Live and Let-7: MicroRNA Plays Surprising Role in Cell Survival 
Researchers at the University of California, San Diego School of Medicine have identified a microRNA molecule as a surprisingly crucial player in managing cell survival and growth. The findings, published in the October 7 issue of Cell Metabolism, underscore the emerging recognition that non-coding RNAs – small molecules that are not translated into working proteins – help regulate basic cellular processes and may be key to developing new drugs and therapies.
Specifically, principal investigator Albert R. La Spada, MD, PhD, professor of cellular and molecular medicine, chief of the Division of Genetics in the Department of Pediatrics and associate director of the Institute for Genomic Medicine at UC San Diego, and colleagues found that a microRNA known as let-7 controls autophagy through the amino acid sensing pathway, which has emerged as the most potent activator of mTORC1 complex activity.
Autophagy is a fundamental process used by cells to degrade unnecessary components in times of starvation, releasing energy stores that help promote cell survival. Cells have further adapted autophagy for other purposes as well, including recycling dysfunctional components, immune response to pathogen invasion, surveillance against cancer and maintenance of protein and organelle control in the central nervous system. MTORC1 is a critical protein complex that regulates energy consumption and growth in cells.
“The ability of let-7 alone to activate autophagy in this way was totally unknown and is very surprising,” said La Spada. “As let-7 is known to be a tumor suppressor, its ability to activate autophagy could be a major component of its anti-tumor forming activity,” though La Spada noted that autophagy may also contrarily promote tumor progression by supporting the altered metabolism of growing cancers.
With let-7 revealed to be a master regulator of metabolism, helping to modulate anabolic growth (the creation of new molecules in cells) with catabolic destruction (the breakdown of molecules in cells), researchers say the overall picture of how cells function becomes more fine-tuned but also more complicated.
“The fact that let-7 is opposing the action of the amino acid sensing pathway provides a glimpse into the complex pathway regulation at work in the cell, with microRNAs emerging as important factors for cells to maintain metabolic set points and overall homeostasis or a healthy equilibrium.”
The therapeutic potential of let-7 remains to be explored. La Spada said he and colleagues have shown that a lentivirus encoding let-7 injected into mouse neurons promotes the autophagic turnover of toxic misfolded proteins associated with neurodegenerative disease.
“We also demonstrate that treatment with anti-let-7 can block autophagy and that this has physiological consequences (weight gain) in mice. It is possible that modulation of let-7 could be pursued for therapeutic application using very carefully targeted delivery systems, but further work will be necessary to see if this is practically possible.”
Pictured: A scanning micrograph of dividing cancer cells. Image courtesy of Thomas Deerinck, National Center for Microscopy and Imaging Research, UC San Diego.

Live and Let-7: MicroRNA Plays Surprising Role in Cell Survival

Researchers at the University of California, San Diego School of Medicine have identified a microRNA molecule as a surprisingly crucial player in managing cell survival and growth. The findings, published in the October 7 issue of Cell Metabolism, underscore the emerging recognition that non-coding RNAs – small molecules that are not translated into working proteins – help regulate basic cellular processes and may be key to developing new drugs and therapies.

Specifically, principal investigator Albert R. La Spada, MD, PhD, professor of cellular and molecular medicine, chief of the Division of Genetics in the Department of Pediatrics and associate director of the Institute for Genomic Medicine at UC San Diego, and colleagues found that a microRNA known as let-7 controls autophagy through the amino acid sensing pathway, which has emerged as the most potent activator of mTORC1 complex activity.

Autophagy is a fundamental process used by cells to degrade unnecessary components in times of starvation, releasing energy stores that help promote cell survival. Cells have further adapted autophagy for other purposes as well, including recycling dysfunctional components, immune response to pathogen invasion, surveillance against cancer and maintenance of protein and organelle control in the central nervous system. MTORC1 is a critical protein complex that regulates energy consumption and growth in cells.

“The ability of let-7 alone to activate autophagy in this way was totally unknown and is very surprising,” said La Spada. “As let-7 is known to be a tumor suppressor, its ability to activate autophagy could be a major component of its anti-tumor forming activity,” though La Spada noted that autophagy may also contrarily promote tumor progression by supporting the altered metabolism of growing cancers.

With let-7 revealed to be a master regulator of metabolism, helping to modulate anabolic growth (the creation of new molecules in cells) with catabolic destruction (the breakdown of molecules in cells), researchers say the overall picture of how cells function becomes more fine-tuned but also more complicated.

