There's no doubt this brazen, beautiful Javan leopard is a male, and he doesn't show any obvious signs of stress ? despite being recently added to the Red List of endangered species.
This prima donna Panthera pardus melas was caught relaxing by a camera trap in Indonesia's Mount Halimun Salak National Park by Age Kridalaksana, an ecologist working with the Center for International Forestry Research.
You can see the leopard come to life in a time-lapse video created from the camera images. Kridalaksana and his colleagues hope to use their new-found knowledge of the big cat's range to work out how best to manage his habitat.
The number of leopards on Java is estimated at 250 to 700, and on average each animal prowls a range of about 1000 hectares. But the island is losing 2000 hectares of rainforest each year to loggers and other causes, and the national park itself has already lost a quarter of its original area ? it's now down to 113,000 hectares. "If their habitat continues to shrink, they could face increasing competition for food and shelter," says Ken Sugimura, head of the project.
If you would like to reuse any content from New Scientist, either in print or online, please contact the syndication department first for permission. New Scientist does not own rights to photos, but there are a variety of licensing options available for use of articles and graphics we own the copyright to.
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YOSEMITE NATIONAL PARK, Calif. (AP) ? Federal investigators probing the hantavirus outbreak blamed for three deaths at Yosemite National Park recommended on Monday that design changes to tent cabins and other privately run lodging first be reviewed by National Park Service officials.
The report released by the Interior Department's Office of Inspector General found that park officials responded to last summer's outbreak appropriately and within department policy.
"When the outbreak was identified, NPS mobilized to contain and remediate the outbreak and to prevent further outbreaks," Mary Kendall, a deputy inspector general, wrote in a letter attached to the report.
Still, the report found that current policy didn't require park officials to approve design changes made to the "Signature tent cabins" by concessionaire Delaware North Companies Parks and Resorts, which added rafters and wall studs to the structures.
Investigators determined that deer mice, which can carry the illness, nested inside the double walls of the new tents in Yosemite's family friendly Curry Village.
At least eight of the nine tourists who fell ill stayed in the tent cabins.
Because the changes to the cabins were considered routine maintenance, current park service policy did not require prior approval, the report found.
The report also recommended that the park service begin cyclical pest monitoring and inspections of all public accommodations.
While there is a current pest monitoring program at Yosemite, Delaware North was responsible for Curry Village, which was not considered at high risk for hantavirus.
The company issued a statement late Monday saying it would follow the recommendations in the report.
"DNC Parks & Resorts at Yosemite has consistently worked hand-in-hand with the National Park Service and public health officials on this issue," spokeswoman Lisa Cesaro said in the statement. "The Signature Tent Cabins have been removed from Curry Village. We are following the recommendations by the National Park Service, which were developed in consultation with the California Department of Public Health and the Centers for Disease Control and Prevention."
Prior to the outbreak, Delaware only responded to pests in the cabins when visitors or housekeeping staff complained, the report said.
Treatment with A1-PI slows the progression of emphysema in Alpha-1 antitrypsin deficiencyPublic release date: 21-May-2013 [ | E-mail | Share ]
Contact: Nathaniel Dunford ndunford@thoracic.org American Thoracic Society
ATS 2013, PHILADELPHIA?Treatment with an Alpha-1 proteinase inhibitor (A1-PI), a naturally occurring protein that protects lung tissue from breakdown and protects the lung's elasticity, is effective in slowing the progression of emphysema in patients with Alpha-1 antitrypsin deficiency (AATD), a life-threatening genetic disorder, according to a new study presented at the 2013 American Thoracic Society International Conference.
The study showed the efficacy of A1-PIin preventing the loss of lung tissue as measured by computed tomography (CT) scan lung density at full inspiration (TLC), which is a more sensitive measure of disease progression than conventional parameters.This is the first prospective study to demonstrate the efficacy and safety of augmentation therapy in a randomized, placebo-controlled trial using this parameter.
"Our experience of the last quarter century has been that augmentation therapy is associated with better preserved lung function and reduced mortality, " said lead author Kenneth R. Chapman, M.D., director of the Asthma and Airway Centre of the University Health Network, in Toronto. "This randomized, placebo-controlled trial using a sensitive measure of lung density adds the most rigorous evidence to date that augmentation therapy slows the progression of emphysema in patients with Alpha-1 antitrypsin deficiency. The effect of A1-PI seen in this trial was both clinically and statistically significant, finally confirming its benefit in preventing the loss of lung tissue in patients with this potentially debilitating disease."
