Earth

Power in the workplace does not stop women's exposure to sexual harassment. On the contrary, women with supervisory positions are harassed more than women employees. These are the results from a new study from the Swedish Institute for Social Research at Stockholm University, which examined the conditions in Sweden, USA and Japan.

By analyzing the responses from three surveys, researchers at the Swedish Institute for Social Research, SOFI, at Stockholm University, together with fellow American and Japanese researchers, have studied the prevalence of sexual harassment across the organizational hierarchy. The study shows that women with supervisory positions experienced between 30 and 100 per cent more sexual harassment than other women employees. This was true across the United States, Japan, and Sweden, three countries with different gender norms and levels of gender equality in the labour market. Comparing levels of leadership, exposure to harassment was greatest at lower levels of leadership, but remained substantial and similar to the level of harassment for the highest positions.

"When we first started to study sexual harassment, we expected a higher exposure for women with less power in the workplace. Instead we found the contrary. When you think about it, there are logical explanations: a supervisor is exposed to new groups of potential perpetrators. She can be harassed both from her subordinates and from higher-level management within the company. More harassment from these two groups is also what we saw when we asked the women who had harassed them," says Johanna Rickne, Professor of Economics at SOFI.

In all three countries, women with supervisory positions were subject to more harassment when their subordinates consisted of mostly men.

"Sexual harassment means that women's career advancement comes at a higher cost than men's, especially in male-dominated industries and firms. Additional survey data from the United States and Japan showed that harassment of supervisors was not only more common than for employees, but was also followed by more negative professional and social consequences. This included getting a reputation of being a 'trouble maker' and missing out on promotions or training," says Olle Folke, affiliated researcher at SOFI and associate professor at Uppsala University.

The study addressed the risk of measurement error from different awareness of sexual harassment among supervisors and employees. Questions on whether or not particular behaviours should, or should not, be defined as harassment showed similar answers in the two groups. This makes it unlikely that the results derive from different perceptions of work interactions, rather than different treatment in those interactions.

Facts: Measurements of sexual harassment

The study used two different measurement tools. The surveys in the United States and Japan included the Sexual Experiences Questionnaire, a survey instrument with a list of behaviours, developed for studies in the US military. All three countries were also surveyed with subjective questions about whether the person had been exposed to sexual harassment. The time span for all questions was the previous 12 months.

Facts: Research method

The Swedish results come from five waves of the Swedish Work Environment Survey, a nationally representative dataset collected biannually by Statistics Sweden (1999, 2001, 2003, 2005, and 2007) and with a total of 23,994 female respondents. In the United States and Japan, the research team collected new survey material during 2019. The US sample included 1,573 employed female citizens, whereof 62 per cent had supervisory positions, while the Japanese sample included 1,573 respondents, of which 17 per cent of the women were in supervisory positions. Apart from questions about sexual harassments, respondents were asked about perpetrators, how they reacted to the harassment, and what social and professional consequences followed the victimization.

Senescent cells, which stop dividing under stress, are long- recognized drivers of multiple diseases of aging. Mouse studies have shown that targeted removal of these cells and the inflammatory factors they secrete, known as the senescence-associated secretory phenotype (SASP), has beneficial results on multiple organ systems and functions. Success in the laboratory has given rise to companies and research projects aimed at developing either senolytics, drugs that clear senescent cells, or senomorphics, drugs that suppress the SASP. But drug development and clinical utilization require simple, reliable biomarkers to assess the abundance of senescent cells in human tissues. Publishing in PLOS Biology, researchers at the Buck Institute have extensively profiled the SASP of human cells and have generated a curated database available for use in the field.

"The stage is now set for the development of clinically-relevant biomarkers of aging," said Judith Campisi, PhD, Buck professor and one of the senior authors on the paper. "This will speed efforts to get safe and effective drugs into the clinic and, in the long term, could enable physicians to give patients a clear read-out of how well, or poorly, their various tissues and organs are aging."

The study, led by postdoc Nathan Basisty, PhD, expanded the number of proteins known to be secreted by human senescent cells by about 10-fold, to over 1000. Researchers show that a 'core' set of senescence factors, which were secreted by all types of senescent cells studied, are significantly increased in human plasma as we age, and may be the basis for developing "whole body" biomarkers of aging, and biomarkers to assess the efficacy of senolytics and senomorphics in human trials. Using advanced proteomic analysis, researchers also propose signatures that identify specific subsets of senescent cells.

"The complexity of the SASP, which is typically monitored by a few dozen secreted proteins, has been greatly underappreciated, and a small set of factors cannot explain the diverse phenotypes senescence produces in vivo," said Basisty who describes the SASP Atlas as a comprehensive proteomic database of soluble and exosome SASP factors originating from multiple senescence inducers and cell types. Each profile consists of hundreds of largely distinct proteins, but also includes a 'core' subset of proteins elevated in all SASPs.

"The work points out how different inducers of senescence and different cells types result in different secretomes," said Campisi. "For the first time we have the capability of measuring the burden of senescent cells in vivo and making educated guesses on how they became senescent and how neighboring cells are being affected."

"Proteomics allowed us to take a totally unbiased approach in this project and is the perfect example of how you can utilize high-end technology to move forward with biological questions," said Birgit Schilling, PhD, senior co-author and assistant professor and director of the Buck Institute's Proteomics and Mass Spectrometry Center. "Our hope is that the SASP Atlas will facilitate identification of proteins that drive specific senescence-associated phenotypes and catalog and develop potential senescence biomarkers to assess the burden and origin of senescent cells in vivo."

This initial research at the Buck utilized senescent human lung fibroblasts and epithelial cells from the kidney. Results were validated by comparing them with markers of aging found in plasma from The Baltimore Longitudinal Study of Aging (BLSA), America's longest-running scientific study of human aging which is maintained by the National Institute on Aging (NIA) and involves more than 3,200 volunteers. "Our research shows that we all age differently," said Luigi Ferrucci, MD, the Scientific Director of the Intramural Research Program at the NIA and one of the co-authors of the study. "The development of senescence-associated biomarkers will allow us to identify factors that drive aging and disease in specific tissues and will hopefully lead to early detection and interventions that will prevent disease progression. We are pleased to partner with the Buck Institute in this effort."