“The fact that let-7 is opposing the action of the amino acid sensing pathway provides a glimpse into the complex pathway regulation at work in the cell, with microRNAs emerging as important factors for cells to maintain metabolic set points and overall homeostasis or a healthy equilibrium.”

The therapeutic potential of let-7 remains to be explored. La Spada said he and colleagues have shown that a lentivirus encoding let-7 injected into mouse neurons promotes the autophagic turnover of toxic misfolded proteins associated with neurodegenerative disease.

“We also demonstrate that treatment with anti-let-7 can block autophagy and that this has physiological consequences (weight gain) in mice. It is possible that modulation of let-7 could be pursued for therapeutic application using very carefully targeted delivery systems, but further work will be necessary to see if this is practically possible.”

Pictured: A scanning micrograph of dividing cancer cells. Image courtesy of Thomas Deerinck, National Center for Microscopy and Imaging Research, UC San Diego.

Prose and chons
In a vague sort of way, the image above looks like the limb of a cephalopod festooned with suckers. Of course it’s not. 
Rather, these are cells called chondrocytes, which are found in healthy cartilage. In this case the outer ear.
Chondrocytes produce and maintain the cartilaginous matrix, which consists mostly of collagen and proteoglycans. Cartilage is the flexible connective tissue found, aside from the ear, in joints, the rib cage, nose, bronchial tubes and intervertebral discs. It’s not as hard and rigid as bone, but stiffer and less flexible than muscle.
In healthy cartilage, there are no cells except chondrocytes. There are no blood vessels to feed them. Instead, chondrocytes are supplied by diffusion – the movement of substances from regions of high concentration to low concentration. This movement is aided by the constant compression of cartilage by various physical activities, but it also means that compared to other kinds of connective tissue, cartilage grows and repairs itself less quickly.
Image courtesy of Ivor Mason, Kings College London and Wellcome Images.

Prose and chons

In a vague sort of way, the image above looks like the limb of a cephalopod festooned with suckers. Of course it’s not. 

Rather, these are cells called chondrocytes, which are found in healthy cartilage. In this case the outer ear.

Chondrocytes produce and maintain the cartilaginous matrix, which consists mostly of collagen and proteoglycans. Cartilage is the flexible connective tissue found, aside from the ear, in joints, the rib cage, nose, bronchial tubes and intervertebral discs. It’s not as hard and rigid as bone, but stiffer and less flexible than muscle.

In healthy cartilage, there are no cells except chondrocytes. There are no blood vessels to feed them. Instead, chondrocytes are supplied by diffusion – the movement of substances from regions of high concentration to low concentration. This movement is aided by the constant compression of cartilage by various physical activities, but it also means that compared to other kinds of connective tissue, cartilage grows and repairs itself less quickly.

Image courtesy of Ivor Mason, Kings College London and Wellcome Images.

Scientists Discover Pain Receptor on T-Cells
Researchers at University of California, San Diego School of Medicine have discovered that T-cells – a type of white blood cell that learns to recognize and attack microbial pathogens – are activated by a pain receptor.
The study, reported online Oct. 5 in Nature Immunology, shows that the receptor helps regulate intestinal inflammation in mice and that its activity can be manipulated, offering a potential new target for treating certain autoimmune disorders, such as Crohn’s disease and possibly multiple sclerosis. 
“We have a new way to regulate T-cell activation and potentially better control immune-mediated diseases,” said senior author Eyal Raz, MD, professor of medicine.
The receptor, called a TRPV1 channel, has a well-recognized role on nerve cells that help regulate body temperature and alert the brain to heat and pain. It is also sometimes called the capsaicin receptor because of its role in producing the sensation of heat from chili peppers.
The study is the first to show that these channels are also present on T-cells, where they are involved in gating the influx of calcium ions into cells – a process that is required for T-cell activation.
“Our study breaks current dogma in which certain ion channels called CRAC are the only players involved in calcium entry required for T-cell function,” said lead author Samuel Bertin, a postdoctoral researcher in the Raz laboratory. “Understanding the physical structures that enable calcium influx is critical to understanding the body’s immune response.”
T-cells are targeted by the HIV virus and their destruction is why people with AIDS have compromised immune function. Certain vaccines also exploit T-cells by harnessing their ability to recognize antigens and trigger the production of antibodies, conferring disease resistance. Allergies, in contrast, may occur when T-cells recognize harmless substances as pathogenic.
TRPV1 channels appear to offer a way to manipulate T-cell response as needed for health. Specifically, in in vitro experiments researchers showed that T-cell inflammatory response could be reduced by knocking down the gene that encodes for the protein that comprises the TRPV1 channel. Overexpression of this gene was shown to lead to a surge in T-cell activation, which in human health may contribute to autoimmune diseases. T-cells also responded to pharmaceutical agents that block or activate the TRPV1 channel.
In experiments with mice models, researchers were able to reduce colitis with a TRPV1-blocker, initially developed as a new painkiller. One of the promising discoveries is that colitis in mice could be treated with much lower doses than what is needed to dull pain. “This suggests we could potentially treat some autoimmune diseases with doses that would not affect people’s protective pain response,” Raz said.
Pictured: An inflammatory response and damage to the intenstinal wall (left) could be prevented by injecting TRPV1-deficient T-cells (right).Credit: Nature Immunulogy, Bertin et al.

