The price of gold is languishing, much like the global economy.
Gold for December delivery fell $10.20 to finish Monday at $1,612.60 per ounce. That's about $10 less than it was on June 1 and nearly $190 less than the high for the year of $1,798.90 per ounce in late February.
The decline came after Japan said its economy grew less than expected during the second quarter. Other Asian-Pacific countries also are experiencing sluggish growth, including China, which is a huge importer of commodities such as oil and copper. That has raised concerns because the region supported the global economy when the U.S. and Europe began to slow.
For much of the summer, gold prices have moved largely based on speculation about whether authorities in the U.S, Europe and China will take additional steps to promote their respective economies.
Stimulus measures can raise demand for commodities, which drives up prices for industrial metals and oil, for example. Gold benefits because it often is used as a hedge against inflation.
The Federal Reserve has pledged to try to bolster economic growth if hiring remains weak but didn't take immediate action after a meeting earlier this month. Now traders are awaiting Fed Chairman Ben Bernanke's remarks Aug. 31 at an annual economic conference in Jackson Hole, Wyo.
The European Central Bank and China are believed to be considering action, too.
"Unless we start to see some effect of stimulus, traders are concentrating on what is now," said George Gero, a vice president at RBC Global Futures. "If traders can't find something positive to point to, they tend to shy away from taking risks."
Concerns about a slowing global economy also weighed on industrial metals and energy products. Volumes were light which often can exaggerate price shifts.
Silver for September delivery fell 29.5 cents to end at $27.767 per ounce, September copper dropped 3.9 cents to $3.3535 per pound, October platinum declined $7.10 to $1,392.80 per ounce and September palladium ended down $7.50 at $574.70 per ounce.
Benchmark oil fell 14 cents to finish at $92.73 per barrel. Heating oil decreased 0.22 cent to $3.0183 per gallon, gasoline dropped 1.32 cents to $2.9907 per gallon and natural gas ended down 4.1 cents at $2.729 per 1,000 cubic feet.
Corn for December delivery fell 17 cents to finish at $7.9225 per bushel, September wheat decreased 28.5 cents to $8.5675 per bushel and November soybeans dropped 43 cents to $16.0075 per bushel.
Two Yale chemists have been awarded $2.5 million from the National Cancer Institute to investigate novel approaches to treating cancers previously thought ?undruggable.?
Professors Alanna Schepartz and Andy Phillips will focus on developing molecules that can enter cells and activate or inhibit genes dependent on the protein p53, often called the ?guardian of the genome? for its important role in preventing cells from becoming cancerous.
Schepartz, the Milton Harris ?29 Ph.D. Professor of Chemistry and director of the Yale Chemical Biology Institute at the West Campus, said much of the research related would take place at West Campus.
The research team also includes Professor Dylan Taatjes of the University of Colorado.
Said Phillips, professor of chemistry, ?I?m excited about this special opportunity to engage two great colleagues on a spectrum of science that we all share a passion for ??the interplay between ?undruggable? targets in cancer biology and the development of new paradigms in chemical biology.?
The highly competitive grant, to be distributed over five years at about $500,000 annually, comes through NCI?s ?Provocative Questions? program. It challenges researchers to focus on important but neglected problems. It also requires researchers to select a specific question to address from a list prepared by NCI.
The Schepartz-Phillips team picked question 18: ?Are there new technologies to inhibit traditionally ?undruggable? target molecules, such as transcription factors, that are required for the oncogenic phenotype??
?Transcriptional deregulation is one of the key features of cancer, and there are many potential points of intervention,? Phillips said. ?A longstanding goal has been to directly modulate erroneous transcription factor function, and an increasing number of genomic characterizations of cancers have underscored the value and impact that such capabilities might have for patients. We had all been thinking about ways to have an impact on this seemingly obvious problem that many others view as impossible. This was a perfect opportunity for us to coordinate our thoughts and address the challenge of ?drugging one of the poster child transcription factors in cancers: p53.?
