Outsourcing is similar to hiring a staff. A business person recognizes the importance of leveraging other people?s time and skills to their advantage. To some, outsourcing is an uncommon name for something that they know all to well. There are very few things that can grow your business faster than outsourcing your work out to people. If your marketing is already producing results then you can have far greater results by hiring workers. The most successful marketers understand this concept very well. Outsourcing is simple but it looks simpler than what it really is. Patience is required with outsourcing because you will not see instant results. Keep reading to discover proven outsourcing methods.
The first thing you can easily outsource is the product creation part. That?s right; you can have your product created by a professional, while you sit back and relax. If there?s a business task that needs to be done, you can find someone who will be happy to get paid to do it. This is extremely common in IM, in fact none of your customers will ever have the slightest clue you didn?t write that great new ebook. No one knows, and if it?s good people will love and send in their testimonials. Even posts to your blog or your newsletter can be hired out. If you choose this route, you just need to be sure you have a good writer on your staff. An important tip to keep in mind when outsourcing your tasks is that you need to offer the worker a test project first to see his/her caliber. This is before you assign the complete project to the worker. This is an effective way to gauge the quality of their work and other factors. For example, if you have to get 20 articles written every month, you can give this writer 5-10 articles first to test the waters and see he/she is good enough to hire for the job. The best approach is to gradually scale-up the level of responsibility, and you?ll be able to filter out anyone or keep them because you know they?ll do well for you. You?ll be able to retain those who do well for you, or keep them on file so you can hire them for future projects. Look at considering Bodybuilding.com Coupons for in-depth advice.
One of the important tasks that you can outsource for your Internet marketing business is customer service. All the customer service needs and responsibilities are very time consuming, to say the least. If you?re established, this can save you a huge amount of time and aggravation. Whatever you do, be very sure you pick someone who will do a great job and never mess up in this important area of your business. That is why so many marketers outsource as much as possible, it gives them time and choices.
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A jury's refusal to convict John Edwards was less a redemption of the former White House hopeful than a rejection of the Justice Department's boldest attempt to make an example of someone in the name of enforcing campaign finance laws.
Thursday's verdict of not guilty on one count and a mistrial on five others bore out criticism from the earliest stages of the case that it was a reach, that prosecutors went after the ex-U.S. senator without the kind of evidence that justified the charges that he masterminded a scheme to use campaign donations to hide his pregnant mistress from the public and his terminally ill wife.
"As noted by nearly every campaign finance lawyer who considered the matter, this was a lousy case," said Melanie Sloan, executive director for the campaign finance watchdog group Citizens for Responsibility and Ethics in Washington. "All the salacious details prosecutors offered up to prove that Edwards is, indeed, despicable, were not enough to persuade the jury to convict him."
Several jurors said there just wasn't enough evidence. On network talk shows Friday, even jurors who thought Edwards was guilty on at least some counts said the prosecution wasn't able to prove it.
"We tried to put our feelings aside and what we were doing was just looking at the facts to come up with a verdict," juror Cindy Aquaro said on NBC's "Today" show.
Edwards faced six felony charges involving nearly $1 million provided by two wealthy political donors that was used to help hide the Democrat's mistress, Rielle Hunter, as he sought the White House in 2008. He faced a maximum sentence of up to 30 years in prison if convicted on all counts.
To convict Edwards, prosecutors needed to show not only that the candidate knew about the secret payments, which he denied, but that he knew he was violating federal law by accepting them. But the government was unable to produce any witness who said Edwards knowingly violated the law. Even former Edwards aide Andrew Young testified that Edwards told him he had consulted campaign finance lawyers who assured him the money was legal.
A former trial lawyer, Edwards was so unimpressed with the testimony against him that when the government rested, he turned to a member of his defense team and asked dismissively, "That's their case?"
When it was their turn, his lawyers presented just two days of evidence. Edwards elected not to take the stand in his own defense.
"This is a case that should define the difference between a wrong and a crime ... between a sin and a felony," Edwards' lead attorney Abbe Lowell told the jury during closing arguments. "John Edwards has confessed his sins. He will serve a life sentence for those."
Presented with no damning evidence and no obvious victim beyond the public's trust, jurors couldn't see their way to convicting the charismatic ex-candidate. Prosecutors are unlikely to retry the case, a law enforcement official told The Associated Press on the condition of anonymity because the decision will undergo review in the coming days.
Kieran Shanahan, a former federal prosecutor and Raleigh defense attorney who attended the trial, said he thought the prosecutors took their best shot with what was ultimately a very weak case.
"They got their best witnesses, their best evidence and the judge ruled in their favor on all major evidentiary issues," Shanahan said. "In the end, the jury just didn't believe them."
