Igor Grant Named Chair of UC San Diego Department of Psychiatry

Igor Grant, MD, FRCP(C), an internationally recognized neuropsychiatrist, whose research interests have ranged from the neurobiology of HIV/AIDS and substance abuse, psychobiology of stress, to the therapeutic potential of medicinal cannabis, has been named the new Chair of the Department of Psychiatry at the University of California, San Diego School of Medicine.

“Dr. Grant embodies the extraordinary scope and depth of research in the Department of Psychiatry. Indeed, he has been fundamental to its rise and enduring excellence,” said David Brenner, MD, vice chancellor for Health Sciences and dean of the School of Medicine. “Dr. Grant has always been at the forefront of his science, pushing for answers to questions in new and sometimes controversial or difficult areas. I have no doubt that the Department of Psychiatry will continue to excel under his leadership.”

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The awe of similars
Cilia are typically tiny, even microscopic, protruberances. They are hairlike – derived in fact from the Latin word for eyelash – but far more complicated, found abundantly throughout nature doing many kinds of jobs.
There are two types: motile and non-motile. The former are employed as a form of locomotion, with groups of cilia undulating in coordinated waves as a method of transportation. Non-motile or primary cilia behave as sensory organelles. Humans feature both types.
Motile cilia, for example, are found in the lining of the trachea, where they sweep mucus and dirt out of the lungs and in the Fallopian tubes, where their rhythmic beating moves the egg from the ovum to the uterus.
Virtually every cell in the human body sports at least one primary cilium, used by the cell to take measure of its surroundings. For some cilia, such as those in the ear or lining the nasal cavity, this job is particularly notable. They are essential elements of our sensory processes.
The images above: Top left, a false-colored scanning electron micrograph of cilia in a human Fallopian tube, courtesy of Steven Gschmeissner; top right, nasal cilia, courtesy of Susumu Nishinaga; lower left, an immature hair bundle of cells in the cochlea of the human ear, courtesy of David Furness, Wellcome Images; and lower right, cilia lining the trachea, courtesy again of Gschmeissner.

The awe of similars

Cilia are typically tiny, even microscopic, protruberances. They are hairlike – derived in fact from the Latin word for eyelash – but far more complicated, found abundantly throughout nature doing many kinds of jobs.

There are two types: motile and non-motile. The former are employed as a form of locomotion, with groups of cilia undulating in coordinated waves as a method of transportation. Non-motile or primary cilia behave as sensory organelles. Humans feature both types.

Motile cilia, for example, are found in the lining of the trachea, where they sweep mucus and dirt out of the lungs and in the Fallopian tubes, where their rhythmic beating moves the egg from the ovum to the uterus.

Virtually every cell in the human body sports at least one primary cilium, used by the cell to take measure of its surroundings. For some cilia, such as those in the ear or lining the nasal cavity, this job is particularly notable. They are essential elements of our sensory processes.

The images above: Top left, a false-colored scanning electron micrograph of cilia in a human Fallopian tube, courtesy of Steven Gschmeissner; top right, nasal cilia, courtesy of Susumu Nishinaga; lower left, an immature hair bundle of cells in the cochlea of the human ear, courtesy of David Furness, Wellcome Images; and lower right, cilia lining the trachea, courtesy again of Gschmeissner.

