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The workplace is ever changing, becoming more diverse, highly regulated and volatile resulting in complex challenges and risks for employers impacting their operations on a global basis. As a result, clients need skilled counsel to manage risk, assist them with labor disputes, litigation avoidance and defense, and to guide them in devising and implementing effective workplace policies and procedures.
Dechert's labor and employment team has the ability to provide rapid, integrated solutions to any employment, benefits or labor matter. We work closely with companies of all sizes in virtually every industry to assure that their interests are protected. Our lawyers navigate clients through the ever-changing landscape of federal, state and local laws and regulations governing the workplace, assisting them with structuring and implementing effective workplace policies and procedures, preserving their intellectual property, addressing the full range of labor and employment law issues, and guiding them through the challenges of litigation.
Dechert represents clients as advisers and advocates, devising solutions to preserve the efficiency and productivity of their workforce. We regularly defend companies against individual claims and class actions, as well represent them before state and federal agencies including the Equal Employment Opportunity Commission, National Labor Relations Board, Department of Labor, Occupational Safety and Health Administration, Office of Federal Contract Compliance, and various state agencies throughout the United States.
Prevention Advice
Clearly, the best solution to an employment problem is prevention. To that end, we counsel clients on establishing and reviewing personnel practices, developing and implementing employee relations programs, and drafting and negotiating employment contracts and policies. We address problems by applying practical, timely strategies to minimize risk and prevent employment disputes from arising in the first place.
Legal Services on Three Continents
Dechert's U.S. labor and employment practice has national presence with offices located in several major U.S. commercial centers, including Boston, Los Angeles, New York and Philadelphia.
We have a strong labor and employment presence in Europe and Asia with attorneys strategically located in Beijing, Brussels, London, Luxembourg, Munich, Moscow and Paris. We advise on domestic employment matters, cross-border matters and issues facing U.S. clients with overseas operations. We have advised on and coordinated many collective consultation programs in the United Kingdom and across Europe and Asia.
A Diverse Practice
Our services include litigation defense, labor-management relations, and preventive and compliance counseling on every conceivable workplace issue including:
We also handle grievance investigations and compliance with regulatory requirements impacting employers. We represent clients of all sizes from those with fewer than 50 employees to those with more than 5,000.
Dechert trial lawyers defend clients in all types and phases of employment actions:
On the traditional labor law side, we represent employers in all aspects of management-union relations, including union avoidance and election campaigns, collective bargaining negotiations, arbitrations and proceedings under the National Labor Relations Act (NLRA) and before the National Labor Relations Board (NLRB) and courts throughout the United States.
Our Approach to Client Service
Our priority is making sure our clients manage their employee relationships effectively with minimal disruption to their day-to-day business operations and long-term business plans. There are times when workplace problems demand immediate attention and action, while other situations call for thorough investigation and careful planning. In some cases, we must defend our clients against workplace-related claims or actions brought by employees. Our legal team works closely with our clients to assess their workplace challenges, legal needs, and business strategies to determine the best course of action.
Our labor and employment attorneys often partner with Dechert lawyers skilled in other areas, such as employee benefits and executive compensation, corporate transactions, restructurings, regulatory, intellectual property and tax matters to provide the most comprehensive, cost-efficient service. Dechert has the resources and geographic reach to provide clients with truly integrated service both in the U.S. and abroad.
The Right Results for Clients
We strive to get the results that best meet our clients' needs effectively and efficiently. We know that not all employment claims are alike. There is no "one size fits all" legal strategy. Our employment lawyers are highly skilled at assessing client matters and determining the strategy and tactics that will produce the best result for each individual client. Experienced in trying some of the most complex and high-stakes matters, we have had great success in obtaining summary judgment and other early dismissal of lawsuits, negotiating settlements, and resolving conflicts using alternative dispute resolution techniques.


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Aaron Cochran is a top-notch 2013 prospect and his brother, Matt, just signed with Cal so the Golden Bears look good in his recruitment but it's not a done deal that he'll sign there.
That's the message from Cochran, that he's still open to all programs and really doesn't plan to make his commitment until after the all-star games next year or possibly even closer to signing day.
Rivals.com rates Cochran as the No. 98 prospect in the new 2013 class rankings.
Article Continues Below
"I feel like it's a family (at Cal) but nothing has really changed," Cochran said. "It's all pretty much the same interest with all the schools recruiting me.
"We don't really talk about it too much as brothers. The last time we really talked about recruiting is when he committed at the Marines game.
"I'm going to take it up until the All-American games, maybe even after that, but I'm not going to make any decisions early on."
So far, Cal, Colorado, Washington and Washington State have offered the 6-foot-6, 320-pound prospect who looked good last year at the Los Angeles NIKE Camp and solid during his junior year.
But Cochran is not rushing things and would like to hear from more programs.
Oregon is showing lots of interest and he is planning a trip to USC at some point this off-season as well. He will be at Cal's junior day on Feb. 18. Many other offers are expected to come in as his senior season gets closer.
"I want to see what interest I get in from the other schools and I want more options," Cochran said. "Colorado is mostly talking to me and I'm obviously hearing from Cal a lot."

subset: commoncrawl


text:
ACParadise Network: American Cosplay Paradise American Cosplay Experience American Cosplay Snapshots
Cosplayer Etaru Kaumoto > Costume of Sara Mudo (Angel Sanctuary)
- Most Recent Photo
- Series
- Angel Sanctuary
- Character
- Sara Mudo
- Special Variation:
- artbook
- Year Completed:
- Construction Difficulty:
- Normal
About this Costume
- Construction Details:
The wings took about a month to make, as they were my first attempt. Although I now know how I'll make the next pair differently, I'm quite proud of them nonetheless. Kailand as Setsuna Mudou Mythrin as Raphael
- Personal Thoughts:
- Sara is such a cute and brave character, I adore her! Thank you to my awesome group who made this shoot possible :)
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text:
Leaving home: City dept. finds timely park location
Hoffman Park: If you're the Parks & Recreation Department, what better place to go if you're forced to relocate?
And so it goes.
On Monday, July 7, Parks & Recreation will shift its office from the confines of the soon-to-be demolished Ingram Center to the "octagon shelter" at Hoffman Park.
Parks & Rec has been at the Ingram Center, 210 Lewis St., since 1980.
That's the same year Danke got hired as a Youth Center recreational aide. Her job was paid for by a federal grant.
When that money ran dry she was taken on to work for Parks & Rec. In 1985 she became department coordinator.
That's a long time ago and Danke, at the end of the interview for this story, got choked up and teary-eyed about leaving the Ingram Center.
"It's an old building but, yes, I feel nostalgic for it," she said, wiping her eyes. "It's been a good place to work and people are used to coming here."
Nostalgia aside, the reality is that Parks & Rec must move. The Ingram Center is being torn down this summer, replaced by a new City Hall.
When that new City Hall opens, Parks & Rec will finally join other city departments under the same roof in that facility.
Meanwhile, between the razing of Ingram and the opening of a new City Hall, Parks & Rec needs new digs.
It was decided to set up temporarily at the eight-sided rental shelter at Hoffman Park. While smaller physically than the current site at Ingram Center, Danke said the Hoffman shelter building offers roughly the same office/work station space.
Unlike the Ingram Center location, the Hoffman Park shelter lacks meeting space for small groups and storage for bats, balls, helmets, rackets, nets, first-aid kits and swimming pool supplies.
But the Hoffman shelter is heated. Throw in a room air-conditioner and it'll be usable for both summer and winter.
Over the years the shelter's been rented for family gatherings and reunions. It was also used as a warming house when youth hockey played out at Hoffman in winter.
For a department that handles more than 2,500 kids and adults who participate in everything from swimming and soccer to baseball and volleyball, Danke said Hoffman Park is a good spot for her department to be.
"This is our busy time of the year, but fortunately we have most everyone already registered for these summer activities," she said. "If this move had been a month earlier when registration was still going on, that would have been a real headache."
Danke also likes being at Hoffman because she'll be able to monitor the 15 overnight camp sites and answer questions about availability just by stepping out her office door.
"And we get questions about field conditions because of rain for softball games," she said. "Again, it will be a lot easier to check on those conditions when I'm right there."
Hoffman Park also has a skateboard area. Safety concerns and conflicts between big and little kids will be easier to control with the Parks & Rec office within view.
Hoffman Park also had much greater visibility for Parks & Rec than the Ingram Center, though Danke said families were so used to going to the Ingram Center that she never considered its location obscure.
"We've been here 28 years. People know how to find us," she said.
The new Hoffman Park office site will not require much renovation. Work stations will be laid out in the open without partitions. A new reception counter will be set up for greeting the public. Phone and computer lines must be installed.
The park has plenty of free parking, which should make the new office site accessible.
Danke said she'll miss the convenience of being close to downtown. In the winter, her department was also close to the River Falls Academy, where Parks & Rec-sponsored basketball, volleyball and dance programs are held.
Vandalism is occasionally a problem at Hoffman Park. Danke said new security measures, possibly adding a surveillance camera, would be needed to safeguard the Parks & Rec office.
"Sure, it's sad to leave here, but I'm also happy to be going to Hoffman," Danke said. "There are so many people using that park that it's an ideal place for us to be."
When Danke says "us," it mostly means just her. She has two part-time staffers and, in the summer, 25-30 part-time employees who oversee the Glen Park pool, along with soccer, tennis, gymnastic, baseball and softball programs.
Right before the transfer to Hoffman park, Danke said there may be a brief disruption of phone service for those calling Parks & Rec. But the packing and moving will go quick and the office won't shut down.
Phone number and office hours at the new location will remain the same: 425-0924; 8 a.m. to 4:30 p.m., Monday through Friday.


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Don't miss a story. Like us on Facebook. Like Dallas News' Facebook Page
Dallas ISD trustees hired former U.S. Attorney Paul Coggins on Monday to investigate allegations that Superintendent Mike Miles tried to manipulate the outcome of a service contract award and then interfered with an investigation into the matter.
DISD trustees approved to hire Coggins in an 8-0 vote. Investigation costs are not to exceed $100,000 without board approval. A final report is expected in 30 days.
More to come.


