We are all painfully aware that falls are not uncommon in hospitalized patients, but I was shocked and appalled to learn that there are approximately 11,000 falls that are ultimately fatal in U.S. hospitals each year, according to the Joint Commission Center for Transforming Healthcare.

Fortunately, there appear to be some very viable solutions at hand.

Hospitals that use the center’s new measuring systems and solution have been able to slash the number of patients who fall by 35%, as well cutting the percentage of patients injured when they fall by 62%. Extrapolating these results to an average 200-bed hospital, an estimated $1 million could be saved each year through fall prevention efforts.

©ERproductions Ltd/thinkstockphotos.com

Hospitals participating in this study ranged from small community-based hospitals with fewer than 200 beds to large medical centers with more than 1,700 beds. All used a data-driven, Lean Six Sigma–inspired "Robust Process Improvement" methodology to determine the causes of falls and create solutions to prevent them. One solution was simply providing hourly rounding which included proactive toileting. When you think about it, this makes perfect sense. Patients with an immediate need may not be able to hold it until it is "their turn" for the nurse to assist them. In their haste to avoid soiling their clothes, a mechanical fall is very understandable, especially if they are impaired due to weakness or medication.

Other solutions included teaching patients how to actively participate in their own safety, engaging patients and family members in their fall safety program, using a validated fall risk assessment tool, and increasing awareness and participation among staff so that patients did not walk alone.

Most of us have received that dreaded call from the nurse about a patient who was injured from a fall. I once had a patient who slipped and fell, breaking a hip while in the hospital for a relatively minor issue. If she had been more stable on her feet, she probably could have caught herself prior to hitting the hard floor. Had a close relative not witnessed the incident, it would have been very difficult (and embarrassing) to explain to the family why their loved one experienced such a traumatic event while in a seemingly protected environment. Her son was very understanding, though the event was very disconcerting all the same.

Based on their staffing, resources, and creativity, different hospitals may develop different innovative solutions to prevent falls. There is room for a wide variety of options. Yes, early ambulation is crucial to help prevent unnecessary complications, such as pneumonia and blood clots, but we should be mindful of the individual patient’s circumstances. A simple order requesting the nurse to ambulate a patient in the room or down the hall two or three times a day may be adequate for some, while in other cases a formal physical therapy consultation may clearly be in order. If there are any concerns over the patient’s ability to ambulate safely and I am not sure if a physical therapy consult is really needed, I sometimes call the nurse into the room and the two of us walk with the patient. That way, I can get an immediate sense of the likelihood of falls, the need for dedicated strengthening exercises, and, on occasion, the impact that medications are having on gait. And for those difficult, unmotivated patients, family members can frequently provide invaluable encouragement, as well as the emotional, and sometimes physical safety net many patients desire.

With safety interventions and highly engaged care teams in place, even steady patients never walk truly alone.

Dr. Hester is a hospitalist with Baltimore-Washington Medical Center who has a passion for empowering patients to partner in their health care. She is the creator of the Patient Whiz, a patient-engagement app for iOS. Reach her at [email protected]

We are all painfully aware that falls are not uncommon in hospitalized patients, but I was shocked and appalled to learn that there are approximately 11,000 falls that are ultimately fatal in U.S. hospitals each year, according to the Joint Commission Center for Transforming Healthcare.

Fortunately, there appear to be some very viable solutions at hand.

Hospitals that use the center’s new measuring systems and solution have been able to slash the number of patients who fall by 35%, as well cutting the percentage of patients injured when they fall by 62%. Extrapolating these results to an average 200-bed hospital, an estimated $1 million could be saved each year through fall prevention efforts.

©ERproductions Ltd/thinkstockphotos.com

Hospitals participating in this study ranged from small community-based hospitals with fewer than 200 beds to large medical centers with more than 1,700 beds. All used a data-driven, Lean Six Sigma–inspired "Robust Process Improvement" methodology to determine the causes of falls and create solutions to prevent them. One solution was simply providing hourly rounding which included proactive toileting. When you think about it, this makes perfect sense. Patients with an immediate need may not be able to hold it until it is "their turn" for the nurse to assist them. In their haste to avoid soiling their clothes, a mechanical fall is very understandable, especially if they are impaired due to weakness or medication.

Other solutions included teaching patients how to actively participate in their own safety, engaging patients and family members in their fall safety program, using a validated fall risk assessment tool, and increasing awareness and participation among staff so that patients did not walk alone.

Most of us have received that dreaded call from the nurse about a patient who was injured from a fall. I once had a patient who slipped and fell, breaking a hip while in the hospital for a relatively minor issue. If she had been more stable on her feet, she probably could have caught herself prior to hitting the hard floor. Had a close relative not witnessed the incident, it would have been very difficult (and embarrassing) to explain to the family why their loved one experienced such a traumatic event while in a seemingly protected environment. Her son was very understanding, though the event was very disconcerting all the same.

Based on their staffing, resources, and creativity, different hospitals may develop different innovative solutions to prevent falls. There is room for a wide variety of options. Yes, early ambulation is crucial to help prevent unnecessary complications, such as pneumonia and blood clots, but we should be mindful of the individual patient’s circumstances. A simple order requesting the nurse to ambulate a patient in the room or down the hall two or three times a day may be adequate for some, while in other cases a formal physical therapy consultation may clearly be in order. If there are any concerns over the patient’s ability to ambulate safely and I am not sure if a physical therapy consult is really needed, I sometimes call the nurse into the room and the two of us walk with the patient. That way, I can get an immediate sense of the likelihood of falls, the need for dedicated strengthening exercises, and, on occasion, the impact that medications are having on gait. And for those difficult, unmotivated patients, family members can frequently provide invaluable encouragement, as well as the emotional, and sometimes physical safety net many patients desire.

With safety interventions and highly engaged care teams in place, even steady patients never walk truly alone.

Dr. Hester is a hospitalist with Baltimore-Washington Medical Center who has a passion for empowering patients to partner in their health care. She is the creator of the Patient Whiz, a patient-engagement app for iOS. Reach her at [email protected]

We are all painfully aware that falls are not uncommon in hospitalized patients, but I was shocked and appalled to learn that there are approximately 11,000 falls that are ultimately fatal in U.S. hospitals each year, according to the Joint Commission Center for Transforming Healthcare.

Fortunately, there appear to be some very viable solutions at hand.

Hospitals that use the center’s new measuring systems and solution have been able to slash the number of patients who fall by 35%, as well cutting the percentage of patients injured when they fall by 62%. Extrapolating these results to an average 200-bed hospital, an estimated $1 million could be saved each year through fall prevention efforts.

©ERproductions Ltd/thinkstockphotos.com

Hospitals participating in this study ranged from small community-based hospitals with fewer than 200 beds to large medical centers with more than 1,700 beds. All used a data-driven, Lean Six Sigma–inspired "Robust Process Improvement" methodology to determine the causes of falls and create solutions to prevent them. One solution was simply providing hourly rounding which included proactive toileting. When you think about it, this makes perfect sense. Patients with an immediate need may not be able to hold it until it is "their turn" for the nurse to assist them. In their haste to avoid soiling their clothes, a mechanical fall is very understandable, especially if they are impaired due to weakness or medication.

Other solutions included teaching patients how to actively participate in their own safety, engaging patients and family members in their fall safety program, using a validated fall risk assessment tool, and increasing awareness and participation among staff so that patients did not walk alone.

