults. They found that the six-week intervention produced slight, but noticeable improvements in exercise capacity and glucose tolerance. The results from the present study suggest that time-restricted eating could reduce health issues that come with age.
These results demonstrate time-restricted eating to be a safe and feasible intervention that may reduce the development of chronic problems as people age. This pilot investigation lays the foundation for future long-term dietary studies examining time-restricted eating in older adults with and without chronic diseases.
An important part of science is sharing the findings, both with the general public, and with fellow scientists. The main method of sharing science is done by writing articles that are published in academic journals. However, most people are not subscribed to the Annals of Thoracic Surgery, and thus may not be aware of the latest articles that came out. This means that a lot of articles never reach the general public, or sometimes even fellow scientists. by the Thoracic Surgery Social Media Network shows that tweeting might be the solution.
Their team divided 112 journal articles into two groups. They only tweeted about the articles in one group, and not in the other, and only sent out one tweet on each article. They then looked at how this changed how much attention the articles had gotten a year later. They found that the articles that they tweeted about received on average more attention, which they measured using , a measure of the amount of interaction with a certain article through social media and the press. So a higher Altmetric score means that more people have heard about the article.
However, tweeting out articles did not just change how many people heard about the science. The study also found that the articles they tweeted about received more citations, on average three times as many, meaning other researchers used the findings in their own studies. This is quite a big deal for scientists, as it reflects how important their work is within their field.
Overall, tweeting about research articles can have a big impact in how far the article reaches and how it impacts future research. So the advice to any researchers who want their articles to be read: Tweet about them!
White sharks may have a guaranteed spot on Shark Week but there is still a lot to learn about this famed fish.
Sharks have been around for millions of years. The earliest fossil of Carcharodons, the of the white shark, dates back to . Yet today, white shark populations are considered to becoming endangered due to .
It isn't just modern populations of sharks that can provide us with useful insight. Understanding how white sharks thrived millions of years ago could help us protect them today.
The researchers collected white shark from three different places. They used measurements of the teeth to estimate the total length of the individual sharks. The total length of a juvenile white shark was considered to be between 175 cm to 300 cm. In Coquimbo, there was a higher proportion of juveniles compared to the other study sites. The researchers also found signs of potential prey species and evidence that this area was once a shallow-water marine habitat.
Nursery habitats helped protect young sharks millions of years ago. Identify and conserving modern nursery habitats could be an important factor in keeping white shark populations stable today.
Adriana L. Romero-Olivares
Guinea pigs are pets, , they're food, they're , and they are . You may have seen or heard of them, and wondered if they're enormous hamsters, or just pigs from Guinea — but they are none of these things. cas and .
Guinea pig trade outside of the Americas, started in the late 15th century when . Three centuries later, , and now, guinea pigs can be found almost anywhere in the world. Because of this, guinea pigs make an excellent tool for understanding human history and our relationship with domesticated animals.
In a , scientists looked at from guinea pig specimens recovered from archaeological sites in Latin America, the Caribbean, Europe, and the United States. They found that guinea pigs left South America, and into the Caribbean, around the 6th century, through existing human networks and trade routes. The work provides some of the earliest evidence of guinea pig domestication and distribution, over thousands of years ago and across long-distance continents far before Europeans arrived in the Americas.
They are charismatic, have their own personalities, are extremely vocal and social, eat a lot, poop a lot, and need to be cleaned a lot. But as a guinea pig pet owner, my life has been brightened by guinea pigs for over 15 years. I plan to have guinea pig pets until the day I die. And in doing so, perpetuating a strong bond and evolutionary history dating back thousands of years. Thank you guinea pigs, for teaching us so much.
When you experience a bacterial infection, knowing the site of infection helps doctors determine a treatment regimen. Today, clinicians figure out where these pathogens are using radiotracers – compounds with that react to the X-rays and magnetic field employed by CT and MRI imaging technology. However, clinicians using these radiotracers, such as those that have radioactive fluorine (18F) or gallium citrate (88Ga), suffer from a distinction problem: they cannot distinguish live infections versus a pathogen-free inflammatory response.
Scientists at the University of California, San Francisco came up with a clever solution: synthesize a radiotracer from the building blocks of bacterial cell walls. That way, as the bacteria grow and replicate at the infection site, each live cell is incorporated with a glowing radiotracer. They proved that their radioactive carbon (11C) radiotracer integrated nicely into the bacterial cell wall in the top pathogenic bacteria for hospital settings, Pseudomonas aeruginosa and Staphlococcus aureus — including MRSA.