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|You are in: Sci/Tech
Wednesday, 16 January, 2002, 19:05 GMT
Formula for quiz show success
Game show contestants on The Weakest Link could win more money by following a set strategy.
According to a US mathematician, banking the winnings after every right answer or after a run of six is the best formula for success. Eight players compete on the TV quiz show, answering questions in turn.
They accumulate money for the team when they answer a question correctly.
At the end of each round one player, dubbed "the weakest link" by acerbic host Anne Robinson, is voted off by the group.
Paul Coe, a mathematician at Dominican University in River Forest, Illinois, reckons players often lose their nerve and go home with less money than they could.
"I am always struck by how little money is actually given away," he told New Scientist.
Under Pressure
According to his team's analysis of a 21-question round, banking the money after six correct answers offers the highest reward ($50,000 in the US).
Banking after three questions ($5,000) is a less successful strategy, says Dr Coe, because strings of three right answers are harder to come by.
Unless a player has a very high success rate (more than 67%), it would be better to bank after each correct answer ($1,000), he says.
But not all mathematicians are convinced. Edward Aboufadel of Grand Valley State University in Allendale, Michigan, says it could take several rounds for a team to get six correct answers. He thinks the wait may prove too hot to handle.
"With Anne Robinson harassing the team for not banking any money, I think people would quickly back out," he says.
See also:
17 Jun 01 | TV and Radio
Weakest Link to battle Millionaire
16 Apr 01 | TV and Radio
Weakest Link hits US screens
28 Sep 01 | Reviews
Weakest Link game: Your views
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text: Hi I recently read an article on FED2 at a website [Through APUG Forums ]where, the author concluded that the RF was out of alignment based on the observation that the RF didnot align to infinity... I have recently acquired a Contax II... I have noticed that it's RF also doesnot align at infinity... However, it doesnot seem off! I have put through 2-3 rolls and all seem fine and alignments upto its before-infinity limit (and beyond as well) are very perfect... For example, you could follow the link below: http://photos1.blogger.com/img/27/1667/640/amravati04_KhadiBhndr_Port0.jpg The shot shown here is taken at f1.5 and under low light; yet, I could focus and the focus seems right-on... Is it that alignment at infinity should be proper!? My RF is great and doesnot seem a least bit misaligned! Kindly Help... Awaiting your replies... Regards Paresh Pandit Mumbai, IN Sept 12, 2004 P.S.: The FED 2 article can be found here : http://open.hr/~dpleic/photo/fed2.html


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Another Voice: Expanding casino gambling will hurt more than help
Editor's note: This is the first of two Another Voice articles on the proposed expansion of casino gambling in New York State. The second piece will appear on Saturday.
By Sam Magavern
In deciding how to vote on Proposition 1, voters should ask a simple question: Will expanded casino gambling create more costs or benefits? The answer, according to decades of research, is that casino gambling generates costs to taxpayers that far outweigh the revenues it provides.
Casinos make most of their money not from casual gamblers but from frequent, problem and pathological gamblers who sit in front of slot machines for hours on end. Depending on the venue, slots are programmed to keep between 2 and 18 cents from every dollar wagered. The more you play, the more you lose, and so, by definition, frequent gamblers lose big. When large numbers of people gamble away large sums of money, all sorts of expensive social problems result: embezzlement, fraud, bankruptcy and mental illness, to name a few.
In addition to being individual tragedies, they impose huge expenses on taxpayers. That is why Maryland concluded that gambling addicts cost the public $1.5 billion per year. That is why professor Earl Grinols reports that casinos create $3 in social costs for every dollar they bring in. That is why professor John Kindt has estimated the socio-economic costs of pathological gambling at $80 billion per year.
In exchange, the public receives very little. Casinos do not produce any valuable goods or services. They do not make our economy smarter, more efficient or more productive – just the opposite. Proponents will tell you that casinos create jobs. Sure, casinos hire people to work at them; but for every job "created" at a casino, more than one job is lost somewhere else. Every dollar spent gambling is a dollar that would have been spent elsewhere: a restaurant, sports arena or theater; or, in the case of problem gamblers, perhaps on a car payment or mortgage. Because casinos are dominated by computerized slot machines, they require only a small number of mostly low-wage employees; as a result, they kill more jobs at other businesses than they create. For a look at what gambling does to a local economy, take a quick drive to downtown Niagara Falls and see how local restaurants, taverns and other businesses have fared in the shadow of the casino.
Pretty much the only people who benefit from casinos are the people who own them (and the politicians to whom they make donations). They absorb the profits while offloading the costs onto state and local taxpayers. They know that expanding casino gambling will work just like the computerized slot machines they operate: the house wins big, and everyone else loses.
Sam Magavern co-directs the Partnership for the Public Good.


text:
With a limited number of scholarships for the 2013 class, it is likely that the Minnesota staff will take only two offensive linemen. One lineman that recently received a Golden Gopher offer was Ir...
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text:
By Angel Verdejo
Killeen Daily Herald
"Look at that little girl - just watch her run."
Alissa Gonzalez isn't that concerned about what other people say when they see her run.
"Most girls are a lot taller than me and back then, people would always say something about it," says the 5-foot Gatesville junior, who admits she stopped growing in the seventh grade. "But since I've lived here all my life, it's kind of something that they're used to now.
"So they look at me (now) and they're like, 'Just watch her run - she'll do something.'"
She's done plenty.
Gonzalez finished second in both the 1,600- and 3,200-meter runs at the District 19-3A meet on April 7 and 11, advancing to the Region III-3A meet beginning Monday at Humble's Turner Stadium. She set a personal best in the 1,600 and is edging ever so closer to the school records Gonzalez hopes to break before she graduates.
"She's just tough," Gatesville girls track coach Katy Kelley said. "Everything she does - whatever athletic event she's doing, she'd going to do it to the full extent. She might not even like it, but she's going to push herself until she can't get anything else out of her."
Gonzalez's 12:21 in the 3,200 is two seconds away from the school record, while her 5:41 in the 1,600 is 10 seconds off the mark.
"I can taste it," she says.
But Gonzalez is a regular at regionals - at least on the track - having advanced every year in high school.
The volleyball letterman and next year's cheerleading captain tried cross country for the first time last fall after coaches kept asking her to give it a try.
"In junior high, I was a sprinter," said Gonzalez, who eventually worked her way to the 1,600 and 1,600 relay by the eighth grade. "So because it was long distance, I didn't know if I could do it."
Gonzalez was the 19-3A runner up, only to run a minute faster at the Region III-3A meet a week later. She ended the season at the state meet.
"She's just an extremely competitive kid - she hates to lose," Gatesville cross country coach Brian Edwards said. "To do what she did for us cross country-wise - along with playing volleyball - to me, was amazing."
The longer distance proved to be relaxing. It also gives Gonzalez more time to do a few other things while running.
"I think about stuff a lot when I run," she said. "I have random trains (of thought) in my head."
During the cross country season, most of Gonzalez's thoughts centered around the ever-popular "Twilight" book and movie series.
"I'm like, 'Oh, we're running through trees. I feel like Bella,'" she said, referring to the lead character. "I like cross country a lot because you're going through things - I enjoy seeing the scenery."
During track, where the scenery is the football field, Gonzalez will sing songs to herself. The singing is in her head though, not out loud.
"People would be like, 'What is she doing?'" Gonzalez joked. "It wouldn't sound like a song."
Then there are the conversations - not in Gonzalez's head - that she'll have, or at least try to, with the other runners or her coaches. It's more frequent during cross country, but not as much on the track with coaches more visible for encouragement and pointers during a race.
"They just think I'm weird, but I can't help it," Gonzalez said. "It's what I do."
Said Kelley: "She talks to me - she'll tell me she's mad at me. But I'll say, 'If you have time to be mad or frustrated and tell me that, then you're not running hard enough.'"
Either way, Gonzalez keeps making believers out of those watching, even though her strides are shorter than others or she has to work that much harder.
"It is something you think about, especially when every day someone has to say something about my height," Gonzalez said. "It just never fails - it's just how things go. So I always just tell people that I'm proud of the way that I am and I'm going to use it.
"If it's something that helps me as motivation, I'll use it."