Most of us have received that dreaded call from the nurse about a patient who was injured from a fall. I once had a patient who slipped and fell, breaking a hip while in the hospital for a relatively minor issue. If she had been more stable on her feet, she probably could have caught herself prior to hitting the hard floor. Had a close relative not witnessed the incident, it would have been very difficult (and embarrassing) to explain to the family why their loved one experienced such a traumatic event while in a seemingly protected environment. Her son was very understanding, though the event was very disconcerting all the same.

Based on their staffing, resources, and creativity, different hospitals may develop different innovative solutions to prevent falls. There is room for a wide variety of options. Yes, early ambulation is crucial to help prevent unnecessary complications, such as pneumonia and blood clots, but we should be mindful of the individual patient’s circumstances. A simple order requesting the nurse to ambulate a patient in the room or down the hall two or three times a day may be adequate for some, while in other cases a formal physical therapy consultation may clearly be in order. If there are any concerns over the patient’s ability to ambulate safely and I am not sure if a physical therapy consult is really needed, I sometimes call the nurse into the room and the two of us walk with the patient. That way, I can get an immediate sense of the likelihood of falls, the need for dedicated strengthening exercises, and, on occasion, the impact that medications are having on gait. And for those difficult, unmotivated patients, family members can frequently provide invaluable encouragement, as well as the emotional, and sometimes physical safety net many patients desire.

With safety interventions and highly engaged care teams in place, even steady patients never walk truly alone.

Dr. Hester is a hospitalist with Baltimore-Washington Medical Center who has a passion for empowering patients to partner in their health care. She is the creator of the Patient Whiz, a patient-engagement app for iOS. Reach her at [email protected]

Acute myeloid leukemia cells

Chromatin conformation can guide the classification of leukemia, according to research published in Genome Biology.

Investigators mapped the conformation of the homeobox A (HOXA) gene cluster—11 genes encoding proteins that are highly relevant to many cancers—in a panel of leukemia cell lines.

And the team found they could use this information to distinguish subtypes of leukemia from one another.

“Previous studies have shown that looking at gene expression—the specific proteins produced by the genes—is a good predictor of whether patients have leukemia,” said study author Mathieu Blanchette, PhD, of McGill University in Montréal, Québec, Canada.

“We found that different types of leukemia cells also have a distinctive chromatin interaction—how the chromatin that makes up the genome is folded.”

The investigators used 5C chromosome conformation capture technology to analyze the HOXA gene cluster and then used the data to train and test a support vector machine classifier called 3D-SP.

They found 3D-SP could distinguish leukemias expressing MLL-fusion proteins from those expressing wild-type MLL. It could also classify leukemia subtypes according to MLL fusion partner.

The team noted that it is not clear whether the genome shape plays a role in causing leukemia or whether the leukemia causes the genome to change shape. And additional studies are needed to determine whether genome shape is as useful for classifying other types of cancer.

“Our study validates a new research avenue: the application of 3D genomics for developing medical diagnostics or treatments that could be explored for diseases where current technologies, including gene expression data, have failed to improve patient care,” said Josée Dostie, PhD, also of McGill University.

“While the use of 3D genomics in the clinic is still remote when considering the technical challenges required for translating the information to the bedside, we discovered a new approach for classifying human disease that must be explored further, if only for what it can reveal about how the human genome works.”

Acute myeloid leukemia cells

Chromatin conformation can guide the classification of leukemia, according to research published in Genome Biology.

Investigators mapped the conformation of the homeobox A (HOXA) gene cluster—11 genes encoding proteins that are highly relevant to many cancers—in a panel of leukemia cell lines.

And the team found they could use this information to distinguish subtypes of leukemia from one another.

“Previous studies have shown that looking at gene expression—the specific proteins produced by the genes—is a good predictor of whether patients have leukemia,” said study author Mathieu Blanchette, PhD, of McGill University in Montréal, Québec, Canada.

“We found that different types of leukemia cells also have a distinctive chromatin interaction—how the chromatin that makes up the genome is folded.”

The investigators used 5C chromosome conformation capture technology to analyze the HOXA gene cluster and then used the data to train and test a support vector machine classifier called 3D-SP.

They found 3D-SP could distinguish leukemias expressing MLL-fusion proteins from those expressing wild-type MLL. It could also classify leukemia subtypes according to MLL fusion partner.

The team noted that it is not clear whether the genome shape plays a role in causing leukemia or whether the leukemia causes the genome to change shape. And additional studies are needed to determine whether genome shape is as useful for classifying other types of cancer.

“Our study validates a new research avenue: the application of 3D genomics for developing medical diagnostics or treatments that could be explored for diseases where current technologies, including gene expression data, have failed to improve patient care,” said Josée Dostie, PhD, also of McGill University.

“While the use of 3D genomics in the clinic is still remote when considering the technical challenges required for translating the information to the bedside, we discovered a new approach for classifying human disease that must be explored further, if only for what it can reveal about how the human genome works.”

Acute myeloid leukemia cells

Chromatin conformation can guide the classification of leukemia, according to research published in Genome Biology.

Investigators mapped the conformation of the homeobox A (HOXA) gene cluster—11 genes encoding proteins that are highly relevant to many cancers—in a panel of leukemia cell lines.

And the team found they could use this information to distinguish subtypes of leukemia from one another.

“Previous studies have shown that looking at gene expression—the specific proteins produced by the genes—is a good predictor of whether patients have leukemia,” said study author Mathieu Blanchette, PhD, of McGill University in Montréal, Québec, Canada.

“We found that different types of leukemia cells also have a distinctive chromatin interaction—how the chromatin that makes up the genome is folded.”

The investigators used 5C chromosome conformation capture technology to analyze the HOXA gene cluster and then used the data to train and test a support vector machine classifier called 3D-SP.

They found 3D-SP could distinguish leukemias expressing MLL-fusion proteins from those expressing wild-type MLL. It could also classify leukemia subtypes according to MLL fusion partner.

The team noted that it is not clear whether the genome shape plays a role in causing leukemia or whether the leukemia causes the genome to change shape. And additional studies are needed to determine whether genome shape is as useful for classifying other types of cancer.

“Our study validates a new research avenue: the application of 3D genomics for developing medical diagnostics or treatments that could be explored for diseases where current technologies, including gene expression data, have failed to improve patient care,” said Josée Dostie, PhD, also of McGill University.

“While the use of 3D genomics in the clinic is still remote when considering the technical challenges required for translating the information to the bedside, we discovered a new approach for classifying human disease that must be explored further, if only for what it can reveal about how the human genome works.”

Thrombus

Credit: Kevin MacKenzie

The US Food and Drug Administration (FDA) has issued a Complete Response Letter to The Medicines Company regarding its new drug application for the antiplatelet agent cangrelor.

The company applied for approval of cangrelor to treat patients undergoing percutaneous coronary intervention (PCI) and those who require bridging from oral antiplatelet therapy to surgery.

The new drug application filing was based on the results of a development program that included 4 randomized trials.

These trials—BRIDGE, CHAMPION PHOENIX, CHAMPION PLATFORM, and CHAMPION PCI—included 25,567 patients with coronary artery disease.

In the Complete Response Letter, the FDA said it cannot approve cangrelor for the PCI indication without additional information.

The agency suggested The Medicines Company conduct a series of clinical data analyses of the CHAMPION PHOENIX study, review certain processes regarding data management, and provide bioequivalence information on the clopidogrel clinical supplies for the CHAMPION trials.

For the bridge indication, the FDA said a prospective, adequate, and well-controlled trial, in which outcomes such as bleeding are studied, is needed. Such a trial could provide the clinical data necessary to assess the benefit-risk relationship of cangrelor in this indication.

