Tech

Animals that do well in urban areas tend to be the ones that learn to make use of resources such as the food humans throw away. But is our food actually good for them? A new study published in The Condor: Ornithological Applications suggests that a diet of human foods such as discarded cheeseburgers might be giving American Crows living in urban areas higher blood cholesterol levels than their rural cousins.

Hamilton College's Andrea Townsend and her colleagues sampled the blood cholesterol levels of 140 crow nestlings along an urban-to-rural gradient in California, returning to track their survival rates after they fledged. They found that the more urban the environment, the higher the blood cholesterol of the crow nestlings raised there. To directly test the effects of human food, the researchers also provided nestlings in a rural New York population with a regular supply of McDonald's cheeseburgers and compared their blood cholesterol levels with those of nearby crows who had to fend for themselves. The crows who were fed cheeseburgers ended up with higher cholesterol levels than their neighbors, similar to those of the urban crows in California.

However, whether all that cholesterol was actually doing the crows any harm is trickier to answer. Survival rates during the first three years of life were lower for urban crows than rural ones, but cholesterol wasn't the culprit--in the New York population, nestlings with higher cholesterol actually scored higher on measurements of their body condition. "Despite all the bad press that it gets, cholesterol has benefits and serves a lot of essential functions," says Townsend. "It's an important part of our cell membranes and a component of some crucial hormones. We know that excessive cholesterol causes disease in humans, but we don't know what level would be 'excessive' in a wild bird."

Still, Townsend doesn't recommend that people start tossing cheeseburgers or other processed foods to the birds at their feeders. "Wild birds haven't evolved to eat processed food, and it might have negative consequences that we didn't measure, or that will only show up over longer periods of time," she says. "Feeding wild birds can be a great way to connect with nature, and it can be a refreshing change to think that we're doing something that helps animals out. At the same time, though, I do worry that some of the foods that humans give to wild animals, and living in an urban environment in general, might not be good for their health."

A recent study indicates that certain physicians who care for patients with cancer do not often promote healthy lifestyle changes to cancer survivors, and they may fear that providing such advice would distress or overwhelm patients. Published early online in CANCER, a peer-reviewed journal of the American Cancer Society, the findings are noteworthy because maintaining a healthy lifestyle is especially important to the long-term well-being of cancer survivors.

Cancer survivors face increased risks of cardiovascular disease and other conditions, and guidelines advise physicians--including oncologists--to encourage cancer survivors to adopt healthy lifestyles to help protect their long-term health.

To investigate the extent to which physicians follow these recommendations, a team led by Tammy Stump, PhD, and Bonnie Spring, PhD, faculty at the Northwestern University Feinberg School of Medicine in Chicago, surveyed 91 physicians: 30 primary care physicians; 30 oncologists; and 31 specialists (urologists, gynecologists, and dermatologists) who treat survivors of prostate cancer, breast cancer, and melanoma, respectively. Interviews also were conducted with 12 of the oncologists who were sent the survey.

Among primary care physicians, 90 percent reported recommending health promotion such as weight loss and smoking cessation to at least some cancer survivors. However, only 26.7 percent of oncologists and 9.7 percent of specialists said they ever did so.

In interviews, oncologists expressed fear that promoting healthy lifestyle changes would distress or overwhelm patients. They also noted that they often lack the time and training to make such recommendations to patients. Most physicians believed that at least half of cancer survivors would take their medications properly to prevent cancer recurrence, but they believed that patients would not do so if they were also trying to lose weight

"Even though oncologists clearly believe that cancer survivors should adopt a healthy lifestyle, they don't have the time to address more than cancer care--that's their expertise," said Dr. Stump. "Ultimately, we believe that healthy lifestyle support can be provided to cancer survivors most effectively as part of integrated survivorship care delivered by health promotionists trained in nutrition, physical activity, and behavioral coaching in a program designed with the input of oncologists to meet the specific needs of cancer survivors," added Dr. Spring.

There is a growing demand for diagnostic markers for early disease detection and prognosis. Exosomes are potential biomarkers for cancer progression and neurodegenerative disease but it can be difficult to identify what tissue a specific exosome comes from. Researchers at Uppsala University and spin-off company Vesicode AB have solved this problem by developing a method that maps surface protein complements on large numbers of individual exosomes.

Exosomes are released from all cells in the body. They convey protein and nucleic acid cargos between the cells as a form of intercellular communication, and they represent potential circulating biomarkers for tumor progression and metastasis, as well as for early detection of neurodegenerative disease.

In order to use exosomes as biomarkers of diseases in different tissues it is vital to distinguish them according to their surface protein complements. Researchers at Uppsala University and Vesicode AB, along with collaborators, have developed a method that can map surface protein complements on large numbers of individual exosomes.

The novel proximity-dependent barcoding assay (PBA) reveals the surface protein composition of individual exosomes using antibody-DNA conjugates and next-generation sequencing. The method identifies proteins on individual exosomes using micrometer-sized, uniquely tagged single-stranded DNA clusters generated by rolling circle amplification.

"This technology will not only benefit researchers studying exosomes, but also enable high-throughput biomarker discovery. We will further develop and validate the PBA technology and provide service to researchers starting later this year. We believe single exosome analysis will allow this exciting class of biomarkers to reach its full potential," says Di Wu, researcher and inventor of the PBA technology and founder of Vesicode AB, commercializing the technique.

"This new technology will allow large-scale screens for biomarkers in disease, complementing a panel of methods for sensitive and specific detection of exosomes that we have previously established," says Masood Kamali-Moghaddam one of the group leaders at the Molecular Tools unit at Uppsala University.

