While destination cities will work to sustainably accommodate swelling populations, aging coastal communities will confront stark new challenges, including an outflow of vital human infrastructure such as health care workers, said Associate Professor of Sociology Matt Hauer, lead author of the study published in the Proceedings of the National Academy of Sciences.

“In the destination communities where populations are increasing you’ll need more dentists, doctors, service workers, construction workers, etc.,” Hauer said. “So by people moving, you affect other people’s likelihood of moving. You get a demographic amplification.”

Previous studies estimated where people are likely to move as a changing climate affects livability. Hauer’s study also incorporates demographic data and secondary effects that revealed a host of challenges awaiting both the coastal “sender” communities and their destination counterparts.

“Imagine young families moving out of areas like Miami and moving to other locations and starting a family there,” he said. “And just by the fact that there’s more people who have moved there, these indirect population processes draw even more people.”

The study concluded that these indirect processes could create 5.3 to 18 times the number of climate migrants as those directly displaced by rising seas. It also found that by 2100, median age in coastal communities could spike as much as 10 years.

“Think about who are more unlikely to move and who will be left behind in these communities; it tends to be the oldest,” Hauer said. “Because migration is most likely to occur in more youthful populations, areas experiencing accelerated out-migration could face accelerated population aging.”

Doctoral student Sunshine Jacobs and computational scientist Scott Kulp co-authored the study with Hauer.

The researchers developed a migration model that uses sea level rise data from Climate Central and information about migration patterns from the U.S. Internal Revenue Service. That tool allowed them to predict migration on a county-by-county basis across the country. Jacobs said the model can be adapted to research different hazards that go beyond encroaching seas.

“We only looked at sea level rise,” she said. “Imagine other hazards that we know cause people to move, like heat events, wildfires and economic hazards. The future uses and implications of the model are amazing.”

This work was supported by the State of Louisiana, the American Society of Adaptation Professionals, the New York State Energy Research Development Authority, and the Great Lakes Integrated Sciences Assessment.

They also found a way to deliver immunotherapy’s cancer-killing impact without the unwelcome side effect.

The findings are published in Science.

“This is a good example of how understanding a mechanism helps you to develop an alternative therapy that’s more beneficial. Once we identified the mechanism causing the colitis, we could then develop ways to overcome this problem and prevent colitis while preserving the anti-tumor effect,” said senior study author Gabriel Nunez, M.D., Paul de Kruif Professor of Pathology at Michigan Medicine.

Immunotherapy has emerged as a promising treatment for several types of cancer. But immune checkpoint inhibitors can also cause severe side effects, including colitis, which is inflammation in the digestive tract.

Colitis can cause severe gastrointestinal discomfort, and some patients will discontinue their cancer treatment because of it.

The problem facing researchers was that while patients were developing colitis, the laboratory mice were not. So researchers couldn’t study what was causing this side effect.

To get past this, the Rogel team, led by first author Bernard C. Lo, Ph.D., created a new mouse model, injecting microbiota from wild-caught mice into the traditional mouse model.

In this model, the mice did develop colitis after administration of antibodies used for tumor immunotherapy. Now, researchers could trace back the mechanism to see what was causing this reaction.

In fact, colitis developed because of the composition of the gut microbiota, which caused immune T cells to be hyper-activated while regulatory T cells that put the brakes on T cell activation were deleted in the gut.

This was happening within a specific domain of the immune checkpoint antibodies.

Researchers then removed that domain, which they found still resulted in a strong anti-tumor response but without inducing colitis.

“Previously, there were some data that suggested the presence of certain bacteria correlated with response to therapy. But it was not proven that microbiota were critical to develop colitis. This work for the first time shows that microbiota are essential to develop colitis from immune checkpoint inhibition,” Nunez said.

To follow up what they saw in mice, researchers reanalyzed previously reported data from studies of human cells from patients treated with immune checkpoint antibodies, which reinforced the role of regulatory T cells in inducing colitis.

The antibody they used to stop the colitis was developed by Takeda Pharmaceuticals.

The Rogel team plans additional studies to further understand the mechanisms causing colitis and seeks clinical partners to move this knowledge to a clinical trial.

Additional authors are Ilona Kryczek, Jiali Yu, Linda Vatan, Roberta Caruso, Masanori Matsumoto, Yosuke Sato, Michael H. Shaw, Naohiro Inohara, Yuying Xie, Yu Leo Lei and Weiping Zou.

