Patients with life-threatening illnesses face challenges in accessing potential therapies at the cutting-edge of research and development, which have not yet been proven in a clinical trial. Some pharmaceutical companies produce and provide medicines on a case-by-case basis through expanded access or “compassionate use” programs. The tension among principles of fairness, equity, and compassion are explored in this podcast through a case study about a social media campaign led to an expedited clinical trial for an investigative antiviral medicine. Guests will explore the provocative and emotional stories of patients, family members, advocates, researchers, physicians, and the regulators charged with keeping medicines in the marketplace safe and effective.
This podcast was a collaboration between The Division of Medical Ethics at NYU School of Medicine and The New York Academy of Sciences.
It’s difficult to imagine a world without antibiotics-since the discovery of penicillin by Alexander Fleming in 1928, antimicrobial drugs and substances have saved millions of lives and controlled the spread of countless infections and diseases. But with the alarming increase in strains of drug-resistant bacteria and questions about the link between antibiotic use in animals and human health, new strategies are needed.
An important element of this holistic approach is to complement the control of antibiotics prescribed to humans with strategies to judiciously use antibiotics consumed by animals in food production. Natural fruit extracts and gasses have been explored as means for curbing the spread of bacteria and initiatives to more accurately track the prevalence of drug-resistant bacteria are just a few of the ideas for reevaluating the use of antibiotics in the food system.
François Malouin, PhD, and colleagues have evaluated cranberries and their compounds as a novel antibiotic alternative for bacteria like methicillin-resistant S. aureus (MRSA), although exactly how the flavonoids work against bacteria is not clear. One poultry study also observed that adding 40mg of cranberry extracts per kilogram of feed led to 40% fewer early deaths in birds. James L. Marsden, PhD, has also analyzed interventions for controlling the genus of bacteria Listeria monocytogenes that is connected to three multistate outbreaks of listeriosis this year alone.
For controlling L. monocytogenes on food-contact surfaces, Ozone may be an effective yet inexpensive means for controlling the spread of potentially dangerous bacteria in food production. Marden’s research showed that when applied to stainless steel surfaces for 15 minutes, an advanced oxidation technology was successful in reducing multiple strains of L. monocytogenes on the previously contaminated surfaces.
A Global Public Health Issue
Antibiotics are also given in feeds for food-producing animals to promote faster growth while also reducing the amount of feed needed. However, in 2006 the European Union banned the use of antibiotics for promoting growth in animal production and since 2013 the Food and Drug Administration has called for the industry to voluntarily phase out the use of antibiotics for food production purposes.
Rebecca Irwin, DVM, MSc, and colleagues from the Canadian Integrated Program for Antimicrobial Resistance Surveillance (CIPARS) reported in 2005 that high levels of cephalosporin-resistant Escherichia coli were detected in chicken samples purchased from grocery stores in Quebec and Ontario and in chicken and human Salmonella Heidelberg samples from humans. Chicken hatcheries in Quebec agreed to a voluntary suspension of ceftiofur, a cephalosporin-type antibiotic. Unfortunately, after the voluntary ban was lifted cephalosporin-resistant E. coli and S. Heidelbergonce again re-emerged in chicken and human samples assessed by CIPARS. As of 2013, CISPARS reported that resistance to ciprofloxacin among S. Typhi human infections increased to 18%, up from 10% in the previous year.
As the demand for animal food products continues to increase while drug-resistant bacteria remain a threat, developing evidence-based interventions and antibiotic alternatives has become a significant public health need at the global level. Although antibiotics may be at times necessary in animals for food production, these alternatives could signal a systemic shift for improved food safety and both animal and human health.
Cancer researcher Christopher Vakoc, PhD, goes “above the genome” in search for leukemia drug targets. His work falls within the emerging field of epigenomics.
Published April 19, 2016
By Diana Friedman
Christopher Vakoc, PhD
If cells in the human body contain identical DNA, why are skin cells so different from lung cells? If identical twins have the same genome, what accounts for differences in their physical characteristics? Enter epigenetics-a term literally meaning “above the genome”- to refer to biological processes that impact gene expression, without altering the underlying DNA sequence. The idea behind epigenetics is that if researchers can first identify the proteins that play a crucial role in tumor cell survival, they may then be able to find means to inhibit these proteins and cut cancer pathways off at the pass.
