There hasn't been a whole lot of news coming out of the Google Zeitgeist event taking place in a posh hotel on the outskirts of London this week, but Google's making some other news in England: its CEO Larry Page has been spotted wearing Google Glasses. The pictures of Page wearing the super-funky augmented reality eyewear are possibly the first -- although his Google co-founder Sergey Brin has also been seen wearing them?in the wild. Today's pictures come courtesy of Google employee Jason Mayes, who posted them -- where else? -- on Google +.
For millions of people around the world, debt has become a big issue. Most people carry some form of debt, but many people have far more debt than they can reasonably handle. The problem for many is that they don?t know how to even begin to tackle the issue and pay down their debt. Luckily, people can turn to a credit counseling service to receive help and information on how to get out of and stay out of debt.
Usually credit counseling programs begin with an educational lesson about how credit works and should be used. It also includes programs that will help you to better be able to deal with the creditors that you currently have. They will often set you up with some kind of debt settlement program. These programs hire people who work on your behalf to negotiate with your creditors in order to get the total amount of money that you owe reduced. Reducing this total can be a crucial step to getting out of debt.
Types of Credit Counseling Services
There are different types of credit counseling that have different levels of success. There are some courses that are offered for free to the public. Typically this kind of course does not go as in-depth as some other courses might. It is more likely that a free course would just give you information about credit and how to use it responsibly. That is not to say that there is no value in free courses. Certainly those who would like to learn more about this subject should take advantage of the course. However, if you are looking for something with a little more immediate impact then you are going to want to enroll in a paid course. The paid courses usually aren?t too expensive to get into since typically people who are drowning in debt don?t have a lot of disposable income.
There are also consumer credit counseling online. This allows an individual to receive debt and credit counseling from the comfort of his or her own home and on their own schedule. This is an attractive option for many people who do not have flexible work schedules, or who may be too self-conscious to do in-person counseling.
Unfortunately, there are unscrupulous companies who take advantage of the desperation of those in debt. When choosing a debt or credit counselor, do some research on the company before you pay anything. Reputable business are often rated, or are members of the Better Business Bureau. BBB members usually display this information right on their home page, or on the front page of any literature they present.
Don?t be Afraid to Ask for Help
Excessive debt is something that affects millions of people worldwide. There is no reason why anyone should feel shame in asking for help dealing with this financial trouble. In fact, it would really be more embarrassing to do nothing and allow yourself to fall farther into the debt trap. Facing the problem head on can be scary, but credit counselors are there to help you face the issue and climb out from under debt. Take the first step to break the cycle that debt has on your financial life by contacting a credit counseling service.?http://www.populararticles.com/
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It seems appropriate that the album cover for Ralph Torrefranca?s new EP, Spare Room Sessions, depicts a man in suit and tie sitting next to an antique radio and black-and-white family photograph, his face obstructed by the image of an antique car and his body partially surrounded by a picture frame. Torrefranca?s lyrics and melodies are notably sincere, yet also convey an age beyond their singer?s 22 years. The effect of basic drums or tambourine outlining the beat and acoustic guitar strumming out the chords is a simple hand-clapping, folksy campfire?feel.
But sincerity doesn?t necessarily imply innocence; the music video to ?The Devil?s Handshake? features a strawberry-haired suburban girl clad in a pink dress, who moves from girl-next-door to bloodthirsty as she searches for the fleeing Torrefranca with a hammer in hand. He speaks of tricky heartbreak and downward decent, while the guitar lingers between resolution and chaos, creating both a disquieting and foot-tapping ambiance. ?5th and Grand? begins with a lazy steel guitar and soft voice conjuring reflection, but instead he sings, ?Stuck my hand in that socket,? calling to mind Conor Oberst?s signature mix of jarring lyrics and tranquil acoustics. This goes to show that Torrefranca isn?t afraid of embracing the darker elements that lie beneath his honest guy?lyricism.
To check out Torrefranca?s music, visit ralphtorrefranca.bandcamp.com.
Study: Heart damage after chemo linked to stress in cardiac cellsPublic release date: 21-May-2012 [ | E-mail | Share ]
Contact: Govindasamy Ilangovan Govindasamy.ilangovan@osumc.edu 614-292-9064 Ohio State University
COLUMBUS, Ohio - Blocking a protein in the heart that is produced under stressful conditions could be a strategy to prevent cardiac damage that results from chemotherapy, a new study suggests.