The Yale Chemical Biology Institute at West Campus promotes innovation at the intersection of chemistry, biology, engineering, physics, and medicine.
Researchers may have discovered a new method to predict solar flares more than a day before they occur, providing advance warning to help protect satellites, power grids and astronauts from potentially dangerous radiation.
The system works by measuring differences in gamma radiation emitted when atoms in radioactive elements "decay," or lose energy. This rate of decay is widely believed to be constant, but recent findings challenge that long-accepted rule.
The new detection technique is based on a hypothesis that radioactive decay rates are influenced by solar activity, possibly streams of subatomic particles called solar neutrinos. This influence can wax and wane due to seasonal changes in the Earth's distance from the sun and also during solar flares, according to the hypothesis, which is supported with data published in a dozen research papers since it was proposed in 2006, said Ephraim Fischbach, a Purdue University professor of physics.
Fischbach and Jere Jenkins, a nuclear engineer and director of radiation laboratories in the School of Nuclear Engineering, are leading research to study the phenomenon and possibly develop a new warning system. Jenkins, monitoring a detector in his lab in 2006, discovered that the decay rate of a radioactive sample changed slightly beginning 39 hours before a large solar flare.
Since then, researchers have been examining similar variation in decay rates before solar flares, as well as those resulting from Earth's orbit around the sun and changes in solar rotation and activity. The new findings appeared online last week in the journalAstroparticle Physics.
"It's the first time the same isotope has been used in two different experiments at two different labs, and it showed basically the same effect," Fischbach said. The paper was authored by Jenkins and Fischbach; Ohio State University researchers Kevin R. Herminghuysen, Thomas E. Blue, Andrew C. Kauffman and Joseph W. Talnagi; U.S. Air Force researcher Daniel Javorsek; Mayo Clinic researcher Daniel W. Mundy; and Stanford University researcher Peter A. Sturrock.
Data were recorded during routine weekly calibration of an instrument used for radiological safety at Ohio State's research reactor. Findings showed a clear annual variation in the decay rate of a radioactive isotope called chlorine 36, with the highest rate in January and February and the lowest rate in July and August, over a period from July 2005 to June 2011.
The new observations support previous work by Jenkins and Fischbach to develop a method for predicting solar flares. Advance warning could allow satellite and power grid operators to take steps to minimize impact and astronauts to shield themselves from potentially lethal radiation emitted during solar storms.
The findings agree with data previously collected at the Brookhaven National Laboratory regarding the decay rate of chlorine 36; changes in the decay rate were found to match changes in the Earth-sun distance and Earth's exposure to different parts of the sun itself, Fischbach said.
Large solar flares may produce a "coronal mass ejection" of highly energetic particles, which can interact with the Earth's magnetosphere, triggering geomagnetic storms that sometimes knock out power. The sun's activity is expected to peak over the next year or so as part of an 11-year cycle that could bring strong solar storms.
Solar storms can be especially devastating if the flare happens to be aimed at the Earth, hitting the planet directly with powerful charged particles. A huge solar storm, called the Carrington event, hit the Earth in 1859, a time when the only electrical infrastructure consisted of telegraph lines.
"There was so much energy from this solar storm that the telegraph wires were seen glowing and the aurora borealis appeared as far south as Cuba," Fischbach said. "Because we now have a sophisticated infrastructure of satellites, power grids and all sort of electronic systems, a storm of this magnitude today would be catastrophic. Having a day and a half warning could be really helpful in averting the worst damage."
Satellites, for example, might be designed so that they could be temporarily shut down and power grids might similarly be safeguarded before the storm arrived.
Researchers have recorded data during 10 solar flares since 2006, seeing the same pattern.
"We have repeatedly seen a precursor signal preceding a solar flare," Fischbach said. "We think this has predictive value."
The Purdue experimental setup consists of a radioactive source - manganese 54 - and a gamma-radiation detector. As the manganese 54 decays, it turns into chromium 54, emitting a gamma ray, which is recorded by the detector to measure the decay rate.