Epigenetics is particularly appealing to cancer researchers because it could give insight into why some patients experience significant side effects, do not respond to conventional cancer treatments, or have recurrent cancer. The emerging field of epigenomics has led to the critical identification of pathways that are not only disrupted in cancer, but are also selective enough to leave the ‘normal’ cells behind, unharmed, while also contributing to treatment response.
Cold Spring Harbor Laboratory’s Christopher Vakoc, PhD, and his research team have been studying the epigenome and acute myeloid leukemia (AML); in 2011, they discovered that a protein called BRD4 (which is known to inhibit proteins responsible for “reading” the epigenome, a key step in the expression of all proteins in a cell) was found in abundance in AML, and was necessary for cancer cell replication. A drug called JQ1 was being tested as a possible treatment for other conditions but Vakoc’s team discovered that it suppressed BRD4, leading to the death of the cancer cells while normal cells survived. How exactly the drug worked was still a mystery.
A Long and Difficult Road Ahead
Vakoc’s lab suspected that the long form of an enzyme called NSD3 played a critical role in BRD4 suppression in AML, but Chen Shen, MD, PhD, a researcher in Vakoc’s lab, conducted a series of experiments with surprising findings. In stark contrast to the dogma, the unassuming NSD3-short was shown to be critical for AML cancer epigenetics. “It’s a David-and-Goliath story,” Vakoc stated. “We figured the long, or full-length, form of NSD3 was of interest because it has a portion, or domain, that enables it to act as an enzyme, and another that suggests its involvement in epigenetic gene regulation.”
When applied to AML cells, JQ1 caused NSD3-short and BRD4 to break apart, along another protein called CHD8. Not only did the researchers gain greater insight into how JQ1 worked, but they also identified CHD8 as an additional protein that could be a target in AML treatment.
Although Vakoc and his team will have a long and difficult road ahead of them in further investigating if JQ1 and other protein inhibitors are effective enough to one day become treatments approved by the Food and Drug Administration for AML, even the most modest of proteins hold promise for epigenetics. In epigenetic research, the epigenome continues to reveal the complexities of tumors but revelations about fighting cancer above and beyond the genome.
This new conference will showcase advances in biomedicine and how they are translating to better treatment options, as well as new avenues for research.
Published March 23, 2016
By Diana Friedman
The New York Academy of Sciences and The Sohn Conference Foundation today announced the inaugural Sohn Conference: Pediatric Cancer in a Post-genomic World, taking place March 30 to April 1, 2016 in New York City. Sponsored by The Sohn Conference Foundation, this conference is the first of its kind to convene leaders in the global pediatric cancer community to share latest developments in research and treatment.
“The Sohn Conference Foundation has brought together elite thought leaders in the global investing community for more than 20 years, and with the launch of this conference in partnership with The New York Academy of Sciences, we strive to do the same in the pediatric cancer space. By breaking down the silos of science and encouraging the industry to collaborate on advancements in research, we can bring life-saving treatments to children battling cancer across the globe,” says Evan Sohn, Vice President, The Sohn Conference Foundation.
The Leading Cause of Death
In the United States, cancer is the leading cause of death by disease for children and globally, more than 250,000 children are diagnosed with cancer each year. Advances in cancer research and treatment have helped more children survive into adulthood, but have also underscored the need for more precise therapeutic options for this vulnerable population. Further, because the genetic profiles of children are less complex than adults, pediatric cancer research is critical not only to children, but to efforts that will unlock the cure for other cancers.
This 2 1/2-day conference will convene leading researchers, clinicians, pediatric cancer advocates, and industry and governmental stakeholders from around the world. The highly-regarded speaker lineup includes scientists who are on the forefront of pediatric cancer research, who will discuss the latest biomedical advancements that will have a tangible impact on children fighting cancer.
“It’s tremendously exciting to be part of this important meeting. The speaker list is a real ‘Who’s Who’ of the leaders in paediatric cancer genomics. The timing for this meeting that will bring the world’s thought leaders together to discuss and debate how best to bring the amazing advances we have made in the lab to the bedside of children with cancer is perfect,” says Richard Gilbertson, MD, PhD, Director, Cambridge Cancer Center, The University of Cambridge. “I am looking forward to the science that will be presented and discussed as well as the ripples of progress that will spread out long after the last talk is over.”