Cancer Stem Cells Linked to Drug ResistanceDiscovery of previously undefined molecular pathway is step toward novel clinical trial
Most drugs used to treat lung, breast and pancreatic cancers also promote drug-resistance and ultimately spur tumor growth. Researchers at the University of California, San Diego School of Medicine have discovered a molecule, or biomarker, called CD61 on the surface of drug-resistant tumors that appears responsible for inducing tumor metastasis by enhancing the stem cell-like properties of cancer cells.
The findings, published in the April 20, 2014 online issue of Nature Cell Biology, may point to new therapeutic opportunities for reversing drug resistance in a range of cancers, including those in the lung, pancreas and breast.
“There are a number of drugs that patients respond to during their initial cancer treatment, but relapse occurs when cancer cells become drug-resistant,” said David Cheresh, PhD, Distinguished Professor of Pathology and UC San Diego Moores Cancer Center associate director for Innovation and Industry Alliances. “We looked at the cells before and after they became resistant and asked, ‘What has changed in the cells?’”
Cheresh and colleagues investigated how tumor cells become resistant to drugs like erlotinib or lapatinib, known as receptor tyrosine kinase inhibitors and commonly used in standard cancer therapies. They found that as drug resistance occurs, tumor cells acquire stem cell-like properties that give them the capacity to survive throughout the body and essentially ignore the drugs.
Specifically, the scientists delineated the molecular pathway that facilitates both cancer stemness and drug resistance, and were able to identify existing drugs that exploit this pathway. These drugs not only reverse stem cell-like properties of tumors, but also appear to re-sensitize tumors to drugs that the cancer cells had developed resistance to. 
“The good news is that we’ve uncovered a previously undefined pathway that the tumor cells use to transform into cancer stem cells and that enable tumors to become resistant to commonly used cancer drugs,” said Cheresh.
Based on these findings, Hatim Husain, MD, an assistant professor who treats lung and brain cancer patients at Moores Cancer Center, has designed a clinical trial to attack this pathway in patients whose tumors are drug-resistant. The trial will be open to patients with lung cancer who have experienced cancer progression and drug resistance to erlotinib. It is expected to begin in the next year.
“Resistance builds to targeted therapies against cancer, and we have furthered our understanding of the mechanisms by which that happens,” said Husain. “Based on these research findings we now better understand how to exploit the ‘Achilles heel’ of these drug-resistant tumors.  Treatments will evolve into combinational therapies where one may keep the disease under control and delay resistance mechanisms from occurring for extended periods of time.”
Although the trial is expected to begin with patients who have already experienced drug resistance, Husain hopes to extend the study to reach patients in earlier stages to prevent initial resistance.
Pictured: When lung cancer cells become drug resistant, tumor cells return, as shown in brown in the photo on the left. Researchers identified an existing drug, bortezomib, that reverses stem cell-like properties of tumors, resensitizing them to drugs as shown in the photo on the right.

Cancer Stem Cells Linked to Drug Resistance
Discovery of previously undefined molecular pathway is step toward novel clinical trial

Most drugs used to treat lung, breast and pancreatic cancers also promote drug-resistance and ultimately spur tumor growth. Researchers at the University of California, San Diego School of Medicine have discovered a molecule, or biomarker, called CD61 on the surface of drug-resistant tumors that appears responsible for inducing tumor metastasis by enhancing the stem cell-like properties of cancer cells.

The findings, published in the April 20, 2014 online issue of Nature Cell Biology, may point to new therapeutic opportunities for reversing drug resistance in a range of cancers, including those in the lung, pancreas and breast.

“There are a number of drugs that patients respond to during their initial cancer treatment, but relapse occurs when cancer cells become drug-resistant,” said David Cheresh, PhD, Distinguished Professor of Pathology and UC San Diego Moores Cancer Center associate director for Innovation and Industry Alliances. “We looked at the cells before and after they became resistant and asked, ‘What has changed in the cells?’”

Cheresh and colleagues investigated how tumor cells become resistant to drugs like erlotinib or lapatinib, known as receptor tyrosine kinase inhibitors and commonly used in standard cancer therapies. They found that as drug resistance occurs, tumor cells acquire stem cell-like properties that give them the capacity to survive throughout the body and essentially ignore the drugs.

Specifically, the scientists delineated the molecular pathway that facilitates both cancer stemness and drug resistance, and were able to identify existing drugs that exploit this pathway. These drugs not only reverse stem cell-like properties of tumors, but also appear to re-sensitize tumors to drugs that the cancer cells had developed resistance to. 

“The good news is that we’ve uncovered a previously undefined pathway that the tumor cells use to transform into cancer stem cells and that enable tumors to become resistant to commonly used cancer drugs,” said Cheresh.

Based on these findings, Hatim Husain, MD, an assistant professor who treats lung and brain cancer patients at Moores Cancer Center, has designed a clinical trial to attack this pathway in patients whose tumors are drug-resistant. The trial will be open to patients with lung cancer who have experienced cancer progression and drug resistance to erlotinib. It is expected to begin in the next year.

“Resistance builds to targeted therapies against cancer, and we have furthered our understanding of the mechanisms by which that happens,” said Husain. “Based on these research findings we now better understand how to exploit the ‘Achilles heel’ of these drug-resistant tumors.  Treatments will evolve into combinational therapies where one may keep the disease under control and delay resistance mechanisms from occurring for extended periods of time.”