Scientists may have found a way to pull down the protective wall that surrounds tumours, potentially re-exposing them to the killing power of the immune system and immunotherapy treatments, according to a study part funded by Cancer Research UK and published in EBioMedicine today (Monday).

Although this is early research in the lab, the findings suggest this approach could help to boost the effects of innovative cancer treatments, such as CAR-T therapy, which so far haven't been used successfully to tackle solid tumours.

Drs Francis Mussai and Carmela De Santo who are based at the University of Birmingham studied immune cells, called myeloid-derived suppressor cells or 'MDSCs', taken from the blood of 200 adults and children newly diagnosed with cancer before they had started treatment.*

These cells send out a barrage of chemical signals that shield tumours cells from the immune system and the effects of treatment, and prevent the activation of T cells that can kill tumour cells.

When MDSCs are present in higher numbers, the outlook for patients is worse as their cancer can become resistant to treatment and is more likely to spread to other parts of the body.

Researchers showed that an antibody drug that is already available for leukaemia, was able to destroy these immune cells, which protect the solid tumour from the immune system.

Dr Francis Mussai, lead author of the study and Cancer Research UK Clinical Scientist Fellow at the University of Birmingham, said: "Treatments that work with the immune system to kill cancer often fail because it can be difficult for our body's defences to get access to the tumour cells. Our research indicates that giving this antibody drug alongside immunotherapies could dramatically increase the number of patients benefitting from the latest innovations in treatment."

Previously, researchers in another group had found a way to break the protective layer around tumours in mice by using antibodies that attach to the MDSC cell surface, marking it for destruction by the immune system. But translating this into clinical trials has been challenging because researchers have been unable to find a drug target that's present on human MDSCs.

In this latest study, the team used blood samples taken from patients and showed that a protein called CD33 is present on the surface of MDSCs** across a wide range of cancers.

By using an antibody drug called gentuzumab ozogamicin that targets CD33, which is already used to treat acute myeloid leukaemia, the researchers were able to kill the MDSCs in the samples and restore the ability of T-cells to attack the tumour cells.

The researchers also showed that active MDSCs prevented CAR-T cells from working - these are T-cells that have been reprogrammed in the lab to make them more effective at killing cancer cells. But when they added the antibody drug, it boosted the activity of the CAR-T cells.

"This is the first time we've been able to effectively target the immune cells that form a barrier around solid tumours," added Dr Mussai. "If this approach works in patients it could improve treatments for many different types of cancer, in both adults and children. We envision our approach will have the most impact in CAR-T therapy, which despite showing lots of promise in blood cancer, so far it's had limited success in solid tumours."

Dr Emily Farthing, research information manager at Cancer Research UK said: "Although this is early research, it's increased our understanding of the way tumours interact with the immune system, and has given us a tantalising insight into how we could make immunotherapies work for more patients in the future. But we are still a long way off in getting this treatment to patients. The next step will be to learn more about the side effects of the antibody drug, and how it works in the body."

In addition to treating a range of cancers, the findings could also be applicable to treating HLH (hemophagocytic lymphohistiocytosis) and MAS (macrophage activation syndrome) - where the body reacts inappropriately to triggers, such as infections. These disorders are extremely rare and as a result there are few treatments available, particularly to children with HLH.

The team are now planning a clinical trial to test the safety and activity of the antibody drug in people with HLH and MAS. The trial will also include people with solid tumours.

SAN DIEGO, Aug. 25, 2019 -- In 2012, Washington and Colorado became the first states to legalize recreational marijuana. Since then, several other states have joined them, and cannabis-infused edibles, including gummy bears, cookies and chocolates, have flooded the market. But these sweet treats have created major headaches for the scientists trying to analyze them for potency and contaminants. Researchers now report that components in chocolate might be interfering with cannabis potency testing, leading to inaccurate results.

The researchers will present their results at the American Chemical Society (ACS) Fall 2019 National Meeting & Exposition. ACS, the world's largest scientific society, is holding the meeting here through Thursday. It features more than 9,500 presentations on a wide range of science topics.

"My research focuses on cannabis potency testing because of the high stakes associated with it," says David Dawson, Ph.D., the project's principal investigator. "If an edible cannabis product tests 10% below the amount on the label, California law states that is must be relabeled, with considerable time and expense. But it's even worse if a product tests 10% or more above the labeled amount -- then the entire batch must be destroyed."

Manufacturers add cannabis to a wide variety of foods, and the composition of these products, also known as the "matrix," can affect potency testing results. Dawson and his colleagues at CW Analytical Laboratories decided to focus on potency testing for cannabis-infused chocolates because they are a very common product. CW Analytical Laboratories is a cannabis testing lab in Oakland, California, where recreational marijuana became legal in 2018. "We also noticed, kind of anecdotally, some weird potency variations depending on how we prepared chocolate samples for testing," he says. So Dawson studied the effects of altering sample prep conditions, such as the amounts of chocolate and solvent, pH and type of chocolate, on the concentration of Δ9-tetrahydrocannabinol (Δ9-THC; the major psychoactive constituent of cannabis) measured by high-performance liquid chromatography (HPLC).

Their results were surprising. "When we had less cannabis-infused chocolate in the sample vial, say 1 gram, we got higher THC potencies and more precise values than when we had 2 grams of the same infused chocolate in the vial," Dawson says. "This goes against what I would consider basic statistical representation of samples, where one would assume that the more sample you have, the more representative it is of the whole." These results suggested that some other component of the chocolate -- a matrix effect -- was suppressing the signal for Δ9-THC.

