Jan Dyer

When clinicians find out that one of their patients died of an overdose of a controlled substance, they are more likely to reduce the number and dose of opioid drugs they prescribe, according to a study funded in part by the National Institute on Aging.

Between July 1, 2015 and June 30, 2016, San Diego County in California reported 222 deaths for which Schedule II, III, or IV drugs were the primary or contributing cause. Of these, 170 deaths were listed in the Controlled Substance Utilization Review and Evaluation System (CURES) database.

In the study of 861 prescribing clinicians, 388 received a notification letter from the chief deputy medical examiner of San Diego County; 438 did not receive a letter. The letter identified the deceased patient by name, address, and age. It also outlined the annual number and types of prescription drug deaths seen by the medical examiner, discussed how to access the state’s prescription drug monitoring program, and reviewed safe prescribing strategies.

Physicians who received the letter wrote 9.7% fewer opioid prescriptions in the 3 months following the intervention.

"Behavioral ‘nudges’ like these letters could be a tool to help curb the opioid epidemic," said NIA Director Richard J. Hodes, MD. "This finding could be very useful in the effort to reduce inappropriate prescribing of opioids without severely restricting availability of legally prescribed opioids for patients who should be getting them."

When clinicians find out that one of their patients died of an overdose of a controlled substance, they are more likely to reduce the number and dose of opioid drugs they prescribe, according to a study funded in part by the National Institute on Aging.

Between July 1, 2015 and June 30, 2016, San Diego County in California reported 222 deaths for which Schedule II, III, or IV drugs were the primary or contributing cause. Of these, 170 deaths were listed in the Controlled Substance Utilization Review and Evaluation System (CURES) database.

In the study of 861 prescribing clinicians, 388 received a notification letter from the chief deputy medical examiner of San Diego County; 438 did not receive a letter. The letter identified the deceased patient by name, address, and age. It also outlined the annual number and types of prescription drug deaths seen by the medical examiner, discussed how to access the state’s prescription drug monitoring program, and reviewed safe prescribing strategies.

Physicians who received the letter wrote 9.7% fewer opioid prescriptions in the 3 months following the intervention.

"Behavioral ‘nudges’ like these letters could be a tool to help curb the opioid epidemic," said NIA Director Richard J. Hodes, MD. "This finding could be very useful in the effort to reduce inappropriate prescribing of opioids without severely restricting availability of legally prescribed opioids for patients who should be getting them."

When clinicians find out that one of their patients died of an overdose of a controlled substance, they are more likely to reduce the number and dose of opioid drugs they prescribe, according to a study funded in part by the National Institute on Aging.

Between July 1, 2015 and June 30, 2016, San Diego County in California reported 222 deaths for which Schedule II, III, or IV drugs were the primary or contributing cause. Of these, 170 deaths were listed in the Controlled Substance Utilization Review and Evaluation System (CURES) database.

In the study of 861 prescribing clinicians, 388 received a notification letter from the chief deputy medical examiner of San Diego County; 438 did not receive a letter. The letter identified the deceased patient by name, address, and age. It also outlined the annual number and types of prescription drug deaths seen by the medical examiner, discussed how to access the state’s prescription drug monitoring program, and reviewed safe prescribing strategies.

Physicians who received the letter wrote 9.7% fewer opioid prescriptions in the 3 months following the intervention.

"Behavioral ‘nudges’ like these letters could be a tool to help curb the opioid epidemic," said NIA Director Richard J. Hodes, MD. "This finding could be very useful in the effort to reduce inappropriate prescribing of opioids without severely restricting availability of legally prescribed opioids for patients who should be getting them."

Obesity not only makes flu more severe, but also lengthens the period of viral shedding for influenza A, according to a study by University of Michigan researchers, partly funded by the National Institute of Allergy and Infectious Diseases.

Over 3 flu seasons, the researchers monitored 1,783 people from 320 households in Managua, Nicaragua. During that time, 87 people became ill with influenza A and 58 with influenza B.

More than 40% of the adults aged > 18 years were obese, as defined by body mass. Obese adults with ≥ 2 symptoms of influenza A (n = 62) shed the virus 42% longer than did nonobese adults, or 5.2 days compared with 3.7 days, respectively. Obese adults with 1 or no symptoms of influenza A (n = 25) shed the virus 104% longer than nonobese adults—3.2 days compared with 1.6 days, respectively.

Obesity was not a risk factor for increased viral shedding duration in children aged 5 to 17 years or for adults with influenza B.

The researchers suggest that chronic inflammation caused by obesity may be responsible for the increased viral shedding. Reducing obesity rates could be an important target to limit the spread of viral infectious diseases, they suggest. The findings may have particular significance in the US, where in 2014 35% of adults were obese compared with 17.4% of adults in Nicaragua.

Obesity not only makes flu more severe, but also lengthens the period of viral shedding for influenza A, according to a study by University of Michigan researchers, partly funded by the National Institute of Allergy and Infectious Diseases.

Over 3 flu seasons, the researchers monitored 1,783 people from 320 households in Managua, Nicaragua. During that time, 87 people became ill with influenza A and 58 with influenza B.

More than 40% of the adults aged > 18 years were obese, as defined by body mass. Obese adults with ≥ 2 symptoms of influenza A (n = 62) shed the virus 42% longer than did nonobese adults, or 5.2 days compared with 3.7 days, respectively. Obese adults with 1 or no symptoms of influenza A (n = 25) shed the virus 104% longer than nonobese adults—3.2 days compared with 1.6 days, respectively.

Obesity was not a risk factor for increased viral shedding duration in children aged 5 to 17 years or for adults with influenza B.