Purdue has filed a U.S. patent application for the concept.
Research findings show evidence that the phenomenon is influenced by the Earth's distance from the sun; for example, decay rates are different in January and July, when the Earth is closest and farthest from the sun, respectively.
"When the Earth is farther away, we have fewer solar neutrinos and the decay rate is a little slower," Jenkins said. "When we are closer, there are more neutrinos, and the decay a little faster."
Researchers also have recorded both increases and decreases in decay rates during solar storms.
"What this is telling us is that the sun does influence radioactive decay," Fischbach said.
Neutrinos have the least mass of any known subatomic particle, yet it is plausible that they are somehow affecting the decay rate, he said.
English physicist Ernest Rutherford, known as the father of nuclear physics, in the 1930s conducted experiments indicating the radioactive decay rate is constant, meaning it cannot be altered by external influences.
"Since neutrinos have essentially no mass or charge, the idea that they could be interacting with anything is foreign to physics," Jenkins said. "So, we are saying something that doesn't interact with anything is changing something that can't be changed. Either neutrinos are affecting decay rate or perhaps an unknown particle is."
Jenkins discovered the effect by chance in 2006, when he was watching television coverage of astronauts spacewalking at the International Space Station. A solar flare had erupted and was thought to possibly pose a threat to the astronauts. He decided to check his equipment and discovered that a change in decay-rate had preceded the solar flare.
Further research is needed to confirm the findings and to expand the work using more sensitive equipment, he said.
Jenkins and Fischbach have previously collaborated with Peter Sturrock, a professor emeritus of applied physics at Stanford University and an expert on the inner workings of the sun, to examine data collected at Brookhaven on the decay rate of radioactive isotopes silicon-32 and chlorine-36. The team reported in 2010 in Astroparticle Physics that the decay rate for both isotopes varies in a 33-day recurring pattern, which they attribute to the rotation rate of the sun's core.
The group found evidence of the same annual and 33-day effect in radium-226 data taken at the Physikalisch-Technische Bundesanstalt (PTB) in Braunschweig, Germany, and those findings were published in 2011. They also found an additional 154-day recurring pattern in both the Brookhaven and PTB data, published in 2011, which they believe to be solar related and similar to a known solar effect called a Rieger periodicity.
###
Purdue University: http://www.purdue.edu/
Thanks to Purdue University for this article.
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New key element discovered in pathogenesis of Burkitt lymphomaPublic release date: 13-Aug-2012 [ | E-mail | Share ]
Contact: bachtler@mdc-berlin.de bachtler@mdc-berlin.de 49-309-406-3896 Helmholtz Association of German Research Centres
MDC scientists develop model for new treatments
Burkitt lymphoma is a malignant, fast-growing tumor that originates from a subtype of white blood cells called B lymphocytes of the immune system and often affects internal organs and the central nervous system. Now Dr. Sandrine Sander and Professor Klaus Rajewsky of the Max Delbrck Center for Molecular Medicine (MDC) Berlin-Buch have identified a key element that transforms the immune cells into malignant lymphoma cells. They developed a mouse model that closely resembles Burkitt lymphoma in humans and that may help to test new treatment strategies (Cancer Cell)*.
Burkitt lymphoma typically develops in childhood and occurs most frequently in equatorial Africa and South America. This tumor originates from germinal centers of the lymphoid organs (Peyer's patches in the small intestine, lymph nodes and spleen). The germinal center reaction is initiated by mature B cells upon detection of a foreign substance (antigen). These B cells modify their DNA in the course of the reaction, resulting finally in a highly specific antibody response against the antigen.
The B cell receptor (BCR), an antibody presented on the surface of mature B cells, plays a crucial role in the germinal center reaction. In order to optimally recognize the respective antigen and initiate an appropriate immune response, the DNA segments encoding the antibody need to be modified and rearranged. While the processes are complex, DNA breaks occur and error-prone repair mechanisms may lead to genetic mutations associated with cancer development.
