WASHINGTON – 4/12/2014 - The U.S. Sentencing Commission voted on April 11 to reduce sentencing guidelines for certain people convicted of nonviolent drug offenses. The amendment would reduce the average sentence for drug traffickers by 11 months, by lowering the drug sentencing guidelines two levels. Attorney General Eric Holder endorsed the change during testimony before the commission last month.
"Our country is slowly but steadily reversing the damage done by the failed, racially biased war on drugs," ACLU Senior Legislative Counse Jesselyn McCurdy said. "The actions taken by the Sentencing Commission . . . are another positive move toward reducing unnecessarily long sentences that have led to bloated, overcrowded prisons. Our criminal justice system is smarter, fairer, and more humane than it was a year ago, and we need to make sure momentum continues in the right direction."
The amendment, along with several others that were passed, will go to Congress for its approval on May 1. Congress has six months to introduce and pass legislation to stop the proposed changes before they become law on November 1.
Source: American Civil Liberties Union
Know Your Rights
SUMMARY: Hear from legal experts at the ACLU of Maine, U.S. Magistrate Judge James Orenstein (Ret.), and former U.S. Attorney Joyce Vance.
Study: Obesity Primes the Colon for Cancer
(NIH) - 4/5/2014 - Obesity, rather than diet, causes changes in the colon that may lead to colorectal cancer, according to a study in mice by the National Institutes of Health. The finding bolsters the recommendation that calorie control and frequent exercise are not only key to a healthy lifestyle, but a strategy to lower the risk for colon cancer, the second leading cause of cancer-related death in the United States.
Paul Wade, Ph.D., and Thomas Eling, Ph.D., scientists at the National Institute of Environmental Health Sciences (NIEHS), part of NIH, led a collaborative team that made the discovery. The study appeared online April 1 in the journal Cell Metabolism.
A large body of scientific literature says people who are obese are predisposed to a number of cancers, particularly colorectal cancer, Eling said. To better understand the processes behind this link, he and his colleagues fed two groups of mice a diet in which 60 percent of the calories came from lard. The first group of mice contained a human version of a gene called NAG-1, which has been shown to protect against colon cancer in other rodent studies. The second group lacked the NAG-1 gene.
The NAG-1 mice did not gain weight after eating the high-fat diet, while mice that lacked the NAG-1 gene grew plump.
The researchers noticed another striking difference between the two groups of animals.
“The obese mice exhibited molecular signals in their gut that led to the progression of cancer, but the NAG-1 mice didn’t have those same indicators,” Eling said.
The researchers looked for molecular clues, by isolating cells from the colons of the mice and analyzing a group of proteins called histones. Histones package and organize DNA in a cell’s nucleus, and sometimes undergo a process known as acetylation, in which chemical tags bind to their surface. The pattern of acetylation varies depending on the chemical processes taking place in the cell.
Wade explained that the acetylation patterns for the obese mice and the thin NAG-1 mice were drastically different. Patterns from the obese mice resembled those from mice with colorectal cancer. The additional weight they carried also seemed to activate more genes that are associated with colorectal cancer progression, suggesting the obese mice are predisposed to colon cancer.
“Any preexisting colon lesions in these animals are more likely to evolve rapidly into malignant tumors,” Wade said. “The same thing may happen in humans.”
Wade and Eling want to find out exactly how obesity prompts the body to develop colorectal cancer. Wade said that the likely candidates for triggering tumor growth in the colon are fat cells, but there are many more possibilities. Finding these cellular switches may give rise to production of medications to keep people from getting colorectal cancer.
“Once we identify the signaling pathways and understand how the signal is transduced, we may be able to design ways to treat colorectal cancer in obese patients,” Wade said.
Source: National Institutes of Health
Paul Wade, Ph.D., and Thomas Eling, Ph.D., scientists at the National Institute of Environmental Health Sciences (NIEHS), part of NIH, led a collaborative team that made the discovery. The study appeared online April 1 in the journal Cell Metabolism.
A large body of scientific literature says people who are obese are predisposed to a number of cancers, particularly colorectal cancer, Eling said. To better understand the processes behind this link, he and his colleagues fed two groups of mice a diet in which 60 percent of the calories came from lard. The first group of mice contained a human version of a gene called NAG-1, which has been shown to protect against colon cancer in other rodent studies. The second group lacked the NAG-1 gene.