The FDA provided additional comments for the company to address, which could affect product labeling, but the company did not disclose them.

“We are grateful for the agency’s review, comments, and suggestions,” said Clive Meanwell, Chairman and Chief Executive Officer of The Medicines Company. “The next steps of review will focus on additional analyses in response to the FDA.”

Cangrelor is an investigational agent not approved for commercial use in any market. The product is a bioavailable, quickly reversible, intravenous antiplatelet agent. It is in development to prevent platelet activation and aggregation that leads to thrombosis in the acute care setting.

Thrombus

Credit: Kevin MacKenzie

The US Food and Drug Administration (FDA) has issued a Complete Response Letter to The Medicines Company regarding its new drug application for the antiplatelet agent cangrelor.

The company applied for approval of cangrelor to treat patients undergoing percutaneous coronary intervention (PCI) and those who require bridging from oral antiplatelet therapy to surgery.

The new drug application filing was based on the results of a development program that included 4 randomized trials.

These trials—BRIDGE, CHAMPION PHOENIX, CHAMPION PLATFORM, and CHAMPION PCI—included 25,567 patients with coronary artery disease.

In the Complete Response Letter, the FDA said it cannot approve cangrelor for the PCI indication without additional information.

The agency suggested The Medicines Company conduct a series of clinical data analyses of the CHAMPION PHOENIX study, review certain processes regarding data management, and provide bioequivalence information on the clopidogrel clinical supplies for the CHAMPION trials.

For the bridge indication, the FDA said a prospective, adequate, and well-controlled trial, in which outcomes such as bleeding are studied, is needed. Such a trial could provide the clinical data necessary to assess the benefit-risk relationship of cangrelor in this indication.

The FDA provided additional comments for the company to address, which could affect product labeling, but the company did not disclose them.

“We are grateful for the agency’s review, comments, and suggestions,” said Clive Meanwell, Chairman and Chief Executive Officer of The Medicines Company. “The next steps of review will focus on additional analyses in response to the FDA.”

Cangrelor is an investigational agent not approved for commercial use in any market. The product is a bioavailable, quickly reversible, intravenous antiplatelet agent. It is in development to prevent platelet activation and aggregation that leads to thrombosis in the acute care setting.

Thrombus

Credit: Kevin MacKenzie

The US Food and Drug Administration (FDA) has issued a Complete Response Letter to The Medicines Company regarding its new drug application for the antiplatelet agent cangrelor.

The company applied for approval of cangrelor to treat patients undergoing percutaneous coronary intervention (PCI) and those who require bridging from oral antiplatelet therapy to surgery.

The new drug application filing was based on the results of a development program that included 4 randomized trials.

These trials—BRIDGE, CHAMPION PHOENIX, CHAMPION PLATFORM, and CHAMPION PCI—included 25,567 patients with coronary artery disease.

In the Complete Response Letter, the FDA said it cannot approve cangrelor for the PCI indication without additional information.

The agency suggested The Medicines Company conduct a series of clinical data analyses of the CHAMPION PHOENIX study, review certain processes regarding data management, and provide bioequivalence information on the clopidogrel clinical supplies for the CHAMPION trials.

For the bridge indication, the FDA said a prospective, adequate, and well-controlled trial, in which outcomes such as bleeding are studied, is needed. Such a trial could provide the clinical data necessary to assess the benefit-risk relationship of cangrelor in this indication.

The FDA provided additional comments for the company to address, which could affect product labeling, but the company did not disclose them.

“We are grateful for the agency’s review, comments, and suggestions,” said Clive Meanwell, Chairman and Chief Executive Officer of The Medicines Company. “The next steps of review will focus on additional analyses in response to the FDA.”

Cangrelor is an investigational agent not approved for commercial use in any market. The product is a bioavailable, quickly reversible, intravenous antiplatelet agent. It is in development to prevent platelet activation and aggregation that leads to thrombosis in the acute care setting.

DNA repair

Credit: Tom Ellenberger

Understanding the interaction between 2 genes may be the key to better treatment of Fanconi anemia, according to a paper published in Cell Cycle.

Researchers investigated the relationship between FANCD2 and DNA2, 2 genes known to play roles in DNA repair.

A defective version of FANCD2 can result in Fanconi anemia. And although DNA2 has not been associated with a Fanconi anemia family

yet, genetic studies have implicated DNA2 in the Fanconi anemia DNA repair pathway.

With the current study, the researchers found that deleting either FANCD2 or DNA2 alone makes cells susceptible to DNA damage. But the deletion of both genes enables DNA repair.

“A key implication of this finding is the potential to manipulate DNA2 to improve the survival of FANCD2-deficient cells, and hopefully, by extension, the survival of [Fanconi anemia] patients,” said study author Kenneth Karanja, PhD, a former postdoctoral scholar at the California Institute of Technology in Pasadena.

To uncover the relationship between the genes, Dr Karanja and his colleagues applied DNA-damaging substances—formaldehyde and cisplatin—to 3 types of cells: those lacking FANCD2, those lacking DNA2, and cells lacking both genes.

The groups of cells in which only 1 of the 2 genes had been deleted quickly succumbed to the substance-induced DNA damage. However, the cells lacking both FANCD2 and DNA2 were able to repair the DNA damage and survive.

So the researchers concluded that depletion of DNA2 in FANCD2-deficient cells reverses the cells’ sensitivity to DNA-damaging substances. And this finding may have implications for Fanconi anemia treatment.

“DNA2 is a well-studied gene, and this recent discovery could potentially become the basis for ameliorating the symptoms of this incurable disorder,” said study author Judith Campbell, PhD, of the California Institute of Technology.

“Since much is known about the mechanism of action of DNA2, it is an attractive target for future drug treatments—like small-molecule inhibitors that could reduce [a Fanconi anemia] patient’s cancer predisposition—as well as a possible gene therapy for aiding a patient’s blood cell development.”

DNA repair

Credit: Tom Ellenberger

Understanding the interaction between 2 genes may be the key to better treatment of Fanconi anemia, according to a paper published in Cell Cycle.

Researchers investigated the relationship between FANCD2 and DNA2, 2 genes known to play roles in DNA repair.

A defective version of FANCD2 can result in Fanconi anemia. And although DNA2 has not been associated with a Fanconi anemia family

yet, genetic studies have implicated DNA2 in the Fanconi anemia DNA repair pathway.

With the current study, the researchers found that deleting either FANCD2 or DNA2 alone makes cells susceptible to DNA damage. But the deletion of both genes enables DNA repair.

“A key implication of this finding is the potential to manipulate DNA2 to improve the survival of FANCD2-deficient cells, and hopefully, by extension, the survival of [Fanconi anemia] patients,” said study author Kenneth Karanja, PhD, a former postdoctoral scholar at the California Institute of Technology in Pasadena.

To uncover the relationship between the genes, Dr Karanja and his colleagues applied DNA-damaging substances—formaldehyde and cisplatin—to 3 types of cells: those lacking FANCD2, those lacking DNA2, and cells lacking both genes.

The groups of cells in which only 1 of the 2 genes had been deleted quickly succumbed to the substance-induced DNA damage. However, the cells lacking both FANCD2 and DNA2 were able to repair the DNA damage and survive.

So the researchers concluded that depletion of DNA2 in FANCD2-deficient cells reverses the cells’ sensitivity to DNA-damaging substances. And this finding may have implications for Fanconi anemia treatment.

“DNA2 is a well-studied gene, and this recent discovery could potentially become the basis for ameliorating the symptoms of this incurable disorder,” said study author Judith Campbell, PhD, of the California Institute of Technology.