The researchers suggest that chronic inflammation caused by obesity may be responsible for the increased viral shedding. Reducing obesity rates could be an important target to limit the spread of viral infectious diseases, they suggest. The findings may have particular significance in the US, where in 2014 35% of adults were obese compared with 17.4% of adults in Nicaragua.

Obesity not only makes flu more severe, but also lengthens the period of viral shedding for influenza A, according to a study by University of Michigan researchers, partly funded by the National Institute of Allergy and Infectious Diseases.

Over 3 flu seasons, the researchers monitored 1,783 people from 320 households in Managua, Nicaragua. During that time, 87 people became ill with influenza A and 58 with influenza B.

More than 40% of the adults aged > 18 years were obese, as defined by body mass. Obese adults with ≥ 2 symptoms of influenza A (n = 62) shed the virus 42% longer than did nonobese adults, or 5.2 days compared with 3.7 days, respectively. Obese adults with 1 or no symptoms of influenza A (n = 25) shed the virus 104% longer than nonobese adults—3.2 days compared with 1.6 days, respectively.

Obesity was not a risk factor for increased viral shedding duration in children aged 5 to 17 years or for adults with influenza B.

The researchers suggest that chronic inflammation caused by obesity may be responsible for the increased viral shedding. Reducing obesity rates could be an important target to limit the spread of viral infectious diseases, they suggest. The findings may have particular significance in the US, where in 2014 35% of adults were obese compared with 17.4% of adults in Nicaragua.

As patients with HIV, hepatitis B (HBV), and hepatitis C (HCV) live longer, more active lives with the help of antiviral treatments, they are now more often having joint replacement surgeries. But HIV, HBV, and HCV can increase the risk of postoperative complications, say researchers from Duke University in North Carolina.

The researchers studied 16,338 patients in 4 cohorts: those with HIV, HBV, HCV, and HIV plus HBV or HCV. They evaluated the patients at 30 days, 90 days, and 2 years after total joint arthroplasty (TJA), comparing their progress with that of a control group.

Patients with HBV and HCV were at risk of both acute and long-term medical and surgical complications. At 90 days and 2 years, the participants had increased risk of pneumonia, sepsis, joint infection, and revision surgery. They also had a greater risk of complications than did patients with HIV, especially for infection, within the first 90 days postsurgery.

Notably, after TJA, patients with HCV had increased risk of acute kidney injury, sepsis, and transfusion at 30 and 90 days. After hip replacement, patients with HBV had a higher risk of acute kidney injury, pneumonia, and transfusion at 30 and 90 days.

Only 364 patients in the study had both HIV and HBV or HBC, but they did have a greater risk of transfusion at 30 and 90 days following both knee and hip surgery.

Following total hip arthroplasty, patients with HIV were more at risk for deep vein thrombosis and transfusion rather than infection. The lower incidence of infection is likely to be related to effective  highly active antiretroviral therapy, the researchers say. HIV patients also were more likely to have mechanical complications, such as loosening, periprosthetic fracture, and revision at 90 days, but not at 2 years. Patients with HIV who underwent total knee arthroplasty (TKA) had a higher risk of death at 30 days and medical complications at 90 days. At 2 years, they had a higher risk of periprosthetic joint infection, irrigation and debridement, and revision. The researchers say the higher incidence of mechanical complications can be explained by the younger, more active, and healthy HIV patients in the cohort—the majority were aged younger than 65 years. They also emphasize that the only risk of infection following TJA in their study was 2 years after TKA.

The researchers suggest that their findings could help prompt future guidelines supporting routine screening prior to elective TJA.

Source:
Kildow BJ, Politzer CS, DiLallo M, Bolognesi MP, Seyler TM. J Arthroplasty. 2018;33(suppl 7):S86-S92.
doi: 10.1016/j.arth.2017.10.061.

As patients with HIV, hepatitis B (HBV), and hepatitis C (HCV) live longer, more active lives with the help of antiviral treatments, they are now more often having joint replacement surgeries. But HIV, HBV, and HCV can increase the risk of postoperative complications, say researchers from Duke University in North Carolina.

The researchers studied 16,338 patients in 4 cohorts: those with HIV, HBV, HCV, and HIV plus HBV or HCV. They evaluated the patients at 30 days, 90 days, and 2 years after total joint arthroplasty (TJA), comparing their progress with that of a control group.

Patients with HBV and HCV were at risk of both acute and long-term medical and surgical complications. At 90 days and 2 years, the participants had increased risk of pneumonia, sepsis, joint infection, and revision surgery. They also had a greater risk of complications than did patients with HIV, especially for infection, within the first 90 days postsurgery.

Notably, after TJA, patients with HCV had increased risk of acute kidney injury, sepsis, and transfusion at 30 and 90 days. After hip replacement, patients with HBV had a higher risk of acute kidney injury, pneumonia, and transfusion at 30 and 90 days.

Only 364 patients in the study had both HIV and HBV or HBC, but they did have a greater risk of transfusion at 30 and 90 days following both knee and hip surgery.

Following total hip arthroplasty, patients with HIV were more at risk for deep vein thrombosis and transfusion rather than infection. The lower incidence of infection is likely to be related to effective  highly active antiretroviral therapy, the researchers say. HIV patients also were more likely to have mechanical complications, such as loosening, periprosthetic fracture, and revision at 90 days, but not at 2 years. Patients with HIV who underwent total knee arthroplasty (TKA) had a higher risk of death at 30 days and medical complications at 90 days. At 2 years, they had a higher risk of periprosthetic joint infection, irrigation and debridement, and revision. The researchers say the higher incidence of mechanical complications can be explained by the younger, more active, and healthy HIV patients in the cohort—the majority were aged younger than 65 years. They also emphasize that the only risk of infection following TJA in their study was 2 years after TKA.

