Fighting dead zones of cancer
Almost all high-risk, poor-prognosis cancers have very low levels of oxygen in the primary tumor’s interior. A marker for this oxygen-depleted state is the presence of a protein known as H1FI alpha. 
In healthy cells, HIF1 alpha is degraded into harmless nothingness in the cytoplasm. In low-oxygen cancer cells however, the normal breakdown goes awry and HiFl alpha is able to enter the nucleus, where it may activate genes that further promote aberrant cell growth.
A new study conducted by researchers at the University of California, San Diego School of Medicine shows that an emerging class of anticancer treatments known as PI-3K inhibitors help to degrade the HIF1 alpha protein and thus may offer a potential therapy for treating deadly hypoxic tumors. The study was published in a recent issue of the Journal of Biological Chemistry.
“Our main finding is that, in the absence of PI-3K signaling, MDM2 proteins cannot go inside the nucleus,” said lead author Shweta Joshi, PhD, postdoctoral researcher. “In the cytoplasm, the MDM2 proteins degrade HIF1 alpha. This is good news because it means that some new cancer therapies may help patients in more ways that was initially realized.”
"These HIF1 proteins are major players in driving the cancer state," said co-author Donald Durden, MD, PhD, professor and vice chair for Research in the Department of Pediatrics and research director, Division of Hematology/Oncology at the UC San Diego Moores Cancer Center. “They control degradation of surrounding tissues, induce a change in metabolism and induce the formation of blood vessels. That is why our observation is so important, because it reveals an entirely new way of HIF1 regulation.”
Pictured: A false-color, scanning electron micrograph of two cultured HeLa cancer cells, courtesy of Thomas Deerinck, National Center for Microscopy and Imaging Research at San Diego.

Fighting dead zones of cancer

Almost all high-risk, poor-prognosis cancers have very low levels of oxygen in the primary tumor’s interior. A marker for this oxygen-depleted state is the presence of a protein known as H1FI alpha.

In healthy cells, HIF1 alpha is degraded into harmless nothingness in the cytoplasm. In low-oxygen cancer cells however, the normal breakdown goes awry and HiFl alpha is able to enter the nucleus, where it may activate genes that further promote aberrant cell growth.

A new study conducted by researchers at the University of California, San Diego School of Medicine shows that an emerging class of anticancer treatments known as PI-3K inhibitors help to degrade the HIF1 alpha protein and thus may offer a potential therapy for treating deadly hypoxic tumors. The study was published in a recent issue of the Journal of Biological Chemistry.

“Our main finding is that, in the absence of PI-3K signaling, MDM2 proteins cannot go inside the nucleus,” said lead author Shweta Joshi, PhD, postdoctoral researcher. “In the cytoplasm, the MDM2 proteins degrade HIF1 alpha. This is good news because it means that some new cancer therapies may help patients in more ways that was initially realized.”

"These HIF1 proteins are major players in driving the cancer state," said co-author Donald Durden, MD, PhD, professor and vice chair for Research in the Department of Pediatrics and research director, Division of Hematology/Oncology at the UC San Diego Moores Cancer Center. “They control degradation of surrounding tissues, induce a change in metabolism and induce the formation of blood vessels. That is why our observation is so important, because it reveals an entirely new way of HIF1 regulation.”

Pictured: A false-color, scanning electron micrograph of two cultured HeLa cancer cells, courtesy of Thomas Deerinck, National Center for Microscopy and Imaging Research at San Diego.

Uh oh!
A diagnosis of prostate cancer can be an “uh oh” moment. After skin cancer, it’s the most common cancer in American men, with more than 238,000 new cases diagnosed each year and almost 30,000 deaths.
However, the confocal micrograph above, produced by Xiaochen Lu and C. Chase Bolt at the University of Illinois at Urbana-Champaign, is not an uh-oh moment. Rather, it may be an “ah-hah!”
It depicts the actual prostate and ureter of an embryonic mouse – a winning image from the 2013 Olympus BioScapes competition.
Mouse models of prostate cancer are widely used, in part because the disease is often very slow progressing in humans and typically not detected in men until their 60s or older.