Although the trial is expected to begin with patients who have already experienced drug resistance, Husain hopes to extend the study to reach patients in earlier stages to prevent initial resistance.

Pictured: When lung cancer cells become drug resistant, tumor cells return, as shown in brown in the photo on the left. Researchers identified an existing drug, bortezomib, that reverses stem cell-like properties of tumors, resensitizing them to drugs as shown in the photo on the right.

To Vape or Not to Vape? We’ve got thee questions for our expert about the supposed safety of e-cigarettes
For the last 50 years cigarette smoking has been on the decline due in large part to aggressive advocacy by health professionals about the risks associated with smoking tobacco, and a once ubiquitous habit has become taboo. Quickly replacing tobacco cigarettes are electronic or e-cigarettes and “vaping” is the new inhaling. E-cigarette availability and popularity are at an all-time high, especially among teens and young adults, with claims of e-cigarette safety driving the trend.
But are e-cigarettes really safe? Recent reports of liquid nicotine poisoning beg to differ and much remains unknown about whether or not inhaling the vapor from e-cigarettes is safer than inhaling smoked tobacco.
We’ve asked John Pierce, PhD, Distinguished Professor of Family and Preventive Medicine, Moores Cancer Center director for population sciences and expert on tobacco cessation three questions about the relative safety of e-cigarettes.
Question: What, if anything, is known about the health effects of nicotine delivery from e-cigarettes versus traditional tobacco cigarettes? Are they, as advocates and tobacco companies suggest, safer?Answer: There is no question that a heavy smoker who stops using cigarettes and switches to e-cigs will have a reduced risk of lung cancer.  However, it is not at all clear that e-cigarettes will not introduce a new health risk to the person who has never smoked or whether it will be a safe alternative for the occasional smoker.
Q: Is there any evidence that it’s easier to quit smoking by shifting to e-cigarettes?
A: No, the evidence that is available suggests that e-cigarettes are not an effective smoking cessation device. The question is how difficult will it be for heavy smokers to substitute e-cigarettes for their regular cigarettes.
Q: How much nicotine from e-cigarettes is released as vapor, potentially to be inhaled by others? Does the vapor represent less of a health threat than secondhand smoke?
A: Plenty. Currently, there is very little standardization in e-cigarettes and lots of potentially harmful chemicals have been measured in it. The first study to report on this did so last December. There is no science that supports allowing e-cigarettes to be used where cigarettes are prohibited.
Image source: The Mercury News

To Vape or Not to Vape?
We’ve got thee questions for our expert about the supposed safety of e-cigarettes

For the last 50 years cigarette smoking has been on the decline due in large part to aggressive advocacy by health professionals about the risks associated with smoking tobacco, and a once ubiquitous habit has become taboo. Quickly replacing tobacco cigarettes are electronic or e-cigarettes and “vaping” is the new inhaling. E-cigarette availability and popularity are at an all-time high, especially among teens and young adults, with claims of e-cigarette safety driving the trend.

But are e-cigarettes really safe? Recent reports of liquid nicotine poisoning beg to differ and much remains unknown about whether or not inhaling the vapor from e-cigarettes is safer than inhaling smoked tobacco.

We’ve asked John Pierce, PhD, Distinguished Professor of Family and Preventive Medicine, Moores Cancer Center director for population sciences and expert on tobacco cessation three questions about the relative safety of e-cigarettes.

Question: What, if anything, is known about the health effects of nicotine delivery from e-cigarettes versus traditional tobacco cigarettes? Are they, as advocates and tobacco companies suggest, safer?

Answer: There is no question that a heavy smoker who stops using cigarettes and switches to e-cigs will have a reduced risk of lung cancer.  However, it is not at all clear that e-cigarettes will not introduce a new health risk to the person who has never smoked or whether it will be a safe alternative for the occasional smoker.

Q: Is there any evidence that it’s easier to quit smoking by shifting to e-cigarettes?

A: No, the evidence that is available suggests that e-cigarettes are not an effective smoking cessation device. The question is how difficult will it be for heavy smokers to substitute e-cigarettes for their regular cigarettes.