Steve Friedland, another former federal prosecutor who watched the case from inside the courtroom, said the jury's verdict was not surprising, considering the government had no smoking gun to prove Edwards guilty beyond a reasonable doubt.
But, he predicted, Edwards won't fare as well in the court of public opinion.
"Regardless of the decision, he still is Exhibit A for how we do not want our leaders to behave," said Friedland, now a professor at Elon University School of Law. "This is a huge victory for him, and big burden off his shoulders, but a hollow one given his astounding fall from grace."
From the start, lawyers for Edwards painted the prosecution as politically motivated. The investigation was originally spearheaded by George Holding, the then-U.S. Attorney for the Eastern District of North Carolina.
Appointed by President George W. Bush, Holding made a name for himself with criminal probes of high profile Democrats, including the state's former governor. When President Barack Obama came into office, Holding managed to forestall being replaced by a Democrat for years while the Edwards investigation was ongoing. He eventually resigned in 2011 as Edwards was indicted and soon announced his candidacy for Congress, winning in the GOP primary last month.
The final decision to prosecute Edwards was made by the Obama administration and the Justice Department's Public Integrity Section. Once highly admired, the section's reputation suffered after a corruption conviction against former U.S. Sen. Ted Stevens of Alaska was overturned in 2009 after it was found prosecutors knowingly concealed exculpatory evidence and allowed false testimony to be presented at trial.
The case against Edwards was tried by three prosecutors sent down from Washington and one prosecutor from Raleigh who had served as Holding's second-in-command. They presented 14 days of testimony and evidence, with Young their star witness.
An aide once so loyal he falsely claimed paternity of Edwards' baby and helped hide his mistress from the media for nearly a year, Young turned against his former boss and testified for the prosecution under an immunity agreement. Though the government's case recounted how Edwards repeatedly lied about his affair to both the American people and his cancer-stricken wife, the defense countered by shredding Young's credibility on the witness stand and using financial records to show the former aide and his wife kept most of the money at issue in the case, funneling it into the construction of the couple's $1.6 million dream home.
Before Edwards' prosecution, no federal candidate had been tried over payments from a third party that flowed to a mistress. Sloan said the lack of resolution in the case will likely leave candidates and regulators confused about what is and is not a legitimate campaign expense.
"The U.S. criminal justice system requires fair notice of what is and is not against the law," Sloan said. "Sadly, the Justice Department seems to have forgotten this fundamental American precept. Luckily, the jury remembered."
In recent years, a growing body of evidence has linked inflammation to the development of insulin resistance. In insulin resistance, the hormone insulin is less effective in promoting glucose uptake from the bloodstream into other tissues. Obesity is a major factor that contributes to insulin resistance, which can eventually lead to type 2 diabetes. Previous studies have shown that proinflammatory molecules found in fat tissue decreases sensitivity of tissues to insulin.
To identify drug targets that will improve insulin sensitivity, Dr. Olivia Osborn and her colleagues from the University of California in San Diego investigated the role of G protein-coupled receptor 21 (GPR21) in insulin resistance and energy homeostasis. The group compared mice without the gene encoding GPR21 to healthy control mice under normal and high-fat diet conditions. They discovered that mice lacking GPR21 had enhanced insulin sensitivity and increased energy expenditure independent of diet. This result was attributed to the reduced migration of inflammatory cells to the liver and fat tissue in the absence GPR21. Under normal diet, absence of GPR21 in the hypothalamus caused a modest decrease in body weight. This is the first study to demonstrate the negative impact of GPR21 on inflammation and insulin sensitivity. Their findings suggest that GPR21 inhibition may improve insulin resistance and enhance energy expenditure, making GPR21 inhibitors promising treatments for diabetes.
TITLE:
G proteincoupled receptor 21 deletion improves insulin sensitivity in diet-induced obese mice
View this article at: http://www.jci.org/articles/view/61953?key=dbc390c7fd2397640830
METABOLISM
Keep metabolism in mind
Metabolic regulation requires activity in the brain that controls glucose balance and food uptake. The hormones insulin, which controls glucose uptake, and leptin, which regulates energy intake and energy expenditure, are critical for mediating energy balance and influence a number of activities in the brain. Dr. Joel Elmquist and colleagues at the University of Texas in Houston wanted to specifically determine which neurons in the brain are required for regulating energy balance. The research team knew that a transcription factor called FOXO1 controlled expression of many genes in response to insulin and leptin signaling. Using genetically modified mice that lack FOXO1 in a specific area of the brain called the ventral medial nucleus of the hypothalamus, they showed that these mice are lean because of increased energy expenditure. Further, these mice had higher sensitivity to insulin in muscle, and were unable to decrease energy expenditure in response to fasting. Their data shows that the action of FOXO1 in the ventral medial nucleus of the hypothalamus is critical for appropriate regulation of energy expenditure and normal glucose balance.