Chapman added that preliminary data from an extension trial suggest that early treatment with A1-PIshows persistent efficacy in patients with AATD and emphysema. In both the A1-PI and placebo groups who elected to continue treatment withA1-PI 60 mg/kg weekly, the benefit in CT scan lung density decline continued.
AATD is a hereditary condition that can severely affect a patient's lung function. The condition is marked by a low level or absence of A1-PI, a natural protein that protects the lung from breakdown by inhibiting neutrophil elastase, and protects lung elasticity. AATD can lead to emphysema at a young age (
There is no cure for AATD, but there are treatments for the symptoms of the disease, including bronchodilators and inhaled steroids, which help open the airways. Augmentation therapy, which is administered intravenously, has been shown to slow or halt the destruction of lung tissue in AATD.
The current trial, the largest clinical trial of this treatment to date, was a randomized, placebo-controlled, double-blind, multinational, multicenter phase III/IV study comparing the efficacy and safety ofA1-PIwith placebo in 180 subjects with emphysema due to AATD. Patients received A1-PIintravenously 60 mg/kg weekly or matching placebo over two years. The effect ofA1-PI on the progression of emphysema, the primary endpoint of the study, was assessed by the decline of lung density, measured by CT scan. Key secondary endpoints included changes in exercise capacity, symptoms score and rate of pulmonary exacerbations over two years.
There was no difference between groups in baseline characteristics: mean age 53.1 +/- 7.4 year; forced expiratory volume in 1 second (FEV1) 48.9 +/- 11.7%. According to study findings, the annual rate of lung density loss was significantly less in A1-PI-treated patients (-1.45 +/- 0.24 units vs. -2.19 +/-0.25 units; p = 0.017, one sided). Secondary outcome variables and the few adverse reactions reported were not significantly different between groups.
"The augmentation treatment used in the current study is not known to have a role in emphysema caused by tobacco smoking unrelated to alpha-1 antitrypsin deficiency, and our findings apply to a particular type of genetically-related emphysema," said Dr. Chapman. "Furthermore, our findings show preservation, but not restoration, of lung tissue. That is, the treatment slows the damage for people with alpha-1 antitrypsin deficiency but does not repair the damage."
"Although augmentation therapy has been well accepted in the United States, it has been slow to gain acceptance in other countries where augmentation therapy may be unavailable and/or unfunded. Our positive findings may encourage more widespread use of this treatment," said Dr. Chapman.
"With 2013 marking the 50th anniversary of the discovery of Alpha-1 antitrypsin deficiency, we are excited to now have confirmation of the clinical efficacy of this therapy in reducing the loss of lung tissue in Alpha-1 patients who have emphysema, " said Gerry McElvaney, professor of medicine at Royal College of Surgeons of Ireland, and principal investigator of the trial.
###
* Please note that numbers in this release may differ slightly from those in the abstract. Many of these investigations are ongoing; the release represents the most up-to-date data available at press time.
Abstract 45385
IV Alpha1 Antitrypsin (A1AT) Preserves Lung Density In Homozygous Alpha1 Antitrypsin Deficiency (A1ATD); A Randomized, Placebo-Controlled Trial
Authors: K.R. Chapman1, J.G.W. Burdon2, E. Piitulainen3, R.A. Sandhaus4, N. Seersholm5, J.M. Stocks6, L. Huang7, J.M. Edelman7, N.G. McElvaney8; 1University Health Network - Toronto/CA, 2St. Vincent's Hospital - Melbourne, VIC/AU, 3Lund University - Malmo/SE, 4National Jewish Health - Denver, CO/US, 5Gentofte Hospital - Hellerup/DK, 6University of Texas Health Science Center at Tyler - Tyler, TX/US, 7CSL Behring - King Of Prussia, PA/US, 8Beaumont Hospital, Royal College of Surgeons in Ireland - Dublin/IE; RAPID Trial Study Group
Abstract Body
Background: Observational studies show slower rates of lung function decline and decreased mortality in A1ATD patients receiving IV augmentation with purified A1AT but efficacy in slowing emphysema progression has not been confirmed by a randomized, placebo-controlled trial. CT scan measured lung density is a more sensitive measure of disease progression in A1ATD emphysema than conventional lung function parameters and is a biomarker of response to therapy. Methods: In a multi-center, multi-national trial, we randomized patients with homozygous A1ATD (ZZ) to receive A1AT (Zemaira, CSL Behring) intravenously 60 mg/kg weekly or placebo over 2 years, measuring CT scan lung density at baseline, 3 months, 1 and 2 years. Secondary endpoints included spirometry, KCO, shuttle walk and reported adverse events. Results: There was no difference between groups in baseline characteristics: mean age 53.1 +/- 7.4 (SD) yr; FEV1 48.9 +/- 11.7 (SD) %; KCO 31.7 +/- 5.8 (SD) %. Of 180 patients randomized (98 men, 82 women), 153 completed the trial (84/93 A1AT, 69/87 placebo, p=0.04). The annual rate of lung density loss was significantly less in A1AT-treated patients (-1.45 +/- 0.24 units vs. -2.19 +/-0.25 units; p = 0.017, one-sided). Secondary outcome variables and adverse events were not significantly different between groups. There was 1 death in the A1AT group and 3 in the placebo group. Conclusions: Purified A1AT augmentation IV slowed the progression of emphysema as measured by CT scan lung density, a more sensitive measure of disease progression in AATD emphysema than conventional lung function parameters. This is the first prospective study demonstrating the efficacy and safety of augmentation therapy in a randomized, placebo-controlled trial using this parameter.
