Earth

Idiopathic pulmonary fibrosis is a potentially lethal disease for which there is currently no cure and that is associated with certain mutations or advanced age. The Telomeres and Telomerase Group at the Spanish National Cancer Research Centre (CNIO) had previously developed an effective therapy for mice with fibrosis caused by genetic defects. Now they show that the same therapy can successfully be used to treat mice with age-related fibrosis.

"With respect to humans, our results indicate that it may be possible to devise a treatment to prevent the development of pulmonary fibrosis associated with ageing," says Maria Blasco, principal investigator of the study that is published in The Journal of Cell Biology.

The treatment tested in mice is a gene therapy that activates the production of telomerase in the body. Telomerase is an enzyme that repairs the telomeres at the end of chromosomes. According to Blasco, this therapy was highly effective in animal models and no side effects were observed.

Telomere dysfunction leading to pulmonary fibrosis

Pulmonary fibrosis affects around 8,000 people in Spain. In this disease, the lung tissue becomes stiff and scarred, and patients develop progressive shortness of breath. It is thought to be caused by a combination of genetic and environmental factors. Exposure to toxic substances plays an important role, but for the disease to manifest itself the patient must be of advanced age or have an underlying genetic condition.

The CNIO team had already shown in previous studies that the genetic factors are associated with telomere dysfunction. Telomeres are structures that, like "end caps", protect the ends of chromosomes in all cells.

Back in 2015, the team generated an animal model for pulmonary fibrosis - a mouse that, among other characteristics, lacked the telomerase gene. In this mouse model, alveolar type II cells or type II pneumocytes - important for lung tissue regeneration - eventually die as a result of telomere dysfunction. As a consequence, the mice develop aggressive pulmonary fibrosis because the respiratory epithelium cannot renew itself periodically; this periodic regeneration keeps the tissue healthy and free from possible damage caused by harmful airborne substances.

Age-related fibrosis

The mouse model that lacks the telomerase gene faithfully mimics the human disease caused by mutations affecting the telomeres. However, specific mutations are found in relatively few pulmonary fibrosis cases. In the vast majority of patients, nothing points to a specific mutation, but all patients have something in common: an advanced age.

Indeed, telomeres can become defective through the mere process of ageing. The team led by Blanco have done ground-breaking research on telomeres and the ageing process. Telomeres are protein structures that cap the ends of chromosomes; they shorten with every cell division. After many rounds of cell division over the lifetime of an individual, they become so short that they can no longer protect the chromosomes. The cells interpret this as an error and stop dividing so that the tissue cannot regenerate anymore.

In the paper now published, the researchers show that telomere dysfunction associated with ageing occurs in alveolar type II cells, which play a primary role in lung tissue regeneration. The team have thus found the molecular basis of the link between pulmonary fibrosis and ageing, a link that is clearly seen in the clinical setting.

Loss of pulmonary surfactant

The new study describes the effects of ageing on lung tissue in detail. One such effect is that alveolar type II cells stop doing their job.

In addition to regenerating tissue, these cells produce and release a lipid-protein complex called pulmonary surfactant that facilitates the mechanical work done by the lungs. "Lung tissue must expand when we breathe in, six to ten times per minute, which means a great deal of physical effort. Pulmonary surfactant plays an important role in lubricating lung tissue, retaining its elasticity, and reducing the amount of work required to expand and contract it. If type II pneumocytes fail to regenerate, the surfactant is not produced, which results in lung stiffness and fibrosis," says Jesús Pérez-Gil of the Complutense University of Madrid, who participated in the study and whose team are experts in this field.

"We have observed a very clear relation between telomere status in type II pneumocytes, pulmonary surfactant production and fibrosis development in animals," Pérez-Gil adds. "Here we address the effects on telomeres at the molecular level, biological and physical changes in cells and tissues, and the consequences for the health of the animal, the whole organism.", indicates Sergio Piñeiro, first author of the study.

A therapy for all types of fibrosis

In 2018, the CNIO group developed a gene therapy that reversed pulmonary fibrosis in mice lacking the telomerase gene. This therapy was based on activating telomerase expression temporarily. A virus used as a telomerase gene carrier was injected intravenously into the mice. The effect - alveolar type II cells with long telomeres - was temporary, but lung tissue regeneration was successfully induced.

The same therapy was now used in ageing mice. And it worked in them too. "The telomerase-activating gene therapy prevented the development of fibrosis in all mice, including the ones without genetic alterations that only underwent physiological ageing," Blasco explains.

This extends the possibility of a cure for pulmonary fibrosis to virtually all cases of fibrosis, as the researchers conclude in their paper: "These findings contribute to a better understanding of the importance of [the telomerase gene] as a potential target for future therapeutic approaches in idiopathic pulmonary fibrosis."

(Boston)-- Since 2008, researchers at Boston University School of Medicine (BUSM) and VA Boston Healthcare System have studied Chronic Traumatic Encephalopathy (CTE), a progressive brain disease associated with repetitive head impacts that has been diagnosed after death in the brains of American football players and other contact sport athletes as well as members of the armed services.

In 2013, these same researchers proposed criteria for the pathological diagnosis of CTE and a methodology for grading the severity of the disease known as the McKee CTE staging scheme. The McKee staging scheme defined four pathological stages of CTE, stages I (mild) to IV (severe), based on the density and regional deposition of hyperphosphorylated tau (p-tau) pathology. The criteria for pathological diagnosis of CTE were adopted and refined by the National Institute of Neurological Disorders and Stroke/National Institute of Biomedical Imaging and Bioengineering consensus panel of expert neuropathologists in 2015. Since then, although the staging scheme has been used widely to characterize the severity of pathology in hundreds of CTE subjects, its effectiveness and accuracy has not been formally tested.