The researchers suggest that their findings could help prompt future guidelines supporting routine screening prior to elective TJA.

Source:
Kildow BJ, Politzer CS, DiLallo M, Bolognesi MP, Seyler TM. J Arthroplasty. 2018;33(suppl 7):S86-S92.
doi: 10.1016/j.arth.2017.10.061.

As patients with HIV, hepatitis B (HBV), and hepatitis C (HCV) live longer, more active lives with the help of antiviral treatments, they are now more often having joint replacement surgeries. But HIV, HBV, and HCV can increase the risk of postoperative complications, say researchers from Duke University in North Carolina.

The researchers studied 16,338 patients in 4 cohorts: those with HIV, HBV, HCV, and HIV plus HBV or HCV. They evaluated the patients at 30 days, 90 days, and 2 years after total joint arthroplasty (TJA), comparing their progress with that of a control group.

Patients with HBV and HCV were at risk of both acute and long-term medical and surgical complications. At 90 days and 2 years, the participants had increased risk of pneumonia, sepsis, joint infection, and revision surgery. They also had a greater risk of complications than did patients with HIV, especially for infection, within the first 90 days postsurgery.

Notably, after TJA, patients with HCV had increased risk of acute kidney injury, sepsis, and transfusion at 30 and 90 days. After hip replacement, patients with HBV had a higher risk of acute kidney injury, pneumonia, and transfusion at 30 and 90 days.

Only 364 patients in the study had both HIV and HBV or HBC, but they did have a greater risk of transfusion at 30 and 90 days following both knee and hip surgery.

Following total hip arthroplasty, patients with HIV were more at risk for deep vein thrombosis and transfusion rather than infection. The lower incidence of infection is likely to be related to effective  highly active antiretroviral therapy, the researchers say. HIV patients also were more likely to have mechanical complications, such as loosening, periprosthetic fracture, and revision at 90 days, but not at 2 years. Patients with HIV who underwent total knee arthroplasty (TKA) had a higher risk of death at 30 days and medical complications at 90 days. At 2 years, they had a higher risk of periprosthetic joint infection, irrigation and debridement, and revision. The researchers say the higher incidence of mechanical complications can be explained by the younger, more active, and healthy HIV patients in the cohort—the majority were aged younger than 65 years. They also emphasize that the only risk of infection following TJA in their study was 2 years after TKA.

The researchers suggest that their findings could help prompt future guidelines supporting routine screening prior to elective TJA.

Source:
Kildow BJ, Politzer CS, DiLallo M, Bolognesi MP, Seyler TM. J Arthroplasty. 2018;33(suppl 7):S86-S92.
doi: 10.1016/j.arth.2017.10.061.

When all 3 original classes of antiretroviral drugs no longer suppress viral load in a patient with HIV, the next step may be a new drug like etravirine (ETR), a nonnucleoside reverse transcriptase inhibitor (NNRTI). And, according to a French study, that could be a good way of keeping patients out of the hospital.

Using data from the French Hospital Database on HIV (FHDH), researchers analyzed hospitalization rates among heavily treated HIV-1 infected patients on failing regimens between 2005 (etravirine became available in France in 2006) and 2011. They compared 2 groups of patients: those who had received ETR plus a ritonavir-boosted protease inhibitor (PI) and those who had not. The primary endpoint of the study was hospitalization, divided by AIDS-defining cause and non–AIDS-defining cause.

Of 3,884 patients who had been exposed to at least 2 nucleoside reverse transcriptase inhibitors (NRTI), 2 PIs, and 1 NNRTI, 838 received ETR + PI.

During 13,986 person-years of follow-up, there were 2,484 hospitalizations among 956 patients: 617 were from an AIDS-defining cause in 301 patients, and 1,867 from a non–AIDS-defining cause in 828 patients.

The ETR + PI was associated with a 20% reduction in the hospitalization rate, mainly due to the reduction in AIDS hospitalizations. The researchers suggest that the clinical benefit of ETR could be explained by a high rate of virologic suppression (62% at month 6) and excellent tolerability. The FHDH did not include adherence data, but adherence is “unlikely” to explain the better outcome, the researchers say, given that ETR is a twice-daily drug, which may lead to slightly lower adherence than does a once-daily regimen.

The is the first study, to their knowledge, the researchers say, to focus on the risk of hospitalizations in current clinical practice and to show a positive effect.

Source:
Potard V, Goujard C, Valantin MA, et al. BMC Infect Dis. 2018;8:326.
doi: 10.1186/s12879-018-3231-5.

When all 3 original classes of antiretroviral drugs no longer suppress viral load in a patient with HIV, the next step may be a new drug like etravirine (ETR), a nonnucleoside reverse transcriptase inhibitor (NNRTI). And, according to a French study, that could be a good way of keeping patients out of the hospital.

Using data from the French Hospital Database on HIV (FHDH), researchers analyzed hospitalization rates among heavily treated HIV-1 infected patients on failing regimens between 2005 (etravirine became available in France in 2006) and 2011. They compared 2 groups of patients: those who had received ETR plus a ritonavir-boosted protease inhibitor (PI) and those who had not. The primary endpoint of the study was hospitalization, divided by AIDS-defining cause and non–AIDS-defining cause.

Of 3,884 patients who had been exposed to at least 2 nucleoside reverse transcriptase inhibitors (NRTI), 2 PIs, and 1 NNRTI, 838 received ETR + PI.