"Simply changing how much sample is in the vial could determine whether a sample passes or fails, which could have a huge impact on the producer of the chocolate bars, as well as the customer who might be under- or overdosing because of this weird quirk of matrix effects," he notes.

Now Dawson is trying to figure out which ingredient of chocolate is responsible for the matrix effects. He has tried spiking a standard solution of Δ9-THC with varying amounts of chocolate bar, cocoa powder, baker's chocolate and white chocolate, all of which have different components, and observing how the HPLC signal changes. "Our best lead right now is that it has something to do with the fats, which makes sense considering that Δ9-THC is fat-soluble," Dawson says.

The team would like to extend their analyses to other cannabinoids, such as cannabidiol (CBD), a non-psychoactive substance that is cropping up in many edible products. Also, they plan to investigate other food matrices, such as chocolate chip cookies. Dawson says that he hopes the research will contribute toward developing standard methods for cannabis potency testing in a variety of edibles. "We owe this research to the scientific community, the producers and the consumers," he says. "We have to be able to provide highly accurate and precise testing across a wide swath of matrices."

SAN DIEGO, Aug. 25, 2019 -- For years, scientists have been trying to solve a medical mystery: Why do people with type 1 or type 2 diabetes have an increased risk of developing some forms of cancer? Today, researchers report a possible explanation for this double whammy. They found that DNA sustains more damage and gets fixed less often when blood sugar levels are high compared to when blood sugar is at a normal, healthy level, thereby increasing one's cancer risk.

The researchers will present their results at the American Chemical Society (ACS) Fall 2019 National Meeting & Exposition. ACS, the world's largest scientific society, is holding the meeting here through Thursday. It features more than 9,500 presentations on a wide range of science topics.

"It's been known for a long time that people with diabetes have as much as a 2.5-fold increased risk for certain cancers," says John Termini, Ph.D., who is presenting the work at the meeting. These cancers include ovarian, breast, kidney and others. "As the incidence of diabetes continues to rise, the cancer rate will likely increase, as well."

Scientists have suspected that the elevated cancer risk for diabetics arises from hormonal dysregulation. "In people with type 2 diabetes, their insulin is not effectively carrying glucose into cells," Termini explains. "So the pancreas makes more and more insulin, and they get what's called hyperinsulinemia." In addition to controlling blood glucose levels, the hormone insulin can stimulate cell growth, possibly leading to cancer. Also, most people with type 2 diabetes are overweight, and their excess fat tissue produces higher levels of adipokines than those at a healthy weight. These hormones promote chronic inflammation, which is linked to cancer. "The most common idea is that the increased cancer risk has to do with hormones," Termini says. "That's probably part of it, but there hasn't been a lot of solid evidence."

Termini, who is at City of Hope, a research and treatment center for cancer and diabetes, had a different idea. He wondered if the elevated blood glucose levels seen in diabetes could harm DNA, making the genome unstable, which could lead to cancer. So Termini and colleagues looked for a specific type of damage in the form of chemically modified DNA bases, known as adducts, in tissue culture and rodent models of diabetes. Indeed, they found a DNA adduct, called N2-(1-carboxyethyl)-2'-deoxyguanosine, or CEdG, that occurred more frequently in the diabetic models than in normal cells or mice. What's more, high glucose levels interfered with the cells' process for fixing it. "Exposure to high glucose levels leads to both DNA adducts and the suppression of their repair, which in combination could cause genome instability and cancer," Termini says.

Recently, Termini and colleagues completed a clinical study that measured the levels of CEdG, as well as its counterpart in RNA (CEG), in people with type 2 diabetes. As in mice, people with diabetes had significantly higher levels of both CEdG and CEG than people without the disease.

But the team didn't stop there. They wanted to determine the molecular reasons why the adducts weren't being fixed properly by the cells. They identified two proteins that appear to be involved: the transcription factor HIF1α and the signaling protein mTORC1, which both show less activity in diabetes. HIF1α activates several genes involved in the repair process. "We found that if we stabilize HIF1α in a high-glucose environment, we increase DNA repair and reduce DNA damage," Termini says. "And mTORC1 actually controls HIF1α, so if you stimulate mTORC1, you stimulate HIF1α."

According to Termini, several drugs that stimulate HIF1α or mTORC1 already exist. The researchers plan to see if these drugs decrease cancer risk in diabetic animal models, and if so, they will test them in humans. Termini notes that metformin, a common diabetes medication that helps lower blood glucose levels, also stimulates DNA repair. "We're looking at testing metformin in combination with drugs that specifically stabilize HIF1α or enhance mTORC1 signaling in diabetic animal models," he says. In the meantime, a more immediate way for diabetics to reduce their cancer risk could be better control of their blood sugar. "That sounds like such an easy solution, but it's extremely difficult for most people to maintain glycemic control," Termini says.

A press conference on this topic will be held Monday, Aug. 26, at 3 p.m. Pacific time in the San Diego Convention Center. Reporters may check-in at the press center, Room 14B, Mezzanine Level, or watch live on Youtube http://bit.ly/acs2019sandiego. To ask questions online, sign in with a Google account.

Tokyo, Japan - Scientists from Tokyo Metropolitan University and Ritsumeikan University have found a link between the "roundness" distribution of tsunami deposits and how far tsunamis reach inland. They sampled the "roundness" of gravel from different tsunamis in Koyadori, Japan, and found a common, abrupt change in composition approximately 40% of the "inundation distance" from the shoreline, regardless of tsunami magnitude. Estimates of ancient tsunami size from geological deposits may help inform effective disaster mitigation.