Funding for this work is from National Institutes of Health grants R01 DK121504, R01 DK095782, R01 DE026728, R01 DE030691, P30 CA046592; Takeda Millennium Pharmaceuticals, Canadian Institutes of Health, Crohn’s and Colitis Foundation, National Science Foundation grant IOS-2107215.

This work was supported by these Rogel Cancer Center Shared Resources: Single Cell Spatial Analysis, Tissue and Molecular Pathology

“Bird mortality has become an unintended consequence of renewable energy development,” said Hannah Vander Zanden, an assistant professor of biology at the University of Florida. “If we want to minimize or even offset these fatalities, especially for vulnerable populations, we need to identify the geographic origin of affected birds. In other words, are the dead birds local or are they coming from other parts of North America?”

Birds can be killed when they collide with wind turbines, fly into solar panels they mistake for bodies of water or become singed by the intense heat from concentrating solar power plants. While the death rate of birds due to these energy facilities is far less than deaths due to domestic cats and collisions with building, efforts to mitigate this problem is important, scientists say.

Vander Zanden and colleagues performed geospatial analyses of stable hydrogen isotope data obtained from feathers of 871 individual birds found dead at solar and wind energy facilities in California, representing 24 species.

Their analysis of natural-occurring markers in the feathers provided information about where the feathers were grown based on the water the birds consumed.

“With these markers, we could determine whether the bird was local or if it was migrating from somewhere else,” said Vander Zanden, who is the principal investigator of UF’s Animal Migration and Ecology Lab.

Results from the study, which were published Friday in the journal Conservation Biology, show that the birds killed at the facilities were from a broad area across the continent. Their geographical origins varied among species and included a mix of local and nonlocal birds.

Researchers found most birds killed at solar facilities were nonlocal and peaked during the migratory periods of April and September through October. The percentage of migratory birds found at wind facilities nearly matched that of local birds, at 51%, Vander Zanden said.

“This kind of data can help inform us about best strategies to use to minimize or mitigate the fatalities,” she said. “For example, facilities management could work with conservationists to improve the local habitat to help protect local birds or improve other parts of the species’ range where the migratory birds originate.”

The results also illustrate the power of stable isotope data to assess future population growth or decline patterns for birds due to a variety of reasons.

“Studying the remains of animals is a noninvasive approach to get information that is otherwise hard to track and apply to conservation,” Vander Zanden said. “It’s a great way to understand the mysteries about animals.”

Now, a study conducted in Japan has revealed the existence of around 11,000 vital genetic switches active in every cell type — housekeeping cis-regulatory elements (HK-CREs) — that play a role in maintaining the stability and function of our cells, far beyond the regulation of housekeeping genes. This study was performed by scientists from the Laboratory of Functional Analysis in silico (Nakai-lab) at The Institute of Medical Science, The University of Tokyo, Japan: Professor Kenta Nakai, head of the laboratory, and Dr. Martin Loza, Assistant Professor, in collaboration with Dr. Alexis Vandenbon, Associate Professor, from the Institute of Life and Medical Sciences, Kyoto University, Japan. Their work was published in Nucleic Acids Research on December 12, 2023.

Discussing his motivation behind this study, Dr. Loza states, “Given the significant association between cancer and mutations in epigenetic components, every small insight we gain could be key in the ongoing battle against this disease, which has tragically claimed innumerable lives. Through extensive bioinformatics analyses, we aimed to emphasize HK-CREs profound impact on fundamental cellular processes, including their potential as essential housekeeping tumor suppressors.” The research team found that HK-CREs were not solely confined to regulating the well-studied housekeeping genes (HKGs), which only constituted less than 20% of the genes associated with these elements. Instead, these elements predominantly resided within core promoter regions of many more genes (around 8,000), indicating a broader regulatory role beyond typical housekeeping gene functions. By employing bioinformatics analyses and levering diverse public datasets, the team validated the robustness of HK-CREs across 50 randomly selected healthy cell types, confirming the location of HK-CREs within the genome. These elements were highly conserved, residing in unmethylated CpG-rich regions, a trait strongly associated with their housekeeping regulatory function.

Sharing his concerns about the analysis, Dr. Lozastates, “By leveraging bioinformatics analyses of multiomics data, we offer an approach to harnessing publicly available datasets for exploring diverse biological mechanisms. We anticipate that employing similar workflows can significantly streamline analyses, cutting back both time and financial investments needed for comprehensive studies involving new data.”