Scientists Discover Pain Receptor on T-Cells

Researchers at University of California, San Diego School of Medicine have discovered that T-cells – a type of white blood cell that learns to recognize and attack microbial pathogens – are activated by a pain receptor.

The study, reported online Oct. 5 in Nature Immunology, shows that the receptor helps regulate intestinal inflammation in mice and that its activity can be manipulated, offering a potential new target for treating certain autoimmune disorders, such as Crohn’s disease and possibly multiple sclerosis. 

“We have a new way to regulate T-cell activation and potentially better control immune-mediated diseases,” said senior author Eyal Raz, MD, professor of medicine.

The receptor, called a TRPV1 channel, has a well-recognized role on nerve cells that help regulate body temperature and alert the brain to heat and pain. It is also sometimes called the capsaicin receptor because of its role in producing the sensation of heat from chili peppers.

The study is the first to show that these channels are also present on T-cells, where they are involved in gating the influx of calcium ions into cells – a process that is required for T-cell activation.

“Our study breaks current dogma in which certain ion channels called CRAC are the only players involved in calcium entry required for T-cell function,” said lead author Samuel Bertin, a postdoctoral researcher in the Raz laboratory. “Understanding the physical structures that enable calcium influx is critical to understanding the body’s immune response.”

T-cells are targeted by the HIV virus and their destruction is why people with AIDS have compromised immune function. Certain vaccines also exploit T-cells by harnessing their ability to recognize antigens and trigger the production of antibodies, conferring disease resistance. Allergies, in contrast, may occur when T-cells recognize harmless substances as pathogenic.

TRPV1 channels appear to offer a way to manipulate T-cell response as needed for health. Specifically, in in vitro experiments researchers showed that T-cell inflammatory response could be reduced by knocking down the gene that encodes for the protein that comprises the TRPV1 channel. Overexpression of this gene was shown to lead to a surge in T-cell activation, which in human health may contribute to autoimmune diseases. T-cells also responded to pharmaceutical agents that block or activate the TRPV1 channel.

In experiments with mice models, researchers were able to reduce colitis with a TRPV1-blocker, initially developed as a new painkiller. One of the promising discoveries is that colitis in mice could be treated with much lower doses than what is needed to dull pain. “This suggests we could potentially treat some autoimmune diseases with doses that would not affect people’s protective pain response,” Raz said.

Pictured: An inflammatory response and damage to the intenstinal wall (left) could be prevented by injecting TRPV1-deficient T-cells (right).
Credit: Nature Immunulogy, Bertin et al.