The NAG-1 mice did not gain weight after eating the high-fat diet, while mice that lacked the NAG-1 gene grew plump.
The researchers noticed another striking difference between the two groups of animals.
“The obese mice exhibited molecular signals in their gut that led to the progression of cancer, but the NAG-1 mice didn’t have those same indicators,” Eling said.
The researchers looked for molecular clues, by isolating cells from the colons of the mice and analyzing a group of proteins called histones. Histones package and organize DNA in a cell’s nucleus, and sometimes undergo a process known as acetylation, in which chemical tags bind to their surface. The pattern of acetylation varies depending on the chemical processes taking place in the cell.
Wade explained that the acetylation patterns for the obese mice and the thin NAG-1 mice were drastically different. Patterns from the obese mice resembled those from mice with colorectal cancer. The additional weight they carried also seemed to activate more genes that are associated with colorectal cancer progression, suggesting the obese mice are predisposed to colon cancer.
“Any preexisting colon lesions in these animals are more likely to evolve rapidly into malignant tumors,” Wade said. “The same thing may happen in humans.”
Wade and Eling want to find out exactly how obesity prompts the body to develop colorectal cancer. Wade said that the likely candidates for triggering tumor growth in the colon are fat cells, but there are many more possibilities. Finding these cellular switches may give rise to production of medications to keep people from getting colorectal cancer.
“Once we identify the signaling pathways and understand how the signal is transduced, we may be able to design ways to treat colorectal cancer in obese patients,” Wade said.
Source: National Institutes of Health
Government Sues Sprint Over Wiretap Charges
SAN FRANCISCO – 3/19/2014 - The United States filed a civil complaint against Sprint Communications, Inc., formerly Sprint Nextel Corporation, under the False Claims Act, 31 U.S.C. §§ 3729-3733, according to a recent announcement by United States Attorney Melinda Haag and the U.S. Department of Justice Office of Inspector General, Special Agent in Charge M. Elise Chawaga.
The complaint seeks treble damages and civil penalties in connection with Sprint’s claims for reimbursement of the expenses it incurred in complying with court orders authorizing wiretaps, pen registers, and trap devices.
Like other telecommunications carriers, Sprint is authorized by statute to bill law enforcement agencies for the reasonable expenses it incurs in providing facilities or assistance to accomplish a court-ordered wiretap, pen register, or trap device. In 1994, Congress passed the Communications Assistance in Law Enforcement Act (“CALEA”), which required telecommunications carriers to upgrade their equipment, facilities, or services to ensure they were capable of enabling the government, pursuant to a court order, to intercept and deliver communications and call-identifying information.
In 2006, the Federal Communications Commission ruled that carriers were prohibited from passing on the costs of its CALEA upgrades to law enforcement agencies in its intercept bills. From 2007 to 2010, in violation of the FCC’s ruling, Sprint included in its intercept charges the hidden costs of financing its CALEA upgrades.
The complaint alleges that Sprint unlawfully inflated its charges by approximately 58 percent, causing federal law enforcement agencies to pay over $21 million in non-allowable costs from January 1, 2007 to July 31, 2010.
“As alleged, Sprint overbilled law enforcement agencies for carrying out court-ordered intercepts, causing a significant loss to the government’s limited resources,” U.S. Attorney Melinda Haag said. “This office will use all available tools to protect the public . . . and we will continue to hold those who present false claims to the government accountable.”
Assistant U.S. Attorney Steven Saltiel is prosecuting the case with the assistance of Legal Assistant Kathy Terry. The prosecution is the result of an investigation by the Department of Justice Office of Inspector General.
Source: United States Attorney's Office - Northern District of California
The complaint seeks treble damages and civil penalties in connection with Sprint’s claims for reimbursement of the expenses it incurred in complying with court orders authorizing wiretaps, pen registers, and trap devices.
Like other telecommunications carriers, Sprint is authorized by statute to bill law enforcement agencies for the reasonable expenses it incurs in providing facilities or assistance to accomplish a court-ordered wiretap, pen register, or trap device. In 1994, Congress passed the Communications Assistance in Law Enforcement Act (“CALEA”), which required telecommunications carriers to upgrade their equipment, facilities, or services to ensure they were capable of enabling the government, pursuant to a court order, to intercept and deliver communications and call-identifying information.