The team remarked on the intricate cooperative interactions among housekeeping core promoters (HK-CPs), forming complex regulatory networks through promoter-promoter interactions. These observations hint at the significant influence of such interactions not only on HKGs but also on genes specific to various cell types. Turning their attention to cancer cells, researchers discovered a subset of HK-CREs displaying reduced activity in diverse cancer subtypes due to aberrant methylation, particularly those linked to zinc finger genes clustered in sub-telomere regions of chromosome 19. Identifying genes such as ZNF135, ZNF154, ZNF667, and ZNF667-AS1 under the influence of these foundational core promoters, the research suggests their potential as housekeeping tumor suppressor genes.

“Genes detected in our study have exhibited decreased activity in multiple cancer cell lines, and survival analysis across various cancer projects have revealed significant increases in survival probability in diverse cancer types like pancreas adenocarcinoma and uveal melanoma,” states Dr. Loza.

In essence, the results of this research have uncovered a previously unknown class of HK-CREs critical for cellular stability, extending their influence beyond housekeeping gene regulation. “Our discovery on housekeeping tumor suppressor genes unveils a novel avenue in cancer therapy, harnessing the intrinsic elements within the DNA of every cell. Future approaches to cancer treatment, focusing on these housekeeping tumor suppressor genes, offer a unique solution that could potentially target a broad range of cancers, sidestepping the challenges associated with personalized medicine,” remarks Dr. Loza. He further adds, “Our findings on housekeeping cis-regulatory elements fill a big gap in the current knowledge regarding gene regulatory processes. We anticipate that our findings will enhance the understanding of these processes and serve as a valuable resource for researchers striving to uncover elements inherent in the genome for combating various diseases.”

Technological advancements have enabled scientists to comprehensively explore genetic control elements, unraveling the complexities of gene activation mechanisms in our genetic code. New evidence challenges the simplistic view that cis-regulatory elements (CREs) are mere on/off switches for genes, emphasizing their ability to exhibit complex behaviors, such as the simultaneous enhancement of gene activity and initiation of gene transcription, e.g., simultaneous enhancer and promoter activities. These switches aren’t only important for the enhancement of specific genes but are crucial for the basic functions that keep our cells healthy. Now, a study conducted in Japan has revealed the existence of around 11,000 vital genetic switches active in every cell type — housekeeping cis-regulatory elements (HK-CREs) — that play a role in maintaining the stability and function of our cells, far beyond the regulation of housekeeping genes. This study was performed by scientists from the Laboratory of Functional Analysis in silico (Nakai-lab) at The Institute of Medical Science, The University of Tokyo, Japan: Professor Kenta Nakai, head of the laboratory, and Dr. Martin Loza, Assistant Professor, in collaboration with Dr. Alexis Vandenbon, Associate Professor, from the Institute of Life and Medical Sciences, Kyoto University, Japan. Their work was published in Nucleic Acids Research on December 12, 2023.

Discussing his motivation behind this study, Dr. Loza states, “Given the significant association between cancer and mutations in epigenetic components, every small insight we gain could be key in the ongoing battle against this disease, which has tragically claimed innumerable lives. Through extensive bioinformatics analyses, we aimed to emphasize HK-CREs profound impact on fundamental cellular processes, including their potential as essential housekeeping tumor suppressors.” The research team found that HK-CREs were not solely confined to regulating the well-studied housekeeping genes (HKGs), which only constituted less than 20% of the genes associated with these elements. Instead, these elements predominantly resided within core promoter regions of many more genes (around 8,000), indicating a broader regulatory role beyond typical housekeeping gene functions. By employing bioinformatics analyses and levering diverse public datasets, the team validated the robustness of HK-CREs across 50 randomly selected healthy cell types, confirming the location of HK-CREs within the genome. These elements were highly conserved, residing in unmethylated CpG-rich regions, a trait strongly associated with their housekeeping regulatory function.

Sharing his concerns about the analysis, Dr. Lozastates, “By leveraging bioinformatics analyses of multiomics data, we offer an approach to harnessing publicly available datasets for exploring diverse biological mechanisms. We anticipate that employing similar workflows can significantly streamline analyses, cutting back both time and financial investments needed for comprehensive studies involving new data.”