Bridging Genomics and Immunotherapy
Gilbertson will kick off the conference with a keynote speech on “The Successes and Future Direction of Pediatric Cancer Research and Therapy.” Craig B. Thompson, MD, President and CEO, Memorial Sloan Kettering Cancer Center, will present a second keynote speech on “The Role of Epigenetic and Metabolic Mutations in Stem Cell Maintenance and Pediatric Cancers.”
The conference agenda includes sessions on emerging cutting-edge basic and clinical research in epigenetics, mechanisms of metastasis and disease recurrence, disease risk factors, and diagnostics in pediatric oncology, as well as novel therapies and strategies to improve clinical development and treatment access.
“Bridging the fields of genomics and immunotherapy together is our greatest hope,” says conference speaker and member of the scientific organizing committee John Maris, MD, Pediatric Oncologist, The Children’s Hospital of Philadelphia and University of Pennsylvania, of his work on neuroblastoma, the most common extracranial solid tumor in childhood. “We will be increasingly individualizing therapy based on the unique features of the patients and their heritable genome and the evolving cancer genome/proteome. The road to translating research findings into novel therapies is long, but we’re working on it.”
Nora D. Volkow and George K. Koob describe how research in biomedical science illuminates the puzzle of addiction, specifically the role of neurobiology.
Expanding addiction studies to include the brain has been challenging for researchers, despite promising results on the neurobiological aspects of addiction. Recently we spoke with two of the speakers from the upcoming event “The Addicted Brain and New Treatment Frontiers: Sixth Annual Aspen Brain Forum,” Nora D. Volkow, MD, of the National Institute on Drug Abuse (NIDA), and George F. Koob, PhD, of the National Institute on Alcohol Abuse and Alcoholism (NIAAA). Here, they described how research in biomedical science illuminates the puzzle of addiction.
How would you expect that new knowledge gained from major initiatives from the NIAAA and the NIDA will help to move forward national efforts to improve prevention, treatment, and policies on addiction issues?
George F. Koob:
A significant milestone was the identification of a framework for the three stages of the addiction cycle (intoxication, withdrawal/negative affect, and craving), which represent neuroadaptations in three neurocircuits. This knowledge provides multiple viable targets for medications to return disrupted neurocircuitry to homeostasis and promote recovery. At the NIAAA, our hope is that our longitudinal research programs will converge to provide us with both genetic and environmental factors that will allow us to promote resilience and avoid vulnerability to alcohol-related problems. We know there is high genetic hereditability in alcohol use disorders but that one is not condemned to contracting a disorder. The current work will allow us to identify what environmental factors exacerbate or remove vulnerability.
Nora D. Volkow:
Addiction is a disease of the brain. So, just like any other disease–cancer, diabetes, or asthma–the more we know about the etiology and trajectory of the disorder, the smarter and more targeted the approaches we will be able to develop. This research helps us, among others, identify promising targets for the development of medications and other treatments.
And this focus will also lead to a better understanding of the factors that influence the trajectory or course of the disease such as genetics and epigenetics, comorbid conditions, social support, treatment access and availability, and social stigma. We are constantly improving the quality of this information, which is helping us translate it into more effective and personalized prevention and treatment interventions.
What are some of the significant obstacles that you have encountered in your research over the course of your career? How have you sought to overcome these hindrances?
Nora D. Volkow, MD, and George F. Koob, PhD.
George F. Koob:
The biggest obstacle in my research work, was, and remains a misunderstanding of the addiction process. Addiction is a brain disease and more importantly it is a disease of the brain motivational systems. However, motivation comes from two sources: positive reinforcement and negative reinforcement. To a large extent convincing the scientific community of the negative reinforcement piece has been a challenge.
I like to say that I spent the first half of my career trying to understand how we feel good and the second half of my career trying to understand how we feel bad. We now know that what I call “motivational withdrawal” (comprised of a reward deficit and a stress surfeit) is a critical part of the addiction cycle and a key part of the neurocircuitry driving compulsive drug seeking and drug taking.