In 2006, the Federal Communications Commission ruled that carriers were prohibited from passing on the costs of its CALEA upgrades to law enforcement agencies in its intercept bills. From 2007 to 2010, in violation of the FCC’s ruling, Sprint included in its intercept charges the hidden costs of financing its CALEA upgrades.
The complaint alleges that Sprint unlawfully inflated its charges by approximately 58 percent, causing federal law enforcement agencies to pay over $21 million in non-allowable costs from January 1, 2007 to July 31, 2010.
“As alleged, Sprint overbilled law enforcement agencies for carrying out court-ordered intercepts, causing a significant loss to the government’s limited resources,” U.S. Attorney Melinda Haag said. “This office will use all available tools to protect the public . . . and we will continue to hold those who present false claims to the government accountable.”
Assistant U.S. Attorney Steven Saltiel is prosecuting the case with the assistance of Legal Assistant Kathy Terry. The prosecution is the result of an investigation by the Department of Justice Office of Inspector General.
Source: United States Attorney's Office - Northern District of California
Subjects
government,
law,
Sprint,
telecommunications,
wiretaps
Mutation Linked to Form of Cushing’s Syndrome
(NIH) - 3/12/2014 - Mutations in a gene containing part of the information needed to make an enzyme that provides energy for governing basic cell functions appear to contribute to a severe form of Cushing’s syndrome, according to researchers at the National Institutes of Health and nine European research institutions.
Cushing’s syndrome results when the body is exposed to too much of the stress hormone cortisol. The syndrome may result when the body itself produces excess cortisol, causing symptoms that may include high blood pressure, muscle weakness or osteoporosis.
The study was published online in the New England Journal of Medicine. In a letter to the editor of the same journal, members of the NIH research team and researchers in Italy reported that a mutation in another gene containing information needed to make yet another portion of the enzyme appears to be central to Carney Complex, a rare disease that causes multiple tumors and which is characterized by increased cortisone levels.
For the study on Cushing’s syndrome, the researchers examined tissue from patients having a subtype of Cushing’s syndrome, in which the source of the excess cortisol is a noncancerous tumor confined to only one of the body’ two adrenal glands. The researcher examined samples from nearly 200 such adrenal gland tumors. They found that 37 percent contained a mutation in the gene known as PRKACA.
“The mutation we identified appears to give rise to one of the most common kinds of adrenal tumors seen in Cushing’s syndrome,” said study co- first author Constantine Stratakis, M.D., D.Sc., director of the Division of Intramural Research and head of the Program on Developmental Endocrinology and Genetics at the Eunice Kennedy ShriverNational Institute of Child Health and Human Development (NICHD), the NIH institute that took part in the study. “The discovery suggests a clear path forward for investigating medications that might block the production of excess cortisol.”
The PRKACA gene contains the information needed to make a portion, or subunit, of the PKA (protein kinase A) enzyme. The enzyme is involved in numerous chemical reactions in the cell.
For these patients, the mutant PRKACA gene was found only in the tumor cells, and not in other cells of the body. Because the gene was not found in other cells of the body, the mutation likely arose spontaneously in the adrenal tissue.
The researchers also examined tissue from patients who had non-cancerous growths on both adrenal glands. In samples from these patients, the researchers found an extra copy of the PRKACAgene. This extra copy, they noted, was present in all of the patients’ cells, and was not limited to the tumor tissue. Because the mutation was found in all the cells of the body, it was likely hereditary.
However, in both the cases involving the spontaneous mutation and the inherited mutation, the activity of the PKA enzyme was increased.
“The mutation appears to spur the activity of this enzyme, Stratakis said. “The result appears to be an increase in cell growth and division in adrenal tissue, and an overproduction of cortisol.”
Stratakis collaborated with the other co-first authors, including Felix Beuschlein, M.D., of the Ludwig-Maximilians-University, in Munich, Germany; Martin Fassnacht, M.D., of Ludwig-Maximilians-University and the University of Wurtzburg, in Wurtzburg, Germany; Guillaume Assie, M.D., Ph.D., of the Paris Descartes University and Cochin Hospital, in Paris; Davide Calebiro, M.D., of the University of Wurtzburg; and 25 other researchers at the NICHD and institutions in France, Germany and Italy.