But if you have an infection in your intestines, where your normal microflora live, will the radiotracer be taken up and incorporated into their cell walls rather than the pathogenic invaders? The researchers answered this question by comparing the radiotracer's location in various organs in normal mice (with normal microbiome) and microbe-free mice. They found that when the radiotracer integrated into the intestines, overall radiotracer incorporation was low, and the difference between microbe-containing and microbe-free organs was minimal. Notably, these 11C amino acids showed significant differences between live cells and dead cells, allowing clinicians to distinguish between live infection sites and sites of inflammatory responses.
Overall, the ease of creating these compounds and great incorporation efficacy into invading pathogens points to an easy translation of this radiotracer from the academic to clinical setting.
The Nelson Bay Cave, near the coast of South Africa, was excavated between the 1960s and the 1970s. It contains Stone Age remains and is also an important site to uncover past climate fluctuations, thanks to the traces of past animals (such as shells and teeth) the archaeologists found inside.
Between twenty-three and twelve thousand years ago, the cave was not facing the ocean, as it does today. During this period, known as the Last Glacial Maximum, sea level was 120 meters below what it is now, and the cave was facing the vast grassland now known as the Agulhas Plains. There are a lot of unknowns about what happened between that time and the beginning of the Holocene, when the ocean rose and submerged the Agulhas Plains.
To study these climatic changes, a team of scientists from the University of Cape Town, the Natural History Museum of Utah, and Nelson Mandela University studied the remains of herbivorous animals, related to cattle, found in the cave to look for changes in their diet. When an animal eats, some of its body tissues record the chemical signatures of food it has eaten. Scientists can measure this with isotopes, which are slightly altered versions of standard chemical elements. By measuring carbon and oxygen isotopes in herbivore teeth, the scientists could understand how the environment the food grew in changed over time. They identified a shift in the vegetation available at that time, which seems to have been caused by a change in rainfall patterns. This finding is another piece the puzzle of what climate around the world was like during the Last Glacial Maximum.
SARS-CoV-2, the coronavirus virus responsible for the COVID-19 pandemic, has infected over 9 million people globally and accounted for nearly 500,000 deaths as of June 23. This has led to a global effort whereby researchers have mobilized their labs to better understand the virus.
However, the exact source of the virus has still not been determined. To understand the origin of the virus causing the COVID-19 pandemic, researchers are screening the environment for all types of coronaviruses, such as those found in bats. These efforts will allow researchers the ability to map out the start of the virus' spread.
To further study coronaviruses in circulation, a group of scientists used samples from 227 bats in the Yunnan Province in southern China. The individual samples were collected between May - October 2019. Researchers next determined the viral strains in the samples and discovered two unique coronaviruses called RmYN01 and RmYN02.
Upon further examination, it was determined that RmYN02’s DNA sequence was very similar to SARS-CoV-2. However, there were significant differences in regions the virus uses to enter human cells. Looking closer, researchers noted the RmYN02 virus had only one of six critical anchors SARS-CoV-2 uses to enter human cells. These results were surprising considering the overall DNA similarity.
However, the DNA sequence of the RmYN02 virus did reveal unique mutations thought to be only found in SARS-CoV-2. This points researchers to the fact that this is a close relative of SARS-CoV-2. The origin of SARS-CoV-2 is still the subject of much debate, and it will be difficult to prove with certainty how it jumped from its host to humans. In the meantime, scientists are gathering data on other coronaviruses in an effort to prevent future pandemics.
The brain is a champion of self isolation. In other parts of your body, drugs and nutrients enter through the lining of blood vessels. While the brain is full of blood vessels, specialized vessel walls tightly regulate what can get in. This “blood-brain barrier” is important for protecting the specialized environment of the brain, but it is also a problem when trying to treat conditions like brain cancer or neurodegeneration as drugs can't get in.
We do know of some drugs that are really good at getting through this barrier, either by slipping in or by breaking the barrier down. A new study, currently published as a pre-print, has found that giving rats a drug that easily crosses the blood-brain barrier helps other drugs get into the brain, even if they aren’t normally able to.
What is this barrier breaking drug? Methamphetamine, also known as meth. Meth’s powerful effects are partly due to its ability to get into your brain. At low doses, it can increase a process called fluid phase transcytosis, in which a drug is packaged and transported into the brain by the cells lining blood vessels. While previous studies have shown this is how low dose meth enters the brain, this new study is the first time it’s been shown that it can bring other drugs along for the ride.
Researchers gave low doses of meth to rats, along with therapeutic drugs that don't easily cross the blood brain barrier. They then looked at the rats' brains to see what molecules were present. The therapeutic drugs got into the brain far more easily if meth was given at the same time. In another experiment, meth was able to help a chemotherapy drug enter the brain, which increased survival in a mouse model of brain cancer.
Meth isn’t often associated with medicine, but it is FDA approved for some uses. In cases such as aggressive brain tumors, it may be worth using a little meth for a lot of chemotherapeutic.