Now a new study for the first time proves that the McKee staging scheme for CTE accurately represents the progression of tau pathology in CTE and correlates with clinical dementia. It also confirms that it correlates with age at death and years of American football play.

To test its effectiveness and accuracy and provide a detailed examination of the regional distribution of p-tau in CTE, researchers from Boston University examined the relationship between the McKee staging scheme and p-tau pathology in regions throughout the brain, age at death, dementia and years of American football play among 366 male brain donors neuropathologically diagnosed with CTE. They found having a higher CTE stage was associated with higher scores on all assessments of p-tau severity and density and ultimately more clinically advanced CTE. Severity and distribution of p-tau in CTE followed an age-dependent progression, meaning older age was associated with increased odds for having a higher CTE stage and CTE stage was independently associated with increased odds for dementia.

In addition, the researchers identified five areas in the brain where there were clusters of increasing p-tau pathology that conformed to CTE stage, age at death, dementia and years of American football play. Tau pathology was consistently most severe in five brain regions: dorsolateral frontal cortex, superior temporal cortex, entorhinal cortex, amygdala and locus coeruleus. In the youngest brain donors with the least advanced CTE stage, tau pathology was most severe in dorsolateral frontal cortex and locus coeruleus.

"These findings further advance our understanding of CTE and lay the groundwork for diagnosis during life using brain imaging techniques that can identify the specific tau of CTE in the brains of living people. This work will also help focus the development of therapies aimed at arresting tau progression," explained corresponding author Ann McKee, MD, chief of neuropathology at VA Boston Healthcare System and director of the BU CTE Center.

While further study is needed to clarify the clinical correlates of CTE across the different stages of disease and identify repetitive head impacts (RHI) and non-RHI related risk factors that enhance susceptibility and course progression, these findings support the usefulness of the McKee CTE staging scheme in assessing CTE pathological severity and support their continued use in the study of CTE.

"This study addresses a key knowledge gap in the field by confirming the usefulness of the McKee CTE staging scheme and directly linking the tau from CTE with age, years of American football play and dementia. The findings will play an important role in guiding both clinical and basic science research on CTE," said lead author Michael Alosco, PhD, associate professor of neurology at BUSM and co-director of the BU Alzheimer's Disease Center Clinical Core.

Corals in the Ocean are made up of coral polyps, a small soft creature with a stem and tentacles, they are responsible for nourishing the corals, and aid the coral's survival by generating self-made currents through motion of their soft bodies.

Scientists from WMG at the University of Warwick, led by Eindhoven University of Technology in the Netherlands, developed a 1cm by 1cm wireless artificial aquatic polyp, which can remove contaminants from water. Apart from cleaning, this soft robot could be also used in medical diagnostic devices by aiding in picking up and transporting specific cells for analysis.

In the paper, 'An artificial aquatic polyp that wirelessly attracts, grasps, and releases objects' researchers demonstrate how their artificial aquatic polyp moves under the influence of a magnetic field, while the tentacles are triggered by light. A rotating magnetic field under the device drives a rotating motion of the artificial polyp's stem. This motion results in the generation of an attractive flow which can guide suspended targets, such as oil droplets, towards the artificial polyp.

Once the targets are within reach, UV light can be used to activate the polyp's tentacles, composed of photo-active liquid crystal polymers, which then bend towards the light enclosing the passing target in the polyp's grasp. Target release is then possible through illumination with blue light.

Dr Harkamaljot Kandail, from WMG, University of Warwick was responsible for creating state of the art 3D simulations of the artificial aquatic polyps. The simulations are important to help understand and elucidate the stem and tentacles generate the flow fields that can attract the particles in the water.

The simulations were then used to optimise the shape of the tentacles so that the floating particles could be grabbed quickly and efficiently.

Dr Harkamaljot Kandail, from WMG, University of Warwick comments:

"Corals are such a valuable ecosystem in our oceans, I hope that the artificial aquatic polyps can be further developed to collect contaminant particles in real applications. The next stage for us to overcome before being able to do this is to successfully scale up the technology from laboratory to pilot scale. To do so we need to design an array of polyps which work harmoniously together where one polyp can capture the particle and pass it along for removal."

Marina Pilz Da Cunha, from the Eindhoven University of Technology, Netherlands adds:

"The artificial aquatic polyp serves as a proof of concept to demonstrate the potential of actuator assemblies and serves as an inspiration for future devices. It exemplifies how motion of different stimuli-responsive polymers can be harnessed to perform wirelessly controlled tasks in an aquatic environment."

A new study from North Carolina State University and the Georgia Institute of Technology finds that the more people know about COVID-19, the less pandemic-related stress they have. The study also found that making plans to reduce stress was also effective for older adults - but not for adults in their 40s or younger.

"COVID-19 is a new disease - it's not something that people worried about before," says Shevaun Neupert, a professor of psychology at NC State and co-author of the study. "So we wanted to see how people were responding to, and coping with, this new source of stress."

To that end, researchers surveyed 515 adults from across the United States. The adults ranged in age from 20-79. The cohort of study participants had an average age of just under 40, and 46 of them were more than 60 years old. The surveys were conducted between March 20 and April 19, 2020.

One part of the survey was a 29-item quiz designed to assess how much study participants knew about COVID-19. Coupled with other elements of the survey, this let researchers assess whether an understanding of COVID-19 made people feel more stress or less.