Tsunamis are one of nature's most devastating hazards; understanding their scale and mechanism is of paramount scientific and socio-economic importance. Nevertheless, despite our best efforts to study and understand them, their infrequent occurrence can make quantitative studies difficult; tsunami-causing seismic events around subduction zones (where one tectonic plate dips underneath another plate) recur once every 100 to 1,000 years, significantly reducing the number of accurately documented events. It is highly desirable that we gain some understanding by looking at geological deposits instead. However, despite some success in finding the number and age of past events, it is not yet possible to estimate the magnitude of ancient tsunamis, particularly in narrow coastal lowlands like the Sanriku Coast in Japan, struck by the 2011 Tohoku earthquake and tsunami.

Therefore, Assistant Professor Daisuke Ishimura from Tokyo Metropolitan University and Postdoctoral Fellow Keitaro Yamada from Ritsumeikan University carried out studies of gravel samples collected from bore holes and the trench in Koyadori, situated in the middle of the Sanriku coastline. Geological samples were taken corresponding to three tsunami events (AD 1611, 1896 and 2011) whose magnitudes are known, specifically their "inundation distance," or how far they reach inland. They used automated image analysis to study how "round" each gravel particle was in their samples, giving 10 to 100 times more data than existing, manual methods. Comparing distributions with measurements of modern beach and fluvial (river) gravels, they found that they could map the number ratio between beach and fluvial gravel. They discovered that this ratio suddenly changed at a certain distance away from the sea. This point was named the "Tsunami Gravel Inflection Point" (TGIP); it is thought to arise from "run-up" (incoming) waves bringing beach material inland and "return" waves drawing inland material towards the sea. Although the TGIP occurred at different locations for each event, they found that it was always approximately 40% of the inundation distance. They applied this finding to samples corresponding to even older tsunamis, providing estimates for the size of events along the Sanriku Coast going back approximately 4,000 years for the first time.

Although the researchers believe this ratio is specific to the local topography, the same analysis may be applied to characterize other tsunami-prone locations. An accurate estimate of the extent of ancient tsunamis will expand the number of events available for future research to study the mechanisms behind tsunamis, helping to inform effective disaster mitigation and the planning of coastal communities.

LA JOLLA--(August 23, 2019) The ability to edit genes in living organisms offers the opportunity to treat a plethora of inherited diseases. However, many types of gene-editing tools are unable to target critical areas of DNA, and creating such a technology has been difficult as living tissue contains diverse types of cells.

Now, Salk Institute researchers have developed a new tool--dubbed SATI--to edit the mouse genome, enabling the team to target a broad range of mutations and cell types. The new genome-editing technology, described in Cell Research on August 23, 2019, could be expanded for use in a broad range of gene mutation conditions such as Huntington's disease and the rare premature aging syndrome, progeria.

"This study has shown that SATI is a powerful tool for genome editing," says Juan Carlos Izpisua Belmonte, a professor in Salk's Gene Expression Laboratory and senior author of the paper. "It could prove instrumental in developing effective strategies for target-gene replacement of many different types of mutations, and opens the door for using genome-editing tools to possibly cure a broad range of genetic diseases."

Techniques that modify DNA--notably the CRISPR-Cas9 system--have generally been most effective in dividing cells, such as those in the skin or the gut, using the cells' normal DNA repair mechanisms. The Izpisua Belmonte lab previously showed that their CRISPR/Cas9-based gene-editing technology, called HITI (for homology-independent targeted integration), could target both dividing and non-dividing cells. Protein-coding regions function like recipes for making proteins, while areas called non-coding regions act as chefs deciding how much food to make. These non-coding regions make up the vast majority of DNA (~98%) and regulate many cellular functions including turning genes off and on, so could be a valuable target for future gene therapies.

"We sought to create a versatile tool to target these non-coding regions of the DNA, which would not affect the function of the gene, and enable the targeting of a broad range of mutations and cell types," says Mako Yamamoto, co-first author on the paper and a postdoctoral fellow in the Izpisua Belmonte lab. "As a proof-of-concept, we focused on a mouse model of premature aging caused by a mutation that is difficult to repair using existing genome-editing tools."

The new gene knock-in method, which the scientists call SATI (short for intercellular linearized Single homology Arm donor mediated intron-Targeting Integration) is an advancement of the previous HITI method to enable it to target additional areas of the genome. SATI works by inserting a normal copy of the problematic gene into the non-coding region of the DNA before the mutation site. This new gene then becomes integrated into the genome alongside the old gene via one of several DNA repair pathways, relieving the organism of the detrimental effects of the original, mutated gene, without risking damage associated with fully replacing it.

The scientists tested the SATI technology in living mice with progeria, which is caused by a mutation in the LMNA gene. Both humans and mice with progeria show signs of premature aging, cardiac dysfunction and dramatically shortened life span due to the accumulation of a protein called progerin. By using SATI, a normal copy of LMNA gene was inserted in the progeria mice. The researchers were able to observe diminished features of aging in several tissues including the skin and spleen, along with an extension of life span (45% increase compared to untreated progeria mice). A similar extension of life span, when translated to humans, would be more than a decade. Thus, the SATI system represents the first in vivo gene correction technology that can target non-coding regions of DNA in multiple tissue types.

Next, the team aims to improve the efficiency of SATI by increasing the number of cells that incorporate the new DNA.

"Specifically, we will investigate the details of the cellular systems involved in DNA repair to refine the SATI technology even further for better DNA correction," says Reyna Hernandez-Benitez, co-first author on the paper and a postdoctoral fellow in the Izpisua Belmonte lab.