Previous research has suggested that up to a quarter of patients who receive the common chemotherapy drug doxorubicin are at risk of developing heart failure later in life. Exactly how that heart damage is done remains unclear.
In this study, scientists identified a protein called heat shock factor-1 (HSF-1) as a likely source of chemotherapy-related heart damage in mice and cell cultures. Heat shock factor-1 is known to be induced by stress - in this case, the chemotherapy treatment itself.
"We have found that a simple stress-related factor could be aggravating chemotherapy's effect on the heart," said Govindasamy Ilangovan, associate professor of internal medicine at Ohio State University and senior author of the study. "The results are leading us toward the idea that any additional stress could hurt the heart more than what chemotherapy itself can do."
The researchers gave doxorubicin to two sets of mice - normal animals and mice that were genetically altered so they could not produce HSF-1. Mice without HSF-1 had healthier hearts and lived longer after the chemotherapy treatment than did normal mice.
A closer examination on the cellular level suggested that when HSF-1 is blocked in the heart, this condition allows for the activation of a gene that produces a protein to pump the chemo medicine out of heart muscle cells, preventing these cells from dying.
Ilangovan and colleagues are working to design drugs that could selectively inhibit HSF-1 in the heart as a potential additional therapy for cancer patients undergoing chemo treatment.
The research appears this week in the Proceedings of the National Academy of Sciences Online Early Edition.
Chemotherapy targets cancer cells, but it also can kill many other kinds of cells in various organs. In most cases, Ilangovan explained, organs can regenerate their cells after this damage has occurred. But cardiomyocytes, or heart muscle cells, cannot be regenerated. The loss of muscle can lead to a disorder known as dilated cardiomyopathy, which reduces the heart's pumping action and leads to heart failure.
"This work arose from that background. We are trying to identify a factor that can be targeted to prevent the cardiomyopathy," said Ilangovan, an investigator in Ohio State's Davis Heart & Lung Research Institute.
Previous research had already shown that doxorubicin leads to activation of HSF-1 in the heart. The Ohio State researchers ran a number of experiments in animals and cell cultures to establish the relationship after chemo treatment between heat shock factor-1 and the gene that helps the heart, called multidrug-resistance-1 or MDR1.
In analyses using heart muscle cells from mice with and without activation of HSF-1, the researchers observed more activation of the MDR1 gene in cells lacking the HSF-1 protein compared to normal mouse heart cells. In addition, they demonstrated that the MDR1 gene prompted production of a protein on these heart cells' surface that actually pumped doxorubicin away from the cells.
"This was an exciting finding. When we knock out the protein, not only is the cell death pathway prevented, but it also induces a multidrug-resistant gene, which pumps the drug away from the cells," Ilangovan said. "So when HSF-1 gets activated by chemo, that leads to cardiomyocyte death. But if we knock it out, that gene comes and protects the heart."
The researchers discovered that interplay in the heart cells between HSF-1 and another protein, NF-kB, could be traced to production of the protective gene.
"They're sort of antagonizing each other. If HSF-1 is lower, the other protein becomes dominant. They compete for the same binding site, and when we knock out HSF-1, NF-kB can go freely bind and activate the MDR1 gene," Ilangovan said. That also means that when HSF-1 is present, it inhibits NF-kB and in turn prevents the protective gene from being activated.
Mice also survived longer after a doxorubicin treatment if they did not produce HSF-1, and images of their hearts showed that chemo-related damage to the heart was reduced in the genetically altered mice compared to normal mice.
The researchers also tested breast cancer cells to be sure that brief silencing of the HSF-1 protein before chemotherapy would not induce the multidrug-resistant gene in those cells, which could be a deadly turn of events.
Proper timing of HSF-1 inhibition and limiting this inhibition to the heart are important steps in designing drugs to target it, Ilangovan said. Multiple studies of this protein have suggested that it can have both beneficial and harmful effects in the body. Researchers appear to be reaching consensus that the timing of its activation helps determine which effect it will have - if it is activated before an injury or other damaging event, HSF-1 can be protective. After an injury - in this case, doxorubicin treatment - the protein is more commonly found to be harmful.