“Since much is known about the mechanism of action of DNA2, it is an attractive target for future drug treatments—like small-molecule inhibitors that could reduce [a Fanconi anemia] patient’s cancer predisposition—as well as a possible gene therapy for aiding a patient’s blood cell development.”

DNA repair

Credit: Tom Ellenberger

Understanding the interaction between 2 genes may be the key to better treatment of Fanconi anemia, according to a paper published in Cell Cycle.

Researchers investigated the relationship between FANCD2 and DNA2, 2 genes known to play roles in DNA repair.

A defective version of FANCD2 can result in Fanconi anemia. And although DNA2 has not been associated with a Fanconi anemia family

yet, genetic studies have implicated DNA2 in the Fanconi anemia DNA repair pathway.

With the current study, the researchers found that deleting either FANCD2 or DNA2 alone makes cells susceptible to DNA damage. But the deletion of both genes enables DNA repair.

“A key implication of this finding is the potential to manipulate DNA2 to improve the survival of FANCD2-deficient cells, and hopefully, by extension, the survival of [Fanconi anemia] patients,” said study author Kenneth Karanja, PhD, a former postdoctoral scholar at the California Institute of Technology in Pasadena.

To uncover the relationship between the genes, Dr Karanja and his colleagues applied DNA-damaging substances—formaldehyde and cisplatin—to 3 types of cells: those lacking FANCD2, those lacking DNA2, and cells lacking both genes.

The groups of cells in which only 1 of the 2 genes had been deleted quickly succumbed to the substance-induced DNA damage. However, the cells lacking both FANCD2 and DNA2 were able to repair the DNA damage and survive.

So the researchers concluded that depletion of DNA2 in FANCD2-deficient cells reverses the cells’ sensitivity to DNA-damaging substances. And this finding may have implications for Fanconi anemia treatment.

“DNA2 is a well-studied gene, and this recent discovery could potentially become the basis for ameliorating the symptoms of this incurable disorder,” said study author Judith Campbell, PhD, of the California Institute of Technology.

“Since much is known about the mechanism of action of DNA2, it is an attractive target for future drug treatments—like small-molecule inhibitors that could reduce [a Fanconi anemia] patient’s cancer predisposition—as well as a possible gene therapy for aiding a patient’s blood cell development.”

Vials of drug

Credit: Bill Branson

The antitumor agent bleomycin can treat a range of cancers, but its disease-fighting properties have been poorly understood.

Now, a pair of researchers have characterized bleomycin’s ability to cut through double-stranded DNA in cancerous cells.

The duo believe their research could help inform efforts to fine-tune the drug, improving its cancer-killing properties and limiting toxicity to healthy cells.

The research appears in the Journal of the American Chemical Society.

Bleomycin is part of a family of structurally related antibiotics produced by the bacterium Streptomyces verticillus. Three potent versions of the drug—labeled A2, A5, and B2—are the primary forms in clinical use against cancers.

Previous research has shown that bleomycin can cause death in aberrant cells by migrating to the cell nucleus, binding with DNA, and subsequently causing breaks in the DNA sequence. Following a binding event, a molecule of bleomycin can effectively slice through one or both strands of DNA.

Cleavage of DNA is believed to be the primary mechanism by which bleomycin kills cancer cells, particularly through double-strand cleavages, which are more challenging for the cellular machinery to repair.

“There are several mechanisms for repairing both single-strand and double-strand breaks in DNA, but double-strand breaks are a more potent form of DNA lesion,” explained study author Basab Roy, a graduate student at Arizona State University in Tempe.

For this study, Roy and Sidney Hecht, PhD, used bleomycin A5, which has similar DNA binding and cleaving properties as bleomycin A2 and B2.

Previous research revealed that bleomycin binds with highly specific regions of the DNA strand, typically G-C sites, where a guanosine base pairs with a cytidine. The strength of this binding is closely associated with the degree of double-strand DNA cleavage.

From a pool of random DNA sequences, the researchers selected a library of 10 hairpin DNAs, based on their strong binding affinity for bleomycin A5. Hairpin DNAs are looped structures that form when a segment of a DNA strand base-pairs with another portion of the same strand. These hairpin DNAs were used to investigate double-strand cleavage.

Each of the 10 DNA samples underwent double-strand cleavage at more than one site. All of the observed cleavage sites were found within or in close proximity to an 8-base-pair-variable region.

Examination of the 10 DNA samples exposed to bleomycin revealed a total of 31 double-strand cleavage sites. Earlier research had described the form of double-strand DNA cleavage bleomycin induced at 14 of these sites. But the remaining 17 cases of double-stranded cleavage occurred through a different mechanism, described for the first time by Roy and Dr Hecht.

The pair used iron (FeII) as a cofactor for bleomycin in the binding events, and they observed 2 types of bleomycin binding and cleavage activity.

In the first, bleomycin and its iron cofactor (Fe.BLM) bind with hairpin DNA at a primary site. Typically, this is a site with a particular sequence: 5´-G-Py-B-3´. (Here, 5´ refers to one end of the DNA hairpin, G refers to the base guanosine, Py refers to a pyrimidinic base—either cytidine or thymidine, B refers to any nucleobase, and 3´ refers to the other DNA end.)

The result of this binding is the abstraction of a hydrogen atom at the primary site. Two results are possible following the primary binding event, one causing a single-strand break in the primary site and the other, failing to produce full cleavage of the strand, producing instead a site lacking either a purine or pyrimidine base. This is known as an AP site.

In the first case—where bleomycin achieves single strand cleavage—the bleomycin molecule can then become reactivated, once more abstracting a hydrogen atom from the opposing DNA strand.

The opposite strand can again follow 1 of 2 pathways, (a) full cleavage of the opposing strand, yielding a double-strand cleavage or (b) formation of an AP site. The researchers noted that this AP site can lead to strand cleavage through the opposing DNA strand with the addition of a mild base like n-butylamine.

The results of this study emphasize the correlation between the strength of bleomycin binding to DNA and the frequency of double-strand cleavage. Of the 10 sample hairpin DNAs, the 2 most tightly bound to bleomycin each showed 5 double-strand cleavages, whereas the least tightly bound samples exhibited just 2 double-strand cleavages.

This suggests a plausible mechanism for DNA cleavage by bleomycin that may lead to tumor cell killing, as well as identifying the most common sequences involved in DNA site binding and subsequent strand breakage.

Roy noted, however, that more research is needed to elucidate the biochemical causes of tight binding by bleomycin. Furthermore, bleomycin’s specificity for cancer cells remains enigmatic.

“Cancer is still a black hole,” Roy said. “We’re trying to make this particular molecule better. There is still so much to learn.”

Vials of drug

Credit: Bill Branson

The antitumor agent bleomycin can treat a range of cancers, but its disease-fighting properties have been poorly understood.

Now, a pair of researchers have characterized bleomycin’s ability to cut through double-stranded DNA in cancerous cells.

The duo believe their research could help inform efforts to fine-tune the drug, improving its cancer-killing properties and limiting toxicity to healthy cells.

The research appears in the Journal of the American Chemical Society.

Bleomycin is part of a family of structurally related antibiotics produced by the bacterium Streptomyces verticillus. Three potent versions of the drug—labeled A2, A5, and B2—are the primary forms in clinical use against cancers.

Previous research has shown that bleomycin can cause death in aberrant cells by migrating to the cell nucleus, binding with DNA, and subsequently causing breaks in the DNA sequence. Following a binding event, a molecule of bleomycin can effectively slice through one or both strands of DNA.