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The neurons in the external segment of the pallidum (GPe) in awake animals maintain a high level of firing activity. The level and pattern of the activity change with the development of basal ganglia disorders including parkinsonism and hemiballism. The GPe projects to most of the nuclei in the basal ganglia. Thus exploring the mechanisms controlling the firing activity is essential for understanding basal ganglia function in normal and pathological conditions. To explore the role of ionotropic glutamatergic and GABAergic inputs to the GPe, unit recordings combined with local injections of receptor antagonists were performed in awake monkeys. Observations on the effects of local application of the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)/kainate antagonist 1,2,3,4-tetrahydro-6-nitro-2, 3-dioxo-benzo[f]quinoxaline-7-sulfonamide, the N-methyl-d-aspartic acid (NMDA) antagonist 3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid, and the GABAA antagonist gabazine as well as the effects of muscimol blockade of the subthalamic nucleus on the spontaneous firing rate, firing patterns, and cortical stimulation induced responses in the GPe suggested the following: sustained glutamatergic and GABAergic inputs control the level of the spontaneous firing of GPe neurons; both AMPA/kainate and NMDA receptors are activated by glutamatergic inputs; some GPe neurons receive glutamatergic inputs originating from areas other than the subthalamic nucleus; no GPe neurons became silent after a combined application of glutamate and GABA antagonists, suggesting that GPe neurons have intrinsic properties or nonionotropic glutamatergic tonic inputs that sustain a fast oscillatory firing or a combination of a fast and a slow oscillatory firing in GPe neurons.
The external segment of the pallidum (GPe) is located at a strategically important locus of the basal ganglia connections and plays key roles in the physiology and pathophysiology of the basal ganglia. The GPe receives major GABAergic inputs from the neostriatum (Str) and the GPe itself through axon collaterals of projection neurons and major glutamatergic projections from the subthalamic nucleus (STN) (Kita 1992, 1994; Kita and Kitai 1991; Kita et al. 1999; Parent and Hazrati 1995; Robledo and Feger 1990). The Str and STN are considered to be input-nuclei of the basal ganglia. Some neurons of the centromedian-parafascicular complex of the thalamus and the frontal cortex also innervate the GPe (Deschenes et al. 1996; Kincaid et al. 1991; Mouroux et al. 1997; Naito and Kita 1994; Sadikot et al. 1992; Yasukawa et al. 2004). The GPe sends GABAergic projections to various nuclei in the basal ganglia including the Str, the internal segment of the pallidum (GPi), STN, and the substantia nigra (Bevan et al. 1998; Hazrati et al. 1990; Kita 1994; Kita and Kita 2001; Kita and Kitai 1994; Kita et al. 1999; Nambu and Llinás 1997). These connections imply that the GPe converges information reaching the basal ganglia and that information processed in the GPe are conveyed to many of the nuclei in the basal ganglia. Thus the GPe might play a significant role in controlling the level and pattern of firing activity of neurons in various nuclei of the basal ganglia and, hence, in movement control (Bolam et al. 2000; Kita 1994; Mink 1996; Mink and Thach 1993).
GPe neurons in awake animals maintain a high level of firing activity (Anderson and Horak 1985; DeLong 1971; Matsumura et al. 1995; Nambu et al. 2000; Tremblay et al. 1989; Yoshida et al. 1993). The level and pattern of firing activity change with the development of basal ganglia diseases including Parkinson's disease and hemiballism (Beric et al. 1996; Boraud et al. 2001; Filion and Tremblay 1991; Lenz et al. 1998; Nini et al. 1995; Pan and Walters 1988; Sterio et al. 1994; Tremblay et al. 1989; Vitek et al. 1999). Thus exploring the mechanisms controlling the firing activity of GPe neurons is important for understanding basal ganglia functions in normal and pathological conditions. STN neurons in awake animals are also highly active (Matsumura et al. 1992; Nambu et al. 2000). Thus it can be expected that both local GABAergic and STN-GPe glutamatergic inputs play crucial roles in the maintenance of the high level of firing activity and the generation of firing patterns of the GPe neurons. Previous studies in rodents have indicated that activation of glutamatergic and GABAergic synapses evoke ionotropic receptor-mediated responses in the GPe (Kita 1992; Nambu and Llinás 1997; Ogura and Kita 2000). The aims of the present study were to explore the role of ionotropic glutamatergic and GABAergic inputs on the level and pattern of the GPe firing activity and also to clarify the glutamatergic and GABAergic components of the responses induced in GPe neurons by the stimulation of the motor cortex in awake monkeys.
Monkey preparation
This study was performed in compliance with the guidelines of National Institutes of Health Guide for Care and Use of Laboratory Animals, the Tokyo Metropolitan Institute for Neuroscience, and the National Institute of Physiological Sciences for the Use and Care of Laboratory Animals in Research. The monkey preparation methods used in the present study were very similar to those reported elsewhere (Nambu et al. 2000, 2002). In short, four Japanese monkeys (Macaca fuscata), named K3, K5, K6, and K8, were trained to sit in a monkey chair quietly. The monkeys received a surgery to fix their heads painlessly to a stereotaxic frame attached to the chair. Under ketamine hydrochloride (10 mg/kg im) and pentobarbital sodium (25 mg/kg iv) anesthesia, the skull of monkeys was widely exposed, and two stainless steel pipes were mounted in parallel over the frontal and occipital areas for head fixation.
A few days after the surgery, the primary motor cortex (M1) along the anterior bank of the central sulcus was mapped by observing body part movements induced by cortical microstimulation and also by unitary responses to somatosensory stimuli (skin touch and passive joint movement) to identify the forelimb region. After mapping, two pairs of stimulating electrodes (made of 200 μm diam enamel-coated stainless steel wire; intertip distance, 2 mm) were implanted chronically in the forelimb region of the M1. In monkey K8, the supplementary motor area (SMA) was also mapped, and a pair of stimulating electrode was implanted in the forelimb region of the SMA. To access the pallidum and STN, two holes (10–15 mm diam) were drilled in the skull. A plastic chamber covering both holes was fixed onto the skull with acrylic resin. Recordings of GPe units began after recovery from the surgery. During the experimental sessions, the monkeys were seated in a monkey chair with their heads restrained. The forelimb region of the GPe was determined by cortical stimulation.
Electrode assembly for local injection of drugs
Single-unit recordings of GPe neurons in combination with local applications of drugs were performed with an electrode assembly consisting of a platinum-iridium wire (No. 7675, A-M Systems, Carlsborg, WA) placed in a silica tube (No. 2000018, 147 μm OD, 74 μm ID, Polymicro Technologies, Phoenix, AZ) for unit recordings, two other silica tubes for drug delivery, and a protective stainless-steel tubing (Fig. 1). These three silica tubes were assembled with a 600 to 700 μm separation between the orifices of the drug-injection tubes and the tip of the metal recording electrode and were glued together with epoxy resin (Fig. 1). The two silica tubes for drug injection, ∼25 cm long, were connected with epoxy resin to the needles of 10- or 25-μl Hamilton microsyringes. These syringes contained the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)/kainate blocker 1,2,3,4-tetrahydro-6-nitro-2,3-dioxo-benzo[f]quinoxaline-7-sulfonamide (NBQX, 1–2 mM), the N-methyl-d-aspartate (NMDA) antagonist 3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP, 1–2 mM), or the GABAA antagonist gabazine (1 mM) dissolved in saline. A total volume of 0.1–0.2 μl was injected at a rate of 0.03 μl/min by advancing the plungers with computer controlled stepping motor-driven actuators.
The method for the muscimol blockade of the STN was the same as that described elsewhere (Nambu et al. 2000). In short, a tungsten wire attached to the 30-gauge needle of a 10-μl Hamilton microsyringe was penetrated vertically in to the STN using a hydraulic microdrive (Fig. 1). Using single-unit recordings, the STN was identified by firing patterns and responses to cortical stimulation and to passive joint movements. The response pattern of STN neurons to M1 or SMA stimulation, in particular, provided important information for locating the nucleus. The STN responses consisted of an early excitation, an inhibition, and a late excitation as reported previously (Nambu et al. 2000). The two clearly distinguishable excitatory responses were observed in the STN but not in the zona incerta or the lateral hypothalamus. Strong responses to passive joint movements were also unique to the STN but not to the zona incerta, hypothalamus, or the substantia nigra. To block the unitary activity of the STN, the GABAA receptor agonist, muscimol (0.5 μg/μl, 0.5–1.0 μl), was injected in the nucleus.
Unit recordings and data analysis
The electrode assembly was penetrated obliquely in to the GPe using a hydraulic microdrive (Narishige Scientific Instrument). The unitary activity was amplified, converted into digital data with a window discriminator and sampled using a computer for on-line data analysis. The unitary activity and converted digital data were also stored on videotapes using a Neurocorder (Neurodata, Delaware Water Gap, PA) for further analysis. The pattern of spontaneous activity and responses to the cortical electrical stimulation (300-μs duration single pulse, strength of 100–800 μA and interval of 1.4–2 s) were recorded in the GPe before and after the injection of drugs. Once an injection was made, the next injection site was separated by ≥1 mm from the previous injection site.
The rates and patterns of firing were analyzed by calculating the mean rates and autocorrelograms (bin width, 0.5 ms) from 50 s of digitized recordings. The regularity of the firing was assessed by the existence of multiple peaks and their height in the autocorrelograms. Slow sweep traces of digitized unitary activity were also used to assess the firing patterns. Cortical stimulation induced responses of GPe neurons were assessed by constructing peristimulus time histograms (PSTHs, bin width: 1 ms) for 100 stimulation trials. Mean values and SDs of the firing rate during 100 ms preceding the time of stimulation were calculated from PSTHs and were considered to be the values for base discharge. The changes in the firing activity in response to cortical stimulation were judged to be significant if the firing rate during at least two consecutive bins (2 ms) reached the statistical level of P < 0.05 (1-tailed t-test). The latency of the response was defined as the time at which the firing rate first exceeded this level.
Before examining the effects of locally applied glutamate and GABA antagonists on cortically evoked responses in each neuron, the stimulating site that produced the largest early response sequence was chosen from the aforementioned stimulating sites. The data obtained by M1 and SMA stimulation were grouped together because the components of responses induced by the stimulation of these two cortices were considered to be the same. As mentioned in discussion, cortical stimulation induced responses in the GPe consist of multiple overlapping excitatory and inhibitory responses. Because of this complexity, the changes in cortical-stimulation-induced responses by local injections of glutamate and GABA antagonists were assessed by simply measuring the peak response amplitude, an average of the two highest for excitation or of the two lowest for inhibition from the mean prestimulus firing level. We considered these measurements to be a simple yet sensitive, although not precise, method for the assessment of excitation and inhibition changes. The changes in the spontaneous firing rate, the amplitudes, and the durations of the responses to cortical stimulation were evaluated by paired t-test.
Several of the recording and drug injection sites were marked by passing a cathodal DC (20 μA for 30 s) through the recording electrode. At the end of the final experiment, the monkeys were killed with pentobarbital sodium (50 mg/kg iv) and perfused transcardially with 2 L of phosphate buffered saline, pH = 7.3, followed by 5 L of 4% paraformaldehyde in 0.1 M phosphate buffer. The monkeys were then perfused with 3 L of 0.1 M phosphate buffer containing 10% sucrose and, finally, with 2 L of the phosphate buffer containing 30% sucrose. The brains were cut serially into 60 μm thick frontal sections on a freezing microtome. These sections were mounted onto gelatin-coated glass slides and stained with 1% Neutral Red. The recording and drug injection sites were reconstructed according to the lesions made by current injections and the traces of the electrode tracks (data not shown).
Pallidal local drug injection procedure
The distance between the orifices of the drug injection tubes and the tip of the metal unit-recording electrode was ∼600–700 μm. This distance was determined after testing various injection tube and electrode assemblies to find the optimum conditions to observe a consistent gabazine blockade of the cortical-stimulation-induced inhibitory responses in GPe neurons. The concentration of gabazine was 1 mM, which was 100–200 times higher than that used for bath application in rat brain-slice experiments (Matsui and Kita 2003; Seutin et al. 1997). A volume of 0.2 μl was slowly injected at a rate of 0.03 μl/min for each injection. The assemblies with a distance between drug tube orifices and the tip of the recording electrode <500 μm gave quicker and stronger gabazine effects than did assemblies with a longer orifice-electrode tip distance. However, with this type of electrode assembly, unit recordings during the injection of gabazine were frequently lost. With the 600 to 700 μm orifice-electrode distance, a total blockade of the inhibitory response was observed 3–10 min after the initiation of the gabazine injection. Even a partial recovery from the gabazine effect took >40–60 min after injection, and many neurons were lost before that time (data not shown). Because of the time restrictions associated with the use of awake monkeys, we opted not to attempt to obtain the drug-recovery data. Instead, the neuronal activity obtained before drug injection was used as a control. All the drugs used in this study were dissolved in saline. Local injection of saline did not change the neuronal activity of any pallidal neurons tested (n = 5). The radius of the effective area of the gabazine was estimated to be ∼1 mm from the orifice of the drug-injection tube because neurons evoking clear inhibitions to cortical stimulation were recorded by advancing the electrode by 300–500 μm.
Firing rate, firing patterns, and responses to cortical stimulation
Previous unit recording studies described two types of GPe neurons in awake monkeys (Anderson and Horak 1985; DeLong 1971; Tremblay et al. 1989). The neurons included in the present report were the high-frequency firing with pause type of GPe neurons, which were the most numerous in monkey GPe (DeLong 1971). The spontaneous firing rate of 35 GPe neurons recorded was 62.6 ± 25.8 (SD) Hz. Stimulation of the M1 evoked a sequence of responses in GPe neurons typically consisting of an early excitation, an inhibition, and a late excitation with latencies shown in Table 1. In monkey K8, electrical stimulation of both the M1 and SMA was performed. SMA stimulation evoked a sequence of responses that was very similar to those evoked after M1 stimulation except that the latency of the early excitation was ∼2 ms longer than those seen after M1 stimulation (Table 1). These latencies were very similar to those published elsewhere (Nambu et al. 2000; Yoshida et al. 1993). In some GPe neurons, a slow inhibition and a slow excitation followed the late excitation (e.g., Fig. 5). As described previously, stimulation of the forearm area of the M1 evoked stronger responses in the neurons that responded strongly to passive movements of the forelimb (Nambu et al. 2000).