"I foresee that perhaps a patient would take a drug to silence HSF-1 in the heart one or two days before chemotherapy. So until the chemo is cleared out, the protein would be in the knock-down stage and no damage to the heart would occur," Ilangovan said.
###
This work is supported by grants from the National Institutes of Health.
Co-authors of this study include Karthikeyan Krishnamurthy, Kaushik Vedam and Ragu Kanagasabai of the Department of Internal Medicine and Lawrence Druhan of the Department of Anesthesiology, all at Ohio State.
Written by Emily Caldwell, (614) 292-8310; caldwell.151@osu.edu
[ | 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.
Study: Heart damage after chemo linked to stress in cardiac cellsPublic release date: 21-May-2012 [ | E-mail | Share ]
Contact: Govindasamy Ilangovan Govindasamy.ilangovan@osumc.edu 614-292-9064 Ohio State University
COLUMBUS, Ohio - Blocking a protein in the heart that is produced under stressful conditions could be a strategy to prevent cardiac damage that results from chemotherapy, a new study suggests.
Previous research has suggested that up to a quarter of patients who receive the common chemotherapy drug doxorubicin are at risk of developing heart failure later in life. Exactly how that heart damage is done remains unclear.
In this study, scientists identified a protein called heat shock factor-1 (HSF-1) as a likely source of chemotherapy-related heart damage in mice and cell cultures. Heat shock factor-1 is known to be induced by stress - in this case, the chemotherapy treatment itself.
"We have found that a simple stress-related factor could be aggravating chemotherapy's effect on the heart," said Govindasamy Ilangovan, associate professor of internal medicine at Ohio State University and senior author of the study. "The results are leading us toward the idea that any additional stress could hurt the heart more than what chemotherapy itself can do."
The researchers gave doxorubicin to two sets of mice - normal animals and mice that were genetically altered so they could not produce HSF-1. Mice without HSF-1 had healthier hearts and lived longer after the chemotherapy treatment than did normal mice.
A closer examination on the cellular level suggested that when HSF-1 is blocked in the heart, this condition allows for the activation of a gene that produces a protein to pump the chemo medicine out of heart muscle cells, preventing these cells from dying.
Ilangovan and colleagues are working to design drugs that could selectively inhibit HSF-1 in the heart as a potential additional therapy for cancer patients undergoing chemo treatment.
The research appears this week in the Proceedings of the National Academy of Sciences Online Early Edition.
Chemotherapy targets cancer cells, but it also can kill many other kinds of cells in various organs. In most cases, Ilangovan explained, organs can regenerate their cells after this damage has occurred. But cardiomyocytes, or heart muscle cells, cannot be regenerated. The loss of muscle can lead to a disorder known as dilated cardiomyopathy, which reduces the heart's pumping action and leads to heart failure.
"This work arose from that background. We are trying to identify a factor that can be targeted to prevent the cardiomyopathy," said Ilangovan, an investigator in Ohio State's Davis Heart & Lung Research Institute.
Previous research had already shown that doxorubicin leads to activation of HSF-1 in the heart. The Ohio State researchers ran a number of experiments in animals and cell cultures to establish the relationship after chemo treatment between heat shock factor-1 and the gene that helps the heart, called multidrug-resistance-1 or MDR1.
In analyses using heart muscle cells from mice with and without activation of HSF-1, the researchers observed more activation of the MDR1 gene in cells lacking the HSF-1 protein compared to normal mouse heart cells. In addition, they demonstrated that the MDR1 gene prompted production of a protein on these heart cells' surface that actually pumped doxorubicin away from the cells.
"This was an exciting finding. When we knock out the protein, not only is the cell death pathway prevented, but it also induces a multidrug-resistant gene, which pumps the drug away from the cells," Ilangovan said. "So when HSF-1 gets activated by chemo, that leads to cardiomyocyte death. But if we knock it out, that gene comes and protects the heart."
The researchers discovered that interplay in the heart cells between HSF-1 and another protein, NF-kB, could be traced to production of the protective gene.
"They're sort of antagonizing each other. If HSF-1 is lower, the other protein becomes dominant. They compete for the same binding site, and when we knock out HSF-1, NF-kB can go freely bind and activate the MDR1 gene," Ilangovan said. That also means that when HSF-1 is present, it inhibits NF-kB and in turn prevents the protective gene from being activated.