Nora D. Volkow:
I began my research career at a time when brain imaging techniques were emerging and providing us, for the first time, the ability to study the human brain’s function and neurochemistry noninvasively. I immediately saw that brain imaging offered a unique opportunity to investigate how drugs affect the human brain and how these changes influence behavior. However, it took us several years to convince the scientific community that the brain of cocaine abusers showed evidence of cerebrovascular toxicity, a finding that now has been corroborated by multiple clinical and preclinical studies.
But, even more challenging was the stigma I had to face regarding my interest on addiction. I had to convince my colleagues of the value and importance of studying the neurobiology of addiction, which was viewed by many, including some scientists and physicians, as a moral failure, thus undeserving of my efforts to use modern medical methodologies to study it.
Are there specific moments from your career that you are particularly proud of, or that stand out to you?
George F. Koob:
I am particularly proud of having trained 80 postdoctoral fellows, most, if not all of whom worked in science for their careers. I am also proud of pushing “the dark side of addiction” and weaving the frameworks of opponent process, stress and self-medication back into the fabric of our understanding of the addiction process.
Nora D. Volkow:
My proudest moments have always been when an addicted person, or their relatives, contact me to thank me for giving them a better understanding of what they or their loved ones are going through, and for giving them hope that their disease can be treated.
Mobile technology is emerging as a powerful tool for transforming the way clinical research is conducted now and in the future. Acquisition of real-time biometric data though the use of wireless medical sensors will allow for around-the-clock patient monitoring, reduce costly clinic visits, and streamline inefficient administrative processes. With the promise of this technology also comes challenges including digital data privacy concerns, patient compliance issues, and practical considerations such as continuous powering of these devices.
This podcast provides an illuminating examination of both the promises and challenges that underpin the implementation of mobile technology into the clinical realm.
Lewis Cantley’s discoveries in the laboratory are changing the way we think about and treat cancer.
Published June 1, 2015
By Siobhan Addie, PhD
Lewis C. Cantley, PhD
The 2015 Ross Prize in Molecular Medicine was awarded to Lewis C. Cantley, PhD, who serves as the Margaret and Herman Sokol Professor in Oncology Research and the Meyer Director of the Sandra and Edward Meyer Cancer Center at Weill Cornell Medical College and New York-Presbyterian Hospital. Dr. Cantley received the award at a scientific symposium held at the Academy on June 8, 2015, in his honor.
Early in his career, Dr. Cantley discovered phosphatidylinositol-3-kinase (PI-3K), an enzyme that is important for cell growth, insulin signaling, and immune cell function. Dr. Cantley’s discovery has led to one of the most promising avenues for the development of personalized medicine. Currently, Dr. Cantley’s lab is investigating new treatments for diseases that result from defects in PI-3K and other genes in this important metabolic pathway. He shared his thoughts on this prestigious award as well as the past, present, and future of cancer treatment.
What is the current focus of your laboratory?
My laboratory is trying to understand why cancer cells have altered metabolism and take up significantly more glucose than normal cells. I initially became interested in this area following our discovery of phosphoinositide-3-kinase (PI-3K), an enzyme that is important for cell growth. We came to the realization that when PI-3K is activated, cells consume glucose at significantly higher rates, which is consistent with the Warburg Effect, first described decades earlier by Otto Heinrich Warburg. [The Warburg Effect is the observation that cancer cells produce the majority of their energy by glycolysis and lactic acid fermentation, as opposed to oxidation of pyruvate in mitochondria, as is observed in healthy cells.]
Mutations in PI-3K and other metabolic genes can cause cancer cells to take up increased amounts of glucose, and understanding this process will hopefully reveal new targets for cancer therapies. Together with Craig Thompson and Tak Mak, I co-founded a company called Agios Pharmaceuticals to further explore this concept. Independent of Agios Pharmaceuticals, my lab continues to investigate the mechanisms of altered cancer cell metabolism, and it is our goal to develop cancer drugs for the targets that we discover.
Who were your role models in science and how did they inspire you?
