As published on 11th june 2008 in Breakthrough digest.
Solid tumor cells not killed by radiation and chemotherapy become stronger
Because of the way solid tumors adapt the body’s machinery to bring themselves more oxygen, chemotherapy and radiation may actually make these tumors stronger.
“In a sense, these therapies can make the tumor healthier,” said Mark W. Dewhirst, D.V.M., Ph.D., professor of radiation oncology at Duke University Medical Center. “Unless the treatment is very effective in killing many if not most tumor cells, you are shooting yourself in the foot.”
Dewhirst and colleagues Yiting Cao, M.D., Ph.D., of Duke Pathology, and Benjamin Moeller, M.D., Ph.D. have introduced this counter-intuitive idea at recent conferences and in a review article featured in the June issue of Nature Reviews Cancer.
Radiation and chemotherapy do kill most solid tumor cells, but in the cells that survive, the therapies drive an increase in a regulatory factor called HIF1 (hypoxia-inducible factor 1), which cells use to get the oxygen they need by increasing blood vessel growth into the tumor. Solid tumors generally have low supplies of oxygen, Dewhirst explained and HIF1 helps them get the oxygen they need.
The review article concludes that blocking HIF1 would provide a clear mechanism for killing solid-tumor cells, particularly cells that are proving resistant to radiation or chemotherapy treatments.
As a part of this work, Dewhirst’s team has been studying the phenomenon of rising and falling oxygen levels in tumors, called cycling hypoxia. Oxygen levels have been found to naturally cycle up and down in individual blood vessels as well as large tumor regions. This instability in the tumor’s oxygen levels can increase HIF-1 production and cause radiation therapy to fail, Dewhirst said.
“It is my opinion that the whole tumor grows more aggressively because of this pulsation of oxygen at low levels,” Dewhirst said. “Most people thought cycling hypoxia was caused by temporary stoppage of blood flow in single blood vessel in tumors. In fact, however, oxygen levels cycle up and down virtually everywhere in the tumor, which is caused by fluctuations in blood flow rate. It has been a challenge to convince people of this.”
Dewhirst and colleagues have made movies of oxygen transport in a tumor of a living animal that show the oxygen levels cycle up and down significantly, pulsing in waves seen as color changes in the movies. (View these movies at the Nature Reviews Cancer site: http://www.nature.com/nrc/journal/v8/n6/suppinfo/nrc2397.html )
The Duke team argues that blocking HIF1 is the consistent answer to tumor growth problems. Blocking HIF1 activity interferes with the tumor’s ability to undergo glycolysis (energy production) in low-oxygen conditions, which blocks tumor growth, the authors wrote. Exactly how to accomplish chemotherapy or radiation treatment in the safest, most effective ways, in combination with HIF1 blockade, is still open for exploration, Dewhirst said.
For example, targeting HIF1 in the early stages of tumor growth, especially in very early cancer spread, may help, Dewhirst said. “For a woman who has had a primary breast tumor removed, and who is at high risk for cancer spread, this might be a situation in which you’d target HIF1,” he explained. “Blocking HIF1 makes sense during the early stages of angiogenesis, which is the accelerated phase of blood vessel formation. In this way, you could keep the early metastasis sites inactive and prevent them from growing.”
The Duke team has completed a phase I trial with a HIF1 inhibitor. “We are actively pursuing this clinically and will be moving this study into Phase 2,” Dewhirst said. “We are interested in other applications of HIF-1 inhibition in combination with radiation and chemotherapy for different diseases.”
Tuesday, June 10, 2008
Saturday, June 7, 2008
Cord Blood Stem Cells in Bone Marrow Transplants
New Technology Enhances and Expands “Homing”and Therapeutic Potential of Cord Blood Stem Cells in Bone Marrow Transplants
A CD26 Inhibitor increases the efficiency and responsiveness of umbilical cord blood for bone marrow transplants and may improve care for blood cancer patients according to research from Rush University Medical Center being presented at the 6th Annual International Umbilical Cord Blood
Transplantation Symposium, June 6-7 in Los Angeles.