Diabetes in a DishWith NIH grant, UC San Diego researchers hope to build bits of miniature pancreas
Although type 1 diabetes can be controlled with insulin injections and lifestyle modifications, major advances in treating the disease have not been made in more than two decades and there remain fundamental gaps in what is understood about its causes and how to halt its progression.
With a 5-year, $4-million grant from the National Institutes of Health, researchers at University of California, San Diego School of Medicine and bioengineers at UC San Diego Jacobs School of Engineering, with colleagues at UC Irvine and Washington University in St. Louis hope to change this.
The team’s goal is to bioengineer a miniature pancreas in a dish, not the whole pancreas but the organ’s irregularly shaped patches – called Islets of Langerhans – that regulate the body’s blood sugar levels.
“The bottleneck to new cures for type 1 diabetes is that we don’t have a way to study human beta cells outside of the human body,” said Maike Sander, MD, professor in  the departments of Pediatrics and Cellular and Molecular Medicine and director of the Pediatric Diabetes Research Center at UC San Diego and Rady Children’s Hospital-San Diego. “If we are successful, we will for the first time be able to study the events that trigger beta cell destruction.”
Beta cells in islets secrete the hormone insulin. In patients with type 1 diabetes, the beta cells are destroyed and the body loses its ability to regulate blood sugar levels. Researchers, however, are unsure of the mechanism by which beta cells are lost. Some researchers believe that the disease may be triggered by beta cell apoptosis (self-destruction); others believe that the body’s immune system initiates attacks on these cells.
To actually bioengineer the pancreas’ endocrine system, researchers plan to induce human stem cells to develop into beta cells and alpha cells, as well as other cells in the islet that produce hormones important for controlling blood sugar levels. These cells will then be co-mingled with cells that make blood vessels and the cellular mass will be placed within a collagen matrix mimicking the pancreas. The matrix was developed by Karen Christman, PhD, associate professor of bioengineering at the Jacobs School of Engineering.
“Our previous work with heart disease has shown that organ-specific matrices help to create more mature heart cells in a dish,” Christman said. “I am really excited to apply the technology to diabetes research.”
If the pancreatic islets can be successfully bioengineered, researchers could conduct mechanistic studies of beta cell maturation, replication, reprogramming, failure and survival. They say new drug therapies could be tested in the 3D culture. It would also be possible to compare beta cells from people with and without the disease to better understand the disease’s genetic component. Such work might eventually lead to treatments for protecting or replacing beta cells in patients.

Diabetes in a Dish
With NIH grant, UC San Diego researchers hope to build bits of miniature pancreas

Although type 1 diabetes can be controlled with insulin injections and lifestyle modifications, major advances in treating the disease have not been made in more than two decades and there remain fundamental gaps in what is understood about its causes and how to halt its progression.

With a 5-year, $4-million grant from the National Institutes of Health, researchers at University of California, San Diego School of Medicine and bioengineers at UC San Diego Jacobs School of Engineering, with colleagues at UC Irvine and Washington University in St. Louis hope to change this.

The team’s goal is to bioengineer a miniature pancreas in a dish, not the whole pancreas but the organ’s irregularly shaped patches – called Islets of Langerhans – that regulate the body’s blood sugar levels.

“The bottleneck to new cures for type 1 diabetes is that we don’t have a way to study human beta cells outside of the human body,” said Maike Sander, MD, professor in  the departments of Pediatrics and Cellular and Molecular Medicine and director of the Pediatric Diabetes Research Center at UC San Diego and Rady Children’s Hospital-San Diego. “If we are successful, we will for the first time be able to study the events that trigger beta cell destruction.”

Beta cells in islets secrete the hormone insulin. In patients with type 1 diabetes, the beta cells are destroyed and the body loses its ability to regulate blood sugar levels. Researchers, however, are unsure of the mechanism by which beta cells are lost. Some researchers believe that the disease may be triggered by beta cell apoptosis (self-destruction); others believe that the body’s immune system initiates attacks on these cells.

To actually bioengineer the pancreas’ endocrine system, researchers plan to induce human stem cells to develop into beta cells and alpha cells, as well as other cells in the islet that produce hormones important for controlling blood sugar levels. These cells will then be co-mingled with cells that make blood vessels and the cellular mass will be placed within a collagen matrix mimicking the pancreas. The matrix was developed by Karen Christman, PhD, associate professor of bioengineering at the Jacobs School of Engineering.

“Our previous work with heart disease has shown that organ-specific matrices help to create more mature heart cells in a dish,” Christman said. “I am really excited to apply the technology to diabetes research.”

If the pancreatic islets can be successfully bioengineered, researchers could conduct mechanistic studies of beta cell maturation, replication, reprogramming, failure and survival. They say new drug therapies could be tested in the 3D culture. It would also be possible to compare beta cells from people with and without the disease to better understand the disease’s genetic component. Such work might eventually lead to treatments for protecting or replacing beta cells in patients.

Today, more than 600 health care and construction workers donned pink hard hats while forming a giant human ribbon at the still-under-construction UC San Diego Jacobs Medical Center in support of National Breast Cancer Awareness month.
Read more about the event here.

Today, more than 600 health care and construction workers donned pink hard hats while forming a giant human ribbon at the still-under-construction UC San Diego Jacobs Medical Center in support of National Breast Cancer Awareness month.