Harold Varmus and Michael Bishop were two of my major role models because of their elegant studies on how viruses cause cancer. It was this work that led to the realization that cancer is caused by mutations in human genes. It was paradigm-shifting science because it made us understand that cancer is driven by sporadic mutations in DNA and that the changes in metabolism that Otto Warburg originally observed were a consequence of mutations in genes (like PI-3K) that control metabolism through complex signaling networks.
What led to your discovery of PI-3K?
The discovery of the Warburg Effect made scientists examine changes in cancer cell metabolism. Much of the 20th century was spent trying to understand how cancers change their metabolism, specifically how they perform anabolic processes at a higher rate. In the late 1970s and early 1980s, work from a number of labs led to the discovery of important oncogenes. In our early work we used viral oncogenes to discover PI-3K.
By immunoprecipitating oncoproteins we were able to isolate PI-3K, and at first we believed PI-3K was producing the well-known lipids, PI(4,5)P2 or PI(4)P. However, once we characterized the product, we found out it was chemically distinct from the two well-known phospholipid forms in that the phosphate was on the 3 position of the inositol ring rather than the 4 or 5 position. We were extremely excited since this species had never previously been described.
Upon your discovery of PI-3K, did you realize how complex the signaling cascades were?
Our work revealed that PI-3K phosphorylates the 3 position of phosphatidylinositol; however, after that initial discovery we realized that many other phosphorylation combinations could be generated by PI-3K. Sure enough, in subsequent years, a whole new group of lipids was discovered, including PI(3)P, PI(3,4)P2, PI(3,5)P2 and PI(3,4,5)P3, although at the time it was not clear what they were doing. Now we know that many of these lipids are important in cells for controlling protein kinase cascades and actin rearrangement, which is critical for cell movement.
I was extremely excited by the importance of PI-3K for human disease. Initially our team was mainly focused on insulin signaling rather than on cancer, but soon we realized that there were commonalities between insulin signaling and the evolution of cancers. The story of PI-3K has certainly turned into a bigger story than I could have ever anticipated.
PI-3K inhibitors work quite well in blood cancers, but show more variable results in solid tumors. Why do you think that is?
The PI-3K gene that is mutated in solid tumors (PIK3CA) encodes the same enzyme that insulin activates so inhibitors of this enzyme cause insulin resistance resulting in hyperglycemia, which limits the dose of drug that can be used for therapy. In contrast the PI-3K inhibitor that was approved for treating B cell lymphomas, idelalisib, targets the enzyme encoded by PIK3CD, which does not mediate insulin responses. Thus there is less toxicity and higher doses of drug can be achieved, allowing more effective killing of tumor cells.
I also think that the total number of cancer cells in the body at the time a patient goes on therapy has a major role in explaining resistance to therapy. We now know that there is tremendous heterogeneity in the mutational events in most solid tumors and the more cells present, the more likely that a few cells in the tumor will be resistant to the therapy. That is why we are exploring the usefulness of neo-adjuvant therapy, the delivery of an anticancer drug prior to surgery. Another option for improving patient outcome is adjuvant therapy, the delivery of an anticancer drug immediately following surgery, even before recurrence is detected.
Generally, when metastatic cancer is diagnosed, the total number of cells in the body can be massive. Bert Vogelstein aptly pointed out that every time a cell divides there is a chance for an error in DNA replication, resulting in genetic aberrations, and the more times that happens the greater the diversity of mutations in the tumor and the lower the probability that a single agent will kill all cells in the tumor. Initial clinical trials in solid tumors are typically done in patients who have metastatic disease and have failed multiple therapies—it’s a high bar to achieve complete responses in this setting.
Why do certain cancer drugs look quite promising in pre-clinical models yet do not perform as well in humans?
New cancer drugs are often tested in mice that have a single, small tumor. Since the tumors in mice contain relatively few cells, the odds that we can kill all those cells are rather good. The clinical setting with human patients is far more challenging and complex because, as I indicated before, human cancer cells have greater genetic diversity and there are at least 100 times more cells than in a mouse tumor.
That is not to say that mouse models are bad, but we need to pay better attention to the mathematics. In normal preclinical studies we give seven mice the experimental drug and seven mice receive the placebo. As pointed out by Bert Vogelstein, these numbers are far too low. We need to increase the number of animals used in preclinical studies and focus on therapies that cure all the mice, then we are far more likely to find drugs or drug combinations that are also effective in humans.