Kent W. Christopherson II, PhD, assistant professor of medicine and researcher in the Sections of Hematology and Stem Cell Transplantation at Rush, is researching a CD26 Inhibitor, a small molecule enzyme inhibitor that enhances directional homing of stem cells to the bone marrow by increasing the responsiveness of donor stem cells to a natural homing signal. Homing is the process by which the donor stem cells find their way to the bone marrow. It is the first and essential step in stem cell transplantation.
Cord blood is increasingly being used by transplant centers as an alternative source of stem cells for the treatment of blood cancers, including myeloma, lymphoma and leukemia. The cells, which are collected from the umbilical cord after the baby is delivered and separated from the cord, are most commonly used for bone marrow transplantation when a donor from a patient’s family or an unrelated donor does not produce an appropriate bone marrow match.
The current drawback to the usage of cord blood cells is that due to the limited volume and cell number, there are generally only enough cells available from a single cord blood collection for children or very small adults. Cord blood cells also usually take longer to engraft, leaving the patient at a high risk
for infection longer than donor matched transplanted marrow or peripheral blood stem cells. The goal of Christopherson’s research is to increase the transplant efficiency of umbilical cord blood and ultimately make transplant safer and available to all patients who require this treatment.
In his discussion on “Strategies to Improve Homing,” Christopherson states that results from his and other laboratories suggest “the beneficial effects of the CD26 Inhibitor usage and the potential of this technology to change hematopoietic stem cell transplantation.”
Christopherson will co-chair the session and review some of his Leukemia & Lymphoma Society funded work at the symposium in a session entitled “Basic Science and Clinical Studies Addressing Obstacles to Successful Umbilical Cord Blood Transplants (UCBT)”. He will be joined by Dr. Patrick Zweidler-McKay of the University if Texas MD Anderson Cancer Center. Zweidler-McKay will discuss his team’s work in the same session on Engraftin™, a human recombinant enzyme technology that increases the efficiency of engraftment and reduces graft failure in transplantation of cord blood derived stem cells.
Research results in animal models by Christopherson and Zweider-McKay show that both Engraftin and CD26 Inhibitor can enhance homing and rate of engraftment, which will result in reduced patient morbidity and mortality in bone marrow transplants. American Stem Cell, Inc., the developer of both technologies, plans to begin human trials in the next few months.
There are over 250,000 new cancer patients per year who require or would benefit from stem cell transplantation and as many as 20% are unable to find a blood or marrow match.
A CD26 Inhibitor increases the efficiency and responsiveness of umbilical cord blood for bone marrow transplants and may improve care for blood cancer patients according to research from Rush University Medical Center being presented at the 6th Annual International Umbilical Cord Blood
Transplantation Symposium, June 6-7 in Los Angeles.
Kent W. Christopherson II, PhD, assistant professor of medicine and researcher in the Sections of Hematology and Stem Cell Transplantation at Rush, is researching a CD26 Inhibitor, a small molecule enzyme inhibitor that enhances directional homing of stem cells to the bone marrow by increasing the responsiveness of donor stem cells to a natural homing signal. Homing is the process by which the donor stem cells find their way to the bone marrow. It is the first and essential step in stem cell transplantation.
Cord blood is increasingly being used by transplant centers as an alternative source of stem cells for the treatment of blood cancers, including myeloma, lymphoma and leukemia. The cells, which are collected from the umbilical cord after the baby is delivered and separated from the cord, are most commonly used for bone marrow transplantation when a donor from a patient’s family or an unrelated donor does not produce an appropriate bone marrow match.
The current drawback to the usage of cord blood cells is that due to the limited volume and cell number, there are generally only enough cells available from a single cord blood collection for children or very small adults. Cord blood cells also usually take longer to engraft, leaving the patient at a high risk
for infection longer than donor matched transplanted marrow or peripheral blood stem cells. The goal of Christopherson’s research is to increase the transplant efficiency of umbilical cord blood and ultimately make transplant safer and available to all patients who require this treatment.