Read more about the event here.

An Unforgettable Feeling
With Alzheimer’s disease (AD), the greatest fear is what will be lost, how accumulating neurofibrillary tangles and amyloid plaques in the brain (like those pictured above, courtesy of Thomas Deerinck at the National Center for Microscopy Imaging and Research) will eventually erase one’s recollected life.
But maybe it’s worse (or better?) than that. Researchers at the University of Iowa suggest that persons with AD may feel lingering emotions about past events even when they no longer remember what actually happened.
In a published study, scientists played clips of sad and happy movies to AD patients. The latter no longer remembered ever seeing the films, but still experienced sustained states of sadness and happiness.
“This confirms that the emotional life of an Alzheimer’s patient is alive and well,” said study author Edmarie Guzman-Velez.
The findings have implications for how AD patients should be treated.
“Our findings should empower caregivers by showing them that their actions toward patients really do matter,” Guzmán-Vélez said. “Frequent visits and social interactions, exercise, music, dance, jokes, and serving patients their favorite foods are all simple things that can have a lasting emotional impact on a patient’s quality of life and subjective well-being.”

An Unforgettable Feeling

With Alzheimer’s disease (AD), the greatest fear is what will be lost, how accumulating neurofibrillary tangles and amyloid plaques in the brain (like those pictured above, courtesy of Thomas Deerinck at the National Center for Microscopy Imaging and Research) will eventually erase one’s recollected life.

But maybe it’s worse (or better?) than that. Researchers at the University of Iowa suggest that persons with AD may feel lingering emotions about past events even when they no longer remember what actually happened.

In a published study, scientists played clips of sad and happy movies to AD patients. The latter no longer remembered ever seeing the films, but still experienced sustained states of sadness and happiness.

“This confirms that the emotional life of an Alzheimer’s patient is alive and well,” said study author Edmarie Guzman-Velez.

The findings have implications for how AD patients should be treated.

“Our findings should empower caregivers by showing them that their actions toward patients really do matter,” Guzmán-Vélez said. “Frequent visits and social interactions, exercise, music, dance, jokes, and serving patients their favorite foods are all simple things that can have a lasting emotional impact on a patient’s quality of life and subjective well-being.”

Suicide risk reduction in medical students
Medical school is grueling so is it any wonder that medical students have high rates of burnout, depression and, tragically, suicide?
Help is on the way.
Researchers at UC San Diego School of Medicine have successfully pilot-tested a two-pronged program, called HEAR, short for Healer Education Assessment and Referral, to educate medical professionals about mental illness and to screen and help medical students at risk of suicide.
The preliminary results,reported in the October issue of Academic Psychiatry, are promising.
The implementation of the HEAR program at one medical school reduced the self-reported percentage of medical students with suicidal tendencies from 8.8 percent to 6.2 percent from 2009 to 2013, almost a 30 percent decrease over the four-year period.
The UC San Diego team also observed an increase in the percentage of at-risk students in counseling, from 11.5 percent to 15 percent during the same period, a more than 30 percent increase. This is a good sign because it means people are seeking help.
The HEAR program involves both educational lectures to de-stigmatize mental illness within the broader medical community and voluntary anonymous participation in an interactive online screening survey, developed by American Foundation for Suicide Prevention. Those screened as having depression or at-risk of suicide are referred to counseling or other treatment options.
“Our goals are to educate, de-stigmatize, identify, refer and treat medical students with depression and at risk of suicide,” said Nancy Downs, MD, a professor in the Department of Psychiatry and lead author. “The next step is to follow medical students through time to document whether early intervention has lasting-long term benefits.”
More than a dozen medical schools across the nation are currently testing the HEAR program.
The statistics speak to the need: Medical students are 15 to 30 percent more likely to suffer depression than others in their age group and rates of suicide are 200 percent greater among female doctors and 40 percent greater among male doctors than other professionals.
Pictured: Image courtesy of Maryam Soltani, a first-year resident at UC San Diego in family psychiatry.

Suicide risk reduction in medical students

Medical school is grueling so is it any wonder that medical students have high rates of burnout, depression and, tragically, suicide?

Help is on the way.

Researchers at UC San Diego School of Medicine have successfully pilot-tested a two-pronged program, called HEAR, short for Healer Education Assessment and Referral, to educate medical professionals about mental illness and to screen and help medical students at risk of suicide.