TITLE:
FOXO1 in the ventromedial hypothalamus regulates energy balance
View this article at: http://www.jci.org/articles/view/62848?key=9c93a1c72137e21a5364
ONCOLOGY
The right combination: overcoming drug resistance in cancer
Overactive epidermal growth factor receptor (EGFR) signaling has been linked to the development of cancer. Several drug therapies have been developed to treat these EGFR-associated cancers; however, many patients have developed resistance to these drugs and are therefore no longer responsive to drug treatment. In a recent research article published in the Journal of Clinical Investigation, Goutham Narla and colleagues at Case Western Reserve University sought to better understand the molecular players in the EGFR signaling pathway in hopes of finding new drug targets for EGFR-associated cancers. Using cancerous human lung tissue and a mouse model of EGFR-associated lung cancer, The Narla team discovered that two tumor suppressor genes, KLF6 and FOXO1, function to disrupt overactive EGFR signaling. After treating the cancerous lung tissue and cancer-prone mice with an FDA-approved drug called trifluoperazine hydrochloride (TFP), which increases the activity of FOXO1, they restored the effectiveness of the anti-EGFR drug erlotinib and reduced tumor growth. Their work identified new drug targets for EGFR-associated cancers and suggests that combinatorial drug therapy regimens may improve treatment outcome.
TITLE:
Targeting the FOXO1/KLF6 axis regulates EGFR signaling and treatment response
AUTHOR CONTACT:
Goutham Narla
Case Western Reserve University and University Hospitals, Cleveland, OH, USA
Phone: 3472550885; E-mail: Goutham.Narla@mssm.edu
View this article at: http://www.jci.org/articles/view/62058?key=9eb9f31baf7df0c3365e
NEUROLOGICAL DISEASE
Finding new treatment options in inflammatory brain diseases
A team of scientist, led by Dr. Azeb Tadesse Argaw from the Corinne Goldsmith Dickinson Center for Multiple Sclerosis, have identified a promising avenue for treating inflammatory brain diseases like multiple sclerosis. When the barrier that protects the brain, known as the blood brain barrier (BBB), becomes weak and permeable, it can lead to brain inflammation, edema and neurotoxicity. In a previous study, the group discovered that inflammatory mediators involved in brain lesion development induced angiogenic proteins in the astrocytes. This finding led them to investigate the impact of a protein that stimulates angiogenesis, vascular endothelial growth factor-A (VEGF-A), on brain permeability and inflammation. In this study, the team generated mice that have inactivated VEGF-A proteins in the astrocytes. This mouse model showed reduced BBB breakdown, decreased inflammatory cell infiltration, and increased mobility following administration of a paralytic agent. Next, the group evaluated the efficacy of a few agents in diminishing the negative effects of VEGF-A on the BBB. They discovered that systemic inhibition of endothelial nitric oxide synthase (eNOS) abolished the effects of VEGF-A on BBB breakdown. Additionally, they found that treatment with a selective eNOS inhibitor reduced drug-induced paralysis in mice. These exciting results indicate that blocking VEGF-A is an effective strategy for treating inflammatory brain diseases. Importantly, eNOS inhibitors can be given peripherally to reduce the harmful effects of VEGF-A on the brain.
TITLE:
Astrocyte-derived VEGF-A drives blood-brain barrier disruption in CNS inflammatory disease
View this article at: http://www.jci.org/articles/view/60842?key=f54bc2cb8432c10cbd88
ONCOLOGY
Tumor growth and chemoresistance are promoted by ribosomal associated protein RACK
In cells, ribosomes are responsible for translating genetic information, in the form of messenger RNA, to proteins. Coordinated translation initiation is coupled with cell cycle progression and cell growth, but excessive ribosome synthesis and translation initiation can promote cancer. Hepatocellular carcinoma is among the most common and aggressive cancers worldwide and generally displays inherently high resistance to chemotherapeutic drugs. Dr. Jianxin Gu and colleagues at Fudan University in Shanghai, China found that RACK1, the receptor for activated C-kinase 1, was highly expressed in normal liver and frequently upregulated in hepatocellular carcinoma. Aberrant expression of RACK1 contributed to chemoresistance as well as to tumor growth of hepatocellular carcinoma, effects that depended on ribosome localization of RACK1. The group went on to show that ribosomal RACK1 promoted preferential translation of the potent factors involved in growth and survival. Their results imply that RACK1 may function as an internal factor involved in the growth and survival of hepatocellular carcinoma and suggest that targeting RACK1 may be an efficacious strategy for hepatocellular carcinoma treatment.