An international team of scientists has synthetically engineered mosquitoes that halt the transmission of the dengue virus.

Led by biologists at the University of California San Diego, the research team describes details of the achievement in Aedes aegypti mosquitoes, the insects that spread dengue in humans, on January 16 in the journal PLOS Pathogens.

Researchers in UC San Diego Associate Professor Omar Akbari's lab worked with colleagues at Vanderbilt University Medical Center in identifying a broad spectrum human antibody for dengue suppression. The development marks the first engineered approach in mosquitoes that targets the four known types of dengue, improving upon previous designs that addressed single strains.

They then designed the antibody "cargo" to be synthetically expressed in female A. aegypti mosquitoes, which spread the dengue virus.

"Once the female mosquito takes in blood, the antibody is activated and expressed--that's the trigger," said Akbari, of the Division of Biological Sciences and a member of the Tata Institute for Genetics and Society. "The antibody is able to hinder the replication of the virus and prevent its dissemination throughout the mosquito, which then prevents its transmission to humans. It's a powerful approach."

Akbari said the engineered mosquitoes could easily be paired with a dissemination system, such as a gene drive based on CRISPR/CAS-9 technology, capable of spreading the antibody throughout wild disease-transmitting mosquito populations.

"It is fascinating that we now can transfer genes from the human immune system to confer immunity to mosquitoes. This work opens up a whole new field of biotechnology possibilities to interrupt mosquito-borne diseases of man," said coauthor James Crowe, Jr., M.D., director of the Vanderbilt Vaccine Center at Vanderbilt University Medical Center in Nashville, Tenn.

According to the World Health Organization, dengue virus threatens millions of people in tropical and sub-tropical climates. Severe dengue is a leading cause of serious illness and death among children in many Asian and Latin American countries. The Pan American Health Organization recently reported the highest number of dengue cases ever recorded in the Americas. Infecting those with compromised immune systems, dengue victims suffer flu-like symptoms, including severe fevers and rashes. Serious cases can include life-threatening bleeding. Currently no specific treatment exists and thus prevention and control depend on measures that stop the spread of the virus.

"This development means that in the foreseeable future there may be viable genetic approaches to controlling dengue virus in the field, which could limit human suffering and mortality," said Akbari, whose lab is now in the early stages of testing methods to simultaneously neutralize mosquitoes against dengue and a suite of other viruses such as Zika, yellow fever and chikungunya.

"Mosquitoes have been given the bad rap of being the deadliest killers on the planet because they are the messengers that transmit diseases like malaria, dengue, chikungunya, Zika and yellow fever that collectively put 6.5 billion people at risk globally," said Suresh Subramani, professor emeritus of molecular biology at UC San Diego and global director of the Tata Institute for Genetics and Society (TIGS). "Until recently, the world has focused on shooting (killing) this messenger. Work from the Akbari lab and at TIGS is aimed at disarming the mosquito instead by preventing it from transmitting diseases, without killing the messenger. This paper shows that it is possible to immunize mosquitoes and prevent their ability to transmit dengue virus, and potentially other mosquito-borne pathogens."

CHAPEL HILL, N.C.-Comparison shopping for airfare, a TV or a car can be straightforward online. The same cannot be said for checking what hospitals charge for a standard radiation treatment for prostate cancer, according to a report published in JAMA Oncology.

Trevor Royce, MD, MS, MPH, of the University of North Carolina Lineberger Comprehensive Cancer Center, is the corresponding author of a study that investigated whether a federal rule that requires hospitals to publicly list standard charges for services and procedures -- the foundation of price transparency -- would enable people to compare prices for care provided at National Cancer Institute-designated cancer centers.

The researchers searched the websites of 63 NCI-designated cancer centers for the listed cost for simple intensity-modulated radiation therapy (IMRT) for prostate cancer, and discovered the information was not consistent or was missing altogether.

While 52 centers, or 83 percent, published the cost, three did not list a cost for a simple IMRT, and eight did not publish costs for any procedure.

In addition, the costs published varied greatly, they were listed for a single procedure and not the entire course of care, and the average price was 10 times the Medicare reimbursement rate. There also wasn't any information provided on discounted rates that private insurance companies may have negotiated.

Royce said the lack of common terminology, unbundled cost reporting, the wide range in pricing from center to center, listing of non-negotiated rates limits the information's value, especially when a person is trying to estimate or compare the cost of care.

"Achieving price transparency can be an important step in helping patients and providers understand potential financial liabilities as it relates to health care," said Royce, who is an assistant professor of radiation oncology at the UNC School of Medicine. "How can consumers and providers be expected to make informed decisions, such as pursuing high-value care, if they do not know the costs?"

Price transparency is seen by some as an approach to address the high cost of care. Knowing the cost would make it possible for a person to budget better for the expense, to apply for assistance when available, to discuss costs with a physician and compare what other hospitals charge.

"Providing cost data that is easy to understand and consistent from one hospital to the next is an important step in helping people to make informed decisions about their care and the associated costs," said Ankit Agarwal, MD, MBA, the paper's first author and co-chief resident of radiation oncology at the UNC School of Medicine. "This information also may lead to a more competitive health care marketplace, which could drive down costs if hospitals compete for patients."

Previous studies have found that medical expenses cause financial distress in one in three Americans, and patients with cancer are twice as likely to file for bankruptcy than patients who don't have cancer.

Royce said a new set of price transparency rules the Centers for Medicare and Medicaid Services released in November may address some of the shortcomings the researchers outlined in their study. Included in the new rules is a requirement for hospitals to publicly post both standard charges for specific services and the actual prices they have negotiated with private insurers.

"This has the potential to be a much more impactful step in achieving health care price transparency, but it is not clear when this will be implemented, as several hospital groups have filed a lawsuit against the U.S. Department of Health and Human Services in federal court regarding this rule," said Royce.