Cleavage of DNA is believed to be the primary mechanism by which bleomycin kills cancer cells, particularly through double-strand cleavages, which are more challenging for the cellular machinery to repair.

“There are several mechanisms for repairing both single-strand and double-strand breaks in DNA, but double-strand breaks are a more potent form of DNA lesion,” explained study author Basab Roy, a graduate student at Arizona State University in Tempe.

For this study, Roy and Sidney Hecht, PhD, used bleomycin A5, which has similar DNA binding and cleaving properties as bleomycin A2 and B2.

Previous research revealed that bleomycin binds with highly specific regions of the DNA strand, typically G-C sites, where a guanosine base pairs with a cytidine. The strength of this binding is closely associated with the degree of double-strand DNA cleavage.

From a pool of random DNA sequences, the researchers selected a library of 10 hairpin DNAs, based on their strong binding affinity for bleomycin A5. Hairpin DNAs are looped structures that form when a segment of a DNA strand base-pairs with another portion of the same strand. These hairpin DNAs were used to investigate double-strand cleavage.

Each of the 10 DNA samples underwent double-strand cleavage at more than one site. All of the observed cleavage sites were found within or in close proximity to an 8-base-pair-variable region.

Examination of the 10 DNA samples exposed to bleomycin revealed a total of 31 double-strand cleavage sites. Earlier research had described the form of double-strand DNA cleavage bleomycin induced at 14 of these sites. But the remaining 17 cases of double-stranded cleavage occurred through a different mechanism, described for the first time by Roy and Dr Hecht.

The pair used iron (FeII) as a cofactor for bleomycin in the binding events, and they observed 2 types of bleomycin binding and cleavage activity.

In the first, bleomycin and its iron cofactor (Fe.BLM) bind with hairpin DNA at a primary site. Typically, this is a site with a particular sequence: 5´-G-Py-B-3´. (Here, 5´ refers to one end of the DNA hairpin, G refers to the base guanosine, Py refers to a pyrimidinic base—either cytidine or thymidine, B refers to any nucleobase, and 3´ refers to the other DNA end.)

The result of this binding is the abstraction of a hydrogen atom at the primary site. Two results are possible following the primary binding event, one causing a single-strand break in the primary site and the other, failing to produce full cleavage of the strand, producing instead a site lacking either a purine or pyrimidine base. This is known as an AP site.

In the first case—where bleomycin achieves single strand cleavage—the bleomycin molecule can then become reactivated, once more abstracting a hydrogen atom from the opposing DNA strand.

The opposite strand can again follow 1 of 2 pathways, (a) full cleavage of the opposing strand, yielding a double-strand cleavage or (b) formation of an AP site. The researchers noted that this AP site can lead to strand cleavage through the opposing DNA strand with the addition of a mild base like n-butylamine.

The results of this study emphasize the correlation between the strength of bleomycin binding to DNA and the frequency of double-strand cleavage. Of the 10 sample hairpin DNAs, the 2 most tightly bound to bleomycin each showed 5 double-strand cleavages, whereas the least tightly bound samples exhibited just 2 double-strand cleavages.

This suggests a plausible mechanism for DNA cleavage by bleomycin that may lead to tumor cell killing, as well as identifying the most common sequences involved in DNA site binding and subsequent strand breakage.

Roy noted, however, that more research is needed to elucidate the biochemical causes of tight binding by bleomycin. Furthermore, bleomycin’s specificity for cancer cells remains enigmatic.

“Cancer is still a black hole,” Roy said. “We’re trying to make this particular molecule better. There is still so much to learn.”

Vials of drug

Credit: Bill Branson

The antitumor agent bleomycin can treat a range of cancers, but its disease-fighting properties have been poorly understood.

Now, a pair of researchers have characterized bleomycin’s ability to cut through double-stranded DNA in cancerous cells.

The duo believe their research could help inform efforts to fine-tune the drug, improving its cancer-killing properties and limiting toxicity to healthy cells.

The research appears in the Journal of the American Chemical Society.

Bleomycin is part of a family of structurally related antibiotics produced by the bacterium Streptomyces verticillus. Three potent versions of the drug—labeled A2, A5, and B2—are the primary forms in clinical use against cancers.

Previous research has shown that bleomycin can cause death in aberrant cells by migrating to the cell nucleus, binding with DNA, and subsequently causing breaks in the DNA sequence. Following a binding event, a molecule of bleomycin can effectively slice through one or both strands of DNA.

Cleavage of DNA is believed to be the primary mechanism by which bleomycin kills cancer cells, particularly through double-strand cleavages, which are more challenging for the cellular machinery to repair.

“There are several mechanisms for repairing both single-strand and double-strand breaks in DNA, but double-strand breaks are a more potent form of DNA lesion,” explained study author Basab Roy, a graduate student at Arizona State University in Tempe.

For this study, Roy and Sidney Hecht, PhD, used bleomycin A5, which has similar DNA binding and cleaving properties as bleomycin A2 and B2.

Previous research revealed that bleomycin binds with highly specific regions of the DNA strand, typically G-C sites, where a guanosine base pairs with a cytidine. The strength of this binding is closely associated with the degree of double-strand DNA cleavage.

From a pool of random DNA sequences, the researchers selected a library of 10 hairpin DNAs, based on their strong binding affinity for bleomycin A5. Hairpin DNAs are looped structures that form when a segment of a DNA strand base-pairs with another portion of the same strand. These hairpin DNAs were used to investigate double-strand cleavage.

Each of the 10 DNA samples underwent double-strand cleavage at more than one site. All of the observed cleavage sites were found within or in close proximity to an 8-base-pair-variable region.

Examination of the 10 DNA samples exposed to bleomycin revealed a total of 31 double-strand cleavage sites. Earlier research had described the form of double-strand DNA cleavage bleomycin induced at 14 of these sites. But the remaining 17 cases of double-stranded cleavage occurred through a different mechanism, described for the first time by Roy and Dr Hecht.

The pair used iron (FeII) as a cofactor for bleomycin in the binding events, and they observed 2 types of bleomycin binding and cleavage activity.

In the first, bleomycin and its iron cofactor (Fe.BLM) bind with hairpin DNA at a primary site. Typically, this is a site with a particular sequence: 5´-G-Py-B-3´. (Here, 5´ refers to one end of the DNA hairpin, G refers to the base guanosine, Py refers to a pyrimidinic base—either cytidine or thymidine, B refers to any nucleobase, and 3´ refers to the other DNA end.)

The result of this binding is the abstraction of a hydrogen atom at the primary site. Two results are possible following the primary binding event, one causing a single-strand break in the primary site and the other, failing to produce full cleavage of the strand, producing instead a site lacking either a purine or pyrimidine base. This is known as an AP site.

In the first case—where bleomycin achieves single strand cleavage—the bleomycin molecule can then become reactivated, once more abstracting a hydrogen atom from the opposing DNA strand.

The opposite strand can again follow 1 of 2 pathways, (a) full cleavage of the opposing strand, yielding a double-strand cleavage or (b) formation of an AP site. The researchers noted that this AP site can lead to strand cleavage through the opposing DNA strand with the addition of a mild base like n-butylamine.

The results of this study emphasize the correlation between the strength of bleomycin binding to DNA and the frequency of double-strand cleavage. Of the 10 sample hairpin DNAs, the 2 most tightly bound to bleomycin each showed 5 double-strand cleavages, whereas the least tightly bound samples exhibited just 2 double-strand cleavages.