TITLE:
Ribosomal RACK1 promotes chemoresistance and growth in human hepatocellular carcinoma
AUTHOR CONTACT:
Jianxin Gu
Gene Research Center, Shanghai Medical College, Fudan University, Shanghai, , CHN
Phone: 8621-54237704; E-mail: jxgu@shmu.edu.cn
View this article at: http://www.jci.org/articles/view/58488?key=b32b824a1904ce6fbd34
Glucocorticoids (GCs) are commonly used to treat autoimmunity, but their normal roles in the immune system are not well known. Noting that GCs are naturally made in the thymus, the site where immune cells called T cells originate, Dr. Jonathan Ashwell and his group at the National Cancer Institute studied the role of GCs in T cell development and activation. They designed a mouse line in which the gene encoding the GC receptor (GR) is deleted in immature T cells. They found that the GR-deficient T cells could not respond appropriately to antigen-induced signaling. T cells generate a diverse repertoire of TCR to respond to foreign antigens in the body. Mittelstadt's group concluded that the defects were due to a shift in the TCR repertoire because they found that GR-deficient T cells responded normally when they forced to express a TCR with a fixed specificity. They demonstrated alterations in the TCR repertoire genetically, reporting a difference in the usage of particular TCR-encoding gene segments between GR-deficient and wild-type cells. The TCR repertoire is selected in the thymus where immature T cells that recognize the body's own proteins are selected against and killed. In the GR-deficient thymus, the numbers of T cells late in the maturation pathway were reduced, suggesting unusually high numbers of T cells were previously eliminated. The group concluded that the GCs in the thymus prevent inappropriate killing of T cells during development, thus providing a sufficient and diverse TCR repertoire.
TITLE:
Thymocyte responsiveness to endogenous glucocorticoids is required for immunological fitness
View this article at: http://www.jci.org/articles/view/63067?key=24fae67ed3776d86f2e0
NEUROLOGICAL DISEASE
Breathing abnormalities uncovered in mouse model of Leigh Syndrome
Leigh syndrome is a progressive neurodegenerative disorder affecting 1 in 40,000 live births. In up to 75% of cases, patient death is caused by respiratory arrest, but the molecular mechanisms behind breathing abnormalities are unclear.
Mutations in Leigh syndrome patients have been reported to occur in components of the mitochondrial complex I, which plays a vital role in cellular energy production, though how these mutations contribute to the development of disease is unknown. Researchers from the Howard Hughes Medical Institute at University of Washington, led by Dr. Richard Palmiter, have developed a mouse model with the hallmarks of Leigh syndrome, including progressive neurodegeneration, behavioral changes, and respiratory apnea. The researchers found that loss of murine Ndufs4, which encodes NADH dehydrogenase (ubiquinone) iron-sulfur protein 4, resulted in compromised activity of mitochondrial complex 1 and causes a fatal progressive encephalopathy. Using magnetic resonance imaging and immunohistochemistry, the researchers located signs of neuroinflammation in a specialized region of the brain known as the dorsal brainstem vestibular nucleus (VN). Selective inactivation of Ndufs4 in the VN resulted in breathing abnormalities and premature death in mice. Restoration of Ndufs4 using gene therapy in the VN corrected breathing deficits and prolonged the lifespan of knockout mice. This genetic murine model of Leigh syndrome provides new insights into the disease, indicating that compromised mitochondrial function within the VN of the brain contributes to respiration abnormalities.
TITLE:
Fatal breathing dysfunction in a mouse model of Leigh Syndrome
View this article at: http://www.jci.org/articles/view/62923?key=69fce563f91f65906283
###
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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.
JCI early table of contents for June 1, 2012Public release date: 1-Jun-2012 [ | E-mail | Share ]
Contact: Sarah Jackson press_releases@the-jci.org Journal of Clinical Investigation
In recent years, a growing body of evidence has linked inflammation to the development of insulin resistance. In insulin resistance, the hormone insulin is less effective in promoting glucose uptake from the bloodstream into other tissues. Obesity is a major factor that contributes to insulin resistance, which can eventually lead to type 2 diabetes. Previous studies have shown that proinflammatory molecules found in fat tissue decreases sensitivity of tissues to insulin.
To identify drug targets that will improve insulin sensitivity, Dr. Olivia Osborn and her colleagues from the University of California in San Diego investigated the role of G protein-coupled receptor 21 (GPR21) in insulin resistance and energy homeostasis. The group compared mice without the gene encoding GPR21 to healthy control mice under normal and high-fat diet conditions. They discovered that mice lacking GPR21 had enhanced insulin sensitivity and increased energy expenditure independent of diet. This result was attributed to the reduced migration of inflammatory cells to the liver and fat tissue in the absence GPR21. Under normal diet, absence of GPR21 in the hypothalamus caused a modest decrease in body weight. This is the first study to demonstrate the negative impact of GPR21 on inflammation and insulin sensitivity. Their findings suggest that GPR21 inhibition may improve insulin resistance and enhance energy expenditure, making GPR21 inhibitors promising treatments for diabetes.