Some things we do appear almost automatic, like opening the fridge when feeling hungry or flipping on the air conditioning when the temperature rises. Although such decisions don't seem to take much thought, they are in fact generated by millions of neurons and numerous interactions among several brain regions--a dynamic system so complex that scientists aren't able to observe it fully and in real time, even in simple organisms.

One exception is the zebrafish, whose decision-making processes is now coming into clearer view. In work published in Cell, researchers were able to track the activity of each neuron in the entire brain of zebrafish larvae and reconstruct the unfolding of neuronal events as the animals repeatedly made "left or right" choices in a behavioral experiment.

The resulting frame-by-frame view of a decision in the making was so detailed that, 10 seconds before the fish responded, the researchers could predict what their next move will be and when they would execute it.

Following a decision

Understanding how a brain makes decisions involves tracking how neurons across multiple brain regions respond and cooperate--which, to be clear, is anything but trivial. Scientists have long been stuck between two options: They can either closely observe the firing of only a subset of neurons, which limits their view of the whole picture, or look at the whole brain activity while averaging the data over multiple trials to reduce noise. Averaging, however, leads to loss of some of the details.

"We wanted to understand how decisions unfold on a trial-by-trial basis," says Alipasha Vaziri, head of the Laboratory of Neurotechnology and Biophysics. To do so, the team paired advanced statistical methods with their recently developed imaging technique, light field microscopy, which enables simultaneous tracking of the activity of every neuron in the brains of zebrafish larvae.

But before subjecting the fish to experiments, the scientists had to teach them a new behavior, one that wasn't merely reflexive but goal-oriented.

The goal, from the fish perspective, was to get relief from heat. The researchers slightly warmed the water around the fish using a laser, and switched off the laser only when the fish made a tail movement to the right. After about 15 repeats, the fish had mastered the trick: They responded to their warming surroundings about 20 seconds after the laser came on. About 80 percent of the time, the fish remembered to flip their tail in the correct direction. (To avoid any direction bias, the whole experiment was also repeated by teaching the fish to turn their tails to the left.)

During the interval after the laser was turned on and before the fish made a movement, the researchers tracked the activity state of about 5,000 of the most active neurons across the entire brain. They then identified which activity patterns reflected the brain sensing the heat or moving the tail, and which appeared decision related. Particularly, they found about 10 seconds before the fish made a movement, its brain patterns differed based on whether the fish was going to make a correct or an incorrect turn.

Having this information, the researchers could look at the brain state of any one little fish, and 80 percent of the time guess correctly what the fish was about to do: They were able to predict the specific time at which the animals would initiate the turn, and its direction, in each trial.

An unexpected player

Having found which clusters of neurons corresponded to different aspects of the task, the researchers then mapped the neurons onto their anatomical regions. "This allowed us to see what brain regions were involved in what aspects of the task as the decision unfolded in each trial," Vaziri says.

Several brain regions participated in transforming sensory information into decision and action, but one region stood out: the cerebellum. The rate of activity of neurons in this brain part determined the exact timing of the tail movement. Moreover, a lopsided activity in the two hemispheres of cerebellum, starting from the heat onset and gradually increasing until the fish moved its tail, predicted the direction in which the fish was about to make a turn.

In other words, the cerebellum--a region best known for its role in coordination, balance, and fine-tuning of movements--appeared to play a major role in shaping up the animals' decisions.

"This was surprising," Vaziri says, adding that a few studies in recent years have pointed in the same direction. "I think we might find more generally that the cerebellum is involved in more cognitive brain functions than what we have traditionally thought."

Boston, Mass. - Interoception is the awareness of our physiological states; it's how animals and humans know they're hungry or thirsty, and how they know when they've had enough to eat or drink. But precisely how the brain estimates the state of the body and reacts to it remains unclear. In a paper published in the journal Neuron, neuroscientists at Beth Israel Deaconess Medical Center (BIDMC) shed new light on the process, demonstrating that a region of the brain called the insular cortex orchestrates how signals from the body are interpreted and acted upon. The work represents the first steps toward understanding the neural basis of interoception, which could in turn allow researchers to address key questions in eating disorders, obesity, drug addiction, and a host of other diseases.

Using a mouse model his lab developed at BIDMC, Mark Andermann, PhD, principal investigator in the Division of Endocrinology, Diabetes and Metabolism at BIDMC and Associate Professor of Medicine at Harvard Medical School, and colleagues recorded the activity of hundreds of individual brain cells in the insular cortex to determine exactly what is happening as hungry animals ate.

The team observed that when mice hadn't eaten for many hours, the activity pattern of insular cortex neurons reflected current levels of hunger. As the mice ate, this pattern gradually shifted over hours to a new pattern reflecting satiety. When mice were shown a visual cue predicting impending availability of food - akin to a person seeing a food commercial or a restaurant logo - the insular cortex appeared to simulate the future sated state for a few seconds, and then returned to an activity pattern related to hunger. These findings provided direct support for studies in humans that hypothesized that the insular cortex is involved in imagining or predicting how we will feel after eating or drinking.

"It is as if the insular cortex is briefly estimating, or simulating, the physiological consequences of eating a meal," said first author Yoav Livneh, PhD, a postdoctoral research fellow in Andermann's lab. "When hungry, this would be a simulation of satiety. But when considering whether to eat in the absence of hunger, for example when eating dessert after a big meal, this would be a simulation of the consequences of overeating. We hypothesized in this paper that when insular cortex activity shifts from a pattern reflecting current bodily state to a pattern reflecting a future satiety state, the size of this shift actually predicts how rewarding it will be to eat the food."

A second experiment in which thirsty mice were presented with water yielded nearly identical results - with an important difference. The patterns of activity related to hunger and thirst were quite different, allowing the insular cortex to monitor multiple body states simultaneously.

"Another surprising finding was that insular cortex activity that reflects bodily state was independent of the hypothalamus, which is normally thought to be a master regulator of physiological need states in the brain," Andermann said. "In contrast, we found that even when we artificially activate hypothalamus in a way that compels sated mice to eat, insular cortex activity isn't fooled, and still reflects the body's current physiological state of satiety."