Researchers from Carnegie Mellon University (CMU) and Nanyang Technological University, Singapore (NTU Singapore) have developed an organ-on-an-electronic-chip platform, which uses bioelectrical sensors to measure the electrophysiology of the heart cells in three dimensions. These 3D, self-rolling biosensor arrays coil up over heart cell spheroid tissues to form an "organ-on-e-chip," thus enabling the researchers to study how cells communicate with each other in multicellular systems such as the heart.

The organ-on-e-chip approach will help develop and assess the efficacy of drugs for disease treatment--perhaps even enabling researchers to screen for drugs and toxins directly on a human-like tissue, rather than testing on animal tissue. The platform will also be used to shed light on the connection between the heart's electrical signals and disease, such as arrhythmias. The research, published in Science Advances, allows the researchers to investigate processes in cultured cells that currently are not accessible, such as tissue development and cell maturation.

"For decades, electrophysiology was done using cells and cultures on two-dimensional surfaces, such as culture dishes," says Associate Professor of Biomedical Engineering (BME) and Materials Science & Engineering (MSE) Tzahi Cohen-Karni. "We are trying to circumvent the challenge of reading the heart's electrical patterns in 3D by developing a way to shrink-wrap sensors around heart cells and extracting electrophysiological information from this tissue."

The "organ-on-e-chip" platform starts out as a small, flat rectangle, not unlike a microscale slap bracelet. A slap bracelet starts out as a rigid, ruler-like structure, but when you release the tension it quickly coils up to band around the wrist.

The organ-on-e-chip starts out similarly. The researchers pin an array of sensors made of either metallic electrodes or graphene sensors to the chip's surface, then etch off a bottom layer of germanium, which is known as the "sacrificial layer." Once this sacrificial layer is removed, the biosensor array is released from its hold and rolls up from the surface in a barrel shaped structure.

The researchers tested the platform on cardiac spheroids, or elongated organoids made of heart cells. These 3D heart spheroids are about the width of 2-3 human hairs. Coiling the platform over the spheroid allows the researchers to collect electrical signal readings with high precision.

"Essentially, we have created 3D self-rolling biosensor arrays for exploring the electrophysiology of induced pluripotent stem cell derived cardiomyocytes," says lead author of the study and BME Ph.D. student Anna Kalmykov. "This platform could be used to do research into cardiac tissue regeneration and maturation that potentially can be used to treat damaged tissue after a heart attack, for example, or developing new drugs to treat disease."

Through collaboration with the labs of BME/MSE Professor Adam Feinberg and former CMU faculty Jimmy Hsia, now Dean of the Graduate College of NTU Singapore, the researchers were able to design a proof of concept and test them on 3D micro-mold formed cardiomyocyte spheroids.

"Mechanics analysis of the roll-up process enables us to precisely control the shape of the sensors to ensure conforming contact between the sensors and the cardiac tissue," says NTU Professor Jimmy Hsia. "The technique also automatically adjusts the level of the delicate 'touch' between the sensors and the tissue such that high quality electric signals are measured without changing in the physiological conditions of the tissue due to external pressure."

"The whole idea is to take methods that are traditionally done in planar geometry and do them in three dimensions," says Cohen-Karni. "Our organs are 3D in nature. For many years, electrophysiology was done using just cells cultured on a 2D tissue culture dish. But now, these amazing electrophysiology techniques can be applied to 3D structures."

Irvine, Calif., Aug. 23, 2019 -- A new study, published in the journal Clinical Psychological Science, suggests that the time adolescents are spending on their phones and online is not that bad.

The study tracked young adolescents on their smartphones to test whether more time spent using digital technology was linked to worse mental health outcomes. The researchers -- Candice Odgers, professor of psychological science at the University of California, Irvine; Michaeline Jensen, assistant professor of psychology at the University of North Carolina at Greensboro; Madeleine George, postdoctoral researcher at Purdue University; and Michael Russell, assistant professor of behavioral health at Pennsylvania State University -- found little evidence of longitudinal or daily linkages between digital technology use and adolescent mental health.

(Link to study: https://journals.sagepub.com/doi/10.1177/2167702619859336)

"It may be time for adults to stop arguing over whether smartphones and social media are good or bad for teens' mental health and start figuring out ways to best support them in both their offline and online lives," Odgers said.

"Contrary to the common belief that smartphones and social media are damaging adolescents' mental health, we don't see much support for the idea that time spent on phones and online is associated with increased risk for mental health problems," Jensen said.

The study surveyed more than 2,000 youth and then intensively tracked a subsample of nearly 400 teens on their smartphones multiple times a day for two weeks. Adolescents in the study were between 10 and 15 years old and represented the economically and racially diverse population of youth attending North Carolina public schools.

The researchers collected reports of mental health symptoms from the adolescents three times a day and they also reported on their daily technology usage each night. They asked whether youth who engaged more with digital technologies were more likely to experience later mental health symptoms and whether days that adolescents spent more time using digital technology for a wide range of purposes were also days when mental health problems were more common. In both cases, increased digital technology use was not related to worse mental health.

When associations were observed, they were small and in the opposite direction that would be expected given all of the recent concerns about digital technology damaging adolescents' mental health. For instance, teens who reported sending more text messages over the study period actually reported feeling better (less depressed) than teens who were less frequent texters.

A video walk-through of the study and the journal article are available online.

Why is it that you can remember the name of your childhood best friend that you haven't seen in years yet easily forget the name of a person you just met a moment ago? In other words, why are some memories stable over decades, while others fade within minutes?