During 13,986 person-years of follow-up, there were 2,484 hospitalizations among 956 patients: 617 were from an AIDS-defining cause in 301 patients, and 1,867 from a non–AIDS-defining cause in 828 patients.

The ETR + PI was associated with a 20% reduction in the hospitalization rate, mainly due to the reduction in AIDS hospitalizations. The researchers suggest that the clinical benefit of ETR could be explained by a high rate of virologic suppression (62% at month 6) and excellent tolerability. The FHDH did not include adherence data, but adherence is “unlikely” to explain the better outcome, the researchers say, given that ETR is a twice-daily drug, which may lead to slightly lower adherence than does a once-daily regimen.

The is the first study, to their knowledge, the researchers say, to focus on the risk of hospitalizations in current clinical practice and to show a positive effect.

Source:
Potard V, Goujard C, Valantin MA, et al. BMC Infect Dis. 2018;8:326.
doi: 10.1186/s12879-018-3231-5.

When all 3 original classes of antiretroviral drugs no longer suppress viral load in a patient with HIV, the next step may be a new drug like etravirine (ETR), a nonnucleoside reverse transcriptase inhibitor (NNRTI). And, according to a French study, that could be a good way of keeping patients out of the hospital.

Using data from the French Hospital Database on HIV (FHDH), researchers analyzed hospitalization rates among heavily treated HIV-1 infected patients on failing regimens between 2005 (etravirine became available in France in 2006) and 2011. They compared 2 groups of patients: those who had received ETR plus a ritonavir-boosted protease inhibitor (PI) and those who had not. The primary endpoint of the study was hospitalization, divided by AIDS-defining cause and non–AIDS-defining cause.

Of 3,884 patients who had been exposed to at least 2 nucleoside reverse transcriptase inhibitors (NRTI), 2 PIs, and 1 NNRTI, 838 received ETR + PI.

During 13,986 person-years of follow-up, there were 2,484 hospitalizations among 956 patients: 617 were from an AIDS-defining cause in 301 patients, and 1,867 from a non–AIDS-defining cause in 828 patients.

The ETR + PI was associated with a 20% reduction in the hospitalization rate, mainly due to the reduction in AIDS hospitalizations. The researchers suggest that the clinical benefit of ETR could be explained by a high rate of virologic suppression (62% at month 6) and excellent tolerability. The FHDH did not include adherence data, but adherence is “unlikely” to explain the better outcome, the researchers say, given that ETR is a twice-daily drug, which may lead to slightly lower adherence than does a once-daily regimen.

The is the first study, to their knowledge, the researchers say, to focus on the risk of hospitalizations in current clinical practice and to show a positive effect.

Source:
Potard V, Goujard C, Valantin MA, et al. BMC Infect Dis. 2018;8:326.
doi: 10.1186/s12879-018-3231-5.

An antibiotic drug used to treat acne, among other things, may turn out to have potential well beyond that. Researchers from University of Antioquiain Medellin, Colombia, suggest that minocycline could be a promising antileukemic drug.

Minocycline is a well-established tetracycline derivative, used clinically since 1971, with a safe track record. But it also has nonantibiotic properties, exerting both antioxidant and antiapoptotic effects. There is even “compelling” preclinical evidence, the researchers say, that minocycline induces apoptosis in an acute myeloid leukemia cell line and a chronic myeloid leukemia cell line. Would the same be true of acute lymphoblastic leukemia (ALL) cells? To test their hypothesis, the researchers examined minocycline’s mechanism of action in the Jurkat cell line, an ALL tumor line established in the 1970s from the peripheral blood of a 14-year-old boy. 

The researchers found that minocycline did in fact induce apoptosis in Jurkat cells through a hydrogen peroxide (H₂O₂)-mediated signaling pathway. Indeed, they add, H₂O₂ triggers a whole cascade of adverse effects, including up-regulation of pro-apoptotic proteins. The researchers suggest that minocycline might even be capable of generating H₂O₂, which could explain the cytotoxic effects not only of minocycline, but of other tetracycline analogues. “Interestingly,” the researchers say, minocycline did all that without inducing oxidative stress or apoptosis makers in human peripheral blood lymphocyte cells.

The significance of their study is twofold, the researchers say: First, that minocycline is a safe and specific apoptosis-inducing drug against Jurkat cells in vitro; second, that it is pharmacologically well characterized and widely available.

The researchers note that no information is available on whether minocycline might efficiently kill ALL cells in vivo. However, they also note that minocycline has been found to be safe and well tolerated in doses up to 10 mg/kg in stroke patients—a dose that could be a sufficient concentration to reduce the viability of leukemia cell lines.

Source:
Ruiz-Moreno C, Velez-Pardo C, Jimenez-Del-Rio M. Toxicol In Vitro. 2018;50:336-346.
doi: 10.1016/j.tiv.2018.03.012

An antibiotic drug used to treat acne, among other things, may turn out to have potential well beyond that. Researchers from University of Antioquiain Medellin, Colombia, suggest that minocycline could be a promising antileukemic drug.

Minocycline is a well-established tetracycline derivative, used clinically since 1971, with a safe track record. But it also has nonantibiotic properties, exerting both antioxidant and antiapoptotic effects. There is even “compelling” preclinical evidence, the researchers say, that minocycline induces apoptosis in an acute myeloid leukemia cell line and a chronic myeloid leukemia cell line. Would the same be true of acute lymphoblastic leukemia (ALL) cells? To test their hypothesis, the researchers examined minocycline’s mechanism of action in the Jurkat cell line, an ALL tumor line established in the 1970s from the peripheral blood of a 14-year-old boy. 