Effects of NBQX
To assess the role of AMPA/kainate receptors on the unitary activity, NBQX (1–2 mM in saline ≤0.2 μl) was injected in the vicinity of the recording neurons. NBQX greatly decreased (56.7 ± 35.6%, n = 16) the mean firing rate of all GPe neurons tested (Fig. 2, A, D, and J). The autocorrelograms of these neurons indicated that NBQX increased the regularity of firing slightly as judged from the prominent humps in the autocorrelogram (compare Fig. 2, B with E). The slow traces of digitized spikes indicated that pauses and group discharges were still present after NBQX injection (Fig. 2, C and F). In 4 of 16 neurons, a few seconds of grouped discharges, referred to as an active phase hereafter, and a few seconds of a completely silent phase began to appear alternately in fairly regular intervals although the interval slowly changed over time (Fig. 3 A). The development of the active and silent phases was similar to that observed after muscimol blockade of the STN (described in the following text) (see also Nambu et al. 2000). In five other neurons, active and silent phases occurred alternately in more irregular intervals as shown by the minor peaks in the autocorrelograms (Fig. 3B). The intervals between peaks were 2–16 s long and changed slowly over time.
Local injection of NBQX greatly attenuated or totally abolished the early and late excitations induced by cortical stimulation (Fig. 2, A and D). The mean attenuation of the early excitation was 84.3 ± 23.2% (n = 16) and was significant (Fig. 2K). In 7 of 16 GPe neurons, the late excitation was totally abolished and the remaining inhibitory response was of a very long duration (365 ± 68.8 ms, P < 0.0001 paired t-test, n = 7, Fig. 2D). In the remaining nine GPe neurons, NBQX greatly reduced but did not completely abolish the late excitation. In these neurons, the duration of the inhibition was significantly increased from 13.8 ± 2.4 to 45.3 ± 25.3 ms (P < 0.01 paired t-test, n = 9). The mean attenuation of the late excitation for all 16 neurons was 84.4 ± 21.8% (Fig. 2L).
NBQX also attenuated or abolished the slow inhibition-excitation sequence that was evoked after the late excitation in some GPe neurons. However, these changes were not evaluated statistically because of a very small sample size (data not shown). The changes in the cortical stimulation induced responses of GPe neurons by NBQX described in the preceding text were very similar to those observed after the muscimol blockade of the STN (compare Fig. 2D with Figs. 7A and 8A).
In six GPe neurons that were pretreated with local NBQX, the effect of gabazine was examined. Gabazine increased the firing rate of all NBQX-treated neurons (Fig. 2, G and M). The mean increase was 116.5 ± 16.7% and was significant. The pauses and silent phases were completely eliminated, and the firing became very regular and oscillatory (Fig. 2, H and I). Gabazine also abolished all responses induced by cortical stimulation (Fig. 2G).
Effects of CPP
To assess the role of NMDA receptors on the unitary activity, the NMDA antagonist CPP (1–2 mM in saline ≤0.2 μl) was injected in the vicinity of the recording neurons. CPP decreased (32.4 ± 14.5%, P < 0.0001, paired t-test, n = 10) the mean firing rate of the GPe neurons (Fig. 4, A, C, and E). Although significantly decreased, the change was less prominent than that with NBQX. CPP had no clear effect on the firing pattern as judged from the autocorrelograms (Fig. 4, B and D) and the slow sweep unit recordings (data not shown).
Local application of CPP attenuated the early and late excitations induced by cortical stimulation (Fig. 4, A and C). The mean attenuation of the early and late excitations in the GPe was 21.8 ± 15.3 and 32.0 ± 19.5% (n = 10), respectively, and was significant (Fig. 4, F and G). These effects were also less prominent than those with NBQX. The duration of the inhibitory response was prolonged from 13.8 ± 2.5 ms in the control to 19.4 ± 9.2 ms after CPP injection, and this change was significant (paired t-test, P < 0.05, n = 10). There were no changes in the amplitude of the inhibition induced by M1 stimulation.
Effects of gabazine
Local application of gabazine (1 mM in saline ≤0.2 μl) increased the firing rate of 10 of the 11 GPe neurons tested (Fig. 5, A, D, and G). One GPe neuron had a slightly decreased firing rate after the gabazine application. The average increase in the firing rate was 115.8 ± 81.5% (P < 0.0005, paired t-test, n = 11). In six GPe neurons, the pauses became more apparent after the gabazine application (e.g., Fig. 5F) although these pauses disappeared in other four neurons.
Local application of gabazine totally abolished the inhibition induced by cortical stimulation in all GPe neurons tested (Fig. 5, D and I). Gabazine had no effects on the early excitation (Fig. 5, D and H, P > 0.5). However, gabazine greatly attenuated or abolished the late excitation (Fig. 5, D and J). The mean attenuation of the late excitation was 77.0 ± 29.2%, (P < 0.001, n = 9). Gabazine had no effect on the slow inhibition-excitation sequence occurring after the late excitation in some GPe neurons (e.g., Fig. 5, A and D).
Effects of NBQX, CPP, and gabazine on GPe neurons after muscimol blockade of the STN
We have shown in a previous study that injection of muscimol in the STN completely blocked the unitary activity of the STN (Nambu et al. 2000). The present study also employed muscimol blockade of the STN to eliminate the glutamatergic STN-pallidal input. The STN blockade was considered successful when the cortical stimulation no longer evoked excitatory responses (e.g., Fig. 7) (also see Nambu et al. 2000). The STN blockade resulted in the following time-dependent changes in the firing pattern of GPe neurons. The STN blockade greatly decreased the firing rate, to complete silence in some neurons. However, 5–10 min after the muscimol injection, the activity began to increase with repeated occurrences of short grouped spike discharges. As time progressed, the activity further increased and developed into repeated occurrences of 2–12 s of a very high-frequency active phase and then 2–12 s of a completely silent period, as has been reported previously (Nambu et al. 2000) (Figs. 6B and 7 D). In most of neurons, the intervals between active phases were fairly regular, as shown in the autocorrelograms with clearly identifiable multiple peaks, although the duration of each active and silent phase varied in some degree (Figs. 6A and 7B). The intervals between the peaks in the autocorrelograms differed from neuron to neuron with the shortest and the longest intervals being 1.8 and 22 s, respectively (n = 22). Also, the intervals slowly changed over time for each neuron. In the GPe neurons with alternately occurring active and silent phase activity, cortical stimulation induced different responses depending on the phase of the neurons at the time of stimulation (Fig. 6, C and D). Stimulation applied during the silent phase triggered the active phase ∼400–800 ms after the stimulation (Fig. 6E). Stimulation applied during the active phase induced different responses depending on the intensity and timing of the stimulation. Low-intensity stimulation and stimulation applied during an early part of the active phase often induced a short inhibition (Fig. 6F). Conversely, strong stimulation and stimulation applied during a late part of the active phase often terminated the active phase (Fig. 6G).
After the muscimol blockade of the STN, six neurons were tested with local application of CPP. CPP caused insignificant changes in the mean firing rate in these neurons with the firing rate decreasing in three neurons, increasing in one, and remaining unchanged in two (Fig. 7M). Seven GPe neurons were tested with NBQX, three of which were tested with CCP prior to NBQX. NBQX decreased the firing rate of all GPe neurons (Fig. 7, I and N). The mean decrease in the firing rate was 51.2 ± 42% and was significant (P < 0.02, paired-t-test). The decrease in the firing rate was accompanied by a decrease in the duration and frequency of the active phases, an increase in the irregularity of the firing during the active phases, and an increase in the irregularity of the intervals of the alternately occurring active and silent phases as judged by the decrease in the height of the prominent peaks in the autocorrelograms (Fig. 7, F–H and J–L). The decrease in the firing rate also appeared to be accompanied by an increase in the duration of the inhibition to cortical stimulation, although precise measurement of the duration was often difficult because of a low spontaneous firing rate (e.g., Fig. 7, E and I).
After the muscimol blockade of the STN, local application of gabazine greatly increased the firing rate of all five GPe neurons tested (Fig. 8G). The mean increase was 198 ± 138% and was significant (P < 0.005, paired-t-test, n = 5). The increase in the firing rate was associated with a great increase in the regularity of the spike intervals (Fig. 8F) as noted by several humps in the autocorrelogram (Fig. 8E). Gabazine also totally abolished the cortical stimulation induced inhibition and the silent periods of the GPe neurons (Fig. 8, A, C, D, and F).
Limitations of the local drug application method
Local application of glutamate and GABAA antagonists should have affected not only the neuron being recorded but also other nearby neurons. Because all GPe projection neurons have local axon collaterals, it is possible that the synaptic actions of these nearby neurons on the recording neuron obscure the direct effects of the antagonists on the neuron. However, we considered this not to be a significant problem. If gabazine, a GABAA antagonist, increased the activity of the nearby neurons by removing GABAergic inhibition to these neurons, the activity of the local axon collaterals innervating the recording neuron might increase. This would not affect the recording neuron, however, because the GABAergic inputs had already been blocked. On the other hand, if the glutamate antagonists, CPP and NBQX, decrease the activity of the surrounding neurons, it would disinhibit the recording neuron and act to increase its activity. However, injection of CPP and NBQX decreased the activity of most of the neurons examined, indicating that the direct effect of the antagonists on the recording neurons was stronger than the effects through the axon collaterals.
The electrode assembly had 600 to 700 μm separations between the orifices of the drug ejection tubes and the tip of the metal recording electrode. This distance was chosen after a preliminary experiment to obtain a consistent and reliable gabazine effect on the inhibitory responses induced by cortical stimulation in GPe neurons. The electrode assembly provided stable recording and also increased the chance of covering the entire somatodendritic space of recorded neurons by the injected drugs. However, the dendrites located far from the drug tube orifice might not be within the effective reach of the drugs. For this reason, we infer that locally injected drugs might have failed to produce maximum effects in some of the neurons. Another limitation of the present method was that the number of neurons recorded was small because of the necessity of the distance and time separations between the drug injections.
Another limitation of the local antagonist application method is that assessment of the actual concentrations of the applied antagonists at receptor sites of the recorded neurons is not possible. However, we assumed that the concentration of the antagonists at the active sites was not excessively high based on the observation of the efficacy of blocking the cortically evoked responses and also by the application method of using a small volume with a very slow injection speed. Nevertheless, we tested the possible effects of NBQX and gabazine that are unrelated to the antagonistic action on rat GPe neurons in slice preparations (Kaneda and Kita, unpublished observations). Bath application of 10 and 100 μM NBQX abolished internal capsule stimulation-induced excitatory responses without altering spontaneous firing of all four neurons tested. Application of 1 mM NBQX depolarized these four neurons ∼10 mV and increased the spontaneous firing. Bath application of gabazine ≤1 mM abolished inhibitory responses to striatum stimulation without altering the excitatory responses, spontaneous firing frequencies or firing pattern of all four neurons tested. The development of long active and silent phases was not observed in any of neurons recorded. These observations suggested that the primary effects of the NBQX and gabazine in the present study were the blockade of AMPA/kainate and GABAA receptor-mediated responses, respectively.
Spontaneous activity
Based on the results of the present study, we assume that the major forces driving the spontaneous activity of GPe neurons include the glutamatergic synaptic inputs, the GABAergic synaptic inputs, and other drives. In the very simplified schematic model provided in Fig. 9B, these three forces were given equal strength, as the relative strength of each was not determined in the present study. A sum of these forces determines the level of spontaneous activity.
Previous studies using rat brain slice preparations indicated that rat GPe neurons have AMPA/kainate and NMDA receptors that can be activated by the stimulation of STN-pallidal glutamatergic inputs (Hanson and Jaeger 2002; Ogura and Kita 2000). The present study revealed that local application of NBQX greatly reduced the level of spontaneous activity of GPe neurons. CPP also reduced the activity, although the effect was not as strong as with NBQX. These results suggest that the high rate of spontaneous activity of GPe neurons in awake monkeys is in part due to glutamatergic inputs activating both AMPA/kainate and NMDA receptors. The major origin of the glutamatergic innervations to the GPe is the STN. STN neurons fire at 20–40 Hz in awake monkeys and can provide continuous inputs to the GPe (Matsumura et al. 1992; Nambu et al. 2000). Indeed, unit recording studies in awake monkeys, including ours, showed that the blockade of the STN by local muscimol injection greatly decreased the firing rate of GPe neurons (Hamada and DeLong 1992; Hamada and Hasegawa 1994; Nambu et al. 2000). However, some GPe neurons started to fire grouped discharges a few minutes after the muscimol blockade and slowly developed into a few seconds of an active phase alternating with a few seconds of a silent phase, as mentioned earlier.
The results of the present study further indicated that local application of NBQX decreased the firing rate of most of the GPe neurons even after the muscimol blockade of the STN. This observation suggested that GPe neurons received sustained glutamatergic inputs not only from the STN but also from other sources. Other possible minor origins include the centromedian-parafascicular nuclear complex of the thalamus, the cerebral cortex, and the pedunculopontine tegmentum (Deschenes et al. 1996; Kincaid et al. 1991; Mouroux et al. 1997; Naito and Kita 1994; Sadikot et al. 1992; Yasukawa et al. 2004). Another possibility was an incomplete blockade of the STN by muscimol injection. Muscimol very effectively silenced the unitary activity of the STN for several hours and blocked the cortical stimulation-induced disynaptic excitations mediated through the STN (Nambu et al. 2000; present data). Based on these observations, we speculate that a wide area of the STN was blocked by the muscimol injection, including even the nuclei surrounding the STN.