Q: How much nicotine from e-cigarettes is released as vapor, potentially to be inhaled by others? Does the vapor represent less of a health threat than secondhand smoke?

A: Plenty. Currently, there is very little standardization in e-cigarettes and lots of potentially harmful chemicals have been measured in it. The first study to report on this did so last December. There is no science that supports allowing e-cigarettes to be used where cigarettes are prohibited.

Image source: The Mercury News

The Ilk of Human KindnessOlder women with gumption score high on compassion
Researchers at the University of California, San Diego School of Medicine report that older women, plucky individuals and those who have suffered a recent major loss are more likely to be compassionate toward strangers than other older adults.
The study is published in this month’s issue of the International Journal of Geriatric Psychiatry.
Because compassionate behaviors are associated with better health and well-being as we age, the research findings offer insights into ways to improve the outcomes of individuals whose deficits in compassion put them at risk for becoming lonely and isolated later in life.
“We are interested in anything that can help older people age more successfully,” said Lisa Eyler, PhD, a professor of psychiatry and co-author. “We know that social connections are important to health and well-being, and we know that people who want to be kind to others garner greater social support. If we can foster compassion in people, we can improve their health and well-being, and maybe even longevity.”
The study, based on a survey of 1,006 randomly selected adults in San Diego County, aged 50 and over, with a mean age of 77, identified three factors that were predictive of a person’s self-reported compassion: gender, recent suffering and high mental resiliency.
Women, independent of their age, income, education, race, marital status or mental health status, scored higher on the compassion test, on average, than men. Higher levels of compassion were also observed among both men and women who had “walked a mile in another person’s shoes” and experienced a personal loss, such as a death in the family or illness, in the last year.
Those who reported higher confidence in their ability to bounce back from hard times also reported more empathy toward strangers and joy from helping those in need.
“What is exciting is that we are identifying aspects of successful aging that we can foster in both men and women,” said co-author Dilip Jeste, MD, Distinguished Professor of Psychiatry and Neurosciences, and director of the Sam and Rose Stein Institute for Research on Aging. “Mental resiliency can be developed through meditation, mindfulness and stress reduction practices. We can also teach people that the silver lining to adversity is an opportunity for personal growth.”

The Ilk of Human Kindness
Older women with gumption score high on compassion

Researchers at the University of California, San Diego School of Medicine report that older women, plucky individuals and those who have suffered a recent major loss are more likely to be compassionate toward strangers than other older adults.

The study is published in this month’s issue of the International Journal of Geriatric Psychiatry.

Because compassionate behaviors are associated with better health and well-being as we age, the research findings offer insights into ways to improve the outcomes of individuals whose deficits in compassion put them at risk for becoming lonely and isolated later in life.

“We are interested in anything that can help older people age more successfully,” said Lisa Eyler, PhD, a professor of psychiatry and co-author. “We know that social connections are important to health and well-being, and we know that people who want to be kind to others garner greater social support. If we can foster compassion in people, we can improve their health and well-being, and maybe even longevity.”

The study, based on a survey of 1,006 randomly selected adults in San Diego County, aged 50 and over, with a mean age of 77, identified three factors that were predictive of a person’s self-reported compassion: gender, recent suffering and high mental resiliency.

Women, independent of their age, income, education, race, marital status or mental health status, scored higher on the compassion test, on average, than men. Higher levels of compassion were also observed among both men and women who had “walked a mile in another person’s shoes” and experienced a personal loss, such as a death in the family or illness, in the last year.

Those who reported higher confidence in their ability to bounce back from hard times also reported more empathy toward strangers and joy from helping those in need.

“What is exciting is that we are identifying aspects of successful aging that we can foster in both men and women,” said co-author Dilip Jeste, MD, Distinguished Professor of Psychiatry and Neurosciences, and director of the Sam and Rose Stein Institute for Research on Aging. “Mental resiliency can be developed through meditation, mindfulness and stress reduction practices. We can also teach people that the silver lining to adversity is an opportunity for personal growth.”