The researchers found that minocycline did in fact induce apoptosis in Jurkat cells through a hydrogen peroxide (H₂O₂)-mediated signaling pathway. Indeed, they add, H₂O₂ triggers a whole cascade of adverse effects, including up-regulation of pro-apoptotic proteins. The researchers suggest that minocycline might even be capable of generating H₂O₂, which could explain the cytotoxic effects not only of minocycline, but of other tetracycline analogues. “Interestingly,” the researchers say, minocycline did all that without inducing oxidative stress or apoptosis makers in human peripheral blood lymphocyte cells.

The significance of their study is twofold, the researchers say: First, that minocycline is a safe and specific apoptosis-inducing drug against Jurkat cells in vitro; second, that it is pharmacologically well characterized and widely available.

The researchers note that no information is available on whether minocycline might efficiently kill ALL cells in vivo. However, they also note that minocycline has been found to be safe and well tolerated in doses up to 10 mg/kg in stroke patients—a dose that could be a sufficient concentration to reduce the viability of leukemia cell lines.

Source:
Ruiz-Moreno C, Velez-Pardo C, Jimenez-Del-Rio M. Toxicol In Vitro. 2018;50:336-346.
doi: 10.1016/j.tiv.2018.03.012

An antibiotic drug used to treat acne, among other things, may turn out to have potential well beyond that. Researchers from University of Antioquiain Medellin, Colombia, suggest that minocycline could be a promising antileukemic drug.

Minocycline is a well-established tetracycline derivative, used clinically since 1971, with a safe track record. But it also has nonantibiotic properties, exerting both antioxidant and antiapoptotic effects. There is even “compelling” preclinical evidence, the researchers say, that minocycline induces apoptosis in an acute myeloid leukemia cell line and a chronic myeloid leukemia cell line. Would the same be true of acute lymphoblastic leukemia (ALL) cells? To test their hypothesis, the researchers examined minocycline’s mechanism of action in the Jurkat cell line, an ALL tumor line established in the 1970s from the peripheral blood of a 14-year-old boy. 

The researchers found that minocycline did in fact induce apoptosis in Jurkat cells through a hydrogen peroxide (H₂O₂)-mediated signaling pathway. Indeed, they add, H₂O₂ triggers a whole cascade of adverse effects, including up-regulation of pro-apoptotic proteins. The researchers suggest that minocycline might even be capable of generating H₂O₂, which could explain the cytotoxic effects not only of minocycline, but of other tetracycline analogues. “Interestingly,” the researchers say, minocycline did all that without inducing oxidative stress or apoptosis makers in human peripheral blood lymphocyte cells.

The significance of their study is twofold, the researchers say: First, that minocycline is a safe and specific apoptosis-inducing drug against Jurkat cells in vitro; second, that it is pharmacologically well characterized and widely available.

The researchers note that no information is available on whether minocycline might efficiently kill ALL cells in vivo. However, they also note that minocycline has been found to be safe and well tolerated in doses up to 10 mg/kg in stroke patients—a dose that could be a sufficient concentration to reduce the viability of leukemia cell lines.

Source:
Ruiz-Moreno C, Velez-Pardo C, Jimenez-Del-Rio M. Toxicol In Vitro. 2018;50:336-346.
doi: 10.1016/j.tiv.2018.03.012

Where you live can determine how safe you are (or feel), where you shop, the kind of food you can buy, and other factors that affect your health. For some people, social factors, like their neighborhood, can disproportionately affect health. “Socioeconomic disadvantage is one of the fundamental factors that result in health disparities,” says Eliseo Pérez-Stable, MD, director of the National Institute on Minority Health and Health Disparities. “Having a tool to better understand social factors impacting health disparities is an important step forward to achieving health equity.”

Such a tool is available now developed by Amy Kind, MD, PhD, at the University of Wisconsin. The Neighborhood Atlas is an online platform that allows researchers to visualize socioeconomic data at local levels. Users can download maps indexed with data ranked according to 17 measures, including income, education, employment, and housing quality.

The Atlas is able to merge with other data sources to foster better understanding of how neighborhood disadvantage influences health, Kind says. For instance, researchers and health and social service providers can use the data to understand the risk factors for diseases, study the impact of health policies, or better align resources. Kind adds that the Atlas and the data can be harnessed to advance disparities-focused research, and to improve translational, clinical and community research by showing ways to aid design, recruitment, retention, and outreach.

Where you live can determine how safe you are (or feel), where you shop, the kind of food you can buy, and other factors that affect your health. For some people, social factors, like their neighborhood, can disproportionately affect health. “Socioeconomic disadvantage is one of the fundamental factors that result in health disparities,” says Eliseo Pérez-Stable, MD, director of the National Institute on Minority Health and Health Disparities. “Having a tool to better understand social factors impacting health disparities is an important step forward to achieving health equity.”

Such a tool is available now developed by Amy Kind, MD, PhD, at the University of Wisconsin. The Neighborhood Atlas is an online platform that allows researchers to visualize socioeconomic data at local levels. Users can download maps indexed with data ranked according to 17 measures, including income, education, employment, and housing quality.

The Atlas is able to merge with other data sources to foster better understanding of how neighborhood disadvantage influences health, Kind says. For instance, researchers and health and social service providers can use the data to understand the risk factors for diseases, study the impact of health policies, or better align resources. Kind adds that the Atlas and the data can be harnessed to advance disparities-focused research, and to improve translational, clinical and community research by showing ways to aid design, recruitment, retention, and outreach.