It is well established that in Burkitt lymphoma, mistakes in the repair of DNA breaks result in the translocation of the c-MYC oncogene. This gene regulates cell division, and thus its expression is tightly controlled in normal cells. The c-MYC translocation leads to its deregulation, and the affected cells divide in an uncontrolled manner. However, c-MYC overexpression also leads to massive cell death. Therefore c-MYC deregulation by itself is unable to transform normal cells into cancer cells. In Burkitt lymphoma, the apoptosis induction of elevated c-MYC expression must be overcome by additional mutations preventing cell death.
Recently, Professor Rajewsky and his colleagues showed that an enzyme called PI3K is critical for the survival of mature B cells. It activates a signaling pathway that regulates cell growth and counteracts programmed cell death. Based on these findings Dr. Sander and Professor Rajewsky investigated an interaction of c-MYC and PI3K in mouse tumorigenesis in their present study. They demonstrated that PI3K is a key element in Burkitt lymphoma development which enables c-MYC to turn germinal center B lymphocytes into lymphoma cells that divide continuously and escape apoptosis.
However, not every B cell co-expressing c-MYC and PI3K transforms into a lymphoma cell, thus the researchers suspected additional genetic mutations that may play a role in Burkitt lymphomagenesis. Indeed they could identify such aberrations in their mouse model, and a study in human Burkitt lymphoma by Professor Louis Staudt (National Cancer Institute, Bethesda, Maryland, USA), which was published simultaneously in Nature (DOI: 10.1038/nature11378), confirmed these results. Staudt and colleagues showed that Burkitt lymphoma patients, besides having mutations resulting in the activation of the PI3K signaling pathway, carry genetic mutations that resemble those in the mouse.
"In addition to c-MYC deregulation, the activation of the PI3K signaling pathway is a key element in the development of Burkitt lymphoma," said Dr. Sander and Professor Rajewsky. "The inhibition of this signaling pathway could therefore be an effective strategy for treating the disease."
###
*Synergy between PI3K signalling and MYC in Burkitt lymphomagenesis
Sandrine Sander,1,2 Dinis P. Calado,1,2 Lakshmi Srinivasan,1 Karl Kchert,2 Baochun Zhang,1 Maciej Rosolowski,3 Scott J. Rodig,4 Karlheinz Holzmann,5 Stephan Stilgenbauer,6 Reiner Siebert,7 Lars Bullinger,6 and Klaus Rajewsky 1,2,#
1 Program of Cellular and Molecular Medicine, Children's Hospital, and Immune Disease Institute, Harvard Medical School, Boston, MA 02115, USA
2 Max Delbrck Center for Molecular Medicine, Berlin-Buch 13092, Germany
3 Institute for Medical Informatics, Statistics and Epidemiology, University of Leipzig, Leipzig 04107, Germany;
4 Department of Pathology, Brigham and Women's Hospital, Boston, MA 02115, USA
5 Microarray Core Facility, University of Ulm, Ulm 89081, Germany
6 Department of Internal Medicine III, University Hospital of Ulm, Ulm 89081, Germany
7 Institute of Human Genetics, University Hospital Schleswig-Holstein Campus Kiel/Christian-
Albrechts University Kiel, Kiel 24105, Germany;
Contact:
Barbara Bachtler
Press Department
Max Delbrck Center for Molecular Medicine (MDC) Berlin-Buch
in the Helmholtz Association
Robert-Rssle-Strae 10; 13125 Berlin, Germany
Phone: +49 (0) 30 94 06 - 38 96; Fax: +49 (0) 30 94 06 - 38 33
e-mail: presse@mdc-berlin.de
http://www.mdc-berlin.de/
[ | 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.
