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Memories Control looking to cause an upset in a Grade A2 event at Hall Green
Memories Control is likely to cause an upset in the 480 metres flat race at Hall Green in England on Monday, September 3, 2012. He has not been in good form in recent times, but his talent cannot be doubted at all. He has got impressive speed and his stamina
is also not bad. Therefore, he will definitely give a tough time to his opponents at the end of the day.
The winner of the Grade A2 event will be awarded a cash prize of ?122 in the end. There are some extremely talented participants lined up to fight for this money in the race, which is scheduled to start at 13:51 GMT.
None of the participants seem to be in dominant form right now, thus the competition will be an interesting one overall. The spectators will definitely enjoy this situation, as they will get a chance to witness some splendid action of greyhound racing.
The bookmakers have predicted a close fight amongst Eden Twister and Westmead Story, as both are in decent shape at the moment. The latter of the two has got more experience, thus he will be more confident of winning the race. He is also carrying the winning
momentum right now, which will encourage the punters to risk some money in his favour.
On the other hand, Eden Twister has been delivering some very good results with consistency, which will put him in strong contention of fighting for a win. He is young and energetic and will be looking to exert a lot of pressure on his opponents.
However, both the favourite greyhounds will face a stiff challenge from Memories Control, who has proved to be highly competitive in the past. His confidence level is low at the moment, but he has the tools to bounce back strongly at Hall Green.
The C. Kyme?s trainee knows the conditions at this venue better than others and should not have any issues in the end. He has not won a single event out of his previous five outings, which will be a worrying sign for his team.
In his most recent race, the black dog finished sixth overall. However, his penultimate outing proved to be a good one, which means that he is not in that bad form at the moment.
Disclaimer: The views expressed in this article are solely of the writer?s and do not reflect bettor.com?s official editorial policy.
Many people are probably off their computers for Labor Day, but I can't help sharing a couple things with you. First up, isn't this sculpture gorgeous? The sculpture, called Survival of Serena by Carole A. Feuerman, is in downtown Manhattan for the summer. It portrays a swimmer taking a break, and passersby have been wowed by its hyper-realism?so much so that one day when it rained, people didn't know which drops were real.
But, to me, this sculpture looks strikingly similar to a woman having a home birth and laboring in a tub. (Like this photo of my friend Leigh!) The same concentration, the same athleticism, the same inward focus. It's almost hard to believe that the artist didn't intent that; at first glance, I thought that's exactly what the sculpture was meant to be.
I'm curious: Would you (or did you) consider having a home birth? Or would you prefer a hospital birth? I loved this recent post by Elizabeth, encouraging every woman to do what she thinks is best for her and her baby.
(Photos by Jenna Fain and Andrea Swalec) Pin It Now!
September 4, 2012 in Featured, Games, PC/Mac, PS3, Review, Xbox 360
I didn?t have high (or any) expectations for this movie tie-in, but then again I never have. These games usually signify the quickest grab for cash possible and while the ads starring Terry Crews certainly were entertaining enough, the end product just doesn?t cut the mustard.
That?s gotta hurt!
The potential was there and a little more spit and poilsh could have made?The Expendables 2 ? Videogame a really fun arcade release especially considering the pure awesomeness of each character?s signature kills (pictured above), but shoddy development and poor shooting mechanics were the nail in the coffin for this bad boy.
?The main problem here is spotty hit recognition, aiming difficulties to get accurate shots off with the right thumbstick (on console) and a temperamental auto-lock. Throw in some weak weaponry (with you wondering if you?re actually doing any damage at all) and many times you find melee is the best and most reliable option. After spending significant time with each character I opted for Gunner or Caesar with Caesar?s auto-shotty best for crowd control and Gunner?s laser scoped sniping the most accurate for pesky rocket launcher dudes. You just don?t feel like you?re laying the serious smack down with the other characters, even with several weapon or heath upgrades.?
Would you like to know more? For my AusGamers review in its entirety click on through here?
Terry Crews was not at all pleased with Dave?s review
Tags: AusGamers, Dave Kozicki, Dolph Lundgren, Jet Li, Review, Sylvester Stallone, Terry Crews, The Expendables 2 Videogame, Ubisoft, ZootFly
NIH-funded researchers restore sense of smell in mice using genetic techniquePublic release date: 2-Sep-2012 [ | E-mail | Share ]
Contact: Robin Latham lathamr@nidcd.nih.gov 301-496-7243 NIH/National Institute on Deafness and Other Communication Disorders
Study could lead way to first therapeutic treatment for people born with anosmia
Scientists funded by the National Institutes of Health have restored the ability to smell in a mouse model of a human genetic disorder that causes congenital anosmiathe inability to smell from birth. The approach uses gene therapy to regrow cilia, cell structures that are essential for olfactory function.
The study was funded by four parts of NIH: the National Institute on Deafness and Other Communications Disorders (NIDCD), the National Institute on Diabetes and Digestive and Kidney Diseases (NIDDK), the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), and the National Eye Institute (NEI). It was published online in the September 2, 2012, issue of the journal Nature Medicine.