Where you live can determine how safe you are (or feel), where you shop, the kind of food you can buy, and other factors that affect your health. For some people, social factors, like their neighborhood, can disproportionately affect health. “Socioeconomic disadvantage is one of the fundamental factors that result in health disparities,” says Eliseo Pérez-Stable, MD, director of the National Institute on Minority Health and Health Disparities. “Having a tool to better understand social factors impacting health disparities is an important step forward to achieving health equity.”

Such a tool is available now developed by Amy Kind, MD, PhD, at the University of Wisconsin. The Neighborhood Atlas is an online platform that allows researchers to visualize socioeconomic data at local levels. Users can download maps indexed with data ranked according to 17 measures, including income, education, employment, and housing quality.

The Atlas is able to merge with other data sources to foster better understanding of how neighborhood disadvantage influences health, Kind says. For instance, researchers and health and social service providers can use the data to understand the risk factors for diseases, study the impact of health policies, or better align resources. Kind adds that the Atlas and the data can be harnessed to advance disparities-focused research, and to improve translational, clinical and community research by showing ways to aid design, recruitment, retention, and outreach.

Hundreds of reports since the 1980s have associated Alzheimer disease with bacteria and viruses. But researchers could not explain the connection. Now new research suggests that viral species, particularly herpes viruses, play a role in Alzheimer disease biology.

The hypotheses that link viruses to brain disease are not new, Richard Hodes, MD, director of the National Institute on Aging, says, but this is the first study to provide “strong evidence” based on unbiased approaches and large datasets.

The study, which was funded by National Institute of Aging (NIA) , originally was intended to find out whether drugs used to treat other diseases can be repurposed for treating Alzheimer. Researchers analyzed large datasets from postmortem brain samples to map and compare biological networks underlying Alzheimer disease. They found that the disease biology is impacted by a “complex constellation” of factors, including the ways the interrelated systems of DNA, RNA, proteins, and metabolites interact with molecular, genetic, and clinical aspects of Alzheimer disease.

Among the key findings: Human herpes virus 6A and 7 were more abundant in Alzheimer disease samples than in non-Alzheimer samples. Researchers also found multiple points of overlap between virus-host interactions and genes associated with Alzheimer risk.

The research “reinforces the complexity of Alzheimer disease,” Hode says, and “highlights the importance of sharing data freely and widely with the research community.”

Hundreds of reports since the 1980s have associated Alzheimer disease with bacteria and viruses. But researchers could not explain the connection. Now new research suggests that viral species, particularly herpes viruses, play a role in Alzheimer disease biology.

The hypotheses that link viruses to brain disease are not new, Richard Hodes, MD, director of the National Institute on Aging, says, but this is the first study to provide “strong evidence” based on unbiased approaches and large datasets.

The study, which was funded by National Institute of Aging (NIA) , originally was intended to find out whether drugs used to treat other diseases can be repurposed for treating Alzheimer. Researchers analyzed large datasets from postmortem brain samples to map and compare biological networks underlying Alzheimer disease. They found that the disease biology is impacted by a “complex constellation” of factors, including the ways the interrelated systems of DNA, RNA, proteins, and metabolites interact with molecular, genetic, and clinical aspects of Alzheimer disease.

Among the key findings: Human herpes virus 6A and 7 were more abundant in Alzheimer disease samples than in non-Alzheimer samples. Researchers also found multiple points of overlap between virus-host interactions and genes associated with Alzheimer risk.

The research “reinforces the complexity of Alzheimer disease,” Hode says, and “highlights the importance of sharing data freely and widely with the research community.”

Hundreds of reports since the 1980s have associated Alzheimer disease with bacteria and viruses. But researchers could not explain the connection. Now new research suggests that viral species, particularly herpes viruses, play a role in Alzheimer disease biology.

The hypotheses that link viruses to brain disease are not new, Richard Hodes, MD, director of the National Institute on Aging, says, but this is the first study to provide “strong evidence” based on unbiased approaches and large datasets.

The study, which was funded by National Institute of Aging (NIA) , originally was intended to find out whether drugs used to treat other diseases can be repurposed for treating Alzheimer. Researchers analyzed large datasets from postmortem brain samples to map and compare biological networks underlying Alzheimer disease. They found that the disease biology is impacted by a “complex constellation” of factors, including the ways the interrelated systems of DNA, RNA, proteins, and metabolites interact with molecular, genetic, and clinical aspects of Alzheimer disease.

Among the key findings: Human herpes virus 6A and 7 were more abundant in Alzheimer disease samples than in non-Alzheimer samples. Researchers also found multiple points of overlap between virus-host interactions and genes associated with Alzheimer risk.

The research “reinforces the complexity of Alzheimer disease,” Hode says, and “highlights the importance of sharing data freely and widely with the research community.”

Platelet-transmitted bacterial infections persist as a cause of transfusion-associated morbidity and mortality, according to researchers writing in Mortality and Morbidity Weekly Report. They describe 2 separate clusters of platelet transfusion-associated bacterial sepsis reported in Utah and California, in which 3 patients died.

Contamination of blood products most commonly happens when skin microbiota is introduced during needle insertion. Because most platelets are stored at room temperature, bacteria can proliferate to clinically important levels by the time the unit is transfused, the CDC says. About 1 in 5,000 platelet collections are contaminated; 1 in 100,000 platelet transfusions results in bacterial sepsis.

In Utah, 2 patients received contaminated apheresis platelet units. One developed rigors 30 minutes after infusion, but transfusion-transmitted bacterial infection was not considered because of the patient’s complex medical history. He died 4 days later.

Less than a day after the first patient’s infusion, the second patient received the other platelet unit. No immediate symptoms of sepsis followed but later that day routine laboratory testing revealed new intravascular hemolysis. She died 11 hours after transfusion.