"We found that knowledge is power," Neupert says. "The more factual information people knew about COVID-19, the less stress they had. That was true across age groups.

"Knowledge reduces uncertainty, and uncertainty can be very stressful," Neupert says. "Although speculative, it is likely that knowledge about this new virus reduced uncertainty, which in turn reduced feelings of pandemic stress."

The researchers went into the study thinking older adults would likely experience more stress related to COVID-19, because the disease was portrayed as particularly dangerous to seniors. But they found that pandemic-related stress levels were the same for all age groups.

"The strongest predictor of stress was concern about getting COVID-19, which isn't surprising," says Neupert. "And the older people were, the more pronounced this effect was."

But older adults also had an advantage: pro-active coping. The use of proactive coping - or making plans to reduce the likelihood of stress - reduced stress in adults over the age of 52. It had no effect for younger adults.

"These results suggest that everyone can benefit from staying engaged with factual information that will increase knowledge about COVID-19," Neupert says. "In addition, older adults who are able to use proactive coping, such as trying to prepare for adverse events, could decrease their pandemic stress."

Tropical Storm Jangmi was exiting the East China Sea and moving toward the Sea of Japan when NASA's Aqua satellite measured the strength of the system.

Jangmi formed as a depression on Aug. 8. At 5 a.m. EDT (0900 UTC), Tropical Depression 05W formed about 377 miles northeast of Manila, Philippines. Locally in the Philippines, the depression was known as Enteng. By 5 a.m. EDT (0900 UTC) on Aug. 9, the depression strengthened into a tropical storm.

On Aug. 9 at 10:20 a.m. EDT (1420 UTC) infrared data from the Moderate Resolution Imaging Spectroradiometer or MODIS instrument that flies aboard NASA's Aqua satellite provided a look at cloud top temperatures in Tropical Storm Jangmi as it was about to move out of the East China Sea. Strongest thunderstorms that reach high into the atmosphere have the coldest cloud top temperatures.

MODIS found the most powerful thunderstorms were around the center of circulation, where temperatures were as cold as or colder than minus 70 degrees Fahrenheit (minus 56.6 Celsius). Cloud top temperatures that cold indicate strong storms with the potential to generate heavy rainfall.

On Aug. 10, the Joint Typhoon Warning Center noted that animated multispectral satellite imagery showed a partially exposed low-level circulation center with building strong thunderstorms in the northwestern quadrant of the storm.

On Monday, August 10, 2020 at 5 a.m. EDT (0900 UTC), the Joint Typhoon Warning Center (JTWC) noted that Tropical storm Jangmi was located near latitude 34.2 degrees north and longitude 128.7 degrees east, approximately 48 nautical miles south of Chinhae, South Korea. Jangmi was moving at 23 knots (26 mph/43 kph) and had maximum sustained winds of 35 knots gusting to 45 knots (52 mph/ 83 kph).

Jangmi is moving northeast past South Korea and is forecast to move into the Sea of Japan where it is forecast to merge with an approaching mid-latitude elongated area of low pressure (trough) and then become extra-tropical.

Tropical cyclones/hurricanes are the most powerful weather events on Earth. NASA's expertise in space and scientific exploration contributes to essential services provided to the American people by other federal agencies, such as hurricane weather forecasting.

By Rob Gutro
NASA's Goddard Space Flight Center

The flu vaccine is considered one of the great achievements in public health, and each year it prevents millions of people from getting sick and thousands of deaths. Even so, social media messages abound with skepticism and falsehoods about vaccination.

What effect, if any, do these social media messages have on actual vaccination behavior?

A new study on this underexplored subject, using big data and survey results from the 2018-19 flu season, finds strong associations between regional social media messages and vaccination attitudes and behavior. But when there are negative associations between social media content and vaccination, real-life discussions with family and friends appear to eliminate them.

The study, published in the journal Vaccine, analyzes 115,330 geolocated tweets about the flu and vaccination along with data from a survey of 3,005 U.S. adults conducted from September 2018 to May 2019. The research was done by Man-pui Sally Chan and Dolores Albarracín of the University of Illinois at Urbana-Champaign and Kathleen Hall Jamieson, director of the Annenberg Public Policy Center (APPC) of the University of Pennsylvania.

"What we find is that some online discussions appear to have a negative influence on people's attitudes and vaccine behavior - which makes the people exposed to them less likely to get a flu shot," said Albarracín, who is also an APPC distinguished research fellow. "That's the case if they do not have real-world discussions about vaccination with family and friends. But if they discuss it with others, that effect goes away."

COVID-19 concerns

The researchers said the study has important implications for the COVID-19 pandemic.

"What's going to happen when we have a COVID-19 vaccine?" Albarracín asked. "If public health officials don't offer clear, consistent messaging on vaccination, whatever circulates on Twitter - however crazy it is - may have an impact. We cannot trivialize it."

In addition, she said, the finding that discussing vaccines with family and friends appeared to eliminate negative effects from social media should encourage public health officials to promote real-world conversations about the benefits of vaccination. "We should be inviting families and communities to have open discussions on these issues. You don't necessarily have to tell people what to do, but that at least puts the issue on the table."

Vaccination and social media

In analyzing the more-than-100,000 tweets, the researchers used unsupervised machine learning to identify 10 topics among flu- and vaccine-related tweets. "Tweets, including retweets, are informative about popular topics and conversations within a community," the researchers noted. Those tweets, which were geotagged, were linked to U.S. counties.

The tweets were analyzed against individual responses gathered in five waves of U.S. survey data from the 2018-19 flu season. The respondents (ranging from 1,591 to 3,005 per wave) answered questions about vaccine attitudes, vaccination, and real-life discussions about vaccination.