Next, Andermann and colleagues plan to directly manipulate specific patterns of activity in the insular cortex with the goal of changing the prediction the brain makes when presented with food or water, thereby making eating and drinking more or less rewarding.

"If successful, this approach might provide an intervention that could reduce seeking of unhealthy rewards (such as unhealthy foods or drugs of abuse) without affecting the seeking of other, healthier rewards," said Andermann. "Such an intervention could potentially have a lot of value in both medicine and psychiatry."

Researchers from the Norwegian Institute of International Affairs and the University of Sussex analysed USD 1.3 trillion of research funding around the world.

Between 1990 and 2018, less than 4.59% of the funding was spent on climate-related research.

Only 0.12% of the research funding was spent on a critical issue: how to change societies to mitigate climate change.

Vast funding goes into research on the impact of climate change and adaptation to it, rather than into trying find out how it can be prevented socially.

A new study shows that there is a huge disproportion in the level of funding for social science research into the greatest challenge in combatting global warming - how to get individuals and societies to overcome ingrained human habits to make the changes necessary to mitigate climate change.

The analysis argues that despite many of the key climate-change puzzles residing in the social sciences (such as anthropology, economics, international relations, human geography, development studies, political science, psychology etc), these fields receive least funding for climate research.

Academics from the Norwegian Institute of International Affairs and the University of Sussex analysed research grants from 332 donors around the world spanning 4.3 million awards with a cumulative value of USD 1.3 trillion from 1950 to 2021.

According to the study's estimates, between 1990 and 2018 the natural and technical sciences received 770% more funding than the social sciences for research on climate change - USD 40 billion compared to only USD 4.6 billion for the social sciences and humanities.

Only 0.12% of all research funding was spent on the social science of climate mitigation.

Even the countries that spent the most on social science climate research in absolute terms - the UK, the USA, and Germany - spent between 500% and 1200% more on climate research in the natural and technical sciences.

The report's co-authors say funding of climate research appears to be based on the assumption that if natural scientists work out the causes, impacts, and technological remedies of climate change, then politicians, officials, and citizens will spontaneously change their behaviour to tackle the problem. The academics argue the evidence from the past decades shows this assumption does not hold.

With the window of opportunity for mitigating climate change narrow and closing, the researchers recommend more funding is made available for social science research on climate mitigation; improved global research funding coordination and transparency; prioritisation around key questions within the social sciences and an increase in the rigorousness of social science research.

Benjamin K Sovacool, Professor of Energy Policy at the University of Sussex, said: "Most people probably think that because climate change is so severe, responsive research would be a core priority. But the opposite is true. And, oddly, the smallest part of the funding goes into solving the most pressing issues."

Indra Overland, who heads the Centre for Energy Research at the Norwegian Institute of International Affairs, said: "The one-sided emphasis on the natural sciences leaves one wondering whether funding for climate research is managed by climate sceptics. It's as if they don't quite believe in climate change, so they keep looking into out how it really works, rather than trying to work out how to actually stop it."

The authors recommend:

Funding for climate mitigation needs to match the magnitude of the threat - Global annual damages from climate change has already reached USD 10 to 40 billion from storm surge alone, and it could surpass USD 100 trillion over the next 80 years. Funding for research on climate mitigation should be increased to address the magnitude of this threat.

Improved funding transparency and coordination - There is a need for better global coordination and oversight of funding for climate research. The lack of oversight can cause significant overlaps in funding in some research areas, while other areas are neglected. More research financing organizations need to make their portfolios available online with standardized tags for such things such as project title, summary and discipline.

More rigorous social science research - While more funding is needed for social research on climate change, the social sciences also need to rise to the challenge. Social scientists need to do a better job of ensuring rigor and validity in their research. Social science research needs to show a greater understanding of the natural sciences and the physical world, move away from obscure theoretical debates and avoid focussing on very small groups of people or sample sizes that are difficult to generalize from.

Better alignment with emissions sources and trends - Prioritise truly problem-solving research on the burning mitigation issues.

Do not lose sight of climate change as a global challenge - Although global solutions also depend on understanding the micro level, it is still surprising how little social science research goes straight for the really big issues. Part of the solution could be to organize future research efforts not around disciplines, but around urgent puzzles linked to pressing social challenges related to climate change mitigation and energy systems. This challenges-based approach to research has been relatively successful in other domains, notably national defence.

Cyanobacteria, also known as blue-green algae, are among the most common organisms on Earth. A research team led by the Leibniz-Institute of Freshwater Ecology and Inland Fisheries (IGB) and Heidelberg University has now shown for the first time that Cyanobacteria produce relevant amounts of methane in oceans, inland waters and on land. Due to climate change, "Cyanobacteria blooms" increase in frequency and extent, amplifying the release of methane from inland waters and oceans to the atmosphere.

Methane generation by microorganisms is traditionally considered to take place only under strictly anoxic conditions by microbes of the domain Archaea. This assumption is refuted by the results of the present study led by Dr. Mina Bizic from IGB. The international research team investigated seventeen cyanobacterial species that occur in the sea, freshwater and soil. "Cyanobacteria in surface water are a previously unknown source of methane and we were able to show for the first time that these bacteria produce the greenhouse gas methane during photosynthesis," states Dr. Mina Bizic. To do so, Thomas Klintzsch from Heidelberg University used isotopically labelled carbon to evaluate how methane is formed in the cell during the conversion of light energy into chemical energy.

In laboratory experiments, the team compared the amount of methane produced by Cyanobacteria with the amounts produced by methanogenic archaea and organisms with cell nuclei (eukaryotes). "Cyanobacteria produce less methane than archaea, but more methane than eukaryotes. It is difficult to estimate the global amount of methane produced by Cyanobacteria because there is a severe lack of detailed data on the biomass of these organisms in water and soil," says co-author Frank Keppler, Professor at the Institute of Earth Sciences at Heidelberg University.