Uh oh!

A diagnosis of prostate cancer can be an “uh oh” moment. After skin cancer, it’s the most common cancer in American men, with more than 238,000 new cases diagnosed each year and almost 30,000 deaths.

However, the confocal micrograph above, produced by Xiaochen Lu and C. Chase Bolt at the University of Illinois at Urbana-Champaign, is not an uh-oh moment. Rather, it may be an “ah-hah!”

It depicts the actual prostate and ureter of an embryonic mouse – a winning image from the 2013 Olympus BioScapes competition.

Mouse models of prostate cancer are widely used, in part because the disease is often very slow progressing in humans and typically not detected in men until their 60s or older.

Charles E. Daniels to be Honored for His Leadership in Health-System Pharmacy
The American Society of Health-System Pharmacists (ASHP) has named Charles E. Daniels, PhD, FASHP, as the recipient of the 2014 John W. Webb Lecture Award. The Webb Award honors health-system pharmacy practitioners or educators who stand apart because of their extraordinary dedication to fostering excellence in pharmacy management and leadership.
“This prestigious award reflects Dr. Daniels international recognition as a leader in expanding pharmacy practices and academic development in health systems to improve patient care,” said James H. McKerrow, MD, PhD, dean of the UC San Diego Skaggs School of Pharmacy and Pharmaceutical Sciences. “Throughout his career, Dr. Daniels has focused on solving issues that regularly confront health system pharmacists, including medication safety, cost-effective use of medications, and increased efficiency of health-system operations.”
Daniels is pharmacist-in-chief for UC San Diego Health System and professor of clinical pharmacy and associate dean at UC San Diego Skaggs School of Pharmacy and Pharmaceutical Sciences. Daniels serves as system-wide pharmacy officer for the university’s hospitals and clinics. His leadership has cultivated an understanding among health system executives and health care providers of the importance of including pharmacists in key leadership and decision-making positions. He also has served as a champion for postgraduate education and training in order to best prepare pharmacists for practice.

Charles E. Daniels to be Honored for His Leadership in Health-System Pharmacy

The American Society of Health-System Pharmacists (ASHP) has named Charles E. Daniels, PhD, FASHP, as the recipient of the 2014 John W. Webb Lecture Award. The Webb Award honors health-system pharmacy practitioners or educators who stand apart because of their extraordinary dedication to fostering excellence in pharmacy management and leadership.

“This prestigious award reflects Dr. Daniels international recognition as a leader in expanding pharmacy practices and academic development in health systems to improve patient care,” said James H. McKerrow, MD, PhD, dean of the UC San Diego Skaggs School of Pharmacy and Pharmaceutical Sciences. “Throughout his career, Dr. Daniels has focused on solving issues that regularly confront health system pharmacists, including medication safety, cost-effective use of medications, and increased efficiency of health-system operations.”

Daniels is pharmacist-in-chief for UC San Diego Health System and professor of clinical pharmacy and associate dean at UC San Diego Skaggs School of Pharmacy and Pharmaceutical Sciences. Daniels serves as system-wide pharmacy officer for the university’s hospitals and clinics. His leadership has cultivated an understanding among health system executives and health care providers of the importance of including pharmacists in key leadership and decision-making positions. He also has served as a champion for postgraduate education and training in order to best prepare pharmacists for practice.