The researchers found that two of the 10 Twitter topics, which they named "Vaccine Science Matters" and "Vaccine Fraud and Children," were prospectively associated with attitudes and behaviors - that is, they anticipated the views and behaviors reported by survey respondents:

"Vaccine Fraud and Children": The language of this topic included the terms "child" and "kid" and "worldwide." It also included tweets describing kidney pathology and references to what are now known to be falsified claims of vaccine fraud made in 2014. In U.S. counties where the tweets on this topic were prevalent, among respondents with no discussions with family and friends, this topic when seen in November-February was associated with negative vaccine attitudes in February-March and negative vaccination behavior in February-March and April-May.

"Vaccine Science Matters": Counties associated with tweets using these terms (including "vaxwithme" and "ivax" and "cancer") in November-February were positively correlated with vaccination attitudes in February-March.

In addition, a third topic, the conspiracy theory "Big Pharma," was associated with negative vaccination attitudes concurrent with the tweets.

The researchers said that while the study found "strong to very strong associations" between the social media topics and vaccine attitudes and behavior, the associations do not necessarily imply causation and await experimental results. But they also said that the results offer important insights - for example, that tweets could be used to convey factual information about vaccines and thereby positively influence attitudes and encourage vaccination.

Chan, the study's lead author, said, "Combating the current 'infodemic' online is critical, but so is getting communities to talk about vaccines in daily life."

PHILADELPHIA -- (Aug. 10, 2020) -- According to a study by The Wistar Institute, breast cancer cells starved for oxygen send out messages that induce oncogenic changes in surrounding normal epithelial cells. These messages are packaged into particles called extracellular vesicles (EVs) and reprogram mitochondrial shape and position within the recipient normal cells to ultimately promote deregulated tissue morphogenesis. These findings were published today in Developmental Cell.

"It is well known that cancer cells 'talk' to their neighboring normal cells all the time and this is important to promote cancer progression," said study lead author Dario C. Altieri, M.D., Wistar president and CEO, director of the Institute's Cancer Center and the Robert & Penny Fox Distinguished Professor. "How that happens and what signals are being transferred from one cell to another are still very much open questions. A better understanding of this process may give us important clues about how tumors hijack nearby normal cells to promote disease recurrence."

For their studies, Altieri's team cultured breast cancer cells in a low-oxygen setting to mimic a condition known as hypoxia, which is a hallmark of the microenvironment surrounding most solid tumors, and studied the EVs released by these cells.

EVs are tiny structures enclosed in a double membrane layer and released by most cells to transfer different molecules and information to other cells. As such, vesicles are an important means of intercellular communication. In this study, researchers focused on small EVs (sEV) that are between 30 and 150?nm in size.

To dissect the effects of sEVs produced by cancer cells on normal neighboring cells, researchers incubated normal breast epithelial cells with sEVs released by cells maintained in hypoxia. They observed an increase in the ability of normal recipient cells to migrate in culture, which in turn correlated with a redistribution of their mitochondria to the cell periphery. This is consistent with the role played by mitochondria in supporting cell motility, previously described by the Altieri lab.

In addition to modulation of mitochondrial behavior, the research team discovered that sEV released by hypoxic breast cancer cells induced major changes in gene expression in the normal recipient cells, with activation of multiple pathways of cell motility, cytoskeletal organization and cell-to-cell contact. Additionally, sEV-treated cells exhibited reduced cell death and increased pro-inflammatory responses.

Altieri and colleagues went on to identify Integrin-Linked Kinase (ILK) as the main signaling component packaged in sEVs, responsible for both mitochondrial changes and increased migration of recipient cells.

In turn, activation of ILK signaling profoundly affected normal tissue morphogenesis. Using 3-D cell models of normal mammary gland development, the team observed that exposure to sEVs from hypoxic cancer cells caused a general disruption of the normal mammary gland architecture and induced multiple traits of oncogenic transformation, including morphological changes, deregulated cell proliferation, reduced cell death, and appearance of markers of epithelial-mesenchymal transition (EMT), a process that confers mobility to cancer cells and the capacity to migrate from the primary site.

"Our findings indicate that breast cancer cells may use sEVs to enable both local and distant disease progression," said Irene Bertolini, Ph.D., first author of the study and a postdoctoral fellow in the Altieri lab. "Based on these observations, we suggest that therapeutic targeting of ILK or mitochondrial reprogramming may provide novel strategies to disrupt these pro-tumorigenic changes in the microenvironment."

How much effort should be spent trying to keep Venice looking like Venice - even as it faces rising sea levels that threaten the city with more frequent extreme flooding?

As climate change threatens cultural sites, preservationists and researchers are asking whether these iconic locations should be meticulously restored or should be allowed to adapt and "transform."

"The traditional preservationist paradigm is the idea of static preservation - materials stay in a constant state, and we protect the values identified at the time they were designated," said Erin Seekamp, first author of a paper that raises these questions and a professor of parks, recreation and tourism management at North Carolina State University.

"However, it's really infeasible to manage all heritage sites and property through persistent adaptation due to the extent of projected climate impacts," Seekamp said. "We are arguing for preservationists to shift toward transformation in some cases."

The paper was co-authored by Eugene Jo, World Heritage Leadership Programme Coordinator at the International Centre for the Study of the Preservation and Restoration of Cultural Property (ICCROM).

Seekamp and Jo presented two ideas for how transformation could take place: adaptively in response to climate change impacts, or in advance of anticipated or projected impacts.