TITLE:
G proteincoupled receptor 21 deletion improves insulin sensitivity in diet-induced obese mice
View this article at: http://www.jci.org/articles/view/61953?key=dbc390c7fd2397640830
METABOLISM
Keep metabolism in mind
Metabolic regulation requires activity in the brain that controls glucose balance and food uptake. The hormones insulin, which controls glucose uptake, and leptin, which regulates energy intake and energy expenditure, are critical for mediating energy balance and influence a number of activities in the brain. Dr. Joel Elmquist and colleagues at the University of Texas in Houston wanted to specifically determine which neurons in the brain are required for regulating energy balance. The research team knew that a transcription factor called FOXO1 controlled expression of many genes in response to insulin and leptin signaling. Using genetically modified mice that lack FOXO1 in a specific area of the brain called the ventral medial nucleus of the hypothalamus, they showed that these mice are lean because of increased energy expenditure. Further, these mice had higher sensitivity to insulin in muscle, and were unable to decrease energy expenditure in response to fasting. Their data shows that the action of FOXO1 in the ventral medial nucleus of the hypothalamus is critical for appropriate regulation of energy expenditure and normal glucose balance.
TITLE:
FOXO1 in the ventromedial hypothalamus regulates energy balance
View this article at: http://www.jci.org/articles/view/62848?key=9c93a1c72137e21a5364
ONCOLOGY
The right combination: overcoming drug resistance in cancer
Overactive epidermal growth factor receptor (EGFR) signaling has been linked to the development of cancer. Several drug therapies have been developed to treat these EGFR-associated cancers; however, many patients have developed resistance to these drugs and are therefore no longer responsive to drug treatment. In a recent research article published in the Journal of Clinical Investigation, Goutham Narla and colleagues at Case Western Reserve University sought to better understand the molecular players in the EGFR signaling pathway in hopes of finding new drug targets for EGFR-associated cancers. Using cancerous human lung tissue and a mouse model of EGFR-associated lung cancer, The Narla team discovered that two tumor suppressor genes, KLF6 and FOXO1, function to disrupt overactive EGFR signaling. After treating the cancerous lung tissue and cancer-prone mice with an FDA-approved drug called trifluoperazine hydrochloride (TFP), which increases the activity of FOXO1, they restored the effectiveness of the anti-EGFR drug erlotinib and reduced tumor growth. Their work identified new drug targets for EGFR-associated cancers and suggests that combinatorial drug therapy regimens may improve treatment outcome.
TITLE:
Targeting the FOXO1/KLF6 axis regulates EGFR signaling and treatment response
AUTHOR CONTACT:
Goutham Narla
Case Western Reserve University and University Hospitals, Cleveland, OH, USA
Phone: 3472550885; E-mail: Goutham.Narla@mssm.edu
View this article at: http://www.jci.org/articles/view/62058?key=9eb9f31baf7df0c3365e
NEUROLOGICAL DISEASE
Finding new treatment options in inflammatory brain diseases
A team of scientist, led by Dr. Azeb Tadesse Argaw from the Corinne Goldsmith Dickinson Center for Multiple Sclerosis, have identified a promising avenue for treating inflammatory brain diseases like multiple sclerosis. When the barrier that protects the brain, known as the blood brain barrier (BBB), becomes weak and permeable, it can lead to brain inflammation, edema and neurotoxicity. In a previous study, the group discovered that inflammatory mediators involved in brain lesion development induced angiogenic proteins in the astrocytes. This finding led them to investigate the impact of a protein that stimulates angiogenesis, vascular endothelial growth factor-A (VEGF-A), on brain permeability and inflammation. In this study, the team generated mice that have inactivated VEGF-A proteins in the astrocytes. This mouse model showed reduced BBB breakdown, decreased inflammatory cell infiltration, and increased mobility following administration of a paralytic agent. Next, the group evaluated the efficacy of a few agents in diminishing the negative effects of VEGF-A on the BBB. They discovered that systemic inhibition of endothelial nitric oxide synthase (eNOS) abolished the effects of VEGF-A on BBB breakdown. Additionally, they found that treatment with a selective eNOS inhibitor reduced drug-induced paralysis in mice. These exciting results indicate that blocking VEGF-A is an effective strategy for treating inflammatory brain diseases. Importantly, eNOS inhibitors can be given peripherally to reduce the harmful effects of VEGF-A on the brain.