In his discussion on “Strategies to Improve Homing,” Christopherson states that results from his and other laboratories suggest “the beneficial effects of the CD26 Inhibitor usage and the potential of this technology to change hematopoietic stem cell transplantation.”
Christopherson will co-chair the session and review some of his Leukemia & Lymphoma Society funded work at the symposium in a session entitled “Basic Science and Clinical Studies Addressing Obstacles to Successful Umbilical Cord Blood Transplants (UCBT)”. He will be joined by Dr. Patrick Zweidler-McKay of the University if Texas MD Anderson Cancer Center. Zweidler-McKay will discuss his team’s work in the same session on Engraftin™, a human recombinant enzyme technology that increases the efficiency of engraftment and reduces graft failure in transplantation of cord blood derived stem cells.
Research results in animal models by Christopherson and Zweider-McKay show that both Engraftin and CD26 Inhibitor can enhance homing and rate of engraftment, which will result in reduced patient morbidity and mortality in bone marrow transplants. American Stem Cell, Inc., the developer of both technologies, plans to begin human trials in the next few months.
There are over 250,000 new cancer patients per year who require or would benefit from stem cell transplantation and as many as 20% are unable to find a blood or marrow match.
Brain stem cells...
Brain stem cells can be awakened?
Study findings promise to help in treatment of brain diseases
Boston, MA-Scientists at Schepens Eye Research Institute have identified specific molecules in the brain that are responsible for awakening and putting to sleep brain stem cells, which, when activated, can transform into neurons (nerve cells) and repair damaged brain tissue. Their findings are published online this week in the Proceedings of the National Academy of Science (PNAS).
An earlier paper (published in the May issue of Stem Cells) by the same scientists laid the foundation for the PNAS study findings by demonstrating that neural stem cells exist in every part of the brain, but are mostly kept silent by chemical signals from support cells known as astrocytes.
³The findings from both papers should have a far-reaching impact,² says principal investigator, Dr. Dong Feng Chen, who is an associate scientist at Schepens Eye Research Institute and an assistant professor of ophthalmology at Harvard Medical School. Chen believes that tapping the brain¹s dormant, but intrinsic, ability to regenerate itself is the best hope for people suffering from brain-ravaging diseases such as Parkinson¹s or Alzheimer¹s disease or traumatic brain or spinal cord injuries.
Until these studies, which were conducted in the adult brains of mice, scientists assumed that only two parts of the brain contained neural stem cells and could turn them on to regenerate brain tissue– the subgranular zone (SGZ) of the hippocampus and the subventricular zone (SVZ). The hippocampus is responsible for learning and memory, while the SVZ is a brain structure situated throughout the walls of lateral ventricles (part of the ventricular system in the brain) and is responsible for generating neurons reponsible for smell. So scientists believed that when neurons died in other areas of the brain, they were lost forever along with their functions.
In the first study, Chen¹s team learned that stem cells existed everywhere in the brain by testing tissue from different parts of adult mice brains in cultures containing support cells (known as astrocytes) from the hippocampus, where stem cells do regenerate.
In the cultures the stem cells from other brain regions came to life and turned into neurons.
When they compared the chemical makeup of the areas known to generate new neurons in the hippocampus with other parts of the brain, the team discovered that astrocytes in the hippocampus were sending one signal to the stem cells and that those from the rest of the brain were sending a different signal to stem cells.
In the second (PNAS) study, the team went on to discover the exact nature of those different chemical signals. They learned that in the areas where stem cells were sleeping, astrocytes were producing high levels of two related molecules–ephrin-A2 and ephrin-A3. They also found that removing these molecules (with a genetic tool) activated the sleeping stem cells.
The team also found that astrocytes in the hippocampus produce not only much lower levels of ephrin-A2 and ephrin-A3, but also release a protein named sonic hedghoc that, when added in culture or injected into the brain, stimulates neural stem cells to divide and become new neurons.