This suggests a plausible mechanism for DNA cleavage by bleomycin that may lead to tumor cell killing, as well as identifying the most common sequences involved in DNA site binding and subsequent strand breakage.

Roy noted, however, that more research is needed to elucidate the biochemical causes of tight binding by bleomycin. Furthermore, bleomycin’s specificity for cancer cells remains enigmatic.

“Cancer is still a black hole,” Roy said. “We’re trying to make this particular molecule better. There is still so much to learn.”

SHM’s Hospitalist Program Peak Performance, HP3 for short, will conclude at the end of 2014, but it will leave a legacy that will continue to improve HM groups everywhere for years to come.

The product of a unique collaboration among SHM, hospitalist consulting firm Nelson/Flores, and others, HP3 was designed as a key component of the Preventing Readmissions through Effective Partnerships (PREP) collaborative, sponsored by BlueCross BlueShield of Illinois in collaboration with the Illinois Hospital Association and Northwestern University Feinberg School of Medicine. The overall goal of the PREP collaborative is to help move Illinois from the bottom quartile to the upper quartile ranking on readmission rates by providing tools and approaches to improve transitions of care.

“HP3 was designed to be a little like getting a personal trainer at the gym,” says John Nelson, MD, MHM, who helped create the program. “Each hospitalist group was assigned an experienced hospitalist leader as a mentor, who in some ways acted like a personal trainer, guiding and encouraging efforts to complete projects to improve their practice.

“I think most groups were surprised and pleased that they were able to accomplish more than they realized. Our hope is that they will continue ‘working out’ to improve their practice even after their participation in HP3 concludes.”

Today, many of the lessons learned from HP3—including the idea that a healthy, high-functioning hospitalist practice is an important part of improving care—have been carried into other important SHM projects, like the recent “Key Principles and Characteristics of an Effective Hospital Medicine Group,” an assessment guide developed by SHM and published in the February 2014 Journal of Hospital Medicine.

Among the ideas presented in the “Key Principles and Characteristics” guide is the concept of hospitalist engagement, which is what Dr. Mark Williams thinks hospitals can also take away from HP3.

“Engaging hospitalists is key to improving care for hospitalized patients,” says Dr. Williams, who notes that engaging hospitalists means engaging much of the entire hospital. “Hospitalists are fully integrated into hospital care delivery for general medicine patients and many—if not most—specialty and surgical patients.”

HP3 faculty Leslie Flores, MHA, SFHM, saw a two-fold benefit from HP3: an outside perspective and an introduction to techniques that will continue beyond HP3.

“It caused them to look critically at their hospitalist program and assess its organization and performance against an objective benchmark. For many, it was the first time they had been challenged to think about their hospitalist program in this way,” Flores says.

She noticed that HP3 “also taught the participants how to use basic quality improvement and project management techniques to improve their own group’s performance—these are skills they can use again and again going forward.”

Flores thinks that HP3 also benefited from another core piece of SHM’s DNA: its award-winning Mentored Implementation (MI) model, which pairs hospital sites with national experts in hospital medicine. But, instead of being focused solely on quality improvement, it broadened the MI approach to operational improvement, opening up the possibility of improved quality outcomes.

As with many SHM educational programs, the learning went in both directions and may continue after the end of HP3, according to Flores.

“I think we [the faculty and mentors], in some cases, learned as much from our participants as they learned from us,” she says. “Some of them are doing some really great things that we can add to our fund of practice management ‘best practices’ and share with others!”

SHM’s Hospitalist Program Peak Performance, HP3 for short, will conclude at the end of 2014, but it will leave a legacy that will continue to improve HM groups everywhere for years to come.

The product of a unique collaboration among SHM, hospitalist consulting firm Nelson/Flores, and others, HP3 was designed as a key component of the Preventing Readmissions through Effective Partnerships (PREP) collaborative, sponsored by BlueCross BlueShield of Illinois in collaboration with the Illinois Hospital Association and Northwestern University Feinberg School of Medicine. The overall goal of the PREP collaborative is to help move Illinois from the bottom quartile to the upper quartile ranking on readmission rates by providing tools and approaches to improve transitions of care.

“HP3 was designed to be a little like getting a personal trainer at the gym,” says John Nelson, MD, MHM, who helped create the program. “Each hospitalist group was assigned an experienced hospitalist leader as a mentor, who in some ways acted like a personal trainer, guiding and encouraging efforts to complete projects to improve their practice.

“I think most groups were surprised and pleased that they were able to accomplish more than they realized. Our hope is that they will continue ‘working out’ to improve their practice even after their participation in HP3 concludes.”

Today, many of the lessons learned from HP3—including the idea that a healthy, high-functioning hospitalist practice is an important part of improving care—have been carried into other important SHM projects, like the recent “Key Principles and Characteristics of an Effective Hospital Medicine Group,” an assessment guide developed by SHM and published in the February 2014 Journal of Hospital Medicine.

Among the ideas presented in the “Key Principles and Characteristics” guide is the concept of hospitalist engagement, which is what Dr. Mark Williams thinks hospitals can also take away from HP3.

“Engaging hospitalists is key to improving care for hospitalized patients,” says Dr. Williams, who notes that engaging hospitalists means engaging much of the entire hospital. “Hospitalists are fully integrated into hospital care delivery for general medicine patients and many—if not most—specialty and surgical patients.”

HP3 faculty Leslie Flores, MHA, SFHM, saw a two-fold benefit from HP3: an outside perspective and an introduction to techniques that will continue beyond HP3.

“It caused them to look critically at their hospitalist program and assess its organization and performance against an objective benchmark. For many, it was the first time they had been challenged to think about their hospitalist program in this way,” Flores says.

She noticed that HP3 “also taught the participants how to use basic quality improvement and project management techniques to improve their own group’s performance—these are skills they can use again and again going forward.”

Flores thinks that HP3 also benefited from another core piece of SHM’s DNA: its award-winning Mentored Implementation (MI) model, which pairs hospital sites with national experts in hospital medicine. But, instead of being focused solely on quality improvement, it broadened the MI approach to operational improvement, opening up the possibility of improved quality outcomes.

As with many SHM educational programs, the learning went in both directions and may continue after the end of HP3, according to Flores.

“I think we [the faculty and mentors], in some cases, learned as much from our participants as they learned from us,” she says. “Some of them are doing some really great things that we can add to our fund of practice management ‘best practices’ and share with others!”

SHM’s Hospitalist Program Peak Performance, HP3 for short, will conclude at the end of 2014, but it will leave a legacy that will continue to improve HM groups everywhere for years to come.

The product of a unique collaboration among SHM, hospitalist consulting firm Nelson/Flores, and others, HP3 was designed as a key component of the Preventing Readmissions through Effective Partnerships (PREP) collaborative, sponsored by BlueCross BlueShield of Illinois in collaboration with the Illinois Hospital Association and Northwestern University Feinberg School of Medicine. The overall goal of the PREP collaborative is to help move Illinois from the bottom quartile to the upper quartile ranking on readmission rates by providing tools and approaches to improve transitions of care.

“HP3 was designed to be a little like getting a personal trainer at the gym,” says John Nelson, MD, MHM, who helped create the program. “Each hospitalist group was assigned an experienced hospitalist leader as a mentor, who in some ways acted like a personal trainer, guiding and encouraging efforts to complete projects to improve their practice.

“I think most groups were surprised and pleased that they were able to accomplish more than they realized. Our hope is that they will continue ‘working out’ to improve their practice even after their participation in HP3 concludes.”