Micro-organisms, especially bacteria, play essential roles in our bodies, especially in our guts. Some bacteria are beneficial, and some like E.coli are harmful. Another Escherichia strain (in the same genus as E. coli) named Escherichia albertii is also pathogenic to humans, causing diarrhea and food-borne illnesses. E. albertii was identified for the first time during an illness outbreak in Bangladesh.
Pathogenic bacteria like E. albertii are very motile, meaning they move around a lot. They are able to do this using hair-like structures called flagella. E. albertii was originally described as non-hairy bacterium and thus far has been considered to be a non-motile pathogenic micro-organism.
A new study led by Tetsuya Ikeda and a team at Hokkaido Institute of Public Health in Japan has found that this may not be true: stressful environments can stimulate E. albertii to make flagella. They showed that, despite the fact of having most of the genes needed for flagella, at normal temperature of 37 degrees Celsius this bacterial strain does not show any motility. But in conditions such as low salt and nutrient concentrations and colder temperatures (20 degrees C), the bacterium's flagellar genes are activated and it becomes motile. More motile cells can survival better under unfavorable conditions, making them more harmful to humans.
Viruses that cause devastating pandemics are not exclusive to humans. Prochlorococcus marinus, a marine photosynthetic bacterium, is infected by many viruses – and this ecological interaction has consequences for all of us.
As the most abundant photosynthetic organism on Earth, P. marinus has a vital role in our ecosystem. Collectively, these bacteria absorb about four gigatons (four billion metric tons) of carbon dioxide every year via photosynthesis.
In a newly published paper, researchers at Rice University in Houston studied how bacteriophages, or viruses that infect bacteria, affect photosynthesis in P. marinus. They were particularly interested in ferredoxin proteins, which are involved in transporting the electrons harvested from light during photosynthesis. The ferredoxin proteins of bacteriophages that infect P. marinus were very similar to the proteins of the bacteria themselves that are involved in taking up nutrients. Much like putting a cable to a car battery and using its energy to cook dinner, phages redirect the electrons harvested by the bacteria for their own purposes.
By redirecting light energy to be used in incorporating nutrients instead of storing carbon, phages can offset the abilities of P. marinus to remove carbon dioxide from the air. Thus future studies on the spread of these viruses and how they might change in warming temperatures might be crucial in our projections of climate change.
Anyone who’s been punctual to a party knows that the first hour is pretty awkward. Some of us even prefer to arrive fashionably late to social events, so we won’t have to endure too much awkward silence until the energy builds up.
New research published in the Journal of Ecology suggests that tardiness can help plants avoid unpleasant situations too. Wood avens are forest herbs that reproduce by seeds. Early summer blooms produce the best seeds. Unfortunately, this is also when fruitworm beetle larvae hatch and feast on the developing seeds.
One way that the flowers can avoid beetle breeding season, ensuring that more of their own offspring survive, is by blooming later in the summer. By tracking wild plants, scientists found that those attacked by beetles in early summer did not compensate for their losses by producing more flowers later that year. Instead, the plants revealed their coping strategy in the following year, when they delayed flowering to avoid being attacked again.
But blooming late comes at a cost. The forest canopy grows dense in late summer, shading the wood avens. Without sufficient light, late bloomers make fewer seeds than beetle-free early bloomers. Blooming early is thus advantageous in places or periods where beetles are relatively few. This trade-off to blooming early or late may be why wood avens have evolved flexibility in their flowering time.
This study is the first to show a plant biding time to avoid negative situations, as a direct response to past experiences. Can other plant species do this too? Science continues to uncover the plant kingdom’s diverse, and often unexpected, defense strategies.
The basement membrane is a thin layer of cells and molecules that divides internal or external body surfaces (like your skin or blood vessels) from connective tissue. Basement membrane invasion is when a cell “invades” or moves across neighboring tissues, and it happens a lot in cancers. While many discoveries about how this process plays a role in cancer have been made in mice and human cells, these studies can take a long time. The nematode Caenorhabditis elegans (C. elegans) is a great alternative because it can quickly reproduce and actually uses basement membrane invasion to make its vulva.
Previous work has found that four genes are needed for basement membrane invasion in C. elegans. However, until now it wasn’t clear how these four genes interacted with each other. A recent study, published in the journal Development, discovered that these genes work in a specific cell called the anchor cell (AC) prior to invasion to regulate its division. The AC is a good cell to study because, in C. elegans, it must invade the vulval cells to form a bridge between the uterus and the nematode's vulva. If the AC does not do this, the nematode can't lay eggs.