Seekamp and Jo argue that some cultural icons "severely impacted" by climate change-related events could remain damaged to serve as a "memory" of that event, and to help communities better understand and learn about the climate-related vulnerabilities of places.

In other cases, they argued that some landmarks at risk of climate change should be allowed to "transform" when the cost of preserving a landmark is too high. Decisions about how these important landmarks can and should change need to be guided by the values of descendants of people and cultures that those sites were originally intended to highlight and preserve, they said.

"Individuals whose heritage is at stake, and who receive benefits from those places as tourist sites, should be part of the discussions about change, and about what preserving values connected with sites should look like," Seekamp said.

Their ideas about transformation were inspired by the concept of resilience in ecology, Seekamp said, in which a landscape can absorb change in response to a disturbance, and populations shift toward a "new state" or reorganize.

"What we're arguing is that the heritage field adopt an ecological framework of resilience to expand the current paradigm of preservation toward transformation to allow for autonomous and anticipatory adaptation to occur," Seekamp said.

They focused their recommendations on cultural landmarks designated as World Heritage Sites, which are landmarks or areas with important cultural, natural or scientific significance that have legal protections through the United Nations Educational, Scientific and Cultural Organization, or UNESCO.

They argued that preservation leaders create a new category for sites facing climate threats called "World Heritage Sites in Climatic Transformation." That list could help gather information and better document sites that face threats from climate change, as well as help channel resources toward them.

"We are argue that policy reform is needed to create the flexibility that would allow for both the continuity of heritage values, and the evolution of place meaning and societal benefits in face of climate change," Seekamp said.

Seekamp also indicated that the new designation could aid a natural landmark like Florida's Everglades National Park. While the park isn't a site recognized for its cultural heritage, which was the focus of Seekamp's viewpoint--it was designated as a World Heritage Site because of its outstanding geologic and natural features--there are material remains of heritage present that are also at risk to rising seas and increasing temperatures.

The park is the traditional lands of the Seminole Tribe of Florida and the Miccosukee Tribe, as well as the Calusa. The designation of the park as a "World Heritage Site in Climatic Transformation" could allow managers to think about alternatives that better integrate culture and cultural values in changing environments, Seekamp said.

"We're not saying that this should open the door for development or tourism," Seekamp added. "We're saying, 'Let's create a new categorization, and enable those places to not just think about persistent adaptation, but about transformative adaptation.' It allows us to think about alternatives."

An analysis of cervical cancers in Ugandan women has uncovered significant genomic differences between tumours caused by different strains of human papillomavirus (HPV), signifying HPV type may impact cervical cancer characteristics and prognosis.

The study--recently published in Nature Genetics--was led by a team of researchers, including scientists at the University of British Columbia and Canada's Michael Smith Genome Sciences Centre (GSC) at BC Cancer, and represents the first comprehensive analysis of molecular characteristics of cervical cancers in an African population.

The researchers compared cervical cancer samples infected by different evolutionary related groups of HPV types, known as clades. They identified previously unknown differences in how HPV clades impact the human genome. HPV-16 and HPV-18, belonging to clades A9 and A7, respectively, are the most common causes of cervical cancer detected in at least 70 per cent of cases. Although both are considered high-risk, HPV-18 was associated with more clinically aggressive cancers.

"We are very grateful to have had the opportunity to engage in a wonderful collaboration, involving teams of researchers from different countries and continents, to use genome science to analyze these very precious samples from Ugandan patients," says Dr. Marco Marra, Director of the GSC and head of UBC's department of medical genetics in the faculty of medicine. "This opportunity speaks to the foresight of those who collaborated with the Uganda Cancer Institute in Kampala to perform sample collection, and the study funders that made it possible. We are especially grateful to the support of the patients, without whom this work could not have happened."

HPV infection is a leading cause of cervical cancer. In B.C., cervical cancer incidence has been decreasing due to HPV vaccination and regular screening. However, cervical cancer is the fourth most common cancer worldwide and is the most common form of cancer-related mortality in sub-Saharan African women, with researchers predicting a 50 per cent increase in cervical cancer mortality by 2040.

It is critically important to study cervical cancer in African populations, and to compare the results obtained to other HPV-associated cancers, such as head and neck cancers, which are being observed with increasing frequency in western populations.

A new study suggests that future reductions in seasonal snowpack as a result of climate change may negatively influence forest growth in semi-arid climates, but less so in wetter climates.

Researchers from Portland State University, U.S. Geological Survey, U.S. Forest Service and the universities of Vermont and Maine found that forest density and snowpack can influence drought stress and forest growth in ways that are important to recognize for managing forests in a changing climate.

Research sites included pine-dominated experimental forests in northern Arizona, South Dakota, and northern Minnesota.

The study -- led by Kelly Gleason, assistant professor of ecohydrology at PSU -- found that forest growth in water-limited, dryland areas is likely to be most dramatically impacted by snowpack reductions. In these semi-arid climates, reduced snowpack may negatively influence forest growth and may increase tree mortality. This was only exacerbated in high-density forests.

"Forests are a lot more vulnerable because of increasing density," Gleason said. "More trees are sharing the same amount of water, and there's less water over time because of climate change impacts."

She said that in arid climates like much of the western U.S. where water availability is driven by snow, reducing forest density through thinning will improve the resilience of these forests amid a changing climate.

By contrast, the study found that in wetter climates like Minnesota, reduced snowpack as a result of future warmer winters may positively influence forest growth, potentially by extending the growing season. The study found that in these forests, thinning would have less of an impact on the snowpack-growth relationship.