TITLE:
Astrocyte-derived VEGF-A drives blood-brain barrier disruption in CNS inflammatory disease
View this article at: http://www.jci.org/articles/view/60842?key=f54bc2cb8432c10cbd88
ONCOLOGY
Tumor growth and chemoresistance are promoted by ribosomal associated protein RACK
In cells, ribosomes are responsible for translating genetic information, in the form of messenger RNA, to proteins. Coordinated translation initiation is coupled with cell cycle progression and cell growth, but excessive ribosome synthesis and translation initiation can promote cancer. Hepatocellular carcinoma is among the most common and aggressive cancers worldwide and generally displays inherently high resistance to chemotherapeutic drugs. Dr. Jianxin Gu and colleagues at Fudan University in Shanghai, China found that RACK1, the receptor for activated C-kinase 1, was highly expressed in normal liver and frequently upregulated in hepatocellular carcinoma. Aberrant expression of RACK1 contributed to chemoresistance as well as to tumor growth of hepatocellular carcinoma, effects that depended on ribosome localization of RACK1. The group went on to show that ribosomal RACK1 promoted preferential translation of the potent factors involved in growth and survival. Their results imply that RACK1 may function as an internal factor involved in the growth and survival of hepatocellular carcinoma and suggest that targeting RACK1 may be an efficacious strategy for hepatocellular carcinoma treatment.
TITLE:
Ribosomal RACK1 promotes chemoresistance and growth in human hepatocellular carcinoma
AUTHOR CONTACT:
Jianxin Gu
Gene Research Center, Shanghai Medical College, Fudan University, Shanghai, , CHN
Phone: 8621-54237704; E-mail: jxgu@shmu.edu.cn
View this article at: http://www.jci.org/articles/view/58488?key=b32b824a1904ce6fbd34
Glucocorticoids (GCs) are commonly used to treat autoimmunity, but their normal roles in the immune system are not well known. Noting that GCs are naturally made in the thymus, the site where immune cells called T cells originate, Dr. Jonathan Ashwell and his group at the National Cancer Institute studied the role of GCs in T cell development and activation. They designed a mouse line in which the gene encoding the GC receptor (GR) is deleted in immature T cells. They found that the GR-deficient T cells could not respond appropriately to antigen-induced signaling. T cells generate a diverse repertoire of TCR to respond to foreign antigens in the body. Mittelstadt's group concluded that the defects were due to a shift in the TCR repertoire because they found that GR-deficient T cells responded normally when they forced to express a TCR with a fixed specificity. They demonstrated alterations in the TCR repertoire genetically, reporting a difference in the usage of particular TCR-encoding gene segments between GR-deficient and wild-type cells. The TCR repertoire is selected in the thymus where immature T cells that recognize the body's own proteins are selected against and killed. In the GR-deficient thymus, the numbers of T cells late in the maturation pathway were reduced, suggesting unusually high numbers of T cells were previously eliminated. The group concluded that the GCs in the thymus prevent inappropriate killing of T cells during development, thus providing a sufficient and diverse TCR repertoire.
TITLE:
Thymocyte responsiveness to endogenous glucocorticoids is required for immunological fitness
View this article at: http://www.jci.org/articles/view/63067?key=24fae67ed3776d86f2e0
NEUROLOGICAL DISEASE
Breathing abnormalities uncovered in mouse model of Leigh Syndrome
Leigh syndrome is a progressive neurodegenerative disorder affecting 1 in 40,000 live births. In up to 75% of cases, patient death is caused by respiratory arrest, but the molecular mechanisms behind breathing abnormalities are unclear.
Mutations in Leigh syndrome patients have been reported to occur in components of the mitochondrial complex I, which plays a vital role in cellular energy production, though how these mutations contribute to the development of disease is unknown. Researchers from the Howard Hughes Medical Institute at University of Washington, led by Dr. Richard Palmiter, have developed a mouse model with the hallmarks of Leigh syndrome, including progressive neurodegeneration, behavioral changes, and respiratory apnea. The researchers found that loss of murine Ndufs4, which encodes NADH dehydrogenase (ubiquinone) iron-sulfur protein 4, resulted in compromised activity of mitochondrial complex 1 and causes a fatal progressive encephalopathy. Using magnetic resonance imaging and immunohistochemistry, the researchers located signs of neuroinflammation in a specialized region of the brain known as the dorsal brainstem vestibular nucleus (VN). Selective inactivation of Ndufs4 in the VN resulted in breathing abnormalities and premature death in mice. Restoration of Ndufs4 using gene therapy in the VN corrected breathing deficits and prolonged the lifespan of knockout mice. This genetic murine model of Leigh syndrome provides new insights into the disease, indicating that compromised mitochondrial function within the VN of the brain contributes to respiration abnormalities.