"These results could lead to one of the first therapeutic options for treating people with congenital anosmia," said James F. Battey, Jr., M.D., Ph.D., director of NIDCD. "They also set the stage for therapeutic approaches to treating diseases that involve cilia dysfunction in other organ systems, many of which can be fatal if left untreated."
Olfactory dysfunction can be a symptom of a newly recognized class of genetic disorders, known as ciliopathies, which include diseases as diverse as polycystic kidney disease and retinitis pigmentosa, an inherited, degenerative eye disease that causes severe vision impairment and blindness. The disorders are caused by defects in cilia, antenna-like projections on cells that help them sense their environment. Scientists believe that nearly every cell in the body has the capacity to grow one or more cilia. In the olfactory system, multiple cilia project from olfactory sensory neurons, sensory cells that are found in the olfactory epithelium, tissue high up in the nasal cavity. Receptors that bind odorants are localized on the cilia, which is why a loss of cilia results in a loss in the ability to smell.
The team of researchers, led by Jeffrey R. Martens, Ph.D., at the University of Michigan, Ann Arbor, and Jeremy C. McIntyre, Ph.D., a post-doctoral fellow in Martens' laboratory, worked with a mouse model carrying a mutation in the IFT88 gene. The mutation causes a decrease in the IFT88 protein, which leads to a dramatic reduction in cilia function in several different organ systems, including the olfactory system.
The researchers used an adenovirus to introduce a healthy copy of the gene as a way to restore IFT88 protein levels in the mice. They wanted to see if the reintroduction of the lost protein could restore cilia to the olfactory sensory neurons and return the ability to smell. For three consecutive days, the mice received intranasal gene delivery therapy and then were allowed 10 days for the infected sensory neurons to express the viral-encoded IFT88 protein. After that time, the mice were tested with increasing concentrations of an odorant (amyl acetate). Their responses were measured at the cellular, tissue, and synaptic levels, which all indicated that the mice had regained olfactory function.
"By restoring the protein back into the olfactory neurons, we could give the cell the ability to regrow and extend cilia off the dendrite knob, which is what the olfactory neuron needs to detect odorants," said McIntyre.
The change in olfactory function also has implications in the feeding behavior of the mice. The mouse model the scientists used is born underweight and its anosmia interferes with the motivation to eat, which in many mammals, including humans, is driven by smell. Treatment with adenovirus therapy increased bodyweight by 60 percent in treated compared to untreated mice, indicating that the restored olfactory function was motivating feeding.
The researchers plan to continue their work by developing another mouse model to look at the impact on olfactory function and the potential for restoring function when the IFT88 gene is completely missing, rather than just mutated. Future studies could begin to plot a way to bring this therapeutic tactic to human study volunteers, which could eventually restore the sense of smell, and a better quality of life, to people who are born with anosmia. Further research could also advance the treatments for other ciliopathies, as these findings show that gene therapy is a viable option for the functional rescue of cilia in established, already differentiated cells.
###
This research was supported with funding by NIH grants R01DC009606, F32DC011990, R01DC004553, R01DC008295, R01DK75996, R01DK072301, R01DK075972, R01HD042601, and R01EY021872.
The NIDCD supports and conducts research and research training on the normal and disordered processes of hearing, balance, taste, smell, voice, speech and language and provides health information, based upon scientific discovery, to the public. For more information about NIDCD programs, see the website at http://www.nidcd.nih.gov.
About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov.
NIH...Turning Discovery Into Health
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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.
NIH-funded researchers restore sense of smell in mice using genetic techniquePublic release date: 2-Sep-2012 [ | E-mail | Share ]
Contact: Robin Latham lathamr@nidcd.nih.gov 301-496-7243 NIH/National Institute on Deafness and Other Communication Disorders
Study could lead way to first therapeutic treatment for people born with anosmia
Scientists funded by the National Institutes of Health have restored the ability to smell in a mouse model of a human genetic disorder that causes congenital anosmiathe inability to smell from birth. The approach uses gene therapy to regrow cilia, cell structures that are essential for olfactory function.
The study was funded by four parts of NIH: the National Institute on Deafness and Other Communications Disorders (NIDCD), the National Institute on Diabetes and Digestive and Kidney Diseases (NIDDK), the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), and the National Eye Institute (NEI). It was published online in the September 2, 2012, issue of the journal Nature Medicine.
"These results could lead to one of the first therapeutic options for treating people with congenital anosmia," said James F. Battey, Jr., M.D., Ph.D., director of NIDCD. "They also set the stage for therapeutic approaches to treating diseases that involve cilia dysfunction in other organ systems, many of which can be fatal if left untreated."
Olfactory dysfunction can be a symptom of a newly recognized class of genetic disorders, known as ciliopathies, which include diseases as diverse as polycystic kidney disease and retinitis pigmentosa, an inherited, degenerative eye disease that causes severe vision impairment and blindness. The disorders are caused by defects in cilia, antenna-like projections on cells that help them sense their environment. Scientists believe that nearly every cell in the body has the capacity to grow one or more cilia. In the olfactory system, multiple cilia project from olfactory sensory neurons, sensory cells that are found in the olfactory epithelium, tissue high up in the nasal cavity. Receptors that bind odorants are localized on the cilia, which is why a loss of cilia results in a loss in the ability to smell.