Just as redeploying a fleet of small British fishing boats helped during the Battle of Dunkirk, marshalling the research equipment and expertise of the many agtech labs around the world could help combat pandemics, say the authors of a just-published article in Nature Biotechnology.

Sophisticated agtech labs and equipment used for crop and animal breeding, seed testing, and monitoring of plant and animal diseases could easily be adapted for diagnostic testing and tracing in a human pandemic or epidemic, the article states.

"If there is anything this current pandemic has shown us, it is that we need to mobilize efforts on a large scale to ramp up diagnostics," said lead author Steven Webb, chief executive officer of the Global Institute for Food Security (GIFS) at the University of Saskatchewan (USask).

"We must mobilize 'large ships' to fight pandemics by exploiting and adapting the screening capacity of high-throughput plant breeding laboratories which can rapidly analyze hundreds of thousands of samples."

The authors urge a national or international effort to co-ordinate rapid redeployment of digital agriculture infrastructure for pandemic preparedness. This approach would relieve the pressure on limited testing tools in the health sector and speed up the ability to respond with treatment and measures to contain the spread and occurrence of disease.

"Agtech has the infrastructure and capacity to support this need through its versatile equipment that can be used for very large-scale and automated applications including genetic testing and sequencing, virus detection, protein analysis, and gene expression," Webb said.

For instance, automated analysis of new plant varieties could be quickly switched to the automated detection of viral RNA or proteins, as well as detection of neutralizing antibodies, in humans. Selection of the fittest plant cultivars for breeding could be replaced by confirmation of patient diagnose of infectious diseases.

"As an example, the Omics and Precision Agriculture Laboratory (OPAL) at GIFS combines the digital data analysis of plant genes and traits with the latest precision agriculture technologies, and can provide a complete profile and data analysis of 3,000 plant samples per day," said Webb.

"Appropriate quality control measures would guide OPAL's switch from plant sample testing and analysis to human sample diagnostics during a pandemic, complying with regulation and using processes personnel are trained to employ."

GIFS has already lent equipment to enable expanded testing of COVID-19 blood samples and has donated materials and supplies to the Saskatchewan Health Authority.

The article notes that pandemics also affect animals and plants, with severe consequences for human food security, the economy, the environment, and society. For instance, the Great Famine in Ireland caused by the potato blight in the 1800s led to one million deaths and the spread of the blight in Europe claimed another 100,000 lives.

The article stresses the need to be able to adapt available agtech infrastructure from 'peacetime' applications to emergency use for diagnostic testing. This requires development of contingency protocols at national and international levels.

"There needs to be comprehensive quality control, standardizing the process and outcomes of this high-capacity testing of pandemic diagnostic samples," Webb said.

As well, there's a need to invest in agricultural technologies that can easily be adapted for medical use during pandemics.

"We need to be proactive to fight the next one. A proactive approach on all fronts will ensure the world is more prepared with the infrastructure and resources needed to respond to a pandemic," said Webb.

There's a paradox within the theory of evolution: The life forms that exist today are here because they were able to change when past environments disappeared. Yet, organisms evolve to fit into specific environmental niches.

"Ever-increasing specialization and precision should be an evolutionary dead end, but that is not the case. How the ability to fit precisely into a current setting is reconciled with the ability to change is the most fundamental question in evolutionary biology," says Alex Badyaev, a University of Arizona professor of ecology and evolutionary biology .

Badyaev is co-author of a paper published in Nature Communications that suggests an explanation based on the evolution of colorful pigments in bird feathers throughout North America. He wrote the paper with two former graduate students - lead author Ahva Potticary, now a UArizona lecturer, and Erin Morrison, now an assistant professor at New York University.

There are two general possible solutions, according to Badyaev. First, the mechanisms that enable organisms to fit well into their current environment and the mechanisms that enable change in adaptations are distinct - the latter are suppressed as organisms fit better and better into their current setting and activated only when the environment changes. The second is that the mechanisms that make organisms fit into current environments are themselves modified during evolution.

"Distinguishing between these possibilities is challenging because in evolutionary biology we necessarily study processes that occurred in the past, the events that we missed," he said. "So, instead, we infer what we missed from comparisons of species that exist today. Although this approach can tell us how well the current organisms fit into their current environment, it cannot tell us how they got here."

Ultimately, the first scenario was supported by the researchers' work. The mechanisms that make organisms locally fit and those responsible for change are distinct and occur sequentially in evolution.

Carotenoid Clues

Badyaev and his team aimed to directly observe adaptation to new environments in action while specifically paying attention to the mechanisms involved. The opportunity was provided by the house finch, a ubiquitous Sonoran Desert bird that over the last century has spread throughout most of North America and now occupies the largest ecological ranges of any living bird species.

Birds color themselves by eating and integrating pigmented molecules called carotenoids into their feathers.

"Carotenoids are large molecules, and stuffing them into growing feather is a messy process, resulting in all kinds of structural modifications and aberrations to feathers," Badyaev said. "This presents a unique opportunity to study how well-characterized developmental mechanisms that produce an intricate feather co-evolve with unpredictable external inputs needed to color them."

In feathers where structural integrity is essential, such as in temperature-regulating down or flight feathers, mechanisms evolve that buffer feather growth from incorporating carotenoids. For this reason, flight feathers or down feathers are almost never colorful in any bird species. On the opposite end of spectrum, ornamental feathers benefit from being colorful and evolve mechanisms that modify their structure to enable greater incorporation of carotenoids and to enhance their presentation.

The authors took advantage of this diversity and studied how this array of mechanisms - from complete buffering of carotenoids to fully embracing them - actually evolves.