If you had a crystal ball that showed you the future of cancer research and treatment, what would you like to know right now?
That’s a tough question! One of the things I would like to know is whether we will have technologies available in the future to detect circulating mutant DNA at very early stages of disease. I think it would be great to have a test that would allow us to intervene with therapies potentially even before a tumor can be felt by a patient or detected by standard imaging techniques.
A test like this would have to be extremely sensitive so that we could detect extremely low levels of circulating mutant DNA. We know that we can pick up circulating mutant DNA in the case of metastatic disease, but it would be fantastic to do this for very early stages of cancer.
Your clinical test sounds like a fantastic idea—what are the pros and cons?
If we were able to develop a test like this and it were cost-effective, it could very well become a routine clinical procedure that takes place during the annual physical every year after the age of 50. If people are at high risk for cancer, they could have the test done starting at age 30. These test results could potentially tell you that you have circulating copies of oncogenic mutant DNA. I believe that if clinicians administered targeted cancer therapy at these early stages of disease, we would have a much higher likelihood of a cure.
The success of this whole plan depends on the development of targeted cancer drugs that are safe and have few off-target effects. Developing these drugs and testing their safety could take as long as 5–10 years. Most of the drugs we currently use for cancer therapy would not be acceptable to use in this setting since they could cause more harm than good and even cause new cancers to occur.
Another caveat to this blood test is the possibility of false positive results, where patients may show the mutant DNA but never actually progress to full-blown disease. I think that personalized medicine is the future. If we truly want to cure cancer, we need to target the cancer cells more effectively and hit them earlier with safe, non-toxic drugs.
PI-3K is at the interface of insulin signaling and cancer; what is the relationship between these two?
Many types of cancer cells express higher levels of insulin receptor (IR) or insulin-like growth factor 1 receptor (IGF1R) than the tissue from which they evolved. If a patient with this type of cancer becomes insulin-resistant, as could happen from a high-sugar, high-carbohydrate diet, there will be high levels of circulating insulin and IGF1in the blood.
his is a very dangerous situation because if the tumor expresses IR or IGF1R, it will be getting a strong signal for activating PI-3K all the time, even if PI-3K is not mutated. This will drive tumor growth and may render the tumor less vulnerable to chemotherapy. If I had a cancer that expressed high levels of IR or IGF1R I would go on a low-carbohydrate diet the very next day.
High levels of dietary sugar can cause insulin-resistance, which results in near-constant elevation of circulating insulin. We know that insulin activates PI-3K, which is almost certainly driving a large fraction of cancer growth. In the United States there is a very high fraction of people who are insulin-resistant, but many of them are undiagnosed. It is a frightening possibility that we will retrospectively regret making sugar cheap and broadly added to foods the same way we now regret making cigarettes cheap and broadly available 70 years ago.
What does winning the Ross Prize in Molecular Medicine mean to you?
I am tremendously honored and excited to win the Ross Prize. I am particularly grateful for this award because it is not given for a single discovery, but rather a body of work where a discovery has been translated into a clinical outcome. That is difficult to do; but I certainly did not do that alone. Hundreds of people collaborated with me at various stages—from the mouse models, to the biochemistry, all the way to carrying out a clinical trial. I have been very fortunate in my career to work closely with passionate people who are focused on a common goal of identifying new cellular targets for cancer drugs.
About the Ross Prize in Molecular Medicine
The annual Ross Prize in Molecular Medicine was established in conjunction with the Feinstein Institute for Medical Research and Molecular Medicine. The winner is an active investigator who has produced innovative, paradigm-shifting research that is worthy of significant and broad attention in the field of molecular medicine. This individual is expected to continue to garner recognition in future years, and their current accomplishments reflect a rapidly rising career trajectory of discovery and invention. The winner receives an honorarium of $50,000.
Experts gather in Barcelona, Spain, to explore the consequences of climate change on human health.
Published April 30, 2015
By Diana Friedman
The New York Academy of Sciences, in partnership with the “la Caixa” Foundation and BIOCAT, will host a 2-day conference, Human Health in the Face of Climate Change: Science, Medicine, and Adaptation, on May 14-15, 2015 in Barcelona, Spain.