The team of researchers, led by Jeffrey R. Martens, Ph.D., at the University of Michigan, Ann Arbor, and Jeremy C. McIntyre, Ph.D., a post-doctoral fellow in Martens' laboratory, worked with a mouse model carrying a mutation in the IFT88 gene. The mutation causes a decrease in the IFT88 protein, which leads to a dramatic reduction in cilia function in several different organ systems, including the olfactory system.
The researchers used an adenovirus to introduce a healthy copy of the gene as a way to restore IFT88 protein levels in the mice. They wanted to see if the reintroduction of the lost protein could restore cilia to the olfactory sensory neurons and return the ability to smell. For three consecutive days, the mice received intranasal gene delivery therapy and then were allowed 10 days for the infected sensory neurons to express the viral-encoded IFT88 protein. After that time, the mice were tested with increasing concentrations of an odorant (amyl acetate). Their responses were measured at the cellular, tissue, and synaptic levels, which all indicated that the mice had regained olfactory function.
"By restoring the protein back into the olfactory neurons, we could give the cell the ability to regrow and extend cilia off the dendrite knob, which is what the olfactory neuron needs to detect odorants," said McIntyre.
The change in olfactory function also has implications in the feeding behavior of the mice. The mouse model the scientists used is born underweight and its anosmia interferes with the motivation to eat, which in many mammals, including humans, is driven by smell. Treatment with adenovirus therapy increased bodyweight by 60 percent in treated compared to untreated mice, indicating that the restored olfactory function was motivating feeding.
The researchers plan to continue their work by developing another mouse model to look at the impact on olfactory function and the potential for restoring function when the IFT88 gene is completely missing, rather than just mutated. Future studies could begin to plot a way to bring this therapeutic tactic to human study volunteers, which could eventually restore the sense of smell, and a better quality of life, to people who are born with anosmia. Further research could also advance the treatments for other ciliopathies, as these findings show that gene therapy is a viable option for the functional rescue of cilia in established, already differentiated cells.
###
This research was supported with funding by NIH grants R01DC009606, F32DC011990, R01DC004553, R01DC008295, R01DK75996, R01DK072301, R01DK075972, R01HD042601, and R01EY021872.
The NIDCD supports and conducts research and research training on the normal and disordered processes of hearing, balance, taste, smell, voice, speech and language and provides health information, based upon scientific discovery, to the public. For more information about NIDCD programs, see the website at http://www.nidcd.nih.gov.
About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov.
NIH...Turning Discovery Into Health
[ | 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 ORLEANS (AP) ? Energy companies have reoccupied nearly 400 of the production platforms in the Gulf of Mexico that were abandoned in advance of Hurricane Isaac, a federal agency said Saturday, though offshore oil production still remains almost entirely shut down.
Oil and gas workers began retaking the offshore sites Friday and federal officials said that 377 of the 596 productions platforms have some staffing on them, up from just 97.
Yet officials estimate that 94 percent of oil production, and about 65 percent of natural gas production in the Gulf of Mexico, remains shut in in the aftermath of the hurricane.
It will take a few days for production to be fully restored, according to energy companies with operations in the gulf.
"Once onsite inspections are complete and facilities deemed safe, they will be restarted, and oil and natural gas production will be recommenced in coming days," BP said in a news release. The company said initial aerial inspections showed no significant damage.
The network of platforms, pipelines and storage facilities is massive, however, and exploration and production companies cannot recommence full operations until the chain of energy infrastructure is reconnected.
"Apache personnel are returning to the platforms and inspecting facilities," Bill Mintz, spokesman for Apache Corp., said in an email. "The process of restoring production will take a number of days and will be impacted by the pace of resumption of activities by the pipelines and processing facilities operated by other companies."
The U.S. Bureau of Safety and Environmental Enforcement said reports on offshore facilities indicated mostly minor damage.
In addition to production platforms, the bureau said, 19 of the Gulf's 76 drilling rigs are still evacuated, down from 48 as the storm approached.
A surge in gasoline prices accompanied Isaac, although the dramatic increases came to an end Friday as the storm moved farther inland. The national average price for gasoline inched up just 0.3 cents Friday to $3.83 per gallon.
Pump prices for gasoline were on the rise even before Isaac arrived. The average price for a gallon of gas rose about 40 cents from July 1 to mid-August because of refinery problems in the Midwest and West Coast, and sharply higher crude oil prices.
Crude has traded between $94 and $97 per barrel for two weeks, after rising from a low near $77 in late June.
On Friday U.S benchmark crude rose $1.85 to end at $96.47 per barrel after Federal Reserve Chairman Ben Bernanke made clear in a speech that the central bank can do more to revive the U.S. economy. That would drive up demand for energy.