The sources of carotenoid pigments differ across the house finch's huge range. In native desert populations, finches obtain their pigments from cactus pollen and fruits, while in urban populations they get them from newly introduced plant species and bird feeders. In northern populations, they incorporate the pigments from grass seeds, buds and berries.

"As expected, within each of these locations finches have evolved precise adaptations to incorporate diverse local carotenoids into their feathers," Badyaev said. But the unique aspect of this study is that "we knew the colonization routes of these birds, which enabled us to observe how they modify these adaptations as they move from one location to the next over the last century."

This approach not only allowed the team to directly study the process of evolution but also enabled them to study repeated evolution in the wild, because birds evolved distinct local adaptations in parallel from known starting points as they spread through the continent.

"We got to replay the tape of evolution of this adaptation, instead of deducing the process from the outcome," Badyaev said.

The team established 45 study populations along colonization routes that the species took from its native southern Arizona to the northwestern United States. They also explored how species changed within regions, such as between Arizona desert populations and urban populations on the University of Arizona campus and in Tucson. In all of these populations they examined microscopic structure and complete carotenoid composition in thousands upon thousands of feather samples. The unprecedented scale and depth of the study - believed to be the largest of its kind in a wild bird species - led to two discoveries.

First, evolution proceeded by remarkably similar sequences from widely diverse starting points. Unfamiliar local carotenoids exerted major modifications in developing feathers at first, but the longer birds persisted in a region and the more familiar they became with local carotenoids, the better there were able to incorporate them into their feathers, eventually evolving precise local adaptations.

Second, and most importantly, although carotenoids and their mixtures differed strongly between locations as distinct as deserts and northern evergreen forests, the mechanisms behind their incorporation into growing feathers were remarkably uniform and not specific to biochemical properties of individual carotenoid compounds. Instead, in all populations, evolution resulted from changes in mechanisms that buffered previous local adaptation from external stressors. These general stress-buffering mechanisms - what Badyaev called "the guardians of local adaptations" - had to be recruited to allow evolution of new adaptations.

In other words, "the boundaries of current adaptations become bridges between successive adaptions in evolution," Badyaev said.

The next step for the authors is to study the origin of molecular and developmental mechanisms they implicated in stress-buffering processes in evolution.

Over the last few decades, the divide between the two major political parties in the United States has deepened. Studies of Congressional voting patterns show that politicians take increasingly polarized positions, and that those positions drift farther and farther apart over time. Not voters, though. Since the 1960s, voters have stayed in the middle, usually preferring centrist or moderate positions to the extremes.

"Most people are still quite moderate on issue positions," says Vicky Chuqiao Yang, an Omidyar Fellow at the Santa Fe Institute. This contrast gives rise to a paradox: If voters gravitate toward the center of the political spectrum, why are the parties drifting farther apart? Political scientists have long sought theoretical models that accurately show how individual voting behavior shapes party positions.

This week in SIAM Review, Yang and her collaborators introduce a new model that accurately describes why politicians become more polarized even as their constituents remain steadfast in the middle. When the researchers tested the model on 150 years' worth of Congressional voting data in the United States, they found that it accurately represented real-world shifts in patterns over time.

Notably, the new model is guided by the idea of "satisficing," which assumes people will settle for a candidate who is "good enough", rather than always voting for the best one. That assumption makes a huge difference, says Yang. "Satisficing is a more reasonable description of people's behavior when it comes to voting," she says.

She points to a model, introduced in the 1950s by economist Anthony Downs, which is popular because of its simplicity but which fails to match empirical data. The Downsian model assumes that everyone votes, and that voters choose the candidate who is ideologically closest to their opinions. That assumption seems logical enough, says Yang. However, the model predicts that political parties should drift toward the center of the political spectrum over time in order to capture the most votes, but that's the opposite of how U.S. politics have changed.

The model by Yang's group takes a different tack. If a person is satisfied with a candidate, then that candidate gets the vote. If a person is satisfied with both of two candidates, then the vote is cast at random. And if a person isn't satisfied with either party, they don't vote.

Test runs of the model showed how sticking to party lines can produce a winning strategy. The researchers found that political parties increased their likelihood of winning votes when they established themselves, ideologically, farther from the middle of the spectrum. Yang says the model may also help explain why people want to identify with divided political groups, even though studies show that parties usually don't accurately represent all the opinions of its members.

The new work shows that satisficing voting behavior is one mechanism that can widen the divide in the current political climate, but Yang cautions that the model doesn't capture the whole story. "In reality, there are many things confounding together, and the answer is never that simple," she says.

BIRMINGHAM, Ala. - Cervical cancer kills more than 300,000 middle-aged women a year, and 19 of the 20 nations with the highest death rates are sub-Saharan countries.

Now an international team, including Akinyemi I. Ojesina, M.D., Ph.D., University of Alabama at Birmingham, has published the first comprehensive genomic study of cervical cancers in sub-Saharan Africa, with a focus on tumors from 212 Ugandan patients with cervical cancer.

Ojesina is one of five researchers who jointly supervised this work, which was published in Nature Genetics.

"Large-scale genomics studies like this are important," the co-authors say in the study, "particularly in under-represented ancestry groups, to understand molecular phenotypes of these cancers, which can lead to improved treatment options."

"This study is novel as the first cervical cancer study in which the majority of patients were positive for HIV -- the virus that causes AIDS," said Ojesina, who is an assistant professor of epidemiology in the UAB School of Public Health, an associate scientist with the O'Neal Comprehensive Cancer Center at UAB and adjunct faculty investigator at the HudsonAlpha Institute for Biotechnology, Huntsville, Alabama. "This allowed identification of genomic features that distinguish HIV-positive and HIV-negative patients."