The results of local gabazine application experiments indicated that GABAergic inputs are continuously suppressing the firing of GPe neurons. The major sources of GABAergic innervations to the GPe are the Str and the GPe itself. An in vitro study suggested that unitary Str-GPe inhibitory postsynaptic potentials (IPSPs) recorded at the somata of GPe neurons are very small (Ogura and Kita 2000). In addition, the activity of Str projection neurons is very low in awake animals. However, a large number of Str neurons project to the GPe, and their axons form ∼80% of the total synaptic boutons on the dendrites of GPe neurons. It is possible that these inputs to the dendrites effectively shunt the driving forces generated at the dendrites. In contrast, GPe local axon collaterals generate large unitary inputs to the postsynaptic neurons (Ogura and Kita 2000). In addition, GPe neurons maintain much higher rates of spontaneous activity than Str neurons in awake animals (Anderson and Horak 1985; DeLong 1971; Matsumura et al. 1995; Nambu et al. 2000; Tremblay et al. 1989; Yoshida et al. 1993; present data). However, the population of local collateral boutons in the GPe is relatively small. Thus the observed gabazine effects on the spontaneous activity of GPe neurons might be due to the blockade of the inhibitions by both Str-GPe axons and GPe local axon collaterals. If this assumption is correct, the degree of the tonic inhibition should correlate positively with the level of the spontaneous activity. In the model, the GABAergic inhibitory force is represented by the height of a blue column, which consists of 50% of each of the Str-GPe and GPe local collateral inhibition. Figure 9E mimics a reduction of the GABAergic driving force by gabazine. The application of a local glutamate antagonist also reduces the inhibitory force because the decrease in the spontaneous activity should decrease the local GABAergic synaptic inputs as mentioned in the preceding text. This makes the effects of glutamate blockers on spontaneous activity less apparent in the GPe (Fig. 9F).
The application of gabazine to the neurons that had been treated with NBQX or the application of gabazine after muscimol blockade of the STN greatly increased the firing rate of GPe neurons. These observations suggested that GPe neurons have intrinsic mechanisms to support high-frequency activity and/or that sustained nonionotropic glutamatergic inputs continuously activate GPe neurons. GPe neurons in rat brain slice preparations have intrinsic mechanisms to support a low level, <20 Hz, of spontaneous firing (Nambu and Llinás 1997; Ogura and Kita 2000; Stanford 2003). Although it is possible that primate GPe neurons have ionic mechanisms that support a higher level of spontaneous firing than rodent GPe neurons, the effects of nonglutamatergic inputs acting in the GPe of unanesthetized animals cannot be ruled out. Such possible inputs include the metabotropic glutamatergic and serotoninergic inputs (Hashimoto and Kita 2002; Poisik et al. 2003). The GPe receives a heavy serotoninergic projection from the dorsal raphe nucleus (Hortnagl et al. 1983; Pasik et al. 1984). Application of serotonin depolarizes and increases the firing rate of GPe neurons in rat brain slice preparations (Hashimoto and Kita 2002). In the model, these other forces are presented as an orange column and provide a constant excitatory force to the spontaneous activity (Fig. 9).
Firing patterns
The firing pattern of most of GPe neurons in awake monkeys is of high frequency with pause type (Anderson and Horak 1985; DeLong 1971; Tremblay et al. 1989). In the neurons pretreated with NBQX or in neurons recorded after the blockade of the STN, firing became very regular after the application of gabazine. Recordings of rat GPe neurons in slice preparations indicated that both Str stimulation-induced IPSPs and local axon collaterals induced large spontaneous unitary IPSPs cause various lengthening of the interspike intervals, depending on the timing of the occurrence of IPSPs between spikes (Kita 1996; Nambu and Llinás 1997; Stanford 2003). These results are consistent with the idea that both Str and local axon collaterals can evoke IPSPs that are powerful enough to produce irregularities in the firing of GPe neurons. Another obvious reason for the increase in the regularity in high-frequency firing neurons is the strong activation of membrane properties that support the high-frequency firing (Bar-Gad et al. 2001). The application of NBQX also increased the regularity of the firing. Although the amplitude of unitary EPSPs evoked by STN-GPe axons is small when recorded at the somata, they are capable of inducing spikes at distal dendrites (Hanson and Jaeger 2002, Hanson et al. 2004). The NBQX effect may be due to blocking both the firing triggered by excitatory postsynaptic potentials (EPSPs) and the recurrent IPSPs evoked by that firing.
Two other observations may be worthy of further discussion. The first was that in some GPe neurons, the pauses of firing became more apparent after local gabazine injection, although these pauses disappeared in other neurons. A very similar observation was reported in a previous study using the local injection of bicuculline, a GABAA antagonist, in the awake-monkey GPe (Matsumura et al. 1995). This raises the possibility that intrinsic mechanisms of GPe neurons may generate the pauses within an appropriate membrane potential range. The second interesting observation was that in some GPe neurons, the application of NBQX induced a few seconds of a strong active phase alternating with a few seconds of a complete silent phase that was very similar to those observed after the muscimol blockade of the STN (Hamada and Hasegawa 1994; Nambu et al. 2000). This suggests the possibility that a loss of the STN-GPe synaptic inputs that were mediated by AMPA/kainate receptors was responsible for the development of the alternately occurring long active and silent phases. Co-application of NBQX and gabazine eliminated the silent phases and made the GPe neurons fire very regularly and oscillate at a high rate. Thus it is conceivable that the membrane properties that support high-frequency oscillations become dominant in neurons that are capable of generating active and silent phases at a particular membrane voltage range (Stanford 2003). After muscimol blockade of the STN, gabazine could also abolish the long silent phases in most, but not all, GPe neurons. Therefore it is likely that GABAergic inputs contribute to the occurrence of the silent phase even though the inputs are not absolutely necessary. The precise mechanisms underlying these responses are still unknown at this time.
Cortical stimulation-induced responses
The common response pattern of GPe neurons to M1 or SMA stimulation was a sequence of early excitation, inhibition, and late excitation, as reported previously both in rats and monkeys (Kita 1992; Nambu et al. 2000; Ryan and Clark 1991). Several excitatory and inhibitory drives forming this response pattern can be considered based on the major synaptic connections between the cortex and the GPe and based on the cortical stimulation induced responses in the Str and the STN that have been reported in previous studies (Kita 1992, 1994; Kita and Kitai 1991; Nambu and Llinás 1997; Nambu et al. 2002, 2003; Ogura and Kita 2000; Tremblay et al. 1989).
The early excitation has been considered to be due to the disynaptic cortico-STN-GPe connection with very fast conducting axons (Fig. 9, A and B) (Kita 1992; Nambu et al. 2000; Ryan and Clark 1991). The present results indicated that the early excitation was mediated mainly by AMPA/kainate receptors and partially by NMDA receptors.
The present study confirmed that GABAA receptors mediated the inhibition following the early excitation. Two synaptic inputs can be considered for the inhibition (Fig. 8B). One is the local axon collaterals of GPe projection neurons. The early excitation in the GPe mentioned in the preceding text should evoke recurrent inhibition in the postsynaptic neurons. Another is the cortico-Str-GPe input. Because the conduction velocity of Str axons is slow (Tremblay et al. 1989; Yoshida et al., 1993), the inhibition should arrive a few milliseconds after the arrival of the early excitation. The relative strength of the GPe and Str inhibitions was not assessed in the present study. However, it was certain that the cortico-Str-GPe inhibition was strong enough to stop the spontaneous firing of GPe neurons as cortical stimulation effectively inhibited GPe activity after elimination of the excitation by local NBQX or muscimol blockade of the STN.
The late excitation was also due to mostly AMPA/kainate and some NMDA receptor activation. The major source of the late excitation might be the STN-GPe inputs for the following two reasons. First, stimulation of the cortex also induced a late excitation in STN neurons with a latency that was a few milliseconds shorter than that of the GPe. Second, muscimol blockade of the STN diminished or abolished the late response in the GPe (Nambu et al. 2000; present study). There are two possible driving forces for the late excitation in the STN. The major force is the activation of the Str-GPe-STN, indirect, pathway that should induce a disinhibition in the STN (Albin et al. 1989; Delong 1990). This possibility was confirmed by recent studies that a local injection of muscimol in the Str or of gabazine in the GPe diminished the late excitation without affecting the early excitation of STN neurons (Nambu et al. 2002, 2003) and also by the present observation that local injection of gabazine diminished or abolished the late excitation of the GPe. The other possible driving force of the late STN excitation is an anodal-brake rebound depolarization that follows the preceding inhibition induced by the cortico-STN-GPe-STN pathway (Fig. 9, A and B) as STN neurons in slice preparations evoke a strong anodal-brake depolarization (Bevan et al. 2002; Nakanishi et al. 1987; Plenz and Kitai 1999). These two driving forces would be dependent on the magnitudes of both the early excitation and the inhibition of the GPe (Fig. 9, B and D). Other excitatory force contributing to the late excitation of the GPe might be the disinhibition of the local collateral inputs with its strength dependent on the strength of the preceding inhibition.
Figure 9D shows a simple numerical simulation in which the amplitudes of the aforementioned excitatory and inhibitory inputs were adjusted to mimic actual unit recording shown in Fig. 9C (for details of the simulation, see the figure legend). Figure 9, E and F, simulates an 80% reduction of both the GABAergic and glutamatergic inputs by selective antagonists, respectively. An incomplete blockade was assumed because the local injection method might not assure the total blockade of the synaptic inputs. The results of the simulations were very similar to the actual data shown in Figs. 2 and 5.
In some GPe neurons, a slow inhibition and a slow excitation followed the late excitation. Similar slow inhibition and slow excitation were observed in the Str and the STN after stimulation of the cortex and were considered to be due to a disfacilitation of cortical inputs and to a rebound excitation, respectively (Fujimoto and Kita 1993; Wilson 1986). The slow inhibition and excitation in the GPe were diminished by both local injection of NBQX and muscimol blockade of the STN, while local gabazine injection was without effect. These observations suggest that the slow responses in the GPe reflect the slow responses in the STN.
Long-lasting inhibition and pauses of GPe neurons observed after the blockade of glutamatergic inputs
As discussed in the preceding text, after the muscimol blockade of the STN or after the local application of glutamate antagonists, some GPe neurons induced alternately occurring active and silent phases. Local application of gabazine eliminated the silent phases in most of the GPe neurons, suggesting that GABAergic inhibitory inputs play a role in inducing these silent phases. After the blockade of the STN, stimulation of the cortex should evoked inhibition through the cortico-Str-GPe disynaptic connections. The Str-GPe inhibition may be augmented after STN blockade because of the removal of the tonic presynaptic suppression of GABA release by group III metabotropic glutamate receptors (Matsui and Kita 2003). Cortical stimulation evoked inhibition that arrived during an active phase could terminate the active phase. It was also observed that stimulation applied during the silent phase could trigger the active phase with a 400- to 800-ms delay. These observations supplement the aforementioned suggestion that the alternately occurring active and silent phases may develop in neurons at a particular membrane potential range and that tonic GABAergic inputs contribute to bring the membrane into that range. The stimulation-induced IPSPs may flip the neurons from an active to a silent phase or vice versa by deactivating or deinactivating inward currents such as the persistent sodium current (Hashimoto and Kita 2003; Stanford 2003). However, the precise mechanisms underlying these responses are still unknown at this time.
Functional implication
The present results suggest that the level and pattern of unitary activity in the GPe are controlled by multiple factors including glutamatergic inputs, GABAergic inputs, membrane properties, and other inputs. These results may be useful in interpreting previous pathophysiological observations. Studies have shown that basal ganglia disorders are accompanied by changes in the level and pattern of GPe activity. The changes reported in the GPe of parkinsonian patients and of experimental parkinsonian animals include a modest decrease in the firing rate, an increase in the irregularity and bursting, and an increase in the sensory response such as to the movement of multiple joints (Beric et al. 1996; Filion and Tremblay 1991; Pan and Walters 1988; Sterio et al. 1994). A widely used basal ganglia model of Parkinson's disease assumes an augmentation of the Str-GPe input (Albin et al. 1989; Delong 1990; Nini et al. 1995). The augmented Str-GPe inputs would increase the firing irregularity in an effect opposite to that of gabazine where the firing pattern was greatly regularized. The model used here also predicts a decrease in the level of the firing when Str-GPe inputs were augmented.
Dyskinesias can be experimentally induced by various treatments including a lesion or a chemical blockade of the STN, application of GABA antagonists in the GPe, or application of glutamate antagonists in the GPi (Crossman et al. 1988; Hamada and DeLong 1992; Hamada and Hasegawa 1994; Nambu et al. 2000; Robertson et al. 1989). Dyskinesias induced by blockade of the STN involve a decrease in the firing activity and changes in the firing pattern of the GPe (Hamada and DeLong 1992; Hamada and Hasegawa 1994; Nambu et al. 2000; Vitek et al. 1999). Based on the present study, it can be inferred that application of a GABA antagonist in the GPe increased the firing rate of GPe neurons, and in turn, decreased the activity of the GPi. Application of a glutamate antagonist in the GPi should also decrease the firing rate of GPi neurons. Therefore one of the common effects of these treatments that induce dyskinesias would be a decrease in the activity of the GPi. The strong active phases alternating with silent phases that developed in GPe neurons after the STN blockade also should contribute to the inhibition of GPi activity and promote the occurrence of dyskinesias, although the precise functional significance of the active and silent phases is unknown at this time. Another common aspect of these treatments is the blockade of the Str-GPe-STN, indirect, pathway. Our present observations are consistent with the idea that the indirect pathway provides significant control over the output of the basal ganglia and that the effectiveness of this pathway is critically dependent on both the early excitation and following inhibition of GPe neurons (Fig. 9).
This study was supported by National Institute of Neurological Disorders and Stroke Grants NS-42762 and NS-47085 and Grants-in-Aid for Scientific Research (to H. Kita) and for Scientific Research on Priority Areas (to A. Nambu) from the Ministry of Education, Culture, Sports, Science and Technology of Japan.
We thank D. Merrick for editing the manuscript.
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
- Copyright © 2004 by the American Physiological Society