³These findings identify a key pathway that controls neural stem cell growth in the adult brain and suggest that it may be possible to reactivate the dormant regenerative potential by adding sonic hedgehoc, or blocking ephrin-A2 or ephrin-A3,² says Dr. Jianwei Jiao, the first author of the two papers.
The next step for the team will be to stimulate the sleeping stem cells in animals who are models of neurodegenerative disorders, such as Parkinson’s disease, to see if the brains can repair themselves and restore their damaged functions.
Study findings promise to help in treatment of brain diseases
Boston, MA-Scientists at Schepens Eye Research Institute have identified specific molecules in the brain that are responsible for awakening and putting to sleep brain stem cells, which, when activated, can transform into neurons (nerve cells) and repair damaged brain tissue. Their findings are published online this week in the Proceedings of the National Academy of Science (PNAS).
An earlier paper (published in the May issue of Stem Cells) by the same scientists laid the foundation for the PNAS study findings by demonstrating that neural stem cells exist in every part of the brain, but are mostly kept silent by chemical signals from support cells known as astrocytes.
³The findings from both papers should have a far-reaching impact,² says principal investigator, Dr. Dong Feng Chen, who is an associate scientist at Schepens Eye Research Institute and an assistant professor of ophthalmology at Harvard Medical School. Chen believes that tapping the brain¹s dormant, but intrinsic, ability to regenerate itself is the best hope for people suffering from brain-ravaging diseases such as Parkinson¹s or Alzheimer¹s disease or traumatic brain or spinal cord injuries.
Until these studies, which were conducted in the adult brains of mice, scientists assumed that only two parts of the brain contained neural stem cells and could turn them on to regenerate brain tissue– the subgranular zone (SGZ) of the hippocampus and the subventricular zone (SVZ). The hippocampus is responsible for learning and memory, while the SVZ is a brain structure situated throughout the walls of lateral ventricles (part of the ventricular system in the brain) and is responsible for generating neurons reponsible for smell. So scientists believed that when neurons died in other areas of the brain, they were lost forever along with their functions.
In the first study, Chen¹s team learned that stem cells existed everywhere in the brain by testing tissue from different parts of adult mice brains in cultures containing support cells (known as astrocytes) from the hippocampus, where stem cells do regenerate.
In the cultures the stem cells from other brain regions came to life and turned into neurons.
When they compared the chemical makeup of the areas known to generate new neurons in the hippocampus with other parts of the brain, the team discovered that astrocytes in the hippocampus were sending one signal to the stem cells and that those from the rest of the brain were sending a different signal to stem cells.
In the second (PNAS) study, the team went on to discover the exact nature of those different chemical signals. They learned that in the areas where stem cells were sleeping, astrocytes were producing high levels of two related molecules–ephrin-A2 and ephrin-A3. They also found that removing these molecules (with a genetic tool) activated the sleeping stem cells.
The team also found that astrocytes in the hippocampus produce not only much lower levels of ephrin-A2 and ephrin-A3, but also release a protein named sonic hedghoc that, when added in culture or injected into the brain, stimulates neural stem cells to divide and become new neurons.
³These findings identify a key pathway that controls neural stem cell growth in the adult brain and suggest that it may be possible to reactivate the dormant regenerative potential by adding sonic hedgehoc, or blocking ephrin-A2 or ephrin-A3,² says Dr. Jianwei Jiao, the first author of the two papers.
The next step for the team will be to stimulate the sleeping stem cells in animals who are models of neurodegenerative disorders, such as Parkinson’s disease, to see if the brains can repair themselves and restore their damaged functions.
Wednesday, June 4, 2008
Autoimmune Disease Treatment
A New Approach to Treating Autoimmune Disease
In autoimmune diseases, the immune system turns against the body’s own tissues and organs, wreaking havoc and destruction for no apparent reason. Partly because the origins of these diseases are so obscure, no effective treatment exists, and the suffering they inflict is enormous. Now Weizmann Institute scientists have developed a method that in the future may make it possible to treat autoimmune diseases effectively without necessarily knowing their exact cause. Their approach is equivalent to sending a police force to suppress a riot without seeking out the individuals who instigated the unrest.