New key element discovered in pathogenesis of Burkitt lymphomaPublic release date: 13-Aug-2012 [ | E-mail | Share ]
Contact: bachtler@mdc-berlin.de bachtler@mdc-berlin.de 49-309-406-3896 Helmholtz Association of German Research Centres
MDC scientists develop model for new treatments
Burkitt lymphoma is a malignant, fast-growing tumor that originates from a subtype of white blood cells called B lymphocytes of the immune system and often affects internal organs and the central nervous system. Now Dr. Sandrine Sander and Professor Klaus Rajewsky of the Max Delbrck Center for Molecular Medicine (MDC) Berlin-Buch have identified a key element that transforms the immune cells into malignant lymphoma cells. They developed a mouse model that closely resembles Burkitt lymphoma in humans and that may help to test new treatment strategies (Cancer Cell)*.
Burkitt lymphoma typically develops in childhood and occurs most frequently in equatorial Africa and South America. This tumor originates from germinal centers of the lymphoid organs (Peyer's patches in the small intestine, lymph nodes and spleen). The germinal center reaction is initiated by mature B cells upon detection of a foreign substance (antigen). These B cells modify their DNA in the course of the reaction, resulting finally in a highly specific antibody response against the antigen.
The B cell receptor (BCR), an antibody presented on the surface of mature B cells, plays a crucial role in the germinal center reaction. In order to optimally recognize the respective antigen and initiate an appropriate immune response, the DNA segments encoding the antibody need to be modified and rearranged. While the processes are complex, DNA breaks occur and error-prone repair mechanisms may lead to genetic mutations associated with cancer development.
It is well established that in Burkitt lymphoma, mistakes in the repair of DNA breaks result in the translocation of the c-MYC oncogene. This gene regulates cell division, and thus its expression is tightly controlled in normal cells. The c-MYC translocation leads to its deregulation, and the affected cells divide in an uncontrolled manner. However, c-MYC overexpression also leads to massive cell death. Therefore c-MYC deregulation by itself is unable to transform normal cells into cancer cells. In Burkitt lymphoma, the apoptosis induction of elevated c-MYC expression must be overcome by additional mutations preventing cell death.
Recently, Professor Rajewsky and his colleagues showed that an enzyme called PI3K is critical for the survival of mature B cells. It activates a signaling pathway that regulates cell growth and counteracts programmed cell death. Based on these findings Dr. Sander and Professor Rajewsky investigated an interaction of c-MYC and PI3K in mouse tumorigenesis in their present study. They demonstrated that PI3K is a key element in Burkitt lymphoma development which enables c-MYC to turn germinal center B lymphocytes into lymphoma cells that divide continuously and escape apoptosis.
However, not every B cell co-expressing c-MYC and PI3K transforms into a lymphoma cell, thus the researchers suspected additional genetic mutations that may play a role in Burkitt lymphomagenesis. Indeed they could identify such aberrations in their mouse model, and a study in human Burkitt lymphoma by Professor Louis Staudt (National Cancer Institute, Bethesda, Maryland, USA), which was published simultaneously in Nature (DOI: 10.1038/nature11378), confirmed these results. Staudt and colleagues showed that Burkitt lymphoma patients, besides having mutations resulting in the activation of the PI3K signaling pathway, carry genetic mutations that resemble those in the mouse.
"In addition to c-MYC deregulation, the activation of the PI3K signaling pathway is a key element in the development of Burkitt lymphoma," said Dr. Sander and Professor Rajewsky. "The inhibition of this signaling pathway could therefore be an effective strategy for treating the disease."