In California, a patient developed vomiting, tachycardia, and hypotension within 15 minutes of an infusion that came from an apheresis blood donation. Although the transfusion was stopped, he died within 5 hours. A second patient developed septic shock approximately 9 hours after infusion but recovered.

Subsequent investigation found that both the Utah and California collection facilities followed current practices. However, the CDC report highlights that even when procedures are followed appropriately, the risk remains. The CDC says evidence-based strategies such as pathogen inactivation, rapid detection devices, and modified screen of bacterial culture protocols can help mitigate that risk.

Platelet-transmitted bacterial infections persist as a cause of transfusion-associated morbidity and mortality, according to researchers writing in Mortality and Morbidity Weekly Report. They describe 2 separate clusters of platelet transfusion-associated bacterial sepsis reported in Utah and California, in which 3 patients died.

Contamination of blood products most commonly happens when skin microbiota is introduced during needle insertion. Because most platelets are stored at room temperature, bacteria can proliferate to clinically important levels by the time the unit is transfused, the CDC says. About 1 in 5,000 platelet collections are contaminated; 1 in 100,000 platelet transfusions results in bacterial sepsis.

In Utah, 2 patients received contaminated apheresis platelet units. One developed rigors 30 minutes after infusion, but transfusion-transmitted bacterial infection was not considered because of the patient’s complex medical history. He died 4 days later.

Less than a day after the first patient’s infusion, the second patient received the other platelet unit. No immediate symptoms of sepsis followed but later that day routine laboratory testing revealed new intravascular hemolysis. She died 11 hours after transfusion.

In California, a patient developed vomiting, tachycardia, and hypotension within 15 minutes of an infusion that came from an apheresis blood donation. Although the transfusion was stopped, he died within 5 hours. A second patient developed septic shock approximately 9 hours after infusion but recovered.

Subsequent investigation found that both the Utah and California collection facilities followed current practices. However, the CDC report highlights that even when procedures are followed appropriately, the risk remains. The CDC says evidence-based strategies such as pathogen inactivation, rapid detection devices, and modified screen of bacterial culture protocols can help mitigate that risk.

Platelet-transmitted bacterial infections persist as a cause of transfusion-associated morbidity and mortality, according to researchers writing in Mortality and Morbidity Weekly Report. They describe 2 separate clusters of platelet transfusion-associated bacterial sepsis reported in Utah and California, in which 3 patients died.

Contamination of blood products most commonly happens when skin microbiota is introduced during needle insertion. Because most platelets are stored at room temperature, bacteria can proliferate to clinically important levels by the time the unit is transfused, the CDC says. About 1 in 5,000 platelet collections are contaminated; 1 in 100,000 platelet transfusions results in bacterial sepsis.

In Utah, 2 patients received contaminated apheresis platelet units. One developed rigors 30 minutes after infusion, but transfusion-transmitted bacterial infection was not considered because of the patient’s complex medical history. He died 4 days later.

Less than a day after the first patient’s infusion, the second patient received the other platelet unit. No immediate symptoms of sepsis followed but later that day routine laboratory testing revealed new intravascular hemolysis. She died 11 hours after transfusion.

In California, a patient developed vomiting, tachycardia, and hypotension within 15 minutes of an infusion that came from an apheresis blood donation. Although the transfusion was stopped, he died within 5 hours. A second patient developed septic shock approximately 9 hours after infusion but recovered.

Subsequent investigation found that both the Utah and California collection facilities followed current practices. However, the CDC report highlights that even when procedures are followed appropriately, the risk remains. The CDC says evidence-based strategies such as pathogen inactivation, rapid detection devices, and modified screen of bacterial culture protocols can help mitigate that risk.

After just 4 months, the National Institute of Alcohol Abuse and Alcoholism (NIAAA) is ending funding for the Moderate Alcohol and Cardiovascular Health (MACH) trial, citing concerns about the study design.

The MACH study was designed as a multicenter randomized trial to determine the effects of 1 serving of alcohol (approximately 15 g) a day compared with no alcohol intake on the rate of new cases of cardiovascular disease and new cases of diabetes among participants free of diabetes at baseline. The study was launched because some epidemiologic research had shown that moderate alcohol consumption had health benefits by reducing risk for coronary artery disease, type 2 diabetes, and rheumatoid arthritis.

The study began enrollment in February 2018 and was suspended on May 10. The NIAAA expected to commit $20 million to the project over 10 years, of which $4 million has been spent; remaining funding came from private donations of $67.7 million, of which $11.8 million has been spent.

The “orderly closeout” is based on recommendations from the advisory committee to the director working group, which found “significant process irregularities in the development of funding opportunities for the MACH funding awards undermined the integrity of the research process.” Additionally, a preliminary report from the National Institutes of Health (NIH) Office of Management Assessment determined that a small number of NIAAA employees violated NIH policies in soliciting gift funding and circumvented standard operating procedures.

After just 4 months, the National Institute of Alcohol Abuse and Alcoholism (NIAAA) is ending funding for the Moderate Alcohol and Cardiovascular Health (MACH) trial, citing concerns about the study design.

The MACH study was designed as a multicenter randomized trial to determine the effects of 1 serving of alcohol (approximately 15 g) a day compared with no alcohol intake on the rate of new cases of cardiovascular disease and new cases of diabetes among participants free of diabetes at baseline. The study was launched because some epidemiologic research had shown that moderate alcohol consumption had health benefits by reducing risk for coronary artery disease, type 2 diabetes, and rheumatoid arthritis.