New Approach to Remove Blood Clots Catheter-based system removes clots without open heart surgery  
When a large blood clot was discovered attached to the end of a catheter inside the right atrial chamber of a patient’s heart, doctors faced a daunting challenge. If the clot came loose, the consequences would likely be catastrophic for the patient, who suffered from pulmonary hypertension – a dangerous narrowing of blood vessels connecting the heart and lungs.
But experts at the UC San Diego Sulpizio Cardiovascular Center (SCVC) are now able to save patients like this one from potentially fatal outcomes by using a new technology capable of removing blood clots, infected masses or foreign bodies from major cardiac blood vessels without performing open-heart surgery.
The SCVC is the first in San Diego County to use the AngioVac system developed by AngioDynamics. The AngioVac is a catheter-based device in which thin tubes are inserted into two major veins in the body through the neck or groin area. Under X-ray guidance, the flexible tubes are advanced to the proximal veins, right-sided heart chambers and/or lung arteries. Each is equipped with an expandable, balloon-shaped funnel tip that, when attached to a bypass circuit, vacuums the targeted material, such as a blood, clot out of the body.
“In some cases, medications can be used to dissolve blood clots, but this treatment option does not work for all patients, especially those who are in a life-threatening situation,” said Mitul Patel, MD, FACC, interventional cardiologist at UC San Diego Health System. “This new device allows our team to safely extract material, preventing the patient from having to undergo invasive, high-risk surgery.”
Open-heart surgery takes much longer to perform and often requires the surgeon to divide the breastbone lengthwise down the middle and spread the halves apart to access the heart. After the heart is repaired, surgeons use wires to hold the breastbone and ribs in place as they heal.
"Removing a blood clot through open-heart surgery results in longer hospitalization, recovery and rehabilitation times compared to the minimally invasive approach provided by this new device," said Victor Pretorius, MBchB, cardiothoracic surgeon at UC San Diego Health System.
Read more here

New Approach to Remove Blood Clots
Catheter-based system removes clots without open heart surgery 

When a large blood clot was discovered attached to the end of a catheter inside the right atrial chamber of a patient’s heart, doctors faced a daunting challenge. If the clot came loose, the consequences would likely be catastrophic for the patient, who suffered from pulmonary hypertension – a dangerous narrowing of blood vessels connecting the heart and lungs.

But experts at the UC San Diego Sulpizio Cardiovascular Center (SCVC) are now able to save patients like this one from potentially fatal outcomes by using a new technology capable of removing blood clots, infected masses or foreign bodies from major cardiac blood vessels without performing open-heart surgery.

The SCVC is the first in San Diego County to use the AngioVac system developed by AngioDynamics. The AngioVac is a catheter-based device in which thin tubes are inserted into two major veins in the body through the neck or groin area. Under X-ray guidance, the flexible tubes are advanced to the proximal veins, right-sided heart chambers and/or lung arteries. Each is equipped with an expandable, balloon-shaped funnel tip that, when attached to a bypass circuit, vacuums the targeted material, such as a blood, clot out of the body.

“In some cases, medications can be used to dissolve blood clots, but this treatment option does not work for all patients, especially those who are in a life-threatening situation,” said Mitul Patel, MD, FACC, interventional cardiologist at UC San Diego Health System. “This new device allows our team to safely extract material, preventing the patient from having to undergo invasive, high-risk surgery.”

Open-heart surgery takes much longer to perform and often requires the surgeon to divide the breastbone lengthwise down the middle and spread the halves apart to access the heart. After the heart is repaired, surgeons use wires to hold the breastbone and ribs in place as they heal.

"Removing a blood clot through open-heart surgery results in longer hospitalization, recovery and rehabilitation times compared to the minimally invasive approach provided by this new device," said Victor Pretorius, MBchB, cardiothoracic surgeon at UC San Diego Health System.

Read more here

Beyond Fish Oil: the hunt for small molecules with a big omega-3 punch
The modern Western diet is abundant in fat, especially omega-6 fatty acids. And while there’s nothing inherently unhealthy about these fats, when the ratio of omega-6 to omega-3 fatty acids in our diet is high our body chemistry shifts to a pro-inflammatory state.
This means that if we have arthritis we may ache a bit more, and if we have type 2 diabetes our cells may become less adept at detecting and responding to insulin. Our bodies may be more prone to obesity, as well.
Although consumption of omega-3 fatty acids found in high concentrations in cold-water marine species such as salmon and krill can help reduce chronic inflammation and insulin resistance, researchers at the University of California, San Diego School of Medicine say that the amount of fish or even fish oil needed to reverse insulin resistance is too high to be practical.
In light of this roadblock, they have taken another tack in their efforts to develop novel anti-diabetic treatments. Specifically, they are working to chemically construct a better fish oil – one that is more effective and specific for human medicine, and which has the added benefit of not depleting marine species.
In previous work, they elucidated the molecular mechanism that makes omega-3 fatty acids effective in reducing chronic inflammation and insulin resistance. In a new paper, published in Nature, they report synthesizing a molecule, dubbed Compound A, in mice that activates the same beneficial pathway as omega-3 fatty acids. Interestingly, Compound A is not present in fish oil but it nonetheless binds to a key protein receptor activated by omega-3 fatty acids.
“What we have done is built a small molecule that sets in motion the same molecular cascade as omega-3 fatty acids,” said lead author Da Young Oh, PhD, an assistant professor in the Division of Endocrinology and Metabolism. “The difference is that the small molecule is more selective and suitable for developing pharmaceutical grade product than fish oil.”
Researchers are now collaborating with a major pharmaceutical company to develop a small-molecule, insulin-sensitizing agent for the treatment of type 2 diabetes and other human insulin-resistant states.