###
*Synergy between PI3K signalling and MYC in Burkitt lymphomagenesis
Sandrine Sander,1,2 Dinis P. Calado,1,2 Lakshmi Srinivasan,1 Karl Kchert,2 Baochun Zhang,1 Maciej Rosolowski,3 Scott J. Rodig,4 Karlheinz Holzmann,5 Stephan Stilgenbauer,6 Reiner Siebert,7 Lars Bullinger,6 and Klaus Rajewsky 1,2,#
1 Program of Cellular and Molecular Medicine, Children's Hospital, and Immune Disease Institute, Harvard Medical School, Boston, MA 02115, USA
2 Max Delbrck Center for Molecular Medicine, Berlin-Buch 13092, Germany
3 Institute for Medical Informatics, Statistics and Epidemiology, University of Leipzig, Leipzig 04107, Germany;
4 Department of Pathology, Brigham and Women's Hospital, Boston, MA 02115, USA
5 Microarray Core Facility, University of Ulm, Ulm 89081, Germany
6 Department of Internal Medicine III, University Hospital of Ulm, Ulm 89081, Germany
7 Institute of Human Genetics, University Hospital Schleswig-Holstein Campus Kiel/Christian-
Albrechts University Kiel, Kiel 24105, Germany;
Contact:
Barbara Bachtler
Press Department
Max Delbrck Center for Molecular Medicine (MDC) Berlin-Buch
in the Helmholtz Association
Robert-Rssle-Strae 10; 13125 Berlin, Germany
Phone: +49 (0) 30 94 06 - 38 96; Fax: +49 (0) 30 94 06 - 38 33
e-mail: presse@mdc-berlin.de
http://www.mdc-berlin.de/
[ | 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.
HONG KONG (AP) ? Hong Kong's Occupy movement needs to find a new home.
A judge on Monday granted a legal motion by HSBC to clear out anti-capitalist protesters from a public space below the bank's headquarters in the southern Chinese financial center.
The judge ruled that the activists must leave by 9 p.m. on August 27. A small group of Occupy activists have set up tents, tables and sofas and have been living in the large open space on the ground floor of the building since the movement began last autumn.
While HSBC owns the land, it's legally designated as a public passageway. The judge ruled that the activists' use of the space goes beyond the land's designated use.
Local commercial real estate professionals said they are seeing an upswing this year in commercial leasing activities and interest.
The value of commercial and industrial building permits throughout the Tri-Cities for the first half of the year was about $137 million, up 3 percent from the same time in 2011, according to statistics compiled by the Tri-Cities Home Builders Association.
And there are several large commercial projects still in the planning stages that are scheduled to begin construction this year.
?I think people have a firm grasp that our economy hasn?t suffered as much in the Tri-Cities and that things are strong here,? said Rob Ellsworth, managing broker, Windermere Real Estate Tri-Cities, Commercial. ?That has prompted a lot of local business.?
In addition, the area has received a lot of national publicity over the past two years touting the strong local economy, growth and livability.
Ellsworth said that has prompted more interest from companies outside the area, as well.
?The come in, see the low cost of living, the low cost of power and that we have water ? that is huge,? he said.
The change in the Washington State liquor laws has also prompted movement in the market and is bringing new businesses to the area, he said.
?New liquor distributors, who have main hubs in Seattle and Spokane, are siting facilities here and using it as a cross-docking area,? he said, noting that Southern Wine & Spirits has signed a lease with the company and will be moving into a space at 501 N. Quay in Vista Field.
Dirk Stricker, of Dirk Stricker Commercial Real Estate, said commercial lease rates in the area have started to stabilize and there seems to be a lot of people looking for space.
?The activity has picked up quite a bit,? he said.
Many people, especially doctors, dentists and others in the medical field are taking advantage of low interest rates on Small Business Administration loans.
Stricker said the SBA rules on those loans require the buildings to be owner occupied, but the low interest rates have spurred more medical office building construction. Often doctors or dentists build a facility capable of housing additional specialists to help offset their mortgage costs.
Lance Bacon, principal at NAI Tri-Cities said he?s been hosting a lot of market tours for people coming from outside the area, like regional and national franchisees and developers.
?Retail seems to be the strongest, followed by the financial and service industries,? he said. ?People are looking to be in strong, visible corridors, like near the mall.?
Another commercial growth hot spot in the Tri-Cities is at the Queensgate-Duportail off Interstate I-182 in Richland, where a new Les Schwab Tire Center is under construction, and the new Sterlings Restaurant and Bobs Burger & Brew opened earlier this year.
