In a new study published in Earth’s Future, scientists looked at future projections of evaporative demand — a measure of how dry the air is — in California and Nevada through the end of the 21st century. They then examined how changes in evaporative demand would impact the frequency of extreme fire danger and three-year droughts, based on metrics from the Evaporative Demand Drought Index (EDDI) and the Standardized Precipitation Evapotranspiration Index (SPEI).

According to their results, climate change projections show consistent future increases in atmospheric evaporative demand (or the “atmospheric thirst”) over California and Nevada. These changes were largely driven by warmer temperatures, and would likely lead to significant on-the-ground environmental impacts.

“Higher evaporative demand during summer and autumn — peak fire season in the region — means faster drying of soil moisture and vegetation, and available fuels becoming more flammable, leading to fires that can burn faster and hotter,” explained lead author Dan McEvoy, Ph.D., Assistant Research Professor of Climatology at DRI.

“Increased evaporative demand with warming enables fuels to be drier for longer periods,” added coauthor John Abatzoglou, Ph.D., Associate Professor with the University of California, Merced. “This is a recipe for more active fire seasons.”

The research team found that days with extreme fire danger in summer and autumn are expected to increase four to 10 times by the end of the century. Their results also showed that multi-year droughts, similar to that experienced in California and Nevada during 2012-2016, were projected to increase three to 15 times by the end of the century.

“One major takeaway was that we can expect to see a lot more days in the summer and autumn with extreme fire danger related to increased temperature and evaporative demand,” McEvoy said. “Another takeaway was that even in locations where precipitation may not change that much in future, droughts are going to become more severe due to higher evaporative demand.”

Study authors say that the cumulative effects of increases in evaporative demand will stress native ecosystems, increase fire danger, negatively impact agriculture where water demands cannot be met, and exacerbate impacts to society during periods of prolonged dryness. Several members of the research team are part of the California-Nevada Applications Program (CNAP), and will use these study results to provide resource managers with a view of possible future scenarios.

“These results provide information to support science-based, long-term planning for fire management agencies, forest management agencies, and water resource managers,” said coauthor Julie Kalansky, Ph.D., Program Manager for CNAP. “We plan to work with partners to help integrate the findings from this paper to support building climate resilience.”

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In the current study published in the journal Science, a team led by researchers at Baylor College of Medicine discovered that rotavirus-infected cells release signaling molecules, identified as adenosine diphosphate (ADP), which binds its cellular receptor P2Y1 on neighboring cells. Activating P2Y1 by ADP results in signals called intercellular calcium waves in these uninfected cells. Disrupting ADP binding to its receptor reduced the severity of diarrhea in a mouse model of the disease, suggesting that targeting the P2Y1 may be an effective strategy to control viral diarrhea in human populations.

“In our previous studies using fluorescent calcium sensors and time-lapse imaging, we discovered that rotavirus-infected cells display aberrant calcium signals that we can visualize as bright pulses of intercellular calcium waves that radiate from the infected cells,” said corresponding author Dr. Joseph Hyser, assistant professor of virology and microbiology and member of the Alkek Center for Metagenomic and Microbiome Research at Baylor. “Calcium signaling was known to be associated with various aspects of rotavirus infection and our work revealed the dynamic nature of the alterations induced by rotavirus.”

In the current study, the researchers conducted the experiments using a lower dose of the virus and noticed that it was not just the virus-infected cells that showed dynamic calcium signaling, but also the adjacent uninfected cells surrounding the infected cells produced pulses of calcium waves that were coordinated with those of the infected cells. This observation suggested that the infected cells could be triggering intercellular calcium waves in the uninfected cells.

The researchers connected their observation to a concept proposed in the mid-90s suggesting that rotavirus-infected cells send signals to neighboring uninfected cells that disrupt their function, promoting diarrhea and vomiting.

“Our videos of live fluorescent microscopy showing intercellular calcium wave signaling in both rotavirus-infected and uninfected cells provided an unprecedented means to investigate the nature of the proposed signal, which had not been identified,” said first author Dr. Alexandra L. Chang-Graham, an M.D./Ph.D. student in the Medical Scientist Training Program who completed her Ph.D. thesis working in the Hyser lab.

Finding the signal

Chang-Graham, Hyser and their colleagues worked with three different laboratory models to identify the signal that triggers intercellular calcium waves on uninfected cells. They used a monkey kidney cell line commonly used to study rotavirus. They also worked with human intestinal enteroids, a cultivation system that recapitulates many of the characteristics of the human infection and a neonatal mouse model of rotavirus infection and diarrhea. Their studies showed that suspected triggers of calcium waves, such as prostaglandin E2 and nitric oxide, did not elicit a calcium response. Then they tested ATP and ADP, known mediators of calcium signaling that had not been previously associated with rotavirus infection. They found that rotavirus-infected cells triggered intercellular calcium waves by releasing ADP that binds to its receptor, P2Y1, on uninfected neighboring cells. Knocking out the P2Y1 gene, which prevents ADP from signaling, reduced intercellular calcium waves.