"It is also novel," Ojesina said, "for the identification of unique genomic features associated with the African cohort compared with The Cancer Genome Atlas." The Cancer Genome Atlas includes genomic analysis of many cancers, including 307 cervical cancer tumors from places other than sub-Saharan Africa.

Cervical cancer develops in the tissues of the cervix, the narrow lower end of the uterus. Persistent infection by human papilloma virus, or HPV, is necessary, but not sufficient, to cause the cancer. The cancer can be prevented with an HPV vaccine, and it can be detected early by Pap smears. But these resources are scarce in lower- and middle-income areas that have a lot of HIV infections.

Genomic analysis of cancers is a complicated business. This study included analyses at many different levels.

Researchers started by looking at mutational changes in the DNA of the tumor cells. Restricting that hunt just to locations in the genome that code for expressed portions of genes is a simpler way to search. But the current study, Ojesina said, "is the first cervical cancer study to focus on whole genome sequencing of all samples -- as opposed to whole exome -- leading to identification of noncoding alterations."

Another level of analysis was looking at expression of gene transcripts to see which genes were overexpressed and which were down-regulated. This helps identify pathways used by the tumor to drive cancer growth, and that, in turn, can suggest possible treatments.

Part of the expression analysis also involved looking at non-mutational, or epigenetic, changes that can affect gene regulation. These included looking for the addition or removal of methyl groups on DNA bases, or changes in the methylation or acetylation of the histone proteins that help compact the human chromosome. Histone variants that can regulate gene expression were found in various tumors of the Ugandan study.

Another part of the genomic analysis was finding which types of HPV were in the tumor. Two HPV types commonly associated with cervical cancer are HPV-16 and HPV-18. Each virus type has variants, all descended from a common ancestor, and those variants that are from a single HPV type are called a clade. The variants for HPV-16 are contained in clade A9, and the variants for HPV-18 are contained in clade A7. The current study was able to describe molecular characteristics associated with each clade, including clusters of differential gene expression and clade-associated dysregulation. The A7-infected tumors, for example, showed gene expression patterns that pointed to pathways linked to extracellular matrix, cell adhesion and migration, which are signs of a more aggressive tumor.

The current study also found differences among the tumors, depending on whether the HPV was inserted into human chromosomes or not. For HPVs that were inserted into the chromosomes, the locations of the insertions differentially affected gene expression.

And finally, the researchers found that certain insertions in the Ugandan tumors led to expression of endogenous retroviral sequences, and upregulation of these sequences was associated with histone modifications. These endogenous retrovirus sequences -- found in normal chromosomes -- are remnants of ancient retroviral infections that make up about 8 percent of the human genome. Normally they are silenced in human cells, but they can be activated in human disease.

Myriad details from all the levels of genomic analysis outlined above are described in the study, "Analysis of Ugandan cervical carcinomas identifies human papillomavirus clade-specific epigenome and transcriptome landscapes."

"This international study was funded by the National Cancer Institute Office of Cancer Genomics under the auspices of the HIV+ Tumor Molecular Characterization Project, or HTMCP," Ojesina said. "The bulk of the analysis was done by Marco Marra, Ph.D., and his colleagues at BC Cancer, Vancouver, British Columbia, Canada. But my team at UAB played a vital role in identifying somatic genomic alterations and unique HPV-associated features. The other UAB personnel involved in the project as members of the HTMCP Cervical Cancer Working group include Vinodh Srinivasasainagendra, Aishwarya Sundaresan and Jianqing Zhang."

On Aug. 9, 2020 NASA's Aqua satellite imaged the Apple Fire near Big Bear Lake in California using its false-color bands in order to be able to distinguish burn scars from the surrounding area more easily. The combination of reflectance bands 7, 2, and 1 on the MODIS instrument are most useful for distinguishing burn scars from naturally low vegetation or bare soil and enhancing floods. The MODIS Corrected Reflectance imagery is available only as near real-time imagery. The imagery can be visualized in Worldview and the Global Imagery Browse Service (GIBS). This image was made using the Worldview Data site. Burned areas or fire-affected areas are characterized by deposits of charcoal and ash, removal of vegetation and/or the alteration of vegetation structure. When bare soil becomes exposed, the brightness in Band 1 may increase, but that may be offset by the presence of black carbon residue; the near infrared (Band 2) will become darker, and Band 7 becomes more reflective. When assigned to red in the image, Band 7 will show burn scars as deep or bright red, depending on the type of vegetation burned, the amount of residue, or the completeness of the burn.

In the image below, the measurement tool on the Worldview app was used to show the size of the burn scar. Using the tool, the scar was measured to be approximately 10.32 miles long and 8.16 miles wide. The Inciweb site is reporting that the Apple Fire is currently 32,905 acres in size and is 45% contained. Significant fire suppression is being provided by fire officials and continued advancement of the containment is the central goal. Fire crews will work on reducing fuel load to further contain the blaze and will also focus on repairing impacts to the landscape from fire suppression efforts. With increased winds forecasted for August 10 firefighters crews will continue to be on the lookout for hotspots and sources of spotting across the fire's edge.

NASA's Earth Observing System Data and Information System (EOSDIS) Worldview application provides the capability to interactively browse over 700 global, full-resolution satellite imagery layers and then download the underlying data. Many of the available imagery layers are updated within three hours of observation, essentially showing the entire Earth as it looks "right now." Actively burning fires, detected by thermal bands, are shown as red points.