Today, many of the lessons learned from HP3—including the idea that a healthy, high-functioning hospitalist practice is an important part of improving care—have been carried into other important SHM projects, like the recent “Key Principles and Characteristics of an Effective Hospital Medicine Group,” an assessment guide developed by SHM and published in the February 2014 Journal of Hospital Medicine.

Among the ideas presented in the “Key Principles and Characteristics” guide is the concept of hospitalist engagement, which is what Dr. Mark Williams thinks hospitals can also take away from HP3.

“Engaging hospitalists is key to improving care for hospitalized patients,” says Dr. Williams, who notes that engaging hospitalists means engaging much of the entire hospital. “Hospitalists are fully integrated into hospital care delivery for general medicine patients and many—if not most—specialty and surgical patients.”

HP3 faculty Leslie Flores, MHA, SFHM, saw a two-fold benefit from HP3: an outside perspective and an introduction to techniques that will continue beyond HP3.

“It caused them to look critically at their hospitalist program and assess its organization and performance against an objective benchmark. For many, it was the first time they had been challenged to think about their hospitalist program in this way,” Flores says.

She noticed that HP3 “also taught the participants how to use basic quality improvement and project management techniques to improve their own group’s performance—these are skills they can use again and again going forward.”

Flores thinks that HP3 also benefited from another core piece of SHM’s DNA: its award-winning Mentored Implementation (MI) model, which pairs hospital sites with national experts in hospital medicine. But, instead of being focused solely on quality improvement, it broadened the MI approach to operational improvement, opening up the possibility of improved quality outcomes.

As with many SHM educational programs, the learning went in both directions and may continue after the end of HP3, according to Flores.

“I think we [the faculty and mentors], in some cases, learned as much from our participants as they learned from us,” she says. “Some of them are doing some really great things that we can add to our fund of practice management ‘best practices’ and share with others!”

Maybe you just returned from HM14 in Las Vegas and are ready to head back. Or maybe you missed out on SHM’s annual meeting but would like to meet up with an important part of the hospitalist team: hospital and health system pharmacists.

Regardless of your motivation, the American Society of Health-System Pharmacist’s (ASHP’s) combination of three meetings in one brings a wealth of information to hospitalists—physicians and pharmacists alike—and now SHM members can register for the Medication Safety Collaborative at the applicable ASHP member rates.

SHM members receive the ASHP member rate at ASHP’s meeting within a meeting for hospital and health system pharmacists, to be held May 31-June 4 in Las Vegas.

Many hospitalists will be especially interested in the Medication Safety Collaborative, which brings the entire hospital team together to share best practices in medication and patient safety.

The Medication Safety Collaborative consists of three meetings:

• ASHP Informatics Institute: An event for informaticists to innovate, interact, and improve the use of information technology in healthcare;
• The Medication Safety Collaborative: For inter-professional teams of health system-based clinicians, coordinators, managers, and administrators who focus on patient safety and quality; and
• Pharmacy Practice Policy: The most relevant issues affecting health system pharmacy practice today at ASHP’s first Pharmacy Practice and Policy Meeting.

Maybe you just returned from HM14 in Las Vegas and are ready to head back. Or maybe you missed out on SHM’s annual meeting but would like to meet up with an important part of the hospitalist team: hospital and health system pharmacists.

Regardless of your motivation, the American Society of Health-System Pharmacist’s (ASHP’s) combination of three meetings in one brings a wealth of information to hospitalists—physicians and pharmacists alike—and now SHM members can register for the Medication Safety Collaborative at the applicable ASHP member rates.

SHM members receive the ASHP member rate at ASHP’s meeting within a meeting for hospital and health system pharmacists, to be held May 31-June 4 in Las Vegas.

Many hospitalists will be especially interested in the Medication Safety Collaborative, which brings the entire hospital team together to share best practices in medication and patient safety.

The Medication Safety Collaborative consists of three meetings:

• ASHP Informatics Institute: An event for informaticists to innovate, interact, and improve the use of information technology in healthcare;
• The Medication Safety Collaborative: For inter-professional teams of health system-based clinicians, coordinators, managers, and administrators who focus on patient safety and quality; and
• Pharmacy Practice Policy: The most relevant issues affecting health system pharmacy practice today at ASHP’s first Pharmacy Practice and Policy Meeting.

Maybe you just returned from HM14 in Las Vegas and are ready to head back. Or maybe you missed out on SHM’s annual meeting but would like to meet up with an important part of the hospitalist team: hospital and health system pharmacists.

Regardless of your motivation, the American Society of Health-System Pharmacist’s (ASHP’s) combination of three meetings in one brings a wealth of information to hospitalists—physicians and pharmacists alike—and now SHM members can register for the Medication Safety Collaborative at the applicable ASHP member rates.

SHM members receive the ASHP member rate at ASHP’s meeting within a meeting for hospital and health system pharmacists, to be held May 31-June 4 in Las Vegas.

Many hospitalists will be especially interested in the Medication Safety Collaborative, which brings the entire hospital team together to share best practices in medication and patient safety.

The Medication Safety Collaborative consists of three meetings:

• ASHP Informatics Institute: An event for informaticists to innovate, interact, and improve the use of information technology in healthcare;
• The Medication Safety Collaborative: For inter-professional teams of health system-based clinicians, coordinators, managers, and administrators who focus on patient safety and quality; and
• Pharmacy Practice Policy: The most relevant issues affecting health system pharmacy practice today at ASHP’s first Pharmacy Practice and Policy Meeting.

SHM estimates that there are more than 44,000 hospitalists in 2014. Here are some other facts and figures about the specialty:

• In 2014, it is estimated that hospitalists have a presence at 72% of U.S. hospitals, with an average group size of 12.3 physicians.
• In the 10-year period between 2003 and 2012, the percentage of hospitals with hospitalists has more than doubled. The overall penetration of hospitals with HM groups grew from 29% to 66%.
• In same 10-year period, the number of hospitalists grew from 11,159 to 38,114.
• Since the development of SHM’s award-winning mentored implementation program, 423 hospitals nationwide have adopted the model to address some of the most pressing hospital-based healthcare issues, such as readmissions, VTE, and glycemic control. SHM’s implementation guides on these issues have been downloaded more than 9,500 times.
• Research published in the Journal of Hospital Medicine in 2013 showed that SHM’s Project BOOST has helped reduce readmissions among hospitals collecting and reporting data.

SHM estimates that there are more than 44,000 hospitalists in 2014. Here are some other facts and figures about the specialty:

• In 2014, it is estimated that hospitalists have a presence at 72% of U.S. hospitals, with an average group size of 12.3 physicians.
• In the 10-year period between 2003 and 2012, the percentage of hospitals with hospitalists has more than doubled. The overall penetration of hospitals with HM groups grew from 29% to 66%.
• In same 10-year period, the number of hospitalists grew from 11,159 to 38,114.
• Since the development of SHM’s award-winning mentored implementation program, 423 hospitals nationwide have adopted the model to address some of the most pressing hospital-based healthcare issues, such as readmissions, VTE, and glycemic control. SHM’s implementation guides on these issues have been downloaded more than 9,500 times.
• Research published in the Journal of Hospital Medicine in 2013 showed that SHM’s Project BOOST has helped reduce readmissions among hospitals collecting and reporting data.