Using mouse models, Caltech researchers have now determined that strong, stable memories are encoded by "teams" of neurons all firing in synchrony, providing redundancy that enables these memories to persist over time. The research has implications for understanding how memory might be affected after brain damage, such as by strokes or Alzheimer's disease.

The work was done in the laboratory of Carlos Lois, research professor of biology, and is described in a paper that appears in the August 23 of the journal Science. Lois is also an affiliated faculty member of the Tianqiao and Chrissy Chen Institute for Neuroscience at Caltech.

Led by postdoctoral scholar Walter Gonzalez, the team developed a test to examine mice's neural activity as they learn about and remember a new place. In the test, a mouse was placed in a straight enclosure, about 5 feet long with white walls. Unique symbols marked different locations along the walls--for example, a bold plus sign near the right-most end and an angled slash near the center. Sugar water (a treat for mice) was placed at either end of the track. While the mouse explored, the researchers measured the activity of specific neurons in the mouse hippocampus (the region of the brain where new memories are formed) that are known to encode for places.

When an animal was initially placed in the track, it was unsure of what to do and wandered left and right until it came across the sugar water. In these cases, single neurons were activated when the mouse took notice of a symbol on the wall. But over multiple experiences with the track, the mouse became familiar with it and remembered the locations of the sugar. As the mouse became more familiar, more and more neurons were activated in synchrony by seeing each symbol on the wall. Essentially, the mouse was recognizing where it was with respect to each unique symbol.

To study how memories fade over time, the researchers then withheld the mice from the track for up to 20 days. Upon returning to the track after this break, mice that had formed strong memories encoded by higher numbers of neurons remembered the task quickly. Even though some neurons showed different activity, the mouse's memory of the track was clearly identifiable when analyzing the activity of large groups of neurons. In other words, using groups of neurons enables the brain to have redundancy and still recall memories even if some of the original neurons fall silent or are damaged.

Gonzalez explains: "Imagine you have a long and complicated story to tell. In order to preserve the story, you could tell it to five of your friends and then occasionally get together with all of them to re-tell the story and help each other fill in any gaps that an individual had forgotten. Additionally, each time you re-tell the story, you could bring new friends to learn and therefore help preserve it and strengthen the memory. In an analogous way, your own neurons help each other out to encode memories that will persist over time."

Memory is so fundamental to human behavior that any impairment to memory can severely impact our daily life. Memory loss that occurs as part of normal aging can be a significant handicap for senior citizens. Moreover, memory loss caused by several diseases, most notably Alzheimer's, has devastating consequences that can interfere with the most basic routines including recognizing relatives or remembering the way back home. This work suggests that memories might fade more rapidly as we age because a memory is encoded by fewer neurons, and if any of these neurons fail, the memory is lost. The study suggests that one day, designing treatments that could boost the recruitment of a higher number of neurons to encode a memory could help prevent memory loss.

"For years, people have known that the more you practice an action, the better chance that you will remember it later," says Lois. "We now think that this is likely, because the more you practice an action, the higher the number of neurons that are encoding the action. The conventional theories about memory storage postulate that making a memory more stable requires the strengthening of the connections to an individual neuron. Our results suggest that increasing the number of neurons that encode the same memory enables the memory to persist for longer."

There are only two northern white rhinos left worldwide, both of them female. Saving this representative of megafauna from extinction seems impossible under these circumstances, yet an international consortium of scientists and conservationists just completed a procedure that could enable assisted reproduction techniques to do just that. On August 22, 2019, a team of veterinarians successfully harvested eggs from the two females who live in Ol Pejeta Conservancy in Kenya -- a procedure that has never been attempted in northern white rhinos before. The eggs will now be artificially inseminated with frozen sperm from a northern white rhino bull, and in the near future the embryo will be transferred to a southern white rhino surrogate mother. The successful procedure was a joint effort by the Leibniz Institute for Zoo and Wildlife Research (Leibniz-IZW) Berlin, Avantea, Dvur Kralove Zoo, Ol Pejeta Conservancy and the Kenya Wildlife Service (KWS).

With neither Najin and Fatu, the two northern white rhino females, able to carry a pregnancy, the future of the northern white rhino now rests solely on pioneering artificial reproduction techniques. The successful harvesting of their eggs means that scientists are one step closer to being able to save the northern white rhino from complete extinction.

The procedure was the result of years of research, development, adjustments and practice. "Both the technique and the equipment had to be developed entirely from scratch," says Prof. Thomas Hildebrandt from Leibniz-IZW and Dr. David Ndeereh from the Kenya Wildlife Service (KWS), who headed the procedure. "We were able to harvest a total of 10 oocytes - 5 from Najin and 5 from Fatu - showing that both females can still provide eggs and thus help to save these magnificent creatures."

The procedure was conducted with a probe, guided by ultrasound, which harvested immature egg cells (oocytes) from the ovaries of the animals when placed under general anaesthetic. "The anaesthesia went smoothly without any complications although these animals had not been immobilized for the last five years," say Frank Goeritz from Leibniz-IZW, Dr. Domnic Mijele from KWS and Dr. Stephen Ngulu of Ol Pejeta.

"The number of harvested oocytes is a wonderful success and proof that the unique cooperation between scientists, experts in zoos and conservationists in field can lead to hopeful prospects even for the animals that are imminently facing extinction," adds Jan Stejskal from Dvur Kralove Zoo, where the two rhinos were born.