text: According to wii.qj.net wii update 4.2 may bricks wii's for some. [QUOTE It seems blocking homebrew isn't the only thing that System Menu 4.2 does. According to some reports from NeoGAF and Nintendo's own tech forums, it's also causing Wiis to get bricked. Not everybody is affected, but it doesn't just happen to HBC-enabled Wiis. Apparently the update has dodgy boot2 code that has a high chance of causing write errors. It looks like this is the cause of the brickage. Nintendo hasn't said anything official yet, although there are complaints that some tech support forum posts about the issue are being deleted [/QUOTE]


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This is the third iteration of Microsoft's handheld entertainment device since the Zune launched in 2006, and it's the strongest competitor on the market to Apple's iPod Touch. The gorgeous 3.3-in. organic LED (OLED) touchscreen puts every other portable device to shame. Access to HD-radio channels ensures a radio-listening experience equal to that of CD-quality sound. Built-in wi-fi gives way to the Zune Marketplace, where with a monthly $15 Zune Pass you can stream and purchase your choice of more than 6 million tracks through the Zune HD or Web browser. A multitude of videos, podcasts, games and apps are also available to help occupy your time.
Price: $219.99 for 16 GB; $289.99 for 32 GB
Next NPR Radio by Livio


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Oman Signs Dhofar Power Complex Contract
Year-long negotiations between the Oman government and Dhofar Power Co (DPCO) bore fruit Saturday with the signing of an ambitious concession to build a fully private, vertically integrated power utility in Salalah by March 2003, The Gulf News reported Sunday.
Under the 20-year concession, the daily said, DPCO and its wholly-owned subsidiary, Dhofar Generation Co, will intially invest $270 million to build a world-class 220MW gas-fired power plant in Salalah, the capital of southern province Dhofar.
The consortium, which also has the mandate to add new generation capacity, will completely modernize the Salalah transmission and distribution network, upgrade the voltage capacity to 132KV and extend the network to Thumrait and the suburbs of Mirbat in Dhofar.
According to the daily, DPCO is obliged to offer 35 percent shares to the public in Oman on the Muscat Securities Market within four years of its operation. It is also committed to have at least 75 percent Omani employees by the end of the 20th year – Albawaba.com
Top Headlines
- GE's Advanced Gas Turbine Technology, Services Selected to Help Southern Oman Meet its Growing Water and Power Needs
- OCTAL welcomes OCCI Salalah branch officials to explore new growth opportunities for local businesses in Dhofar
- Indian firm chosen to build $233 million Oman power plant
- SCECO signs $16 million contracts upgrading southern network
- Oman Inaugurates Huge Gas Complex