In healthy people, a small but crucial group of immune cells called regulatory T cells, or T-regs, keeps autoimmunity in check, but in people with inflammatory bowel disease (IBD), one of the most common autoimmune disorders, too few of these cells appear in the diseased intestine, and the ones that do fail to function properly. The new Weizmann Institute approach consists of delivering highly selective, genetically engineered functioning T-regs to the intestine. The study was conducted by Dr. Eran Elinav, a physician from Tel Aviv Sourasky Medical Center’s gastroenterology institute who is working toward his Ph.D. at the Weizmann Institute, and lab assistant Tova Waks, in the laboratory of Prof. Zelig Eshhar of the Immunology Department.
Relying on Eshhar’s earlier work in which he equipped a different type of T cell to zero in on cancerous tumors, the team genetically engineered T-regs, outfitting these cells with a modular receptor consisting of three units. One of these units directed the cells to the intestine while the other two made sure they became duly activated. As reported in the journal Gastroenterology, the approach proved effective in laboratory mice with a disease that simulates human IBD: Most of the mice treated with the genetically-engineered T-regs developed only mild inflammation or no inflammation at all.
The cells produced what the scientists called a ‘bystander’ effect: They were directed to the diseased tissue using neighboring, or ‘bystander’ markers that identified the area as a site of inflammation, and suppressed the inflammatory cells in the vicinity by secreting soluble suppressive substances.
The scientists are currently experimenting with human T-regs for curing ulcerative colitis and believe that in addition to IBD, their ‘bystander’ approach could work in other autoimmune disorders, even if their causes remain unknown. They also think the method could be valuable in suppressing unwanted inflammation in diseases unrelated to autoimmunity, as well as in preventing graft rejection and certain complications in bone marrow and organ transplantation, in which inflammation is believed to play a major role.
Prof. Zelig Eshhar’s research is supported by the M.D. Moross Institute for Cancer Research; the Phyllis and Joseph Gurwin Fund for Scientific Advancement; and the Friends of Assaf Harofeh Medical Center. Prof. Eshhar is the incumbent of the Marshall and Renette Ezralow Professorial Chair of Chemical and Cellular Immunology.
The Weizmann Institute of Science in Rehovot, Israel, is one of the world’s top-ranking multidisciplinary research institutions. Noted for its wide-ranging exploration of the natural and exact sciences, the Institute is home to 2,600 scientists, students, technicians and supporting staff. Institute research efforts include the search for new ways of fighting disease and hunger, examining leading questions in mathematics and computer science, probing the physics of matter and the universe, creating novel materials and developing new strategies for protecting the environment.
In autoimmune diseases, the immune system turns against the body’s own tissues and organs, wreaking havoc and destruction for no apparent reason. Partly because the origins of these diseases are so obscure, no effective treatment exists, and the suffering they inflict is enormous. Now Weizmann Institute scientists have developed a method that in the future may make it possible to treat autoimmune diseases effectively without necessarily knowing their exact cause. Their approach is equivalent to sending a police force to suppress a riot without seeking out the individuals who instigated the unrest.
In healthy people, a small but crucial group of immune cells called regulatory T cells, or T-regs, keeps autoimmunity in check, but in people with inflammatory bowel disease (IBD), one of the most common autoimmune disorders, too few of these cells appear in the diseased intestine, and the ones that do fail to function properly. The new Weizmann Institute approach consists of delivering highly selective, genetically engineered functioning T-regs to the intestine. The study was conducted by Dr. Eran Elinav, a physician from Tel Aviv Sourasky Medical Center’s gastroenterology institute who is working toward his Ph.D. at the Weizmann Institute, and lab assistant Tova Waks, in the laboratory of Prof. Zelig Eshhar of the Immunology Department.