The preliminary results,reported in the October issue of Academic Psychiatry, are promising.

The implementation of the HEAR program at one medical school reduced the self-reported percentage of medical students with suicidal tendencies from 8.8 percent to 6.2 percent from 2009 to 2013, almost a 30 percent decrease over the four-year period.

The UC San Diego team also observed an increase in the percentage of at-risk students in counseling, from 11.5 percent to 15 percent during the same period, a more than 30 percent increase. This is a good sign because it means people are seeking help.

The HEAR program involves both educational lectures to de-stigmatize mental illness within the broader medical community and voluntary anonymous participation in an interactive online screening survey, developed by American Foundation for Suicide Prevention. Those screened as having depression or at-risk of suicide are referred to counseling or other treatment options.

“Our goals are to educate, de-stigmatize, identify, refer and treat medical students with depression and at risk of suicide,” said Nancy Downs, MD, a professor in the Department of Psychiatry and lead author. “The next step is to follow medical students through time to document whether early intervention has lasting-long term benefits.”

More than a dozen medical schools across the nation are currently testing the HEAR program.

The statistics speak to the need: Medical students are 15 to 30 percent more likely to suffer depression than others in their age group and rates of suicide are 200 percent greater among female doctors and 40 percent greater among male doctors than other professionals.

Pictured: Image courtesy of Maryam Soltani, a first-year resident at UC San Diego in family psychiatry.

Disease Without BordersBioregional approach to healthy living involves health care, city planning and ecological restoration
In a paper published this week online in Global Society, researchers with University of California, San Diego School of Medicine and the Urban Studies and Planning Program, also at UC San Diego, present a bioregional guide that merges place-based (territorial) city planning and ecosystem management along the United States-Mexico border as way to improve human and environmental health.
Issues like climate change, economic crisis, natural disasters and disease outbreaks do not stop at national borders, compelling public health officials, academics and researchers to think differently about how to address wide-ranging human health challenges.
“City planners, health officials and researchers are combining knowledge and action in new ways to promote healthy placemaking,” said Keith Pezzoli, PhD, UC San Diego Department of Communication and director of the Urban Studies and Planning Program. “Our health is not entirely hardwired genetically. It is also affected by environmental exposures, stress, diet, urban design and behavior. In our region, we can’t think about health on just one side of the border because animals, sick people and pollutants move back and forth.”
In border towns, health risks are common on both sides of the border. In the paper, Pezzoli, with co-authors Wael K. Al-Delaimy, MD, PhD, professor and chief of the Division of Global Health in the UC San Diego Department of Family and Preventive Medicine, and Catherine Wood Larsen, staff research associate in the Department of Family and Preventive Medicine, recommend supporting ecological restoration in transborder metropolitan areas where urban sprawl is taking place, such as in the canyon communities of Tijuana, Baja California.
In a related paper, published in the International Journal of Environmental Research and Public Health on Sept. 15, Pezzoli, Al-Delaimy and Larsen looked at the impact of the environment on residents of Tijuana’s rapidly urbanizing settlement called Los Laureles Canyon. This was the first large scale investigation evaluating the health of this population.
In one decade, the area grew from zero residents to 70,000, forming multiple communities called “colonias.” These settlements do not typically comply with standard building codes and are without basic infrastructure, such as a sewer system, trash collection or paved roads. Many unregulated dumpsites dot the area, often containing a variety of hazardous waste from industry, construction and household garbage.
With Alter Terra (a binational non-governmental organization), the UC San Diego Superfund Research Center, the Center for U.S.-Mexican Studies and the Universidad Autonoma de Baja California, researchers interviewed residents of Los Laureles Canyon about their well-being and any symptoms of illness. The occupants of the 4.6-square-mile area, a sub-basin of the bi-national Tijuana River Basin, reported skin problems, stomach discomforts, eye irritation, confusion/difficulty concentrating and extreme fatigue, which are symptoms commonly associated with exposure to environmental toxins.
“We have people who are living in dismal situations surrounded by dump sites,” said Al-Delaimy, who was the principal investigator on the study. “Their houses are made of garage doors brought from the U.S. and other materials that are mismatched. This is an environmental injustice that is impacting their health and has consequences for the San Diego region as well.”
For example, the ecological health of the Tijuana River Estuary in San Diego County depends upon what happens in the Tijuana River Basin. Toxins in upstream soils can contaminate rain runoff from Los Laureles Canyon, which eventually drains north to the U.S. and into the Pacific Ocean.
“We are joined together to Mexico through the watershed,” said Pezzoli. “We are in it together because of land, buildings and streets, but also from a health perspective because disease doesn’t stop at the border. The failure of control measures in one country has the potential to put neighboring communities at risk.”
To achieve an interconnected healthy bioregion, the scientists said public health professionals need training in global health diplomacy and cooperation. In addition, universities, through programs like the UC San Diego Superfund Research Center, must integrate community engagement and basic research translation through a cross-border approach. Creating sustainable and resilient communities, even across national borders, is possible by fostering investment in natural resources, rooted livelihoods and institutions, they said.
Image courtesy of UC San Diego Superfund Research Center