When the four genes were individually turned off in healthy worms, instead of having one AC that could invade, they had many ACs that couldn’t invade the basement membrane, suggesting that turning off the genes prevents the AC from stopping itself from dividing. The researchers wondered if these mutations could be fixed by adding a protein called CKI-1, which is required to control cell division. Adding CKI-1 into the AC solved the problem when some combinations of the four genes were switched off, but not others, a hint that those other genes might perform different functions. But they work together to help the AC invade the vulval cells, a process which mirrors the way cancer cells invade other parts of the body.
Although these findings may sound incredibly specific and complex (and they are!), because the genomes of C. elegans are so similar to ours, they provide a roadmap for finding human genes that may be involved in cancer.
Biomarkers are quantifiable indicators of illnesses (such as levels of certain proteins in blood) that may otherwise be difficult to diagnose. Researchers are actively searching for biomarkers for Alzheimer’s disease (AD). Current approaches focus on designating people as “positive” or “negative” for AD based on the amount of two proteins, amyloid-beta (Aβ) and phosphorylated tau (p-tau), in their brains. Patients with more Aβ and p-tau than a certain threshold are considered positive, indicating that they are likely to develop AD.
But more and more, clinicians are discovering exceptions to this yes/no designation system. For example, there have been many cases of those with significant Aβ plaque formation who remain “cognitively intact”, meaning they don't develop dementia or other symptoms of AD, throughout their lives. These exceptions highlight a disconnect between the total accumulation of these biomarkers and the impact on cognitioon.
Scientists have challenged this static system in a new paper, published in a specialized journal for AD research, by introducing time-inclusive categories. Instead of focusing on protein levels, they categorized individuals by how rapidly their brains accumulated Aβ and p-tau. To demonstrate the utility of their system, the researchers analyzed a group of 250+ cognitively normal individuals to see if they could identify the Aβ and p-tau biomarker accumulation rate and their association with AD risk factors, like the APOE4 allele. Their system successfully separated volunteers into distinct groups for both biomarkers. They could also identify timepoints of “escalating accumulation” within each group.
This system provides greater context for at-risk individuals and opens the door for earlier treatment of AD in people who were not considered positive for AD under previously used biomarkers. As more research points to the spread of the “amyloid burden” much earlier in life than the onset of cognitive decline, this new categorization can create more realistic diagnosis timelines for the currently incurable disease. To draw their final conclusions on the efficacy of their system, these researchers must continue monitoring study participants to determine when and if they develop AD. In its current state, their system is an untested theory beholden to the same master as those potentially afflicted with AD: time.
One of the most important tasks for forensic scientists after a body is found is to determine the exact time of death. This is key in piecing together the events that led up the death and is especially important when a crime is suspected. The typical signs of post-mortem change in human bodies are often extremely hard to read if a body has been submerged in water, making it even harder to determine the time of death.
New research from a team at Northumbria University, UK, has revealed a new method to calculate time of death of a body found in water, based on proteins found in bones. The team found that several common bone proteins underwent a chemical change called deamidation when a corpse was submerged in water. More importantly, they found that the longer a corpse was submerged in water, the more deamidation was taking place. They also showed that some types of water, such as pondwater, had a noticeably different impact on protein deamidation in bone after death.
These studies were performed in mice, and obviously must be replicated using human cadavers before the findings are translated into forensic practice. But they have identified some very promising biomarkers for determination of how long bodies have been submerged in water, and their chemical method can be replicated in other labs.
Imagine you live in Canada and it is December. The cold has started to creep in. It takes layers of warm clothes and central heating to keep you from shivering. You look outside the window, see birds fluttering around and think to yourself, “How do animals survive out there?”
Many mammals (like rodents and bears) and birds (like hummingbirds) have the amazing ability to undergo ‘torpor’, during which they slow down their bodily functions to conserve energy. Animals make use of this to survive harsh environmental conditions. However, the mechanism by which animals sense the surrounding temperature and exhibit such a response is not known.
Researchers from Yale University explored this in a recent study published in eLife. They describe how a group of cells called POA neurons in the hypothalamus region of the mouse brain sense cold and get activated to relay the signal forward.
To understand what sets POA neurons apart from other cells, the scientists looked at the different components they are composed of. All neurons receive information with the help of small pores on their surface, which open only when their partner molecule sticks to them. What makes POA neurons special is the abundance of one such pore, which becomes increasingly likely to open as temperatures drop and it becomes more attracted to its partner. Once open, it allows the neuron to become active and pass on the message. The property of the pore to unlock for low concentrations of the partner molecule at cold, but not warm temperatures, is what makes it a cold sensor.
Findings from this study shed light on one possible mechanism of cold temperature sensing. But in order to fully understand how animals survive frigid conditions, we still need to tease apart the steps from sensing temperature to regulating it.