Relying on Eshhar’s earlier work in which he equipped a different type of T cell to zero in on cancerous tumors, the team genetically engineered T-regs, outfitting these cells with a modular receptor consisting of three units. One of these units directed the cells to the intestine while the other two made sure they became duly activated. As reported in the journal Gastroenterology, the approach proved effective in laboratory mice with a disease that simulates human IBD: Most of the mice treated with the genetically-engineered T-regs developed only mild inflammation or no inflammation at all.
The cells produced what the scientists called a ‘bystander’ effect: They were directed to the diseased tissue using neighboring, or ‘bystander’ markers that identified the area as a site of inflammation, and suppressed the inflammatory cells in the vicinity by secreting soluble suppressive substances.
The scientists are currently experimenting with human T-regs for curing ulcerative colitis and believe that in addition to IBD, their ‘bystander’ approach could work in other autoimmune disorders, even if their causes remain unknown. They also think the method could be valuable in suppressing unwanted inflammation in diseases unrelated to autoimmunity, as well as in preventing graft rejection and certain complications in bone marrow and organ transplantation, in which inflammation is believed to play a major role.
Prof. Zelig Eshhar’s research is supported by the M.D. Moross Institute for Cancer Research; the Phyllis and Joseph Gurwin Fund for Scientific Advancement; and the Friends of Assaf Harofeh Medical Center. Prof. Eshhar is the incumbent of the Marshall and Renette Ezralow Professorial Chair of Chemical and Cellular Immunology.
The Weizmann Institute of Science in Rehovot, Israel, is one of the world’s top-ranking multidisciplinary research institutions. Noted for its wide-ranging exploration of the natural and exact sciences, the Institute is home to 2,600 scientists, students, technicians and supporting staff. Institute research efforts include the search for new ways of fighting disease and hunger, examining leading questions in mathematics and computer science, probing the physics of matter and the universe, creating novel materials and developing new strategies for protecting the environment.
CFC propelled inhalers....
FDA Advises Patients to Switch to HFA-Propelled Albuterol Inhalers Now CFC-propelled inhalers no longer available as of Dec. 31, 2008
The U.S. Food and Drug Administration today issued a public health advisory to alert patients, caregivers and health care professionals to switch to hydrofluoroalkane (HFA)-propelled albuterol inhalers because chlorofluorocarbon (CFC)-propelled inhalers will not be available in the United States after Dec. 31, 2008.
CFC-propelled albuterol inhalers are being phased out because they are harmful to the environment by contributing to depletion of the ozone layer above the Earth's surface.
Three HFA-propelled albuterol inhalers have been approved by the FDA: Proair HFA Inhalation Aerosol, Proventil HFA Inhalation Aerosol, and Ventolin HFA Inhalation Aerosol. In addition, an HFA-propelled inhaler containing levalbuterol, a medicine similar to albuterol, is available as Xopenex HFA Inhalation Aerosol.
"Concern about the environment stimulated the need to phase out CFCs," said Janet Woodcock, M.D., director of the FDA's Center for Drug Evaluation and Research. "The FDA wants to emphasize that HFA-propelled albuterol inhalers are safe and effective replacements for CFC-propelled albuterol inhalers."
Albuterol inhalers are used to treat bronchospasm (wheezing) in patients with asthma and chronic obstructive pulmonary disease (COPD), which includes chronic bronchitis and emphysema. Patients use albuterol inhalers to deliver medicine directly into the lungs.
The FDA is urging patients to talk with their health care professionals now about switching to HFA-propelled albuterol inhalers. These products are safe and effective replacements for CFC-propelled albuterol inhalers.
Manufacturers have been increasing production of HFA albuterol inhalers, so an adequate supply is available now.