The team remarked on the intricate cooperative interactions among housekeeping core promoters (HK-CPs), forming complex regulatory networks through promoter-promoter interactions. These observations hint at the significant influence of such interactions not only on HKGs but also on genes specific to various cell types. Turning their attention to cancer cells, researchers discovered a subset of HK-CREs displaying reduced activity in diverse cancer subtypes due to aberrant methylation, particularly those linked to zinc finger genes clustered in sub-telomere regions of chromosome 19. Identifying genes such as ZNF135, ZNF154, ZNF667, and ZNF667-AS1 under the influence of these foundational core promoters, the research suggests their potential as housekeeping tumor suppressor genes.

“Genes detected in our study have exhibited decreased activity in multiple cancer cell lines, and survival analysis across various cancer projects have revealed significant increases in survival probability in diverse cancer types like pancreas adenocarcinoma and uveal melanoma,” states Dr. Loza.

In essence, the results of this research have uncovered a previously unknown class of HK-CREs critical for cellular stability, extending their influence beyond housekeeping gene regulation. “Our discovery on housekeeping tumor suppressor genes unveils a novel avenue in cancer therapy, harnessing the intrinsic elements within the DNA of every cell. Future approaches to cancer treatment, focusing on these housekeeping tumor suppressor genes, offer a unique solution that could potentially target a broad range of cancers, sidestepping the challenges associated with personalized medicine,” remarks Dr. Loza. He further adds, “Our findings on housekeeping cis-regulatory elements fill a big gap in the current knowledge regarding gene regulatory processes. We anticipate that our findings will enhance the understanding of these processes and serve as a valuable resource for researchers striving to uncover elements inherent in the genome for combating various diseases.”

The evidence suggests that the long-term solution to elephant survival requires not only that areas are protected but that they are also connected to allow populations to stabilize naturally, an international research team says.

Their study, published on January 5th in the peer-reviewed journal Science Advances, collected survey estimates and calculated growth rates for more than 100 elephant populations in southern Africa between 1995 and 2020, accounting for an estimated 70% of the global savanna elephant population.

“This is the most comprehensive analysis of growth rates for any large mammal population in the world,” said co-author Rob Guldemond, director of the Conservation Ecological Research Unit (CERU) at the University of Pretoria, in South Africa.

Overall, the survey’s results are positive: There are the same number of elephants now as there were 25 years ago, a rare conservation win at a time when the planet is rapidly losing biodiversity. However, the pattern is not consistent across regions. Some areas, such as south Tanzania, eastern Zambia, and northern Zimbabwe, experienced severe declines due to illegal ivory poaching. In contrast, populations in other regions like north Botswana are booming.

“Unchecked growth isn’t necessarily a good thing, however,” says study co-author Stuart Pimm, the Doris Duke Professor of Conservation at Duke University in North Carolina. “Rapidly increasing populations can outgrow and damage their local environment and prove hard to manage — introducing a threat to their long-term stability,” Pimm says.

In addition to documenting local growth rates, the team also looked at the features of the local populations to identify what makes them stable, that is neither growing nor declining.

Elephant populations in well-protected but isolated parks, sometimes called “fortress conservation,” grow rapidly in the absence of threats but are unsustainable in the long term. These elephants will likely need future conservation interventions, such as translocation or birth control, which are both costly and intensive endeavors.

The team found that the most stable populations occur in large, core areas that are surrounded by buffer zones. The core areas are defined by their strong levels of environmental protection and minimal human impact, whereas the buffers allow some activities such as sustainable farming, forestry, or trophy hunting. Unlike the insular fortresses, core areas are connected to other parks, allowing herds to move naturally.

“What’s crucial is that you need a mix of areas with more stable core populations linked to more variable buffer areas,” said lead author Ryan Huang, a Duke Ph.D. now doing postdoctoral research at CERU.

“These buffers absorb immigrants when core populations get too high, but also provide escape routes when elephants face poor environmental conditions or other threats such as poaching,” Huang said.

Connecting protected areas means elephants can freely move in and out. This allows a natural equilibrium to occur without human intervention, sparing conservationists from using their limited resources to maintain balance.

“Calling for connecting parks isn’t something new. Many have done so,” Huang said. “But surprisingly, there has not been a lot of published evidence of its effectiveness so far. This study helps quantify why this works.”

“Connecting protected areas is essential for the survival of African savanna elephants and many other animal and plant species,” said Celesté Maré, co-author and doctoral student at Aarhus University in Denmark. “Populations with more options for moving around are healthier and more stable, which is important given an uncertain future from climate change.”