Mutant Protein in Muscle Linked to Neuromuscular DisorderA new therapeutic target for Kennedy’s disease and a potential treatment 
Sometimes known as Kennedy’s disease, spinal and bulbar muscular atrophy (SBMA) is a rare inherited neuromuscular disorder characterized by slowly progressive muscle weakness and atrophy. Researchers have long considered it to be essentially an affliction of primary motor neurons – the cells in the spinal cord and brainstem that control muscle movement.
But in a new study published in the April 16, 2014 online issue of Neuron, a team of scientists at the University of California, San Diego School of Medicine say novel mouse studies indicate that mutant protein levels in muscle cells, not motor neurons, are fundamentally involved in SBMA, suggesting an alternative and promising new avenue of treatment for a condition that is currently incurable.
SBMA is an X-linked recessive disease that affects only males, though females carrying the defective gene have a 50:50 chance of passing it along to a son. It belongs to a group of diseases, such as Huntington’s disease, in which a C-A-G DNA sequence is repeated too many times, resulting in a protein with too many glutamines (an amino acid), causing the diseased protein to misfold and produce harmful consequences for affected cells. Thus far, human clinical trials of treatments to protect against these repeat toxicities have failed.
In the new paper, a team led by principal investigator Albert La Spada, MD, PhD, professor of pediatrics, cellular and molecular medicine, and neurosciences, and the associate director of the Institute for Genomic Medicine at UC San Diego, propose a different therapeutic target. After creating a new mouse model of SBMA, they discovered that skeletal muscle was the site of mutant protein toxicity and that measures which mitigated the protein’s influence in muscle suppressed symptoms of SBMA in treated mice, such as weight loss and progressive weakness, and increased survival.   
In a related paper, published in the April 16, 2014 online issue of Cell Reports, La Spada and colleagues describe a potential treatment for SBMA. Currently, there is none.
The scientists developed antisense oligonucleotides – sequences of synthesized genetic material – that suppressed androgen receptor (AR) gene expression in peripheral tissues, but not in the central nervous system. Mutations in the AR gene are the cause of SBMA, a discovery that La Spada made more than 20 years ago while a MD-PhD student.
La Spada said that antisense therapy helped mice modeling SBMA to recover lost muscle weight and strength and extended survival. 
“The main points of these papers is that we have identified both a genetic cure and a drug cure for SBMA – at least in mice. The goal now is to further develop and refine these ideas so that we can ultimately test them in people,” La Spada said.
Pictured: striated human skeletal muscle.

Mutant Protein in Muscle Linked to Neuromuscular Disorder
A new therapeutic target for Kennedy’s disease and a potential treatment

Sometimes known as Kennedy’s disease, spinal and bulbar muscular atrophy (SBMA) is a rare inherited neuromuscular disorder characterized by slowly progressive muscle weakness and atrophy. Researchers have long considered it to be essentially an affliction of primary motor neurons – the cells in the spinal cord and brainstem that control muscle movement.

But in a new study published in the April 16, 2014 online issue of Neuron, a team of scientists at the University of California, San Diego School of Medicine say novel mouse studies indicate that mutant protein levels in muscle cells, not motor neurons, are fundamentally involved in SBMA, suggesting an alternative and promising new avenue of treatment for a condition that is currently incurable.

SBMA is an X-linked recessive disease that affects only males, though females carrying the defective gene have a 50:50 chance of passing it along to a son. It belongs to a group of diseases, such as Huntington’s disease, in which a C-A-G DNA sequence is repeated too many times, resulting in a protein with too many glutamines (an amino acid), causing the diseased protein to misfold and produce harmful consequences for affected cells. Thus far, human clinical trials of treatments to protect against these repeat toxicities have failed.

In the new paper, a team led by principal investigator Albert La Spada, MD, PhD, professor of pediatrics, cellular and molecular medicine, and neurosciences, and the associate director of the Institute for Genomic Medicine at UC San Diego, propose a different therapeutic target. After creating a new mouse model of SBMA, they discovered that skeletal muscle was the site of mutant protein toxicity and that measures which mitigated the protein’s influence in muscle suppressed symptoms of SBMA in treated mice, such as weight loss and progressive weakness, and increased survival.   

In a related paper, published in the April 16, 2014 online issue of Cell Reports, La Spada and colleagues describe a potential treatment for SBMA. Currently, there is none.

The scientists developed antisense oligonucleotides – sequences of synthesized genetic material – that suppressed androgen receptor (AR) gene expression in peripheral tissues, but not in the central nervous system. Mutations in the AR gene are the cause of SBMA, a discovery that La Spada made more than 20 years ago while a MD-PhD student.