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Foxconn, the Taiwan-based company that manufactures gadgets for Apple, Microsoft, Cisco, and others, aims to become a major force in Taiwan's emergent market for 4G.
The gadget supplier will buy a stake worth $390 million in Asia Pacific Telecom, a Taiwanese mobile telecoms operator, reports Reuters. Foxconn will acquire 582.9 million shares in Asia Pacific, according to stock exchange filings. Asia Pacific intends to merge with a unit of Foxconn by June 20.
Foxconn previously won a license to operate part of Taiwan's 4G spectrum, which is expected to become commercially available later this year.
Foxconn, also known as Hon Hai Precision Industry Co Ltd, is one of the world's largest electronics manufacturers. It makes computers, mobile devices, and components for the world's tech giants in factories spanning several countries (though its Vietnamese units ran into some trouble recently). In the last few years, Foxconn has started to expand into other areas, including cloud computing.


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I am a second year teacher working on my Masters in Literacy from Walden University. Blogging is new to me and I am excited to get started. I seek to be the best teacher I can be,so by joining this blog, I hope to aqcuire valuable advice and suggestions from other teachers to improve my practices. :) I am currently certified to teach Pre-K through 6 and have a concentration in History. I enjoy my position as a preschool teacher, but am looking to obtain a job in a public school!
Areas of Interest:
Social Studies


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necklace woman jewellery Ippocampo Botticelli
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This article is no longer produced by parent company and so the purchase does not guarantee the necessary spare parts and technical assistance.
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Jewel Material: 925 Silver


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December 3, 2010 BY Aaron Hope
"Li-Ning; it's a company that's going to be the future; everyone's going to be talking about it."
SoCal basketball fans have been supporting Baron Davis since his days as a UCLA Bruin, but it'd be a mistake to dismiss the above claim as hometown hype. Chinese footwear brand Li-Ning continues to expand into the American market and have had some good success in the LA area and anywhere people appreciate affordable performance footwear, with the Li-Ning BD Doom. Davis launched the Doom himself by taking a murked-out ice cream truck to the South Bay Galleria in Redondo Beach where Baron held a meet-n-greet with fans at the Champs Sports. Fans seemed impressed by all the new things Davis and Li-Ning are bringing to the table, and you can see the entire video when you click on the jump below.
Filed under: Basketball Promo


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US International Taxation
15 July 2009
Stafford Smiley, a member in Caplin & Drysdale's Washington, DC office and a Visiting Professor in the Graduate Tax LLM Program at Georgetown University Law Center, will teach US International Taxation in semester two 2009 as an intensive unit of study.
The unit examines in detail the most important legislative and treaty rules of the US as they apply to cross-border business and investment transactions, both inbound and outbound.
The unit is available to study through the following Sydney Law School degree programmes:
This unit of study meets the training and development requirements of the Institute of Chartered Accountants Australia (ICAA).
Candidates can also enrol in the subject on a Legal Professional Development (LPD), Single Unit Enrolment or Cross-Institutional basis.
For further enquiries or to apply or enrol, please contact the Postgraduate Team.
Contact: Greg Sherington
Phone: +61 2 9351 0202
Email: 742857016a2025284a0e00201d1f17112604214f4f1c5336013847


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Guy Gets Beat Down By Baby Momma's Big Brother [Video]
After being abused by her baby daddy this chick calls up her big brother for some street justice and this dude gets dragged all around the house!
Nothing is more satisfying then seeing a piece of trash get what he deserves. Most people would say " why didn't she just call the cops?" Well my answer would be, why would you do that when you can get big bro to come and handle it?
The only thing I see wrong with this is that his beatdown didn't last long enough.


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Van Buren Theatre
Main Street,
No one has favorited this theater yet
The Van Buren Theatre first opened in 1932, and was named in honor of President Martin Van Buren (1837-41), a native son of the region. One of his distant relations, Mrs. L.J. Van Buren, built the cinema because the Catskill Mountains town lacked one and had no competition for many miles around.
Cairo had a resident population of only 900 or so, but the area had a constant flow of tourists to its many hotels and boarding houses, especially in summer. How the Van Buren Theatre managed to survive the Depression is unknown to this writer, but it was still open in 1941, although closed by 1943.
More information is needed about its history and the current status of the site. According to one report, the building still existed as recently as the 1990's.
Recent comments (view all 1 comments)
also called Love Star Theatre
Just login to your account and subscribe to this theater