Beyond Fish Oil: the hunt for small molecules with a big omega-3 punch

The modern Western diet is abundant in fat, especially omega-6 fatty acids. And while there’s nothing inherently unhealthy about these fats, when the ratio of omega-6 to omega-3 fatty acids in our diet is high our body chemistry shifts to a pro-inflammatory state.

This means that if we have arthritis we may ache a bit more, and if we have type 2 diabetes our cells may become less adept at detecting and responding to insulin. Our bodies may be more prone to obesity, as well.

Although consumption of omega-3 fatty acids found in high concentrations in cold-water marine species such as salmon and krill can help reduce chronic inflammation and insulin resistance, researchers at the University of California, San Diego School of Medicine say that the amount of fish or even fish oil needed to reverse insulin resistance is too high to be practical.

In light of this roadblock, they have taken another tack in their efforts to develop novel anti-diabetic treatments. Specifically, they are working to chemically construct a better fish oil – one that is more effective and specific for human medicine, and which has the added benefit of not depleting marine species.

In previous work, they elucidated the molecular mechanism that makes omega-3 fatty acids effective in reducing chronic inflammation and insulin resistance. In a new paper, published in Nature, they report synthesizing a molecule, dubbed Compound A, in mice that activates the same beneficial pathway as omega-3 fatty acids. Interestingly, Compound A is not present in fish oil but it nonetheless binds to a key protein receptor activated by omega-3 fatty acids.

“What we have done is built a small molecule that sets in motion the same molecular cascade as omega-3 fatty acids,” said lead author Da Young Oh, PhD, an assistant professor in the Division of Endocrinology and Metabolism. “The difference is that the small molecule is more selective and suitable for developing pharmaceutical grade product than fish oil.”

Researchers are now collaborating with a major pharmaceutical company to develop a small-molecule, insulin-sensitizing agent for the treatment of type 2 diabetes and other human insulin-resistant states.

“Den” of leaves
Dendritic cells get their name from their surface projections, which somewhat resemble the dendrites of neurons, the branchlike extensions that increase the surface of a cell body and receive information from other neurons.
Dendritic cells are found in most tissues of the body, most abundantly in those that interface between internal and external environments, such as the skin, lungs and lining of the gastrointestinal tract. Here, they’re suitably placed to serve their primary function, which is to continuously sample their surroundings for antigens, such as dead cells or invasive microbes. They are a key player in the body’s immune response system.
Once exposed to an antigen, say a virus, the sheets of the dendritic cell entrap it so that it can be degraded by internal lysosomes into peptide fragments and then redisplayed to circulating T cells, which develop the appropriate immune response. 
The image above is an artistic rendering, based on ion abrasion scanning electron microscopy developed at the National Institutes of Health.

“Den” of leaves

Dendritic cells get their name from their surface projections, which somewhat resemble the dendrites of neurons, the branchlike extensions that increase the surface of a cell body and receive information from other neurons.

Dendritic cells are found in most tissues of the body, most abundantly in those that interface between internal and external environments, such as the skin, lungs and lining of the gastrointestinal tract. Here, they’re suitably placed to serve their primary function, which is to continuously sample their surroundings for antigens, such as dead cells or invasive microbes. They are a key player in the body’s immune response system.