Jeff Fairchild of Fairchild Cinemas purchased 11 acres from the Kennewick Irrigation District north of I-182 and south of Duportail, behind Gold?s Gym, Wal-Mart and Home Depot, where he plans to build a multi-plex theater. The Richland Planning Commission conditionally approved a site plan for the project in late June.
Bacon said he is also seeking a lot of activity in the Southridge area, where Kennewick General Hospital recently broke ground on its new facility.
A new 52,000-sq.-ft. Yoke?s store is planned at 380 Keene Road, just west of Badger Mountain Park. Glen Englehard, the site developer, also plans to build a 14,000-sq.-ft. strip mall at the 17.4-acre site, where other commercial pads are available.
Two new hotels are currently under construction in Richland. A $6.5 million Marriott Towneplace Suites at 591 Columbia Point Dr. and The Hilton Homewood Suites Extended Stay Hotel at 1060 George Washington Way.
Five other hotels are in the planning stages in Richland. Tom Drumheller, CEO of Escape Lodging and owners of Cousin?s Restaurant in Pasco, is planning to build a boutique hotel at Columbia Point between Anthony?s Restaurant and the Marriott Courtyard.
Kadlec Medical System has an agreement with a private developer to build a hotel within walking distance of the hospital campus to serve patient family members.
Stew Stone, a Portland developer, has ambitious plans to build two hotels, including an Embassy Suites by Hilton and an extended stay hotel, at Horn Rapids Golf Course.
And in June, the Richland Planning Commission approved a site plan submitted by Gramor Development Washington LLC for a new four-story La Quinta hotel at 355 Bradley Blvd., across from the Shilo Inn.
Ellsworth said the robust commercial real estate movement is a good sign for the area, which has experienced large layoffs since stimulus money provided to Hanford through the American Reinvestment and Recovery Act has been used.
?We?re just seeing a lot of activity, but none of it is directly related to Hanford,? Ellsworth said. ?As the rest of the country starts to recover, the perception of all regions is improving.?
by Mary Hopkin Tri-Cities Area Journal of Business
This entry was posted
on Monday, August 13th, 2012 at 3:11 pm and is filed under Construction & Development, Tri-Cities News.
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As if updating and expanding its in-ear headphone lineup wasn't enough, Klipsch has gone ahead and unveiled its revamped Image One on-ear set here at Irving Plaza in NYC. As we're told, the new Image One is acoustically similar to its predecessor, but now it has a more stylish and robust design that should hold up better over time. Notably, the headphones only have a single cable leading into the left earcup (rather than splitting into both cups like the original), and it's also of the flat variety to prevent tangling. The earcups can still fold flat, but now they can fold into the headband as well, making a smaller footprint for storage in a stuffed bag. In terms of comfort, the leather earpads are now a totally flat to provide an improved seal and better comfort. Beyond that, an Apple-certified inline remote / mic will help you control your music and calls on the go. An airliner converter, 1/4-inch adapter and soft-shell carrying case are naturally included, and best of all, pricing still remains set at 150 bones.
Rather than just tweaking the original, however, Klipsch has decided to finally enter the wireless headphone game by offering a $250 Bluetooth-equipped variant for those who hate cords. This version looks nearly identical, with the subtle tweak of having the playback and volume controls positioned as buttons on the outside of the right earcup. The Image One Bluetooth also sports a built-in rechargeable battery, yet the set only gains 10 grams of weight (180 grams total) on top of its wired sibling -- should the battery die, a detachable cable allows for passive functionality. What's more, audiophiles will pleased to know that aptX and A2DP support is baked-in for high-quality lossless audio streaming. If your ears are already tingling with excitement, the updated Image One and Image One Bluetooth are set to hit shelves by the end of the month. We're already putting both sets of cans through their paces here at the event, so check back soon as we'll be updating this post with our initial impressions.
Update: You'll find images of the headphones below and our brief ears-on after the break.
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Public release date: 13-Aug-2012
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by Mary Hopkin