The study began enrollment in February 2018 and was suspended on May 10. The NIAAA expected to commit $20 million to the project over 10 years, of which $4 million has been spent; remaining funding came from private donations of $67.7 million, of which $11.8 million has been spent.

The “orderly closeout” is based on recommendations from the advisory committee to the director working group, which found “significant process irregularities in the development of funding opportunities for the MACH funding awards undermined the integrity of the research process.” Additionally, a preliminary report from the National Institutes of Health (NIH) Office of Management Assessment determined that a small number of NIAAA employees violated NIH policies in soliciting gift funding and circumvented standard operating procedures.

After just 4 months, the National Institute of Alcohol Abuse and Alcoholism (NIAAA) is ending funding for the Moderate Alcohol and Cardiovascular Health (MACH) trial, citing concerns about the study design.

The MACH study was designed as a multicenter randomized trial to determine the effects of 1 serving of alcohol (approximately 15 g) a day compared with no alcohol intake on the rate of new cases of cardiovascular disease and new cases of diabetes among participants free of diabetes at baseline. The study was launched because some epidemiologic research had shown that moderate alcohol consumption had health benefits by reducing risk for coronary artery disease, type 2 diabetes, and rheumatoid arthritis.

The study began enrollment in February 2018 and was suspended on May 10. The NIAAA expected to commit $20 million to the project over 10 years, of which $4 million has been spent; remaining funding came from private donations of $67.7 million, of which $11.8 million has been spent.

The “orderly closeout” is based on recommendations from the advisory committee to the director working group, which found “significant process irregularities in the development of funding opportunities for the MACH funding awards undermined the integrity of the research process.” Additionally, a preliminary report from the National Institutes of Health (NIH) Office of Management Assessment determined that a small number of NIAAA employees violated NIH policies in soliciting gift funding and circumvented standard operating procedures.

The only 2 medicines currently approved for young people with type 2 diabetes—long-acting insulin and metformin—do not slow the progression of diabetes in young people, according to a study funded in part by the National Institute of Diabetes and Digestive and Kidney Diseases.

A substudy of the Restoring Insulin Secretion (RISE) study, the RISE Pediatric Medication Study looked at the effects of insulin and metformin in 91 patients aged 10 to 19 years. The participants were randomly assigned to 1 of 2 treatment groups. The first received 3 months of glargine, a long-acting insulin, followed by 9 months of metformin. The second group received only metformin for 12 months. The participants were followed for 3 more months after treatment ended. The pediatric study found that beta-cell function declined in both groups during treatment and worsened after treatment ended.

Researchers also compared the pediatric participants with their adult counterparts in 2 other RISE trials and found the young people had more insulin resistance and other signs of disease progression at the same stage in the disease. Moreover, at baseline, the younger patients responded to the severe insulin resistance with a greater insulin response than did the adults, which the researchers say may be a reason for their more rapid loss of beta-cell function.

However, the study also found modest improvement in blood glucose with metformin in both groups. But metformin alone is not a long-term solution for many youth, said Dr. Kristen Nadeau, principal investigator for the pediatric study. Their findings underscore the “urgent and growing need,” she says, for more options.

The only 2 medicines currently approved for young people with type 2 diabetes—long-acting insulin and metformin—do not slow the progression of diabetes in young people, according to a study funded in part by the National Institute of Diabetes and Digestive and Kidney Diseases.

A substudy of the Restoring Insulin Secretion (RISE) study, the RISE Pediatric Medication Study looked at the effects of insulin and metformin in 91 patients aged 10 to 19 years. The participants were randomly assigned to 1 of 2 treatment groups. The first received 3 months of glargine, a long-acting insulin, followed by 9 months of metformin. The second group received only metformin for 12 months. The participants were followed for 3 more months after treatment ended. The pediatric study found that beta-cell function declined in both groups during treatment and worsened after treatment ended.

Researchers also compared the pediatric participants with their adult counterparts in 2 other RISE trials and found the young people had more insulin resistance and other signs of disease progression at the same stage in the disease. Moreover, at baseline, the younger patients responded to the severe insulin resistance with a greater insulin response than did the adults, which the researchers say may be a reason for their more rapid loss of beta-cell function.

However, the study also found modest improvement in blood glucose with metformin in both groups. But metformin alone is not a long-term solution for many youth, said Dr. Kristen Nadeau, principal investigator for the pediatric study. Their findings underscore the “urgent and growing need,” she says, for more options.

The only 2 medicines currently approved for young people with type 2 diabetes—long-acting insulin and metformin—do not slow the progression of diabetes in young people, according to a study funded in part by the National Institute of Diabetes and Digestive and Kidney Diseases.

A substudy of the Restoring Insulin Secretion (RISE) study, the RISE Pediatric Medication Study looked at the effects of insulin and metformin in 91 patients aged 10 to 19 years. The participants were randomly assigned to 1 of 2 treatment groups. The first received 3 months of glargine, a long-acting insulin, followed by 9 months of metformin. The second group received only metformin for 12 months. The participants were followed for 3 more months after treatment ended. The pediatric study found that beta-cell function declined in both groups during treatment and worsened after treatment ended.

Researchers also compared the pediatric participants with their adult counterparts in 2 other RISE trials and found the young people had more insulin resistance and other signs of disease progression at the same stage in the disease. Moreover, at baseline, the younger patients responded to the severe insulin resistance with a greater insulin response than did the adults, which the researchers say may be a reason for their more rapid loss of beta-cell function.

However, the study also found modest improvement in blood glucose with metformin in both groups. But metformin alone is not a long-term solution for many youth, said Dr. Kristen Nadeau, principal investigator for the pediatric study. Their findings underscore the “urgent and growing need,” she says, for more options.