“The threat of climate change to health will take many forms – from a more dangerous physical environment to the worsening quality of air and water to the spread of infectious diseases,” says Christopher Dye, DPhil, FMedSci, FRS, Director, Strategy, Office of the Director General at the World Health Organization, as well as a conference organizer and keynote speaker.
The conference is being convened in light of new research that seeks to provide a deeper understanding of the health consequences of climate change on humans – including better quantification of these effects – to improve health preparedness and protect vulnerable populations.
“Many infectious and non-communicable diseases are climate sensitive. They may be associated with specific seasons; respond to extreme events such as droughts, heatwaves, or flood; or shift in their distribution according to shifts in the long-term climate,” says Madeleine Thomson, PhD, Senior Research Scientist, International Research Institute for Climate and Society at Columbia University, as well as a conference organizer and speaker.
Empowering the Health Community
“Climate knowledge and information can be used to understand, predict, and better manage climate-sensitive health outcomes and can also help us to assess the impact of many health interventions. With a changing climate, understanding these connections and empowering the health community to use this knowledge is key to effective adaptation,” adds Thomson.
“We need to move forward effectively and quickly as our actions as humans are moving our climate to dangerous and unprecedented states that will for sure exert a strong pressure on the health status of people globally,” says Xavier Rodó, PhD, ICREA & Catalan Institute of Climate Sciences (IC3), as well as a conference organizer and speaker. “We need new science that teaches us how to face and respond to this challenge. This conference attempts to highlight those areas that require new science, as well as methods to spur policymakers into action by working together,” adds Rodó.
Topics to be explored at this multidisciplinary conference include: changes in the distribution of extreme climate events, vulnerability due to extreme weather events, land-use change and agricultural production, variable epidemiology of parasites and infectious diseases, and climate-altering pollutants.
The conference is designed to be of interest to climate scientists, atmospheric/oceanic scientists, ecologists, evolutionary biologists, epidemiologists, public health specialists, and policymakers, among others, as well as members of the media.
“The impact on human health is among the most significant measures of the harm done by climate change – and health can be a driving force for public engagement in climate solutions,” says Dye.
In honor of Batman’s 75th anniversary, DC Entertainment declared July 23 Batman Day. What does this have to do with science? More than you might expect, with a little imagination. For psychologist Andrea Letamendi, PhD, the Batman world, with its roster of criminally insane villains, is a fictional window onto very real issues. Her podcast series, The Arkham Sessions (named for the asylum where Batman’s enemies usually wind up after the hero thwarts their plots) analyzes characters and interactions from Batman: The Animated Series to explore subjects such as coping with trauma, mental disorders, patient treatment, and stigmatization of people with mental illnesses.
According to National Library of Medicine historian Dr. Michael Sappol, “It’s a powerful technology for forming public opinion. It [doesn’t] just reason with the audience, it recruit[s] the audience’s emotions.” Dr. Letamendi leverages a balance between that emotional resonance and the relative security of fiction to engage her audience in consideration of challenging themes. “It’s a way to educate people about psychological science and address important topics in a way that feels safe—less threatening or less personal,” she says. “At the same time, many people feel very connected to these fictional narratives and the stories actually help us to tune in.”
Dr. Letamendi spoke with The New York Academy of Sciences (the Academy) from Comic-Con in San Diego about superheroes and psychology.
Why apply psychological analysis to fictional characters?
As a psychologist, I’m invested in broadening public knowledge about the psychological sciences. I find that one way I can do that is to speak to my passion and the passion of many others: comic books, science fiction, and fantasy. I’ve had wonderful opportunities to speak at universities and at Comic-Con and other cultural conventions to utilize these narratives that people can really relate to—the stories, heroes, and villains that people already know—to examine important health issues. It’s fun but it’s also an educational advantage.
Are there useful parallels between cartoon characters and real people?
Yes! For example, my first experience speaking on a panel was talking about how comic book heroes are actually really similar to real life heroes, specifically soldiers who have experienced combat-related trauma. I used to practice at a veterans hospital and have a lot of experience working with soldiers and veterans returning from Iraq and Afghanistan with physical and psychological injuries.