More blue-green algal blooms mean higher methane emissions

It may be that Cyanobacteria have been producing the greenhouse gas methane already since the early days of Earth. Cyanobacteria are well known for the Great Oxygenation event that took place 2.5 billion years ago, but the oldest known fossils (stromatolites) are deposits of Cyanobacteria¬-like organism found in 3.5 billion-year-old rocks in Western Australia.

Cyanobacteria are widespread all over the world occurring in almost any illuminated environment. Some species develop particularly well in seawater or fresh water with high nutrient loads and warm temperatures. As a result of climate change, mass developments, so-called cyanobacteria or blue-green algae blooms, already occur more frequently and will do so to a greater extent in the future. "According to our current findings, this will also increase the emission of the greenhouse gas methane from various aquatic systems, which in turn increases climate change," says senior author Prof. Hans-Peter Grossart, researcher at IGB.

Cell-to-cell contacts are necessary for the survival of human cells under protein-damaging conditions and stress. This was one of the conclusions made by a research team working under the leadership of Lea Sistonen, Professor in Cell and Molecular Biology at Åbo Akademi University. The results of their research were recently published in the Cell Reports journal.

The researchers were surprised by the findings because the molecules they studied are usually linked with other cellular functions.

"Our results show, for the first time, that the contacts between cells, known as cell adhesion, are essential for cells to survive stress. The findings also suggest that impaired cell adhesion may sensitize cancer cells to drugs that damage cell proteins and cause stress", Sistonen explains.

The research project focused on heat shock factor 2 (HSF2), a specialized gene regulating protein, and its impact on cells' capacity to survive protein-damaging stress. Protein-damaging stress is caused by, for example, high temperatures, virus infections and certain anti-cancer medications.

The results showed that HSF2 contributes to protecting cells against stress by regulating those genes that mediate cell adhesion contacts.

The results were obtained by studying, among other things, how cancer cells respond to certain commonly used anti-cancer drugs. Cancer cells with impaired cell adhesion contacts were significantly less successful in surviving the drug treatment than the cells showing intact cell adhesion.

"Cell-to-cell contacts are essential for normal tissue functioning and mechanisms. Cancer cells are known to utilize these contacts to form aggressive tumours and metastases. Our results show, indeed, that cancer cells become more vulnerable to drug treatment, when their cell contacts are weakened", says Sistonen.

"Cell adhesion contacts are mediated by proteins known as cadherins, which serve as the source of message chains regulating cell death, but understanding of the molecular basis for these processes calls for further research. Individual differences in these particular cell processes may partly explain why certain drugs work effectively for some patients but not for others."

The research headed by Professor Sistonen is part of the CellMech project, an internal Center of Excellence project in Cellular Mechanostasis (2019-2023) at Åbo Akademi University, which studies the impacts of mechanical stress on the signalling and functioning of cells and tissues. The CellMech project is led by Cecilia Sahlgren, Professor in Cell Biology. Drug Development and Diagnostics is one of the focal research areas at Åbo Akademi University.

Optical sensing in the mid to long infrared (5microns - um) is becoming of utmost importance in different fields since it is proving to be an excellent tool for environmental monitoring, gas sensing, thermal imaging as well as food quality control or the pharmaceutical industry, to name a few. The amount of information hidden within this very rich spectral window opens new possibilities for multi or even hyperspectral imaging. Even though there are technologies that can address these challenges, they are very complex and expensive.

Even though there is a strong market need in bringing such functionalities to the consumer market, this would require a technology that is low-cost, CMOS compatible and does not impose severe regulatory concerns.

PbS Colloidal Quantum Dots (CQDs) have emerged as a cost-competitive and high performance photodetector technology, compatible with CMOS technology, which has demonstrated recently to be successful in the short-wave infrared (1-2 um). However, so far, there has been a fundamental limit: such quantum dots have relied on interband absorption of light (photons excite carrier across the bandgap of the material) and as a result there is a lower energy limit that this technology can operate: the bandgap of the material.

In a study recently published in Nanoletters, ICFO researchers Iñigo Ramiro, Onur Ozdemir, Sotirios Christodoulou, Shuchi Gupta, Mariona Dalmases, Iacopo Torre, led by ICREA Prof. at ICFO Gerasimos Konstantatos, now report the development of a colloidal quantum dot photodetector that is capable of detecting light in the long infrared range, from 5 um - 10 um (microns), using PbS CQDs that, for the first time, are made with mercury-free material.

In their experiment, the researchers used a technique to electronically dope the quantum dots robustly and permanently. This heavy doping approach allowed them to enable a new regime for transitions of electrons: instead of relying on transitions across the bandgap of the material, they found a way to facilitate transitions amongst higher excited states, known as intersubband (or intraband) transitions. By achieving this, they were able to excite electrons by absorbing photons with photon energies much lower than before in the mid and long wave infrared. They also demonstrated that the spectral coverage of such detectors can be tuned by changing the size of the dots, that is, the larger the quantum dots, the farther the absorption in the infrared.

The results of this study have reported a novel and unique material platform, based on heavily doped PbS CQDs covering a broad range of light, which could address and solve the challenges that the field of photodetector technologies is facing nowadays. This newly discovered property of light absorption in the long infrared together with a low-cost and maturing CQD technology may bring about a revolution to extreme broadband as well as multispectral CMOS compatible photodetectors.

COLUMBUS, Ohio -- Scientists studying fossils collected 35 years ago have identified them as the oldest-known scorpion species, a prehistoric animal from about 437 million years ago. The researchers found that the animal likely had the capacity to breathe in both ancient oceans and on land.

The discovery provides new information about how animals transitioned from living in the sea to living entirely on land: The scorpion's respiratory and circulatory systems are almost identical to those of our modern-day scorpions -- which spend their lives exclusively on land -- and operate similarly to those of a horseshoe crab, which lives mostly in the water, but which is capable of forays onto land for short periods of time.

The researchers named the new scorpion Parioscorpio venator. The genus name means "progenitor scorpion," and the species name means "hunter." They outlined their findings in a study published today in the journal Scientific Reports.