[ | E-mail | Share ]
?
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
Treatment with A1-PI slows the progression of emphysema in Alpha-1 antitrypsin deficiencyPublic release date: 21-May-2013 [ | E-mail | Share ]
Contact: Nathaniel Dunford ndunford@thoracic.org American Thoracic Society
ATS 2013, PHILADELPHIA?Treatment with an Alpha-1 proteinase inhibitor (A1-PI), a naturally occurring protein that protects lung tissue from breakdown and protects the lung's elasticity, is effective in slowing the progression of emphysema in patients with Alpha-1 antitrypsin deficiency (AATD), a life-threatening genetic disorder, according to a new study presented at the 2013 American Thoracic Society International Conference.
The study showed the efficacy of A1-PIin preventing the loss of lung tissue as measured by computed tomography (CT) scan lung density at full inspiration (TLC), which is a more sensitive measure of disease progression than conventional parameters.This is the first prospective study to demonstrate the efficacy and safety of augmentation therapy in a randomized, placebo-controlled trial using this parameter.
"Our experience of the last quarter century has been that augmentation therapy is associated with better preserved lung function and reduced mortality, " said lead author Kenneth R. Chapman, M.D., director of the Asthma and Airway Centre of the University Health Network, in Toronto. "This randomized, placebo-controlled trial using a sensitive measure of lung density adds the most rigorous evidence to date that augmentation therapy slows the progression of emphysema in patients with Alpha-1 antitrypsin deficiency. The effect of A1-PI seen in this trial was both clinically and statistically significant, finally confirming its benefit in preventing the loss of lung tissue in patients with this potentially debilitating disease."
Chapman added that preliminary data from an extension trial suggest that early treatment with A1-PIshows persistent efficacy in patients with AATD and emphysema. In both the A1-PI and placebo groups who elected to continue treatment withA1-PI 60 mg/kg weekly, the benefit in CT scan lung density decline continued.
AATD is a hereditary condition that can severely affect a patient's lung function. The condition is marked by a low level or absence of A1-PI, a natural protein that protects the lung from breakdown by inhibiting neutrophil elastase, and protects lung elasticity. AATD can lead to emphysema at a young age (
There is no cure for AATD, but there are treatments for the symptoms of the disease, including bronchodilators and inhaled steroids, which help open the airways. Augmentation therapy, which is administered intravenously, has been shown to slow or halt the destruction of lung tissue in AATD.
The current trial, the largest clinical trial of this treatment to date, was a randomized, placebo-controlled, double-blind, multinational, multicenter phase III/IV study comparing the efficacy and safety ofA1-PIwith placebo in 180 subjects with emphysema due to AATD. Patients received A1-PIintravenously 60 mg/kg weekly or matching placebo over two years. The effect ofA1-PI on the progression of emphysema, the primary endpoint of the study, was assessed by the decline of lung density, measured by CT scan. Key secondary endpoints included changes in exercise capacity, symptoms score and rate of pulmonary exacerbations over two years.
There was no difference between groups in baseline characteristics: mean age 53.1 +/- 7.4 year; forced expiratory volume in 1 second (FEV1) 48.9 +/- 11.7%. According to study findings, the annual rate of lung density loss was significantly less in A1-PI-treated patients (-1.45 +/- 0.24 units vs. -2.19 +/-0.25 units; p = 0.017, one sided). Secondary outcome variables and the few adverse reactions reported were not significantly different between groups.