La Spada said that antisense therapy helped mice modeling SBMA to recover lost muscle weight and strength and extended survival. 

“The main points of these papers is that we have identified both a genetic cure and a drug cure for SBMA – at least in mice. The goal now is to further develop and refine these ideas so that we can ultimately test them in people,” La Spada said.

Pictured: striated human skeletal muscle.

Congratulations to our very own Dr. Quyen T. Nguyen, who received the Presidential Early Career Award for Scientists and Engineers (PECASE) at a ceremony in Washington, D.C. yesterday. She received this award for her work testing fluorescently labeled probes for nerve imaging during surgery. 
More here

Congratulations to our very own Dr. Quyen T. Nguyen, who received the Presidential Early Career Award for Scientists and Engineers (PECASE) at a ceremony in Washington, D.C. yesterday. She received this award for her work testing fluorescently labeled probes for nerve imaging during surgery.

More here

Breaking Bad MitochondriaMechanism helps explain persistence of hepatitis C virus
Researchers at the University of California, San Diego School of Medicine have identified a mechanism that explains why people with the hepatitis C virus get liver disease and why the virus is able to persist in the body for so long.
The hard-to-kill pathogen, which infects an estimated 200 million people worldwide, attacks the liver cells’ energy centers – the mitochondria – dismantling the cell’s innate ability to fight infection. It does this by altering cells mitochondrial dynamics.
The study, published in today’s issue of the Proceedings of the National Academy of Sciences, suggests that mitochondrial operations could be a therapeutic target against hepatitis C, the leading cause of liver transplants and a major cause of liver cancer in the U.S.
“Our study tells us the story of how the hepatitis C virus causes liver disease,” said Aleem Siddiqui, PhD, professor of medicine and senior author. “The virus damages mitochondria in liver cells. Cells recognize the damage and respond to it by recruiting proteins that tell the mitochondria to eliminate the damaged area, but the repair process ends up helping the virus.”
Mitochondria are organelles in a cell that convert energy from food (glucose) into a form of energy that can be used by cells called adenosine triphosphate.
Specifically, the researchers discovered that the virus stimulates the production of a protein (Drp 1) that induces viral-damaged mitochondria to undergo asymmetric fragmentation. This fragmentation (fission) results in the formation of one healthy mitochondrion and one damaged or bad mitochondrion, the latter of which is quickly broken down (catabolized) and dissolved in the cell’s cytoplasm.
More here
Pictured: Mitochondria in hepatitis C-infected cells (bottom row) are self-destructing. The self-annihilation process explains the persistance and virulence of the virus in human liver cells.

Breaking Bad Mitochondria
Mechanism helps explain persistence of hepatitis C virus

Researchers at the University of California, San Diego School of Medicine have identified a mechanism that explains why people with the hepatitis C virus get liver disease and why the virus is able to persist in the body for so long.

The hard-to-kill pathogen, which infects an estimated 200 million people worldwide, attacks the liver cells’ energy centers – the mitochondria – dismantling the cell’s innate ability to fight infection. It does this by altering cells mitochondrial dynamics.

The study, published in today’s issue of the Proceedings of the National Academy of Sciences, suggests that mitochondrial operations could be a therapeutic target against hepatitis C, the leading cause of liver transplants and a major cause of liver cancer in the U.S.

“Our study tells us the story of how the hepatitis C virus causes liver disease,” said Aleem Siddiqui, PhD, professor of medicine and senior author. “The virus damages mitochondria in liver cells. Cells recognize the damage and respond to it by recruiting proteins that tell the mitochondria to eliminate the damaged area, but the repair process ends up helping the virus.”

Mitochondria are organelles in a cell that convert energy from food (glucose) into a form of energy that can be used by cells called adenosine triphosphate.

Specifically, the researchers discovered that the virus stimulates the production of a protein (Drp 1) that induces viral-damaged mitochondria to undergo asymmetric fragmentation. This fragmentation (fission) results in the formation of one healthy mitochondrion and one damaged or bad mitochondrion, the latter of which is quickly broken down (catabolized) and dissolved in the cell’s cytoplasm.

More here

Pictured: Mitochondria in hepatitis C-infected cells (bottom row) are self-destructing. The self-annihilation process explains the persistance and virulence of the virus in human liver cells.

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