"We're looking at the oldest known scorpion -- the oldest known member of the arachnid lineage, which has been one of the most successful land-going creatures in all of Earth history," said Loren Babcock, an author of the study and a professor of earth sciences at The Ohio State University.

"And beyond that, what is of even greater significance is that we've identified a mechanism by which animals made that critical transition from a marine habitat to a terrestrial habitat. It provides a model for other kinds of animals that have made that transition including, potentially, vertebrate animals. It's a groundbreaking discovery."

The "hunter scorpion" fossils were unearthed in 1985 from a site in Wisconsin that was once a small pool at the base of an island cliff face. They had remained unstudied in a museum at the University of Wisconsin for more than 30 years when one of Babcock's doctoral students, Andrew Wendruff -- now an adjunct professor at Otterbein University in Westerville -- decided to examine the fossils in detail.

Wendruff and Babcock knew almost immediately that the fossils were scorpions. But, initially, they were not sure how close these fossils were to the roots of arachnid evolutionary history. The earliest known scorpion to that point had been found in Scotland and dated to about 434 million years ago. Scorpions, paleontologists knew, were one of the first animals to live on land full-time.

The Wisconsin fossils, the researchers ultimately determined, are between 1 million and 3 million years older than the fossil from Scotland. They figured out how old this scorpion was from other fossils in the same formation. Those fossils came from creatures that scientists think lived between 436.5 and 437.5 million years ago, during the early part of the Silurian period, the third period in the Paleozoic era.

"People often think we use carbon dating to determine the age of fossils, but that doesn't work for something this old," Wendruff said. "But we date things with ash beds -- and when we don't have volcanic ash beds, we use these microfossils and correlate the years when those creatures were on Earth. It's a little bit of comparative dating."

The Wisconsin fossils -- from a formation that contains fossils known as the Waukesha Biota¬ -- show features typical of a scorpion, but detailed analysis showed some characteristics that were not previously known in any scorpion, such as additional body segments and a short "tail" region, all of which shed light on the ancestry of this group.

Wendruff examined the fossils under a microscope, and took detailed, high-resolution photographs of the fossils from different angles. Bits of the animal's internal organs, preserved in the rock, began to emerge. He identified the appendages, a chamber where the animal would have stored its venom, and -- most importantly -- the remains of its respiratory and circulatory systems.

This scorpion is about 2.5 centimeters long -- about the same size as many scorpions in the world today. And, Babcock said, it shows a crucial evolutionary link between the way ancient ancestors of scorpions respired under water, and the way modern-day scorpions breathe on land. Internally, the respiratory-circulatory system has a structure just like that found in today's scorpions.

"The inner workings of the respiratory-circulatory system in this animal are, shape-wise, identical to those of the arachnids and scorpions that breathe air exclusively," Babcock said. "But it also is incredibly similar to what we recognize in marine arthropods like horseshoe crabs. So, it looks like this scorpion, this lineage, must have been pre-adapted to life on land, meaning they had the morphologic capability to make that transition, even before they first stepped onto land."

Paleontologists have for years debated how animals moved from sea to land. Some fossils show walking traces in the sand that may be as old as 560 million years, but these traces may have been made in prehistoric surf -- meaning it is difficult to know whether animals were living on land or darting out from their homes in the ancient ocean.

But with these prehistoric scorpions, Wendruff said, there was little doubt that they could survive on land because of the similarities to modern-day scorpions in the respiratory and circulatory systems.

A massive research effort over more than a quarter century has tried to make personalized blood stem cells for use in treating leukemias, among many other uses. One way researchers have gone about this is to sample a patient's adult cells and then "deprogram" them to create induced pluripotent stem cells (iPSCs), which are capable of forming any of the body's cell types, including blood cells. Unfortunately, these iPSCs also have the potential to become cancer. So researchers have largely refocused their efforts on making hematopoietic stem cells (HSCs), which can't make any cell type, but can produce many types of blood cells. The good news is that HSCs don't seem to cause cancer like iPCs. The bad news is that researchers have been unable to create HSCs that can take hold and grow in the body.

Now a University of Colorado Cancer Center study identifies a possible new way to convince pluripotent cells to make HSCs. And, ironically, a possible way to do this lies in magnifying a gene that causes a form of childhood leukemia.

"My lab was working on a gene called MLL that, when accidentally fused together with another gene, causes childhood leukemia," says Patricia Ernst, PhD, CU Cancer Center investigator and Professor in the CU School of Medicine Departments of Pediatrics.

In other words, this malfunctioning form of the gene MLL is bad and Ernst (among others) hoped to discover how to mute the function of this cancer-causing fusion gene. But to understand how to counteract malfunctioning MLL, Ernst and her team needed to know how regular MLL works.

"Half my lab was studying MLL's role in leukemia and the other half was exploring what MLL normally does," Ernst says. "When we knocked out this gene, we saw that hematopoietic stem cells couldn't retain their 'stemness' - instead of being HSCs, they would differentiate to become like normal cells of the blood system. So we wondered what would happen if we increased it," Ernst says.

The current paper, highlighted on the cover of the current issue of the journal Stem Cell Reports, is the result of that question.

What Ernst's studies show is that doubling the amount of the regular MLL protein in pluripotent stem cells, can push these cells to produce more blood cells. The finding may help to develop usable HSCs that could regrow a leukemia patient's blood system after the chemotherapy and irradiation used to kill the cancer.

Second, the finding has important ramifications for ongoing drug development against MLL-rearranged childhood leukemia, namely that drugs affecting the healthy MLL gene along with the rearranged form of the MLL gene may have negative consequences for blood functions.

"It's about selective targeting," Ernst says. "We want to selectively turn off the cancer-causing MLL fusion gene without affecting the regular form of the MLL gene."

With a pilot grant from the CU Cancer Center RNA Biosciences Initiative, Ernst and her team were able to drill down to see the function of MLL at a single-cell level.

"As pluripotent cells differentiate, they enter a kind of transitional state in which they still have the potential to become many different cell types. Single-cell sequencing let us watch the fate of these transitional cells, and we saw that activating MLL led to more of these transitional cells becoming blood cell types," Ernst says.