"The augmentation treatment used in the current study is not known to have a role in emphysema caused by tobacco smoking unrelated to alpha-1 antitrypsin deficiency, and our findings apply to a particular type of genetically-related emphysema," said Dr. Chapman. "Furthermore, our findings show preservation, but not restoration, of lung tissue. That is, the treatment slows the damage for people with alpha-1 antitrypsin deficiency but does not repair the damage."
"Although augmentation therapy has been well accepted in the United States, it has been slow to gain acceptance in other countries where augmentation therapy may be unavailable and/or unfunded. Our positive findings may encourage more widespread use of this treatment," said Dr. Chapman.
"With 2013 marking the 50th anniversary of the discovery of Alpha-1 antitrypsin deficiency, we are excited to now have confirmation of the clinical efficacy of this therapy in reducing the loss of lung tissue in Alpha-1 patients who have emphysema, " said Gerry McElvaney, professor of medicine at Royal College of Surgeons of Ireland, and principal investigator of the trial.
###
* Please note that numbers in this release may differ slightly from those in the abstract. Many of these investigations are ongoing; the release represents the most up-to-date data available at press time.
Abstract 45385
IV Alpha1 Antitrypsin (A1AT) Preserves Lung Density In Homozygous Alpha1 Antitrypsin Deficiency (A1ATD); A Randomized, Placebo-Controlled Trial
Authors: K.R. Chapman1, J.G.W. Burdon2, E. Piitulainen3, R.A. Sandhaus4, N. Seersholm5, J.M. Stocks6, L. Huang7, J.M. Edelman7, N.G. McElvaney8; 1University Health Network - Toronto/CA, 2St. Vincent's Hospital - Melbourne, VIC/AU, 3Lund University - Malmo/SE, 4National Jewish Health - Denver, CO/US, 5Gentofte Hospital - Hellerup/DK, 6University of Texas Health Science Center at Tyler - Tyler, TX/US, 7CSL Behring - King Of Prussia, PA/US, 8Beaumont Hospital, Royal College of Surgeons in Ireland - Dublin/IE; RAPID Trial Study Group
Abstract Body
Background: Observational studies show slower rates of lung function decline and decreased mortality in A1ATD patients receiving IV augmentation with purified A1AT but efficacy in slowing emphysema progression has not been confirmed by a randomized, placebo-controlled trial. CT scan measured lung density is a more sensitive measure of disease progression in A1ATD emphysema than conventional lung function parameters and is a biomarker of response to therapy. Methods: In a multi-center, multi-national trial, we randomized patients with homozygous A1ATD (ZZ) to receive A1AT (Zemaira, CSL Behring) intravenously 60 mg/kg weekly or placebo over 2 years, measuring CT scan lung density at baseline, 3 months, 1 and 2 years. Secondary endpoints included spirometry, KCO, shuttle walk and reported adverse events. Results: There was no difference between groups in baseline characteristics: mean age 53.1 +/- 7.4 (SD) yr; FEV1 48.9 +/- 11.7 (SD) %; KCO 31.7 +/- 5.8 (SD) %. Of 180 patients randomized (98 men, 82 women), 153 completed the trial (84/93 A1AT, 69/87 placebo, p=0.04). The annual rate of lung density loss was significantly less in A1AT-treated patients (-1.45 +/- 0.24 units vs. -2.19 +/-0.25 units; p = 0.017, one-sided). Secondary outcome variables and adverse events were not significantly different between groups. There was 1 death in the A1AT group and 3 in the placebo group. Conclusions: Purified A1AT augmentation IV slowed the progression of emphysema as measured by CT scan lung density, a more sensitive measure of disease progression in AATD emphysema than conventional lung function parameters. This is the first prospective study demonstrating the efficacy and safety of augmentation therapy in a randomized, placebo-controlled trial using this parameter.
[ | E-mail | Share ]
?
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
One reason the Internet has become so popular thing to use is because of how easy it is to reach out or share things with other individuals. This is extremely beneficial for new business online. Read the following article for article advertising tips and techniques which can help you boost your business.
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WASHINGTON (AP) ? The president and CEO of The Associated Press says the government's seizure of AP journalists' phone records was "unconstitutional" and already has had a chilling effect on newsgathering.
Gary Pruitt says the Justice Department's secret subpoena of reporters' phone records has made sources less willing to talk to AP journalists.
The Justice Department disclosed the seizure of two months of phone records in a letter the AP received May 10. The letter did not state a reason, but prosecutors had said they were conducting a leaks investigation into how the AP learned about an al-Qaida bomb plot in Yemen before it was made public last year. Pruitt said the AP story contradicted the government's claim at the time there was no terrorist plot.