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Broca's Brain on the North Dateline CC Meeting Field Trips: Cephlomorphometrics as an indicator of mental prowess has slipped out of fashion (see Gould's The Mismeasures of Man). But contemporary fashion, the baseball cap with the little 7-button plastic fastener on the back, permits observations of cranial perimeters in an unobtrusive manner. Such a survey was taken of members of the LTER coordinating committee and fellow travelers at the LTER CC Big-Alaska Shootout!
Here is how it works (the methods section of this little report). You count the number of buttons on the hat fastener that show. The possibilities are 0, 1, 2, 3, 4, 5, and 6. Twenty cap wearers were approached from behind by this reporter (N=20) and tabulated on the spot! The mean was 2.4 beads showing plus or minus 1.273 (kurtosis -.582; skewness .151). Better run to the closet and check your hat to see where you fit. The histogram below gives the frequency distribution. Not bad for N=20. Y=frequency of buttons showing.
The NSF leadership on the field trip was approached from behind and tabulated as well. Results: smaller heads than the total population (mean = 2.0) and a variable lot (SD = 1.581). They have a large coefficient of variation compared to the total population 79.057 vs 53.050. But have zero skewness. Surprise! The NSF leadership group had the only 0 button subject (pinhead?) and the only 5 button subject (fathead?) Organizers of the CC meeting and field trips were also isolated and tabulated. 1.333 +/- .577 with a coefficient of variation of 43.301 (on the pinheadish side). It is noteworthy that the graduate student minions at Toolik lake scored a robust 3.667 +/- .577 with a 15.746 coefficient of variation. A number of the field trip participants were sans billed baseball cap. Observations indicate considerable cranial girth and a dullness of eyes thus indicating that a hats-that-don't-have-buttons hypothesis that would merit study. Statistics on gender or subfield of ecology were not taken (not PC), nor on family-way status. Because individual egos are involved, the data base for this study will not be put in network archives. You will have to live with the "meta data" in this report. As to the significance of the findings your really should read Gould's The Mismeasures of Man.
One of the Alaska CC meeting participants passes on this to all concerned about the hat-button classification. "I looked at all the hats in my closet and found that the number of buttons showing varied a lot." My. My. Here are some explanations.
The CED cephlometric survey taken on the Alaska Pipeline Highway and in the environs of Toolik Lake has been called into question. The question comes from a closet survey. An intrepid CED reader went to his closet and found ballcaps for all occasions. His caps with the plastic cephlometer for the one-size-fits-all cap-attribute were not identical. He found that some of his cap gave a cranial estimate of three hole others said as much as six hole. As a result it will be necessary to bring to Estes Park an official CED cephlometer. It will be displayed in the poster hall and all can come, measure and rejoice. Results will appear in the following CED.
The question mark in the title of this piece is to help facilitate the pronunciation of Hu. With the ? (interrogative) the pronunciation of Hu becomes Huh!
Hu stands for the Hobbie Unit.
#!!@$&^ @#*! on the other hand is a Pacific Northwest peculiarity.
Some explanation is obviously required. The Hobbie Unit is measured in radians and was determined at the 1993 LMER annual meeting to be 0.052 radians. This yet-to-be-proved constant is one-half of the difference in baseball cap sizes required by John Hobbie when he is
It is a measure of radial deformation and is equal to one post unit in a Portland Trail Blazers baseball cap. The Portland Trail Blazers are not a baseball team. CED readers of my writings on cephlomorphometrics at the All Scientist Meeting in Estes Park will recall that some LTER participants refused to wear the University of North Carolina baseball cap I used in that cranial survey. The reasons had to do with hubris and chauvinism and Duke's recent national championships in basketball.
At the LMER annual meeting in Seaside, Oregon (that is near Astoria at the mouth of the Columbia River) there was concern about wearing any baseball cap at all. It didn't matter what logo rested above the brim. In Ecotopia the baseball cap has become very not-PC! Apparently, loggers have been seen wearing them! In Ecotopia it is not green to be seen wearing our national hat. The greener-than-Thou types in Ecotopia call our national hat the #!!@$&^ @#*!
(Cryptographers. The last "! " is real, a punctuation mark, while the first two stand for letters used by literate people in constructing words).
For non-cryptographers, Stephanie Martin, Si Simenstad and all the Columbia River LMER graduate students know the solution to this little puzzle because they found the time, wearing aren't-we-bad grins, to tell me about the lexicon of this homegrown Ecotopian bigotry.
It was my good luck that the actual cranium-fitting and size-recording took place in the basement of the Shilo Hotel at Seaside and LMER participants from the northwest were not likely to be seen wearing the national hat. John Hobbie, who commissioned this cephlomorphometry, on setting his eyes on the Portland Trail Blazer baseball cap and contemplating his own fitting, said, "This isn't going to be big enough." It was. John's head was 0.1560 Hu? smaller than he thought it was. I continued my work. Measurements were taken, statistics were calculated, overheads were made and an after-dinner cephlo-talk given.
A good time was had by all at the Hobbie Roast.
The Carolina and Blazers hats were subject to the tape measure and caliper and were cross-calibrated. The Blazers Hu? of 0.052 was matched against a Carolinian Hu? of 0.055. Hobbie in the Blazers cap locked in on the third post. My records indicate that Hobbie in Carolina locked in on the 5th post.
With these constants I converted LTER Estes Park truth into LMER Shilo truth. I have been contacted by the Educational Testing Service in Princeton, N. J. to submit this math-teaser for the 1994 edition of the SAT. Any of you have juniors in High School this year? LTER graduate students had on average 0.01265 Hu? smaller heads than PIs. LMER graduate students also showed pinheadedness relative to their PIs. Our best data is for the Columbia LMER site. They were the home team and brought lots of van-driving graduate students. These upstarts were a big 0.1040 Hu? smaller than their mentors! No LTER had such a cap-gap for the student-mentor chasm. It seem clear that there is a yet-to-be-consumated brain-filling marathon needed in Spotted Owl country. The Andrews LTER site was the most fatheaded of all the LTER sites and were deemed obvious candidates to fill Washington NSF posts where they would feel at home. LMER's fatheads were the folks at the Columbia River site. The Pacific Northwest is clearly the home of the fatheads. Andrews graduate students came in at a 0.0760 Hu?, a significant but not worrisome cap-gap. CDR's LTER won the pointed contest for most pinheaded among sites with 0.0183 Hu? smaller crainal deformation than the next most small-minded of sites Arctic Tundra. Please remember that these numbers are relative to John Hobbie's head. It is sort of a departure from Hobbieness.
Two LMERs were locked in a dead, pinhead heat: Chesapeake Bay and Waquiot Bay both came in 0.0728 Hu? smaller than John Hobbie. It should be noted that John Hobbie was only 0.0208 Hu? more fatheaded than the average 120 guests sampled at the Estes Park All Scientist meeting. This means that LMER heads relative to LTERites, with the exception of the Columbia River site, could audition for Saturday Night Live Cone-Head skits. This pinheadedness of LMERhood can only mean that streamlining is selected-for at marine sites.
Managed by LTER LTER Network Communications Office, NCEAS, UCSB, 735 State Street, Suite 300, Santa Barbara, CA 93101Except where otherwise noted, material may be re-used under a Creative Commons BY-SA 4.0 license.
This material is based upon work supported by the National Science Foundation under Cooperative Agreements #DEB#9634135 (3/15/97 - 2/29/04), DEB#0236154 (3/1/03 - 2/28/10), DEB#0832652 (5/1/09 - 4/30/15), DEB#0936498 (9/1/09 - 8/31/14), DEB#1545288, 10/1/2015-9/30/19). Any opinions, findings, conclusions, or recommendations expressed in the material are those of the author(s) and do not necessarily reflect the views of the National Science Foundation.Contact Us | Privacy Policy (pdf)
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Dirt and mud is kicked into the air as runners participate in the Muddy Mayhem 8K run sponsored by The Athlete's Foot on Saturday. Over 1,000 runners participated in the fun yet mucky mess. Proceeds went to Wounded Warrior Project, which provides support to severely injured service members as they transition to civilian life.
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text: Dr Luan Linden Phillips PhD, MSc, BSc (Hons) Institute of Applied Health ResearchHonorary Research Fellow Contact details Telephone+44 (0)121 414 email@example.com AddressDepartment of Public Health, Epidemiology & BiostatisticsInstitute of Applied Health ResearchUniversity of Birmingham Edgbaston Birmingham B15 2TT UK Luan Linden-Phillips is a honorary Honorary Research Fellow in the Institute of Applied Health Research. Luan was previously a senior analyst at the NIHR Horizon Scanning Research & Intelligence Centre (HSRIC), which provided information about selected new and emerging technologies to NICE, the Department of Health and national policy makers. As well as managing the drug topic selection process, Luan leads external engagement with the pharmaceutical industry and other horizon scanning organisations across the UK, including NICE, the Medicines and Prescribing Centre, NHS England, UKMi, Scottish Medicines Consortium and the All Wales Medicines Strategy Group. Luan is also Co-chair of the User Group committee for UK PharmaScan, a joint Department of Health and ABPI project that provides an essential tool for the managed entry of medicines into the NHS. As part of her external engagement role, Luan has represented the Centre at NICE conferences, led on the delivery of UK PharmaScan Masterclasses for Industry delegates and has been responsible for advancing interdepartmental collaboration at the University of Birmingham, where the Centre is based. Luan is an experienced analyst with a broad knowledge of the policy and market access issues that confront innovative new health technologies. She has previously held other, senior positions at the Centre, including specific work on devices and diagnostics. Working with stakeholders, including health professionals and commercial developers, Luan has produced and supervised a diverse range of tailored disease and technology-specific reports to assist in NHS policy and commissioning decisions. In 2014 she completed a PhD on the diffusion of pharmaceutical innovations, which involved accessing and engaging with senior pharmaceutical industry personnel. Qualifications PhD, Diffusion of Pharmaceutical Innovations, University of Birmingham, 2014 MSc in Toxicology, University of Birmingham, 2000 BSc (Hons) in Biosciences (Microbiology), University of Birmingham, 1999 Biography Luan qualified with a first class degree in microbiology in 1999, followed by a Masters degree in toxicology from the University of Birmingham in 2000. She continued to specialise in this field, spending two years as a poisons specialist at the National Poisons Information Service, before joining the Horizon Scanning Centre in 2002. During her time at the NIHR HSRIC, Luan has worked across all areas of the Centre's remit holding senior positions in all sub-teams including Drugs, MedTech and Research and Reviews. This has provided the basis for a unique knowledge of the Centre's work in its entirety. Luan also recently completed a PhD alongside her horizon scanning roles, researching influences on pharmaceutical diffusion. Luan has produced many reports covering a diverse selection of health technologies, disease areas, patient groups and settings and has participated in conferences and panel sessions discussing the challenges affecting the use of new health technologies, which she was able to explore further through her PhD. As part of a wider university role, Luan teaches public health and epidemiology to medical students at undergraduate and graduate entry level, and is involved in training other health professionals in the methods of horizon scanning. Research RESEARCH THEMES Diffusion and uptake of new health technologies; influence of the pharmaceutical industry in drug diffusion; early awareness and alert activities; health services research. RESEARCH ACTIVITY Luan's area of research includes the adoption and diffusion of new innovative health technologies. In addition to having published and presented on the subject, she has also completed a PhD on diffusion of innovations, specifically researching the area of pharmaceutical diffusion. PhD title: Pharmaceutical industry perspectives on factors that influence the adoption and diffusion of drugs in the UK: Four case studies Outline: A predominantly qualitative project utilising in depth interviews with senior pharmaceutical marketing personnel across multiple case studies to explore industry opinions on adoption influences that affect the uptake of new drugs in the UK. Publications Linden-Phillips L, Bitner-Glindzicz M, Lench N, Steel KP, Dawson S, Davis A, Simpson S, Packer C. The future role of genetic screening to detect newborns at risk of childhood-onset hearing loss. International Journal of Audiology 2012; 1-10. Tayo A, Ellis, J, Linden-Phillips L, Simpson S, Ward DJ. Emerging point of care tests for influenza: Innovation or Status quo. Influenza and Other Respiratory Viruses 2011; 6 (4) 291-298. Plüddemann A, Heneghan C, Thompson M, Roberts N, Summerton N, Price C, Linden-Phillips L, Packer C. Prioritisation criteria for the selection of new diagnostic technologies for evaluation. BMC Health Services Research 2010; 10:109. Linden L, Vondeling H, Packer C, Cook A. Does NICE only appraise new pharmaceuticals? International Journal of Technology Assessment in Health Care 2007; 23(3): 349-353. Gao L, Linden L, Parsons NJ, Cole JA, Smith H. Uptake of metabolites by gonococci grown with a lactate in a medium containing glucose: evidence for a surface location of the sialyltransferase. Microbial Pathogenesis 2000; 28 (5); 257-266


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University of Texas Arlington
UTA In The News — Friday, May 25, 2012
Conference move approved
The UT Board of Regents on Thursday unanimously approved UT Arlington's move to the Sun Belt Conference starting July 2013, The Associated Press, Sports Illustrated, the Fort Worth Star-Telegram, KXAS/NBC 5, San Antonio Express-News and several other television and print outlets reported. Jim Baker, the University's director of athletics called Thursday "another milestone day for UT Arlington athletics" and said: "This move to the Sun Belt will allow us to continue to showcase our athletics program on a national level and create further awareness for our university." The Mavericks are wrapping up their final season in the Southland Conference, where they have been since the conference was created in 1963. Next year they will play one season in the Western Athletic Conference before joining the Sun Belt.
Saving energy
Vedero Software has announced a new agreement with The University of Texas at Arlington to automatically reduce energy usage during emergency events on the Texas electric grid, according to the Houston Chronicle, Yahoo!News and Green Technology World. Beyond economic benefits to the University, this program improves reliability of the Texas electric grid during power shortages and defers or avoids the costly build out of additional electrical capacity needed to deal with peak periods.


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Nice rustic villa close to the natural park Montgó presented by your Estate Agent for luxury homes at the Costa Blanca: ENGEL & VÖLKERS.
This single-storey villa with a huge covered terrace and solarium is located on a plain plot of 430 m2. The ample living dining area and open separate kitchen offers a lot of space to enjoy with the whole family. A corridor leads to the private part of the chalet that consists of two bathrooms, a guest or children's room and the big main bedroom. The very private outer space offers a spacious uncovered terrace with BBQ and access to the big community pool, a covered parking and lovely gardens of easy maintenance.
With a small invest this villa will be the ideal holiday home or even a nice place for all-season living.
Dénia the main town of the Marina Alta at the north of the Costa Blanca disposes of a fishing port, a ferry port and different marinas. The majority of the more than 20 kilometres of coastline are sandy beaches but as well there is a rocky part at the foothill of the Mongó. The historic centre with a great variety of bars and restaurants invites to enjoy life during the whole year. It is just one hour by car to the international airports of Alicante and Valencia. Recently Denia has been denominated by the UNESCO, creative gastronomy city.
Availability upon agreement. Engel & Völkers does not accept responsibility as the information provided in this brochure is for information only and it is subject to errors, omissions, change of price or withdrawal without notice. Taxes, notary and registry fees must be paid by purchaser, the commission by the selleras stipulated by Spanish regulations.


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