It was the partnership between Dvur Kralove Zoo, Ol Pejeta Conservancy and KWS that led to the translocation of Najin, Fatu and two male northern white rhinos from the Czech Republic to Kenya in December 2009, when it was hoped that breeding would be stimulated by the rhinos being closer to their natural environment. Although mating attempts were witnessed, there were no pregnancies. "We came to the conclusion after a health assessment in 2014 that, owing to various health issues, neither Najin or Fatu are able to carry a pregnancy," explains Dr. Robert Hermes from the Leibniz-IZW. Two males - Suni and Sudan - died of natural causes in 2014 and 2018 respectively. Their sperm was cryo-preserved in the hope that assisted reproduction techniques would advance enough so that they could pass on their genome to a new generation.

"On the one hand Ol Pejeta is saddened that we are now down to the last two northern white rhinos on the planet, a testament to the profligate way the human race continues to interact with the natural world around us. However we are also immensely proud to be part of the ground breaking work which is now being deployed to rescue this species. We hope it signals the start of an era where humans finally start to understand that proper stewardship of the environment is not a luxury but a necessity," said Richard Vigne, Managing Director of Ol Pejeta.

"The concerted efforts to save the last northern white rhinos should guide the resolutions the world makes at the ongoing CITES meeting in Geneva. The assisted reproductive technique should galvanize the world's attention to the plight of all rhinos and make us avoid decisions that undermine law enforcement and fuel demand for the rhino horn," says Hon. Najib Balala, Kenya's Cabinet Secretary for Tourism and Wildlife.

"We are delighted that this partnership gets us one step closerto prevent extinctionofthe northern white rhinos. This is particularly touching given the heartbreakingdeath of Sudan, the lastmale, who died of old age last year in Kenya," says Brig. (Rtd) John Waweru, the Kenya Wildlife Service Director General.

"Yesterday's operation means that producing a northern white rhino embryo in vitro - which has never been done before - is a tangible reality for the first time," says Cesare Galli from Avantea, the Italian laboratory of advanced technologies for biotechnology research and animal reproduction. Avantea will now fertilise the eggs in vitro using the cryo-preserved semen of Suni and Saut.

The procedure is part of an international research project named "BioRescue", a consortium to which Leibniz-IZW, Avantea, and Dvur Kralove Zoo are a part, and which is funded by the German Federal Ministry of Education and Research (BMBF). As well as harnessing the collective knowledge and expertise of the consortium to conduct the in vitro procedure, the project will also lead the development of techniques and procedures to create artificial gametes from stem cells. This will involve transforming stored tissue from northern white rhinos into induced pluripotent stem cells, and then into primordial germ cells. Germ cells can then be matured to develop into eggs or sperm cells - essentially widening the genetic basis and the quantity of the gametes. The stem cell approach is primarily carried out by BioRescue consortium members Max Delbrueck Center for Molecular Medicine (Germany), Kyushu University (Japan) and Northwestern University (USA).

The whole procedure was conducted within an ethical framework that has been developed beforehand by ethicists and the other scientists and veterinarians involved in the procedure. "We developed a dedicated ethical risk analysis in order to prepare the team for all possible scenarios of such an ambitious procedure and to make sure that the welfare of the two individuals was totally respected," says Barbara de Mori, the conservation and animal welfare ethics expert from Padua University. In addition, the procedure was conducted in compliance with Kenyan laws, policies and the relevant international requirements.

WOODS HOLE, Mass. - Deep in the waterlogged peat of salt marshes, carbon is stored at much greater rates than in land ecosystems, serving as an offset to climate change due to carbon dioxide (CO2) build-up in the atmosphere.

However, a new study indicates that a common pollutant of coastal waters, nitrate, stimulates the decomposition of organic matter in salt marsh sediments that normally would have remained stable over long periods of time. This increase in decomposition, which releases CO2, could alter the capacity of salt marshes to sequester carbon over the long term. The study, led by scientists at the Marine Biological Laboratory (MBL), Woods Hole, and Northeastern University, is published in Global Change Biology.

"Traditionally, we have viewed salt marshes as resilient to nitrogen pollution, because the microbes there remove much of the nitrogen as gas through a process called denitrification," writes first author Ashley Bulseco, a postdoctoral scientist at the MBL.

"But this research suggests that when nitrate is abundant, a change occurs in the microbial community in salt marsh sediments that increases the microbes' capacity to degrade organic matter. This potentially reduces the ability of the marsh to store carbon," Bulseco writes.

As global temperatures continue to rise, a number of carbon capture strategies have been proposed, including sequestering CO2 in "blue carbon" habitats such as salt marshes, mangroves and seagrass meadows. However, coastal nitrogen pollution is also still rising in many areas due to agricultural and urban runoff, and sewage.

"Given the extent of nitrogen loading along our coastlines, it is imperative that we better understand the resilience of salt marsh systems to nitrate, especially if we hope to rely on salt marshes and other blue carbon systems for long-term carbon storage," the authors write.

The next phase of this research, already in progress, is to analyze the microbial community responsible for degrading carbon in a salt marsh ecosystems, especially when exposed to high concentrations of nitrate.

A new Canadian study suggests that individuals who take anti-depressants and/or anti-psychotics and participate in a weight management program can lose weight whether or not they take psychiatric medications, according to a report published online today in Obesity, the flagship journal of The Obesity Society. The study is the first to examine weight loss outcomes in individuals taking anti-depressants or anti-psychotics alone, in combination or not at all.

"The results of this study are relevant not only to the healthcare professionals providing care to those who have both excess weight and mental illness, but also to the patients who experience these comorbidities themselves," said Rebecca Christensen, a PhD student at the University of Toronto's Dalla Lana School of Public Health in Canada. Christensen served as the study's lead and corresponding author.