SHM estimates that there are more than 44,000 hospitalists in 2014. Here are some other facts and figures about the specialty:

• In 2014, it is estimated that hospitalists have a presence at 72% of U.S. hospitals, with an average group size of 12.3 physicians.
• In the 10-year period between 2003 and 2012, the percentage of hospitals with hospitalists has more than doubled. The overall penetration of hospitals with HM groups grew from 29% to 66%.
• In same 10-year period, the number of hospitalists grew from 11,159 to 38,114.
• Since the development of SHM’s award-winning mentored implementation program, 423 hospitals nationwide have adopted the model to address some of the most pressing hospital-based healthcare issues, such as readmissions, VTE, and glycemic control. SHM’s implementation guides on these issues have been downloaded more than 9,500 times.
• Research published in the Journal of Hospital Medicine in 2013 showed that SHM’s Project BOOST has helped reduce readmissions among hospitals collecting and reporting data.

Editor’s note: Originally posted to SHM’s blog, The Hospital Leader, on February 25. Visit www.hospitalleader.org for more insight from leaders in the specialty.

Imagine for a second that, instead of being defined by what you are at work, you were defined by what you aren’t. What if hospitalists were called “non-executive caregivers” or “non-janitorial staff?” Confusing, at best—and potentially even demeaning, depending on the context.

That’s what happens to many nurse practitioners, physician assistants, pharmacists, and other valuable members of the hospital care team all the time. Instead of being called by the titles that they’ve worked hard to earn, some in the hospital use terms that define them by what they aren’t, like “non-physician provider,” “allied health provider,” “physician extender,” or “mid-level.” More to the point, nurse practitioners (NP), physician assistants (PA), and pharmacists are a critical part of the hospitalist teams working to deliver exceptional care to hospitalized patients.

This is not a fringe issue. Today, nearly 800 SHM members identify themselves as NPs, PAs, pharmacists, pharmacy technicians, registered nurses, registered dietitians, physical therapists, research managers, or program coordinators.

That’s why, effective this month, SHM has begun to phase out the following terms in its future materials:

• “Allied health”;
• “Non-physician provider”;
• “Physician extender”; and
• “Mid-level.”

Instead, we plan to use the names for individual groups, like “physician assistants,” “nurse practitioners,” or “pharmacists.”

For a firsthand perspective on how deeply these kinds of terms are felt by NPs and PAs, please read SHM NP/PA Committee Chair Tracy Cardin’s recent blog post on The Hospital Leader.

Admittedly, there may be times when terms like “allied health” are more expedient, and it will take some time for us to fully adjust some of our internal nomenclature (in things like our databases and meeting registration systems) to the change, but the potential for alienating members of the hospitalist family outweighs the need for convenience.

SHM is committed to properly identifying all of SHM’s members. Identity is important in medicine, to the caregivers and their patients. Just 18 years ago, Bob Wachter, MD, coined the word “hospitalist”; the term now applies to more than 44,000 in healthcare.

Today, we’re taking one step toward helping everyone in healthcare better describe the value and expertise of the members of the hospitalist team.

How do you use your titles to convey your contribution to patient care? Let us know in the comments, or join the conversation on HMX (http://connect.hospitalmedicine.org/home).

Blog post author Brendon Shank is SHM’s associate vice president of communications.

Editor’s note: Originally posted to SHM’s blog, The Hospital Leader, on February 25. Visit www.hospitalleader.org for more insight from leaders in the specialty.

Imagine for a second that, instead of being defined by what you are at work, you were defined by what you aren’t. What if hospitalists were called “non-executive caregivers” or “non-janitorial staff?” Confusing, at best—and potentially even demeaning, depending on the context.

That’s what happens to many nurse practitioners, physician assistants, pharmacists, and other valuable members of the hospital care team all the time. Instead of being called by the titles that they’ve worked hard to earn, some in the hospital use terms that define them by what they aren’t, like “non-physician provider,” “allied health provider,” “physician extender,” or “mid-level.” More to the point, nurse practitioners (NP), physician assistants (PA), and pharmacists are a critical part of the hospitalist teams working to deliver exceptional care to hospitalized patients.

This is not a fringe issue. Today, nearly 800 SHM members identify themselves as NPs, PAs, pharmacists, pharmacy technicians, registered nurses, registered dietitians, physical therapists, research managers, or program coordinators.

That’s why, effective this month, SHM has begun to phase out the following terms in its future materials:

• “Allied health”;
• “Non-physician provider”;
• “Physician extender”; and
• “Mid-level.”

Instead, we plan to use the names for individual groups, like “physician assistants,” “nurse practitioners,” or “pharmacists.”

For a firsthand perspective on how deeply these kinds of terms are felt by NPs and PAs, please read SHM NP/PA Committee Chair Tracy Cardin’s recent blog post on The Hospital Leader.

Admittedly, there may be times when terms like “allied health” are more expedient, and it will take some time for us to fully adjust some of our internal nomenclature (in things like our databases and meeting registration systems) to the change, but the potential for alienating members of the hospitalist family outweighs the need for convenience.

SHM is committed to properly identifying all of SHM’s members. Identity is important in medicine, to the caregivers and their patients. Just 18 years ago, Bob Wachter, MD, coined the word “hospitalist”; the term now applies to more than 44,000 in healthcare.

Today, we’re taking one step toward helping everyone in healthcare better describe the value and expertise of the members of the hospitalist team.

How do you use your titles to convey your contribution to patient care? Let us know in the comments, or join the conversation on HMX (http://connect.hospitalmedicine.org/home).

Blog post author Brendon Shank is SHM’s associate vice president of communications.

Editor’s note: Originally posted to SHM’s blog, The Hospital Leader, on February 25. Visit www.hospitalleader.org for more insight from leaders in the specialty.

Imagine for a second that, instead of being defined by what you are at work, you were defined by what you aren’t. What if hospitalists were called “non-executive caregivers” or “non-janitorial staff?” Confusing, at best—and potentially even demeaning, depending on the context.

That’s what happens to many nurse practitioners, physician assistants, pharmacists, and other valuable members of the hospital care team all the time. Instead of being called by the titles that they’ve worked hard to earn, some in the hospital use terms that define them by what they aren’t, like “non-physician provider,” “allied health provider,” “physician extender,” or “mid-level.” More to the point, nurse practitioners (NP), physician assistants (PA), and pharmacists are a critical part of the hospitalist teams working to deliver exceptional care to hospitalized patients.

This is not a fringe issue. Today, nearly 800 SHM members identify themselves as NPs, PAs, pharmacists, pharmacy technicians, registered nurses, registered dietitians, physical therapists, research managers, or program coordinators.

That’s why, effective this month, SHM has begun to phase out the following terms in its future materials:

• “Allied health”;
• “Non-physician provider”;
• “Physician extender”; and
• “Mid-level.”

Instead, we plan to use the names for individual groups, like “physician assistants,” “nurse practitioners,” or “pharmacists.”

For a firsthand perspective on how deeply these kinds of terms are felt by NPs and PAs, please read SHM NP/PA Committee Chair Tracy Cardin’s recent blog post on The Hospital Leader.

Admittedly, there may be times when terms like “allied health” are more expedient, and it will take some time for us to fully adjust some of our internal nomenclature (in things like our databases and meeting registration systems) to the change, but the potential for alienating members of the hospitalist family outweighs the need for convenience.

SHM is committed to properly identifying all of SHM’s members. Identity is important in medicine, to the caregivers and their patients. Just 18 years ago, Bob Wachter, MD, coined the word “hospitalist”; the term now applies to more than 44,000 in healthcare.

Today, we’re taking one step toward helping everyone in healthcare better describe the value and expertise of the members of the hospitalist team.

How do you use your titles to convey your contribution to patient care? Let us know in the comments, or join the conversation on HMX (http://connect.hospitalmedicine.org/home).

Blog post author Brendon Shank is SHM’s associate vice president of communications.