The panel was a chance to talk openly about the impact of recent wars on the people who fight in them, and how the field of psychology is struggling with how to meet the needs of the men and women coming back from those conflicts. It’s a really serious topic, but we can draw upon these fictional narratives that simulate and evoke real tensions and interests in a way that feels safe and remains relatable.
How does your series, named for the Arkham Asylum for the Criminally Insane, avoid associations between mental illness and criminal behavior?
It’s really important to us to always make that distinction. When we started the show we knew we’d be examining the psychology of a lot of villains, but we’re not just trying to come up with labels or diagnoses for them. Every episode of the Batman series has a lot of psychological elements to it. We end up talking about such a wide range of subjects—memory loss, substance abuse, anxiety, family issues, patient care and hospitalization, childhood trauma.
We speak about these issues in a way that deliberately doesn’t stigmatize, but rather helps to normalize these experiences. The result is that we’re very inclusive in a way that let’s everyone relate. We include Batman in our analyses, not just villains, and he’s a character with a lot of issues as well. My hope is that it combats the idea that people with mental health problems are villains or criminals.
Do you have a favorite character?
I like the villains who are overlooked because they’re just seen as being big and burly, like Killer Croc or Clayface. They’re like onions. When you unravel them you realize there’s a deep psychological history and trajectory there that got them to where they are [by the time you meet them in the series].
Are there lessons from Gotham City that might apply to real cities’ policies on mental health care?
There are real barriers to appropriate, evidence-based care. In big cities with diverse populations, we deal with issues of underserved populations that don’t have access to care. There are groups of people with structural and psychosocial barriers to getting care. Sometimes we struggle to provide care that’s culturally or linguistically appropriate. We need to think about all of these psychosocial elements to ensure that people have opportunities to heal.
Any parting thoughts?
It is Comic-Con week! If you’re coming, please keep in mind that you can put together a curriculum of educational panels on really interesting topics like psychology, underrepresentation, and gender equality. Comic-Con is fun and a celebration of superheroes, but it’s also an opportunity for education and to demystify and reduce some of the myth around science.
Scientists at the University of East Anglia have figured out a flaw in bacterial armor, potentially paving the way for novel drug development at a time when antibiotic resistance is becoming a critical global health problem.
According to the World Health Organization, “antibiotic resistance—when bacteria change so antibiotics no longer work in people who need them to treat infections—is now a major threat to public health.” In short, disease-causing microbes are evolving molecular countermeasures to drugs at a far faster rate than we’re discovering new interventions.
However, a group of scientists at the University of East Anglia recently scored a point for Team Humans by mapping the structure of a protein used by a large class of bacteria to construct a defensive outer membrane. Gram-negative bacteria cause a swath of illnesses including pneumonia, salmonella, meningitis, and bloodstream and wound infections. They’re also exceptionally difficult to kill because the outer membrane provides protection from immune cells and antibiotics.
A key component of this natural armor is a molecule called lipopolysaccharide, which gets delivered to its place in the protective layer by transporter proteins called LptD and LptE. Researchers at UEA collaborated with scientists at the Diamond synchrotron to blast these transporters with super high-powered x-rays, the diffraction pattern of which reveals the atomic structure of the protein.
The Atomic Blueprint
When it comes to proteins, form and function go firmly hand in hand. Using the atomic blueprint as a guide, the team was able to model the function of the LptDE complex.
“We have identified the path and gate used by the bacteria to transport the barrier building blocks to the outer surface. Importantly, we have demonstrated that the bacteria would die if the gate is locked,” says lead researcher Prof. Changjiang Dong in this press release. “If the bacteria do not have the outer membrane, they cannot withstand environmental changes. It also makes it easier for the human immune system to kill them.”
Now that researchers understand the structure and mechanisms of the bacterial defenses, it may be possible to develop drugs to interfere with their function. “The really exciting thing about this research is that new drugs will specifically target the protective barrier around the bacteria, rather than the bacteria itself,” says study author Haohoa Dong. “Because new drugs will not need to enter the bacteria itself, we hope that the bacteria will not be able to develop drug resistance in the future.”