TITLE:
Fatal breathing dysfunction in a mouse model of Leigh Syndrome
View this article at: http://www.jci.org/articles/view/62923?key=69fce563f91f65906283
###
[ | 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.
The current National Flood Insurance program has been extended until July 31, 2012.? The National Association of Realtors has been working with Congress to help pass a 5-year National Flood Insurance Program reauthorization and reform bill.? The bill has passed the House of Representatives and is awaiting action in the United States Senate.?
The name of the bill is H.R. 1309 the Flood Insurance Reform Act of 2011.? You can read the details of this bill on The Library of Congress web site at:? http://thomas.loc.gov/cgi-bin/bdquery/z?d112:h.r.1309:.?? The goals are to extend the authorization of the national flood insurance program, to achieve reforms to improve the financial integrity and stability of the program, and to increase the role of private markets in the management of flood insurance risk, and for other purposes.?
Without this extension may home buyers would have been put on hold and would be unable to purchase flood insurance or close on their new homes.? This would have put another glitch in the real estate market recovery.?? Flood insurance is required by law to obtain a mortgage in more than 21,000 communities nationwide.?
To keep up to date with the latest information visit the FEMA web site at: http://www.fema.gov/business/nfip/.?? If you are considering purchasing a home and want to know what the flood rating is of that particular property, you can go to www.floodsmart.gov and type in the address.? It will give you a flood rating, range of rates, and insurance companies nearby to contact for homeowner insurance quotes.?
Inmarsat Mobile Satellite Communication Technology
And the International Maritime Satellite Organization (INternational MARitime SATelliteorganization; Inmarsat) in late 2003 by the signing of the Declaration, the global voice communications and digital information will be expected to upgrade from the satellite to be delivered. The cooperation between the two means will be entering a No matter vessels in the open sea, in the 30000? High-flying aircraft, or even any one of the world?s human feet can tread upon the environment can be voice communications era. The future, by the International Maritime Satellite Organization-led broadband global area network system (broadband global area network system; BGAN) In addition to the European Space Agency?s technical support, but also to the European Space Agency on the BGAN system, 50% of the funds sponsorship.
? With the country?s economic development, information communication technology has become to improve the management level, and enhance the efficiency of the basic conditions for effective face of China?s vast economic imbalance caused by the small total area covered by conventional communication, service area differences and are subject to major problems affecting the natural situation, with comprehensive coverage of mobile satellite communications service no difference, stable, and reliable communication quality advantages of a conventional communications network available to complement and extend the powerful, including Inmarsat mobile satellite communication system 20 years of operations for its reliable, safe, technologically advanced, cost-effective and reasonable global mobile satellite communications industry recognized best choice.
First of all, reliable communication is a basic requirement.
Inmarsat mobile satellite communications, as IMO (International Maritime Organization) designated for maritime distress and safety communications system for help, hormone known for its stable and reliable communications. The entire communications network to rely on five-synchronous orbit satellites, and is equipped with a backup satellite, to ensure 365 days, 24 hours / day business without disruption. Second, the security requirements. Inmarsat mobile satellite as an international business and public safety communications systems to provide users with reliable and transparent transmission channel, on the one hand to protect the smooth transmission of various information, on the other hand to meet the needs of the user encryption to ensure the freedom of uninterrupted communication. Inmarsat mobile satellite communications business continued to expand the root causes of the technical research and development of its excellent work. It is always tracking new technologies combined with industry?s need for dynamic new products and services, including telecommunications services in the transplant, and the integration of 3G, broadband and other aspects of the business meeting to go in the mobile satellite communications industry?s first end. In addition, the system according to the amount of talk time or communications billing, no monthly fees, one-way charges, charges at the level of total transport sector based on the amount of peak operation period varies, ?use more support, less a small branch do not expend ?great to meet the economic emergency communication requirements.
Beijing Marine Communication and Navigation for Inmarsat in China?s sole legitimate operators, construction and operation and maintenance only ground station in China ? Beijing station, for up to 15 years of service to maintain the system?s advanced technology, R & D value-added services to promote the Inmarsat mobile satellite system to become the largest user base in China, using the industry?s most extensive, most system application integration for mobile satellite communication network, in the following areas have achieved good results.