In a letter to the editor of the same issue of the New England Journal of Medicine, Orsetta Zuffardi of the University of Pavia, in Pavia, Italy and Stratakis and other colleagues in Italy and at the NIH discovered that a patient with Carney Complex, who had a tumor in the pituitary gland and elevated growth hormone, had an extra copy of the PRKACBgene. This gene codes for another subunit of Protein Kinase A. In addition to elevated growth hormone levels, people with Carney Complex often have skin spots and increased risk of tumors in the pituitary, adrenals as well as other parts of the body.
“It’s likely that the extra copy of this gene also increases the activity of protein kinase A, essentially setting the stage for increased cell proliferation and higher production of hormones,” Stratakis said.
Source: National Institutes of Health release of 2/26/2014
Cushing’s syndrome results when the body is exposed to too much of the stress hormone cortisol. The syndrome may result when the body itself produces excess cortisol, causing symptoms that may include high blood pressure, muscle weakness or osteoporosis.
The study was published online in the New England Journal of Medicine. In a letter to the editor of the same journal, members of the NIH research team and researchers in Italy reported that a mutation in another gene containing information needed to make yet another portion of the enzyme appears to be central to Carney Complex, a rare disease that causes multiple tumors and which is characterized by increased cortisone levels.
For the study on Cushing’s syndrome, the researchers examined tissue from patients having a subtype of Cushing’s syndrome, in which the source of the excess cortisol is a noncancerous tumor confined to only one of the body’ two adrenal glands. The researcher examined samples from nearly 200 such adrenal gland tumors. They found that 37 percent contained a mutation in the gene known as PRKACA.
“The mutation we identified appears to give rise to one of the most common kinds of adrenal tumors seen in Cushing’s syndrome,” said study co- first author Constantine Stratakis, M.D., D.Sc., director of the Division of Intramural Research and head of the Program on Developmental Endocrinology and Genetics at the Eunice Kennedy ShriverNational Institute of Child Health and Human Development (NICHD), the NIH institute that took part in the study. “The discovery suggests a clear path forward for investigating medications that might block the production of excess cortisol.”
The PRKACA gene contains the information needed to make a portion, or subunit, of the PKA (protein kinase A) enzyme. The enzyme is involved in numerous chemical reactions in the cell.
For these patients, the mutant PRKACA gene was found only in the tumor cells, and not in other cells of the body. Because the gene was not found in other cells of the body, the mutation likely arose spontaneously in the adrenal tissue.
The researchers also examined tissue from patients who had non-cancerous growths on both adrenal glands. In samples from these patients, the researchers found an extra copy of the PRKACAgene. This extra copy, they noted, was present in all of the patients’ cells, and was not limited to the tumor tissue. Because the mutation was found in all the cells of the body, it was likely hereditary.
However, in both the cases involving the spontaneous mutation and the inherited mutation, the activity of the PKA enzyme was increased.
“The mutation appears to spur the activity of this enzyme, Stratakis said. “The result appears to be an increase in cell growth and division in adrenal tissue, and an overproduction of cortisol.”
Stratakis collaborated with the other co-first authors, including Felix Beuschlein, M.D., of the Ludwig-Maximilians-University, in Munich, Germany; Martin Fassnacht, M.D., of Ludwig-Maximilians-University and the University of Wurtzburg, in Wurtzburg, Germany; Guillaume Assie, M.D., Ph.D., of the Paris Descartes University and Cochin Hospital, in Paris; Davide Calebiro, M.D., of the University of Wurtzburg; and 25 other researchers at the NICHD and institutions in France, Germany and Italy.
In a letter to the editor of the same issue of the New England Journal of Medicine, Orsetta Zuffardi of the University of Pavia, in Pavia, Italy and Stratakis and other colleagues in Italy and at the NIH discovered that a patient with Carney Complex, who had a tumor in the pituitary gland and elevated growth hormone, had an extra copy of the PRKACBgene. This gene codes for another subunit of Protein Kinase A. In addition to elevated growth hormone levels, people with Carney Complex often have skin spots and increased risk of tumors in the pituitary, adrenals as well as other parts of the body.
“It’s likely that the extra copy of this gene also increases the activity of protein kinase A, essentially setting the stage for increased cell proliferation and higher production of hormones,” Stratakis said.
Source: National Institutes of Health release of 2/26/2014