Once exposed to an antigen, say a virus, the sheets of the dendritic cell entrap it so that it can be degraded by internal lysosomes into peptide fragments and then redisplayed to circulating T cells, which develop the appropriate immune response

The image above is an artistic rendering, based on ion abrasion scanning electron microscopy developed at the National Institutes of Health.

New Reprogramming Method Makes Better Stem Cells
A team of researchers from the University of California, San Diego School of Medicine, Oregon Health & Science University (OHSU) and Salk Institute for Biological Studies has shown for the first time that stem cells created using different methods produce differing cells. The findings, published in the July 2, 2014 online issue of Nature, provide new insights into the basic biology of stem cells and could ultimately lead to improved stem cell therapies.
Capable of developing into any cell type, pluripotent stem cells offer great promise as the basis for emerging cell transplantation therapies that address a wide array of diseases and conditions, from diabetes and Alzheimer’s disease to cancer and spinal cord injuries. In theory, stem cells could be created and programmed to replace ailing or absent cells for every organ in the human body.
The gold standard is human embryonic stem cells (ES cells) cultured from discarded embryos generated by in vitro fertilization, but their use has long been limited by ethical and logistical considerations. Scientists have instead turned to two other methods to create stem cells: Somatic cell nuclear transfer (SCNT), in which genetic material from an adult cell is transferred into an empty egg cell, and induced pluripotent stem cells (iPS cells), in which adult cells are reverted back to a stem cell state by artificially turning on targeted genes.
Until now, no one had directly and closely compared the stem cells acquired using these two methods. The scientists found they produced measurably different results. “The nuclear transfer ES cells are much more similar to real ES cells than the iPS cells,” said co-senior author Louise Laurent, PhD, assistant professor in the Department of Reproductive Medicine at UC San Diego. “They are more completely reprogrammed and have fewer alterations in gene expression and DNA methylation levels that are attributable to the reprogramming process itself.”
Read more here
Pictured: Scanning electron micrograph of cultured human neuron from induced pluripotent stem cell. Image courtesy of Mark Ellisman and Thomas Deerinck, National Center for Microscopy and Imaging Research, UC San Diego

New Reprogramming Method Makes Better Stem Cells

A team of researchers from the University of California, San Diego School of Medicine, Oregon Health & Science University (OHSU) and Salk Institute for Biological Studies has shown for the first time that stem cells created using different methods produce differing cells. The findings, published in the July 2, 2014 online issue of Nature, provide new insights into the basic biology of stem cells and could ultimately lead to improved stem cell therapies.

Capable of developing into any cell type, pluripotent stem cells offer great promise as the basis for emerging cell transplantation therapies that address a wide array of diseases and conditions, from diabetes and Alzheimer’s disease to cancer and spinal cord injuries. In theory, stem cells could be created and programmed to replace ailing or absent cells for every organ in the human body.

The gold standard is human embryonic stem cells (ES cells) cultured from discarded embryos generated by in vitro fertilization, but their use has long been limited by ethical and logistical considerations. Scientists have instead turned to two other methods to create stem cells: Somatic cell nuclear transfer (SCNT), in which genetic material from an adult cell is transferred into an empty egg cell, and induced pluripotent stem cells (iPS cells), in which adult cells are reverted back to a stem cell state by artificially turning on targeted genes.

Until now, no one had directly and closely compared the stem cells acquired using these two methods. The scientists found they produced measurably different results. “The nuclear transfer ES cells are much more similar to real ES cells than the iPS cells,” said co-senior author Louise Laurent, PhD, assistant professor in the Department of Reproductive Medicine at UC San Diego. “They are more completely reprogrammed and have fewer alterations in gene expression and DNA methylation levels that are attributable to the reprogramming process itself.”

Read more here

Pictured: Scanning electron micrograph of cultured human neuron from induced pluripotent stem cell. Image courtesy of Mark Ellisman and Thomas Deerinck, National Center for Microscopy and Imaging Research, UC San Diego

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