Mice also survived longer after a doxorubicin treatment if they did not produce HSF-1, and images of their hearts showed that chemo-related damage to the heart was reduced in the genetically altered mice compared to normal mice.
The researchers also tested breast cancer cells to be sure that brief silencing of the HSF-1 protein before chemotherapy would not induce the multidrug-resistant gene in those cells, which could be a deadly turn of events.
Proper timing of HSF-1 inhibition and limiting this inhibition to the heart are important steps in designing drugs to target it, Ilangovan said. Multiple studies of this protein have suggested that it can have both beneficial and harmful effects in the body. Researchers appear to be reaching consensus that the timing of its activation helps determine which effect it will have - if it is activated before an injury or other damaging event, HSF-1 can be protective. After an injury - in this case, doxorubicin treatment - the protein is more commonly found to be harmful.
"I foresee that perhaps a patient would take a drug to silence HSF-1 in the heart one or two days before chemotherapy. So until the chemo is cleared out, the protein would be in the knock-down stage and no damage to the heart would occur," Ilangovan said.
###
This work is supported by grants from the National Institutes of Health.
Co-authors of this study include Karthikeyan Krishnamurthy, Kaushik Vedam and Ragu Kanagasabai of the Department of Internal Medicine and Lawrence Druhan of the Department of Anesthesiology, all at Ohio State.
Written by Emily Caldwell, (614) 292-8310; caldwell.151@osu.edu
[ | 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.
Businesses are constantly on the lookout for ways to improve their current processes. Improving their more routine practices means better productivity, a more streamlined workflow and happier employees.
In this modern age, no monetary value can be placed on your time, as it seems to be the one commodity that no one can trade or sell. With time clock software you can not only start saving yourself copious amounts of time, but money as well, thereby increasing your output and maximizing the productivity of your workplace.
If you?re looking for a simple solution, which enables you to monitor your employee?s time in and out of the office, or you?re a bigger corporation that has complicated overtime requirements, time clock software works for you.
Paper time cards and manual time clocks are a thing of the past since the birth of the time clock calculator, which provides a virtual interface for the users to work within. Much like the antiquated time clock, time clock software allows users to log in securely by using their assigned identification code as well as their unique PIN. When a staff member arrives at work, they log in and their virtual time card will receive a time stamp, much like a paper time card would.
The difference being however, that a mechanical time clock is subject to manipulation. Employees have become wise to the fact that the actual time on the time clock can be adjusted to reflect them having come in to work on time when in reality, they were late. Time clock software subverts these problems by automatically checking an employee in and preventing unauthorized changes to the schedule without the approval of the administrator.
Whether you realize it or not, these small changes will start saving you money instantly. Missed punches and longer than scheduled breaks account for a large amount of the revenues you put towards wages being lost. You may even find that with the money you save, you finally have the ability to hire on an assistant or a new supervisor.
Real-time updating will let you know when and where your employees are at any given point in the day. Time clock software has the capacity to show you if an employee clocked in late, on time, or even not at all.
You can forget about having to sift through paper time cards in an effort to amalgamate your operating expenses into a spreadsheet document, as the time clock calculator will do this for you. You will get a detailed analysis of hours worked by department as well as a comprehensive breakdown of overtime hours, so you can ensure that your staff members are scheduled accordingly.
It has never been easier to make great gains in the productivity of your small or large business. Time clock software offers employers the ultimate solution in flexibility and long-terms savings and is an incredible asset for any department.
About the Author: Marko is a marketing associate and writer for ShiftPlanning Inc. In this article he explains how to use time clock software in order to maximize productivity.
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There hasn't been a whole lot of news coming out of the Google Zeitgeist event taking place in a posh hotel on the outskirts of London this week, but Google's making some other news in England: its CEO Larry Page has been spotted wearing Google Glasses. The pictures of Page wearing the super-funky augmented reality eyewear are possibly the first -- although his Google co-founder Sergey Brin has also been seen wearing them?in the wild. Today's pictures come courtesy of Google employee Jason Mayes, who posted them -- where else? -- on Google +.
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Public release date: 21-May-2012
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