“Across the three model systems we consistently found evidence that rotavirus-infected cells signal uninfected cells with ADP and that this contributes to the severity of the disease,” Chang-Graham said. “We consider it paradigm shifting that the actual signal, ADP, was not even on the radar before.”

ADP signaling is involved in triggering severe rotavirus symptoms

Further studies revealed previously unknown roles of ADP on rotavirus infection and replication, shining a spotlight on ADP as an important trigger of the multiple factors involved in severe diarrhea and vomiting caused by rotavirus. For instance, the researchers found evidence that ADP signaling increases rotavirus infection, the expression of inflammatory cytokine IL1-alpha and the secretion of serotonin, an inducer of diarrhea. ADP signaling also increases the expression of enzymes that produce prostaglandin and nitric oxide, potentially causing the increases in those compounds observed in rotavirus infection. Preventing ADP signaling and intercellular calcium waves reduced the production of the compounds mentioned above.

“Finally, we determined that inhibiting the P2Y1 receptor reduced the severity of rotavirus-induced diarrhea in a mouse model,” Chang-Graham said. “Using intercellular calcium waves, rotavirus amplifies its ability to cause disease beyond the cells it directly infects. This is the first virus identified to activate ADP-mediated intercellular calcium waves. This may be a strategy that other viruses also use to cause disease in their hosts.”

“Our findings add a new and very potent signaling pathway into the causative mechanisms of rotavirus diarrhea,” Hyser said. “In terms of treatment, this is exciting because currently some drugs targeting P2Y1 are undergoing preclinical testing as anticlotting drugs. It’s possible that such drugs could be repurposed, if proven to be safe for children, to be used to treat diarrhea caused by rotavirus infection.”

Other contributors to this work include Jacob L. Perry, Kristen A. Engevik, Francesca J. Scribano, J. Thomas Gebert, Heather A. Danhof, Joel C. Nelson, Joseph S. Kellen, Alicia C. Strtak, Narayan P. Sastri, Mary K. Estes and Robert A. Britton at Baylor College of Medicine. Melinda A. Engevik and James Versalovic are affiliated with Baylor and Texas Children’s Hospital.

“This is a retrospective study of prospective data,” said Dr. Kjersti Aagaard, professor of obstetrics and gynecology at Baylor and Texas Children’s Hospital. “We developed a biobank and data repository called PeriBank where we consistently asked our pregnant patients a set of questions about their familial history. We were able to take that detailed data and determine if that specific woman’s family history did or did not predict her delivering preterm.”

Once familial information was gathered, the research team was able to answer questions to quantify estimates of risk for preterm birth based on the pregnant patient’s family history of preterm birth in herself, her sister(s), her mother, grandmothers and aunts and great-aunts. Their findings showed scenarios for women who have previously given birth (multiparous), as well as women who have never given birth (nulliparous). If a nulliparous woman herself was born preterm, her relative risk for delivering preterm was 1.75-fold higher. If her sister delivered preterm, her relative risk was 2.25-fold higher. If her grandmother or aunt delivered preterm, there was no significant increase of risk. If a multiparous mother with no prior preterm births was born preterm herself, her risk was 1.84-fold higher. However, if her sister, grandmother or aunt delivered preterm, there was no significant increase.

“We’ve managed over the years to collect data from a very large population of pregnant women that reflect Houston. There was considerable diversity by race, ethnicity, culture and socioeconomic status. This was a key strength of our study. With this breadth and depth of data reflective of the diversity of Houston, we were able to ask some good questions, which gave us really important information about ‘heritability’ of risk,” Aagaard said.

The research team showed that preterm births cannot be fully attributed to genetics, Aagaard said. Family members may share DNA or genetic code, but the same generation of family members are more likely to share social determinants or have experienced systemic racism and bias. This was best demonstrated by their finding that a history of preterm birth in the pregnant woman or her sister was significantly associated with preterm birth, while a grandmother or aunt was not. These same-generation predictors are generally thought to reflect more about common environmental or social exposures (or a combination of limited genetics plus common exposures) than genetic linkages.

“We know that for the majority of women who deliver a baby preterm, we cannot say that the cause of that preterm birth was in whole or in part genetics. Rather, this study provides subtle but important clues that it is more likely the shared familial background and its exposures that render risk,” Aagaard said. “We hope others will similarly be mindful of those subtle characteristics when looking at heritability and risk. We remain committed to finding the underlying true causal and driving factors. In the meantime, we provide for the first time some reliable risk estimates for first time moms based on their and their family history of preterm birth.”

Other contributors to this work include Amanda Koire and Derrick Chu.

This work was funded by the March of Dimes Preterm Birth Research Initiative (KA) and the NIH (1R01NR014792; KA).

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