One way to activate MLL in a population of pluripotent cells would be with genetic engineering, adding additional copies of the MLL gene to the pluripotent cells' genome. However, that approach is not practical in human patients. Instead, Ernst plans to pursue development of a drug-based method to amplify the level of existing MLL.

The goal is to "make customizable stem cell products that could be adapted to any particular patient," Ernst says.

The finding of MLL's role in stem cell differentiation and maintenance provides an important new starting point in a field of study that has seen many dead ends.

EAST LANSING, Mich. - When it comes to certain parts of the brain, bigger doesn't necessarily equate to better memory. According to a new study led by Michigan State University, a larger hippocampus, a curved, seahorse-shaped structure embedded deep in the brain, does not always reliably predict learning and memory abilities in older adults.

It's normal for the hippocampus to shrink as we age, but it's much more pronounced in people with mild cognitive impairment or Alzheimer's disease. Scientists long believed that a bigger hippocampus meant a better memory until a 2004 study showed that its size does not always matter for memory in older adults. But scientists are only now starting to understand why.

This latest study published online in the journal Cerebral Cortex shows the size or volume of the hippocampus is only a meaningful marker of learning for older people with more intact limbic white matter - the neural circuitry that connects the hippocampus to the rest of the brain.

"Our findings highlight the need to measure not just the size of the hippocampus but also how well it's connected to the rest of the brain when we look for physical markers of memory decline in older adults," said Andrew Bender, lead author on the study and assistant professor of epidemiology and biostatistics, and neurology and ophthalmology at MSU's College of Human Medicine.

The study has potential implications for earlier diagnosis of aging-related memory disorders such as Alzheimer's disease. Some older adults whose brain scans show a larger hippocampus - perhaps due to high levels of education, physical activity, or social and cognitive engagement - could have their cognitive decline overlooked or mischaracterized if physicians do not also consider their white matter connectivity.

Bender, and colleagues at Harvard University, the Hungarian Academy of Sciences and the Max Planck Institute for Human Development, analyzed two different types of MRI brain scans: one that evaluated hippocampal size and another that evaluated the white matter circuitry that connects the hippocampus with other brain regions involved in learning. The scans came from more than 330 older adults who are part of the Berlin Aging Study-II, or BASE-II, a large, population-based investigation of aging in Germany.

The BASE-II participants also took learning and memory tests in which they heard a list of 15 words and then had to record as many words as they could remember. Each participant repeated the exact same test five times to gauge how they learn through repetition.

Bender and colleagues then analyzed the relationships between how quickly the participants learned and the size of their hippocampus and white matter structure. They reported that faster learning was found only in older adults who had both a larger hippocampus and more uniform white matter circuitry connecting it to other parts of the brain.

"Our findings reinforce a growing perspective that studying age-related changes in learning and memory from a systems perspective appears far more informative in understanding different patterns of brain and cognitive declines than focusing on any single brain region," Bender said.

Next, he and his colleagues plan to analyze new data from BASE-II ¬- participants who returned for a second round of brain scans and memory recall tests two to three years after their first visits.

"By following people over time," Bender said, "we can see if there is actually change in older adults' brain structure and whether that is linked with observable declines in learning and memory."

Although coming from a disadvantaged background, experiencing violence within the family, having a negative school environment or consuming violent media such as films and computer games have little or no direct influence on potential criminal behaviour among adolescents and young adults. These factors do often result in young people regarding violent acts as harmless and spending their time with friends with similar attitudes - and this, in turn, is clearly linked to crime.

These are two of the most important results of the long-term study "Crime in the modern City" headed by criminologist Prof. Klaus Boers (University of Münster, Germany) and sociologist Prof. Jost Reinecke (University of Bielefeld, Germany). The study - funded over a period of almost 20 years by the German Research Foundation (DFG) - is the only long-term study in Germany, and one of the few internationally, to examine delinquent behaviour from late childhood through to early adulthood. The study differs from previous ones predominantly inasmuch as the latter included one-off interviews which provided 'snapshots' but said nothing about the development of criminal behaviour.

Between 2002 and 2019 the researchers questioned around 3,000 people in Duisburg aged from 13 to 30 - initially every year, and later every two years - not only on crimes they had committed themselves, but also on attitudes, values and lifestyles. The researchers gained insights into the dark field of crime as a result of the young peoples' reports of offences which do not appear in any official statistics. In addition, they evaluated (light-field) data relating to convictions and cases which were dismissed. The information and the data contained in the study relate exclusively to Duisburg - although the researchers are convinced that many of the results can be applied to other German cities.

Overview of the most important results:

Occasional acts of theft or low-level violent crime are not unusual, especially in boys, from late childhood (28 percent) to mid-teens (25 percent) - but they are also committed by girls (22 percent and 14 percent respectively for the two age groups). However, from the end of adolescence onwards, most of the young people no longer display delinquent behaviour - with girls stopping earlier than boys. "This sharp reduction in juvenile crime is normal, and its success is due to standard educational processes and socialization," says Klaus Boers. "With attentiveness on the part of parents and teachers, and with the youngsters being among friends and in clubs, things sort themselves out in the end."

Young people accept social norms especially when society reacts in a pedagogically appropriate way to any infringements of the rules, says Boers. For this reason, he adds, something that is welcome and which makes sense is the fact that criminal law relating to juveniles allows for public prosecutors and courts to give priority to the corrective efforts undertaken by parents, teachers and other groups and to drop cases involving short-term offences committed by young people. This is one reason, Klaus Boers says, why, since the first decade of this century, crime amongst juveniles has decreased by one-third, and violent crime by as much as one-half. "A so-called zero-tolerance strategy - in other words, convictions for minor first offences - would counteract such positive developments," comments Jost Reinecke.

It's a small group of habitual offenders that are the problem. They account for five to eight percent in their respective age groups and commit half of all offences and three-quarters of all violent crimes in these age groups. Habitual offenders are active predominantly in adolescence, but the vast majority of them leave delinquency behind them at the end of this period of their lives. Nor does being an habitual offender in early years necessarily lead to a development of long-term delinquency. Half of such offenders active in late childhood commit noticeably fewer crimes in adolescence. These findings - which have been confirmed in international studies - support the theory that preventive measures and treatment programmes can also make habitual offenders turn their backs on crime.