Christensen and colleagues explain that individuals who have mental health conditions are at an increased risk of having obesity. Many of the medications used to treat mental health disorders are known to cause weight gain. However, it has remained unclear, if taking these medications would put people at a disadvantage for weight loss.

To determine their findings, researchers reviewed data from 17,519 patients enrolled in a life-style weight loss program at the Wharton Medical Clinic (WMC) in Ontario, Canada. For referrals to the weight management clinic, patients needed to have a body mass index (BMI) of greater than 27 kg/m2 with at least one weight-related comorbidity or a BMI of greater than 30 kg/m2. Participants consented to have their medical data used, and the data collected spanned from July 2008 to July 2017.

Because of known sex differences in weight loss and prevalence in mental health conditions, the study's authors conducted separate analyses for male and female patients. Researchers examined differences in absolute and percent weight change by psychiatric medication group, and weight gain potential. Participants were categorized as taking an antidepressant(s) alone, antipsychotic(s) alone, a combination of both, or no psychiatric medication. The authors also conducted a sub-analysis among patients taking psychiatric medication, where patients were categorized as taking psychiatric medications that are known to cause weight gain, or psychiatric medication that is weight neutral and/or cause weight loss.

Height and weight measurements were taken by a trained medical professional, and patients met with a physician and/or bariatric educator monthly for dietary and physical activity suggestions based on current life-style practices. WMC staff provided treatment in accordance with Canadian clinical practice guidelines on the management and prevention of obesity in adults and children and the National Institutes of Health guidelines on the identification, evaluation and treatment of overweight and obesity in adults.

According to the study's authors, more than 23 percent of patients were taking at least one psychiatric medication. Results showed that while men lost a significant amount of weight regardless of the type of psychiatric medication they were taking, men taking anti-depressants alone lost slightly less weight than men taking both anti-depressants and anti-psychotics, and men taking neither medication. Women lost a similar amount of weight regardless of their psychiatric medication use. Christensen and colleagues also observed that both men and women were able to lose a significant amount of weight regardless of the weight gain potential of their mental health medication.

"The results of this study are promising," said Christensen.

"Significant strengths of the study included a large sample size and treatment with no additional cost to patients as part of the Canadian healthcare system, " said Robert I. Berkowitz, MD, FTOS, Professor of Psychiatry and Pediatrics at the Center for Weight and Eating Disorders, Perlman School of Medicine at the University of Pennsylvania, and at the Children's Hospital of Philadelphia.

Berkowitz, who was not part of the study, added that "future research is needed to increase the duration of treatment, as well as to consider adding other treatment methods to the lifestyle modification program in order to increase the amount of weight loss obtained in this important population of patients typically excluded from weight loss trials, those who have psychiatric disorders." Christensen agreed that additional research is needed to corroborate the results.

Foods fried in vegetable oil are popular worldwide, but research about the health effects of this cooking technique has been largely inconclusive and focused on healthy people. For the first time, UMass Amherst food scientists set out to examine the impact of frying oil consumption on inflammatory bowel disease (IBD) and colon cancer, using animal models.

In their paper published Aug. 23 in Cancer Prevention Research, lead author and Ph.D. student Jianan Zhang, associate professor Guodong Zhang, and professor and department head Eric Decker showed that feeding frying oil to mice exaggerated colonic inflammation, enhanced tumor growth and worsened gut leakage, spreading bacteria or toxic bacterial products into the bloodstream.

"People with colonic inflammation or colon cancer should be aware of this research," says Jianan Zhang.

Guodong Zhang, whose food science lab focuses on the discovery of new cellular targets in the treatment of colon cancer and how to reduce the risks of IBD, stresses that "it's not our message that frying oil can cause cancer."

Rather, the new research suggests that eating fried foods may exacerbate and advance conditions of the colon. "In the United States, many people have these diseases, but many of them may still eat fast food and fried food," says Guodong Zhang. "If somebody has IBD or colon cancer and they eat this kind of food, there is a chance it will make the diseases more aggressive."

For their experiments, the researchers used a real-world sample of canola oil, in which falafel had been cooked at 325 F in a standard commercial fryer at an eatery in Amherst, Massachusetts. "Canola oil is used widely in America for frying," Jianan Zhang says.

Decker, an expert in lipid chemistry performed the analysis of the oil, which undergoes an array of chemical reactions during the frying process. He characterized the fatty acid profiles, the level of free fatty acids and the status of oxidation.

A combination of the frying oil and fresh oil was added to the powder diet of one group of mice. The control group was fed the powder diet with only fresh oil mixed in. "We tried to mimic the human being's diet," Guodong Zhang says.

Supported by grants from the U.S. Department of Agriculture, the researchers looked at the effects of the diets on colonic inflammation, colon tumor growth and gut leakage, finding that the frying oil diet worsened all the conditions. "The tumors doubled in size from the control group to the study group," Guodong Zhang says.

To test their hypothesis that the oxidation of polyunsaturated fatty acids, which occurs when the oil is heated, is instrumental in the inflammatory effects, the researchers isolated polar compounds from the frying oil and fed them to the mice. The results were "very similar" to those from the experiment in which the mice were fed frying oil, suggesting that the polar compounds mediated the inflammatory effects.

While more research is needed, the researchers hope a better understanding of the health impacts of frying oil will lead to dietary guidelines and public health policies.

"For individuals with or prone to inflammatory bowel disease," Guodong Zhang says, "it's probably a good idea to eat less fried food."