HFA-propelled albuterol inhalers may taste and feel different than the CFC-propelled albuterol inhalers. The spray of an HFA-propelled albuterol inhaler may feel softer than that of a CFC-propelled albuterol inhaler. Patients must also prime and clean HFA-propelled albuterol inhalers. Doing so prevents buildup of the drug in the inhalation device, and buildup can block the medicine from reaching the lungs. Each HFA-propelled albuterol inhaler has different priming, cleaning, and drying instructions, and patients should read and understand the instructions first before using the inhaler.
The phaseout of CFC-propelled inhalers is the result of the Clean Air Act and an international environmental treaty, the Montreal Protocol on Substances that Deplete the Ozone Layer. Under this treaty, the United States has agreed to phase out production and importation of ozone depleting substances including CFCs. No CFC-propelled albuterol inhalers may be produced, marketed or sold in the United States after Dec. 31, 2008.
The U.S. Food and Drug Administration today issued a public health advisory to alert patients, caregivers and health care professionals to switch to hydrofluoroalkane (HFA)-propelled albuterol inhalers because chlorofluorocarbon (CFC)-propelled inhalers will not be available in the United States after Dec. 31, 2008.
CFC-propelled albuterol inhalers are being phased out because they are harmful to the environment by contributing to depletion of the ozone layer above the Earth's surface.
Three HFA-propelled albuterol inhalers have been approved by the FDA: Proair HFA Inhalation Aerosol, Proventil HFA Inhalation Aerosol, and Ventolin HFA Inhalation Aerosol. In addition, an HFA-propelled inhaler containing levalbuterol, a medicine similar to albuterol, is available as Xopenex HFA Inhalation Aerosol.
"Concern about the environment stimulated the need to phase out CFCs," said Janet Woodcock, M.D., director of the FDA's Center for Drug Evaluation and Research. "The FDA wants to emphasize that HFA-propelled albuterol inhalers are safe and effective replacements for CFC-propelled albuterol inhalers."
Albuterol inhalers are used to treat bronchospasm (wheezing) in patients with asthma and chronic obstructive pulmonary disease (COPD), which includes chronic bronchitis and emphysema. Patients use albuterol inhalers to deliver medicine directly into the lungs.
The FDA is urging patients to talk with their health care professionals now about switching to HFA-propelled albuterol inhalers. These products are safe and effective replacements for CFC-propelled albuterol inhalers.
Manufacturers have been increasing production of HFA albuterol inhalers, so an adequate supply is available now.
HFA-propelled albuterol inhalers may taste and feel different than the CFC-propelled albuterol inhalers. The spray of an HFA-propelled albuterol inhaler may feel softer than that of a CFC-propelled albuterol inhaler. Patients must also prime and clean HFA-propelled albuterol inhalers. Doing so prevents buildup of the drug in the inhalation device, and buildup can block the medicine from reaching the lungs. Each HFA-propelled albuterol inhaler has different priming, cleaning, and drying instructions, and patients should read and understand the instructions first before using the inhaler.
The phaseout of CFC-propelled inhalers is the result of the Clean Air Act and an international environmental treaty, the Montreal Protocol on Substances that Deplete the Ozone Layer. Under this treaty, the United States has agreed to phase out production and importation of ozone depleting substances including CFCs. No CFC-propelled albuterol inhalers may be produced, marketed or sold in the United States after Dec. 31, 2008.
Rapid Wound Healing....
Rapid wound healing
A new type of wound dressing made of silica gel fibers will soon help to heal difficult wounds caused by burns or diabetes. The dressing forms a supporting matrix for newly growing skin cells and is fully absorbed by the body during the healing process.
In Germany alone, about three million – mostly elderly – patients suffer from poorly healing large-area wounds caused by complaints such as diabetes, burns or bedsores. The wounds can be treated with conventional collagen dressings or polylactic acid dressings, but the success rate is not as good as it should be. A new type of dressing made of silica gel fibers, developed by scientists at the Fraunhofer Institute for Silicate Research ISC in Würzburg, shall solve the problem. This novel dressing has many advantages: it is shape-stable, pH-neutral and 100 percent bioresorbable. Once applied it remains in the body, where it gradually degrades without leaving any residues. What’s more, the fibre fleece provides the healthy cells around the edges of the wound with the structure they additionally need for a proper supply of growth-supporting nutrients. To prevent any infection, treatment of the wound must be absolutely sterile. “As only the outer bandage needs to be changed, the risk of contaminating the wound is low,” explains Dr. Jörn Probst of the ISC. And thanks to the supporting
matrix for the cells, the chances of a scar-free natural closure of the wound are very good.