One, using Inmarsat-C satellite radio and navigation systems development, telemetry and data acquisition, vehicle fleet management, remote tracking and monitoring of business
Inmarsat-C system is a pure data communication system, in addition to ordinary telex, data, text, fax, communication and positioning system, according to C double-entry feature, water conservancy, energy, transportation logistics, ocean transportation, fisheries, marine and weather information research industry to develop a variety of application integration system: With a good water Rain Fade telemetry functions necessary to develop CSCADA data acquisition systems used in water industry, widely used in rivers, lakes, water level forecasting, the full replacement of the water level of the manual measurement, as The first line of digital water products; used in the energy sector on oil, gas pipeline monitoring the situation and realize the whole network of regular inspections, traffic control, to ensure the security situation along the route and automation; used in the exploration industry to realize the no man?s land and danger zone at any time the data extraction, to facilitate data access to ensure the accuracy of the results, but also to ensure the personal safety of exploration; developed CTrack moving target monitoring system, combined with electronic maps, GPS, GIS (geographic information system) function, used in the logistics industry, to achieve seamless worldwide mobile communications and surveillance targeting the management teams of the business on the one hand to ensure contact with the company, to help drivers to locate, understand the navigation information, the other companies or by regular Extraction of the team at any time the location and travel path of vehicle fleet monitoring the situation, the vehicle alarm or control vehicle, to ensure vehicle safety, the company can provide goods to customers information inquiry service conditions, and improve service grades; used in ocean shipping industry, has been as distress and safety information systems and fleet anti-terrorism system, essential equipment, but also can be fleet management and monitoring; using the integrated systems and electronic charts used in fisheries management, fishing vessels fishing areas on the implementation of monitoring, but also to Using enhanced EGC (data broadcasting) functions released fish, ocean currents, weather information bulletin to help fishermen raise income, the effective protection of life and safety; meteorological and oceanographic research departments are using Inmarsat-C system and the corresponding analysis device integration, to achieve the survey data collection and extraction.
Depending on company / sector circumstances, Beijing Marine Communication and Navigation Company offers different solutions to achieve these system functions: for government departments, large vehicle fleet company monitoring center in the headquarters building, the electronic chart / map and information control information integration, and the Beijing ground station line or Internet network connection, to provide proprietary software release orders and announcements, will feedback directly reflected in the electronic map, and appropriate (such as leaving the designated area, the direction is wrong, etc.) options (warning, alarm, control); also use MCN development CMail, C-SMS, C-IGW business of Email, SMS, fax forwarding, etc. designated phone free way of receiving information; for data acquisition, energy trade to increase the remote control software and data analysis device interface, can control the system and extract data analysis; and for small companies, Beijing Marine Communication and Navigation Company provides digital map has a vector site, the site can publish instructions , display data and other functions, will also support the mobile phone users to text message form of simple
NEW YORK (AP) ? Oracle Corp. received another setback Thursday as a federal judge in San Francisco undermined a central part of the company's multimillion dollar case against Google Inc. over its Android software for mobile devices.
Oracle had accused Google of copyright infringement in using "application programming interfaces," or APIs, that help Oracle's Java software work effectively. A jury found Google infringed on those APIs on May 7, but it couldn't agree on whether Google was covered under "fair use" protections in U.S. law. Without a fair-use determination, Oracle wasn't able to extract huge sums from Google.
Now, U.S. District Judge William Alsup said Google's use of the APIs wasn't covered by copyright law in the first place.
The effect of Thursday's ruling is limited because a jury had earlier reached an impasse on the issue of fair use. But the ruling could be important in any appeals.
Oracle said it will appeal the ruling.
Android now powers more than 300 million smartphones and tablet computers. Those devices are the chief competitors to Apple's iPhones and iPads. Google has driven the adoption of Android by giving the software away to manufacturers of phones and tablets. That would have been more difficult for Google to keep doing if the court had found that Google needed to pay Oracle millions of dollars to license Java technology.
The jury in the case had been asked to rule on the infringement and fair use questions on the assumption that the APIs were copyrightable. Alsup deferred a ruling on the broader copyright question until after the trial, which ended May 23.
Alsup ruled Thursday that Google didn't use Oracle's exact programming code in Android, but rather wrote its own code to produce the same functions. Although Google used some of the same phrases in the code, Alsup said it had to do so to maintain interoperability. Names, titles and short phrases aren't covered by copyright, and Google's use of those phrases amounted to that, he said.
"In sum, Google and the public were and remain free to write their own implementations to carry out exactly the same functions of all methods in question, using exactly the same method specifications and names," Alsup said.
In a statement, Google said "the court's decision upholds the principle that open and interoperable computer languages form an essential basis for software development. It's a good day for collaboration and innovation."
Oracle countered that Alsup's ruling would "make it far more difficult to defend intellectual property rights against companies anywhere in the world that simply takes them as their own."
Alsup's ruling does not affect the jury's determination that Android infringed on nine lines of Java coding, but the penalty for that violation is confined to statutory damages no higher than $150,000. Oracle had been seeking hundreds of millions of dollars from Google on the API questions.
The jury has also cleared Google of infringing two Oracle patents.
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Public release date: 1-Jun-2012
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