What is especially helpful, says the report, are good relationships, based on attentiveness and trust, between schoolchildren, teachers, family members and friends. In contrast, only rarely does any contact with the police or the courts which ends in leniency have an immediate effect on adolescents' further behaviour. In the case of more drastic measures, the solidarity provided by cliques - with their particular attitudes - may be strengthened. Anyone who is known to the judicial system, the report continues - regardless of the actual extent of any offences they go on to commit - runs a higher risk of again being the focus of attention.

According to the report, adolescents who are the children of immigrants* do not commit more theft than young Germans. Girls with a Turkish heritage - a group for which the researchers in Duisburg had a good quantity of data available - commit fewer offences than German girls. In the 1990s, however, male adolescents from immigrant families committed substantially more violent crimes and they were more frequently habitual offenders. It was only in the first decade of this century, however, that no significant differences could be observed any longer between male juveniles with a German, Turkish or eastern European background. This could be attributed to successful integration of third-generation immigrants into the education system. Moreover, as regards young Germans who have social deficits comparable to those of youngsters with a Turkish heritage, both groups show similar levels of violence.

Conclusion: Even problematic offenders frequently stop committing offences - and, especially, violent crimes - at the latest when they reach early adulthood. This positive development can be supported by means of pedagogical measures and appropriate reactions on the part of the police and the courts. There is a good chance that these young people can build positive ties and attitudes in later life.

AUGUSTA, Ga. (Jan. 15, 2020) - A stroke appears to create a sticky situation inside the blood vessels of the brain that can worsen damage days, even months later, scientists report.

They have found that after stroke, exosomes -- nanosized biological suitcases packed with an assortment of cargo that cells swap, like proteins and fats -- traveling in the blood get activated and sticky and start accumulating on the lining of blood vessels, according to a collaborative study by the Medical College of Georgia and the University of Oxford.

Like a catastrophic freeway pileup, platelets, also tiny cells that enable our blood to clot after an injury, start adhering to the now- sticky exosomes, causing a buildup that can effectively form another clot, further obstruct blood flow to the brain and cause additional destruction, they report in the journal Scientific Reports.

One thing traveling exosomes typically aren't is sticky rather, much like our real suitcases, they have a smooth label that marks their intended destination, says Dr. Zsolt Bagi, vascular biologist in the MCG Department of Physiology. He and Dr. Daniel C. Anthony, professor of experimental neuropathology/pharmacology in the Department of Pharmacology at the University of Oxford, are co-corresponding authors of the new study.

But when these external destination tags become inexplicably sticky following a stroke, not only do exosomes not reach their
destination, they can worsen stroke outcome, he notes.

In a bit of a perfect storm, the scientists have shown in both stroke models and human blood vessels that exosomes cruising through the blood then pick up RGD, the unique and normally sticky peptide sequence, arginine-glycine-aspartate, which is key to the pileup that can cause additional brain damage.

More typically, exosomes carry a negligible amount of RGD, a protein that's important in holding together the extracellular matrix that helps cells connect and form tissue. In the aftermath of a stroke, cells and the extracellular matrix both get damaged, and sticky RGD is effectively set free.

Platelets normally aren't exposed to RGD, which should mostly be sequestered in the extracellular matrix, so they become angry, activated and also sticky in response. "There is always a problem when platelets become activated," Bagi says.

Another piece of this sticky situation is that a receptor called αvβ3, which is important to new blood vessel growth and the relationship between the endothelial cells that line blood vessels and the extracellular matrix that supports them. Avβ3 also is found on the lining of blood vessels and naturally binds to sticky RGD as part of its role with the extracellular matrix. There was already evidence that in heart attack, for example, when the lining of blood vessels is activated by inflammation, these αvβ3 receptors become key sites for cells to pile up inside the blood vessel.

The new stroke study shows the RGD carrying exosomes also target these receptors. In fact, when scientists gave antibodies to αvβ3, the binding to the blood vessel lining was blocked. Conversely, when they exposed a human blood vessel to tumor necrosis factor, which increases inflammation, adhesion increased.

A bottom line of the new work is that RGD sequences are a key contributor to the secondary damage from stroke, says Bagi.

"We can't prevent the initial stroke, but what we are trying to do is prevent further damage," he says, which likely makes removing or masking the stickiness a good future strategy. Synthetic exosomes given right after a stroke that compete for the same binding sites or that help internalize abnormal sticky labels, may one day be treatment options, Bagi says.

Normally, few platelets bind to the endothelium, and when they do it's generally not a good sign. The Oxford investigators have shown increased platelet binding, for example, in the microvasculature of mice with cerebral malaria, a severe complication of the infection that can result in a coma. But just how platelets start accumulating on interior blood vessel walls has been an unknown.

The studies at MCG and Oxford actually started in the blood of stroke patients, where the scientists found this sticky conversion of exosomes and their picking up of now-free RGD, and the findings held in stroke models. Anthony's lab develops synthetic exosomes, and the scientists used one of these that was both sticky and contained a contrast agent so they could more easily track exosome movement.

"We were able to see they bind and that once they bind, they trap the platelets," says Bagi. They even watched the exosomes with RGD on their surface, pull platelets out of the blood then stick to the blood vessel lining.

When they put exosomes from an animal model of stroke into a healthy brain blood vessel, platelets started piling up there as well.

Future explorations include whether this process also contributes to the initial stroke in the face of inflammation-producing conditions like high blood pressure or high cholesterol.

Bagi notes that the secondary damage altered exosomes clearly help instigate may in reality be part of an effort to be helpful that goes awry. "I think exosomes are not supposed to stick to the surface of the endothelium but when damage happens they may try to pick up the damage and take it to the liver for elimination," Bagi says.

Circulating exosomes are known to increase in number following an ischemic stroke, the most common stroke type.