Disease Without Borders
Bioregional approach to healthy living involves health care, city planning and ecological restoration

In a paper published this week online in Global Society, researchers with University of California, San Diego School of Medicine and the Urban Studies and Planning Program, also at UC San Diego, present a bioregional guide that merges place-based (territorial) city planning and ecosystem management along the United States-Mexico border as way to improve human and environmental health.

Issues like climate change, economic crisis, natural disasters and disease outbreaks do not stop at national borders, compelling public health officials, academics and researchers to think differently about how to address wide-ranging human health challenges.

“City planners, health officials and researchers are combining knowledge and action in new ways to promote healthy placemaking,” said Keith Pezzoli, PhD, UC San Diego Department of Communication and director of the Urban Studies and Planning Program. “Our health is not entirely hardwired genetically. It is also affected by environmental exposures, stress, diet, urban design and behavior. In our region, we can’t think about health on just one side of the border because animals, sick people and pollutants move back and forth.”

In border towns, health risks are common on both sides of the border. In the paper, Pezzoli, with co-authors Wael K. Al-Delaimy, MD, PhD, professor and chief of the Division of Global Health in the UC San Diego Department of Family and Preventive Medicine, and Catherine Wood Larsen, staff research associate in the Department of Family and Preventive Medicine, recommend supporting ecological restoration in transborder metropolitan areas where urban sprawl is taking place, such as in the canyon communities of Tijuana, Baja California.

In a related paper, published in the International Journal of Environmental Research and Public Health on Sept. 15, Pezzoli, Al-Delaimy and Larsen looked at the impact of the environment on residents of Tijuana’s rapidly urbanizing settlement called Los Laureles Canyon. This was the first large scale investigation evaluating the health of this population.

In one decade, the area grew from zero residents to 70,000, forming multiple communities called “colonias.” These settlements do not typically comply with standard building codes and are without basic infrastructure, such as a sewer system, trash collection or paved roads. Many unregulated dumpsites dot the area, often containing a variety of hazardous waste from industry, construction and household garbage.

With Alter Terra (a binational non-governmental organization), the UC San Diego Superfund Research Center, the Center for U.S.-Mexican Studies and the Universidad Autonoma de Baja California, researchers interviewed residents of Los Laureles Canyon about their well-being and any symptoms of illness. The occupants of the 4.6-square-mile area, a sub-basin of the bi-national Tijuana River Basin, reported skin problems, stomach discomforts, eye irritation, confusion/difficulty concentrating and extreme fatigue, which are symptoms commonly associated with exposure to environmental toxins.

“We have people who are living in dismal situations surrounded by dump sites,” said Al-Delaimy, who was the principal investigator on the study. “Their houses are made of garage doors brought from the U.S. and other materials that are mismatched. This is an environmental injustice that is impacting their health and has consequences for the San Diego region as well.”

For example, the ecological health of the Tijuana River Estuary in San Diego County depends upon what happens in the Tijuana River Basin. Toxins in upstream soils can contaminate rain runoff from Los Laureles Canyon, which eventually drains north to the U.S. and into the Pacific Ocean.

“We are joined together to Mexico through the watershed,” said Pezzoli. “We are in it together because of land, buildings and streets, but also from a health perspective because disease doesn’t stop at the border. The failure of control measures in one country has the potential to put neighboring communities at risk.”

To achieve an interconnected healthy bioregion, the scientists said public health professionals need training in global health diplomacy and cooperation. In addition, universities, through programs like the UC San Diego Superfund Research Center, must integrate community engagement and basic research translation through a cross-border approach. Creating sustainable and resilient communities, even across national borders, is possible by fostering investment in natural resources, rooted livelihoods and institutions, they said.

Image courtesy of UC San Diego Superfund Research Center

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