The fibers are produced by means of wet-chemical material synthesis, a sol-gel process in which a transparent, honey-like gel is produced from tetraethoxysilane (TEOS), ethanol and water in a multi-stage, acidically catalyzed synthesis process. The gel is processed in a spinning tower: “We press it through fine nozzles at constant temperatures and humidity levels,” explains Walther Glaubitt, the inventor of the silica gel fibers. “This produces fine endless threads which are collected on a traversing table and spun in a specific pattern to produce a roughly A4-sized multi-layer textile web.” The dressings are then cut, packed and sterilized. Dr. Jörn Probst and Dipl.-Ing. Walther Glaubitt will receive the Joseph von Fraunhofer Prize 2008 for developing the biocompatible dressing.
A partner to support the development and market the dressing has already been found: Bayer Innovation GmbH BIG, a wholly owned subsidiary of Bayer AG. “We anticipate that hospitals will start to use the silica gel wound dressing in 2011,” states Iwer Baecker, project manager at Bayer Innovation GmbH. And that is by no means the end of the story. The scientists plan to integrate active substances such as antibiotics or painkillers in the dressing to improve and accelerate the healing process.
A new type of wound dressing made of silica gel fibers will soon help to heal difficult wounds caused by burns or diabetes. The dressing forms a supporting matrix for newly growing skin cells and is fully absorbed by the body during the healing process.
In Germany alone, about three million – mostly elderly – patients suffer from poorly healing large-area wounds caused by complaints such as diabetes, burns or bedsores. The wounds can be treated with conventional collagen dressings or polylactic acid dressings, but the success rate is not as good as it should be. A new type of dressing made of silica gel fibers, developed by scientists at the Fraunhofer Institute for Silicate Research ISC in Würzburg, shall solve the problem. This novel dressing has many advantages: it is shape-stable, pH-neutral and 100 percent bioresorbable. Once applied it remains in the body, where it gradually degrades without leaving any residues. What’s more, the fibre fleece provides the healthy cells around the edges of the wound with the structure they additionally need for a proper supply of growth-supporting nutrients. To prevent any infection, treatment of the wound must be absolutely sterile. “As only the outer bandage needs to be changed, the risk of contaminating the wound is low,” explains Dr. Jörn Probst of the ISC. And thanks to the supporting
matrix for the cells, the chances of a scar-free natural closure of the wound are very good.
The fibers are produced by means of wet-chemical material synthesis, a sol-gel process in which a transparent, honey-like gel is produced from tetraethoxysilane (TEOS), ethanol and water in a multi-stage, acidically catalyzed synthesis process. The gel is processed in a spinning tower: “We press it through fine nozzles at constant temperatures and humidity levels,” explains Walther Glaubitt, the inventor of the silica gel fibers. “This produces fine endless threads which are collected on a traversing table and spun in a specific pattern to produce a roughly A4-sized multi-layer textile web.” The dressings are then cut, packed and sterilized. Dr. Jörn Probst and Dipl.-Ing. Walther Glaubitt will receive the Joseph von Fraunhofer Prize 2008 for developing the biocompatible dressing.
A partner to support the development and market the dressing has already been found: Bayer Innovation GmbH BIG, a wholly owned subsidiary of Bayer AG. “We anticipate that hospitals will start to use the silica gel wound dressing in 2011,” states Iwer Baecker, project manager at Bayer Innovation GmbH. And that is by no means the end of the story. The scientists plan to integrate active substances such as antibiotics or painkillers in the dressing to improve and accelerate the healing process.
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