text:
EATON TWP. — Columbia found itself in a situation Saturday night it had yet to experience this season.
"Not until tonight," Zach Stopper said when asked if he and his teammates had ever had to end a game without star point guard Jay Banyasz.
Banyasz, Columbia's primary ball handler and one of the Raiders' most reliable scorers, fouled out with 2:22 to go and his team holding a six-point lead that had dwindled from a 15-point advantage only 2½ minutes earlier.
"We all had to be strong with the ball, and be smart," Stopper said. "We were prepared to step up."
Step up the Raiders did, not committing a turnover the rest of the way and not permitting Midview another point as Columbia beat the host Middies 63-52 to win the championship of the 12th annual Bob DiFranco Memorial Holiday Tournament.
The victory kept Columbia undefeated through eight games. Midview fell to 5-4.
Banyasz fouled out via an offensive foul, giving the ball back to Midview and handing the Middies — who were on an 11-2 run at the time — a big window of opportunity to grab the lead.
The window slammed shut. Wes Davic, who had scored 13 straight Midview points, couldn't get one to fall on the Middies' ensuing possession. Stopper, who led Columbia with 17 points, scored with 1:21 to play. He hit one of a pair of free throws 28 seconds later following a technical foul.
Brandon Severo secured the victory with two successful free throws 18 seconds after that.
"We are fortunate to have other guys who can handle the ball," Columbia coach Larry Babics said. "They remained calm and we survived. This is a big win for our program. It's a momentum builder."
The Raiders led the entire way. Columbia jumped ahead 11-3 and was in front 19-8 early in the second quarter.
Midview made a couple runs, cutting Columbia's lead from 10 points to six in the last four minutes of the first half and getting as close as seven points on a 7-2 run in the third period.
"Every time we had a run, they had an answer for us," Midview coach Troy DiFranco said. "They hit big shot after big shot. Our goal was to keep them to no more than four 3-point baskets. Their shooters would get one pass and make a three."
The Raiders hit eight 3-pointers — Jacob Simon buried four of them, all in the second half, and finished with 16 points. Banyasz also had 16 points, 14 of them in the first half, and led Columbia with four assists.
Davic led all scorers with 27 points and all rebounders with 16. For four minutes of the last quarter Davic, a 6-foot-5 senior, was unstoppable with 13 points and five rebounds.
"The kid is a heck of a player," Babics said of Davic. "(Midview) is a hard team to guard. They've got shooters and they have post people. We have been giving up about 50-52 points a game, so we were there where we needed to be on defense."
"I was not happy with the offense in the first half," DiFranco said. "We were too individualistic. We settled down in the second half, but we didn't get the ball to (Davic) at the end."
Two Middies substitutes came in to provide major contributions. Matt Randolph led Midview with four assists and scored eight points. Jack Duffner was second to Davic in points (10) and rebounds (four).
Contact Steve Byrne at 329-7135 or email@example.com.
Columbia 63, Midview 52
COLUMBIA (63): Brandon Severo 2-2-8, Jay Banyasz 7-1-6, Jacob Simon 6-0-16, Kevin Simon 1-0-2, Zach Stopper 6-5-17, Michael Boey 1-1-4, Tyler Edmisten 0-0-0. Totals 23-9-63.
MIDVIEW (52): Wes Davic 10-6-27, Devin Dombrowski 0-0-0, Steve Gott 0-0-0, Grant Overy 1-0-3, Kyle Warner 0-2-2, Matt Randolph 3-0-8, Jacob Wells 1-0-2, Dylan Eason 0-0-0, Tyler Pasenow 0-0-0, Jack Duffner 4-2-10. Totals 19-10-52.
Columbia 14 14 20 15 — 63
Midview 8 14 14 16 — 52
Three-point goals: Columbia 8 (J. Simon 4 Severo 2, Banyasz, Boey), Midview 4 (Randolph 2, Overy, Davic). Rebounds: Columbia 21 (Banyasz, J. Simon, Stopper 4), Midview 27 (Davic 16). Turnovers: Columbia 9, Midview 18. Total fouls: Columbia 17, Midview 20. Fouled out: Banyasz, Eason.


text:
Training Buddy in Sydney?
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I just recently joined bodybuilding.net in the hope of finding a training buddy. I am 20 and have been going to the gym for the last year but really need to improve on my exercise routine and form, among other things. I am writing this message in the hope of finding someone who could join me at the gym, preferably somewhere near glebe/camperdown. Feel free to contact me privately if you wish. My email address is email@example.com
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text: i currently own a sti spartan, i have been bitten with the 1911 bug, thanks! anyhow i just sold my glock 30 and looking to replace it with a springfield trp i see you can order one with a bull barrel or a match barrel with bushing. i will be target shooting mainly. i am more accurate with the 1911 over the glocks and i enjoy shooting the 1911 over the glock i'm just looking for some suggestions and help thanks john


text:
Owls Head awards bid on sewer line easement survey
Rockland — Owls Head selectmen on Nov. 5 awarded a sole bid of $1,800 to Landmark Construction Co. of Warren to survey a proposed easement for a sewer line.
Selectmen also voted to contact the owner of a vacant mobile home on Ash Point Drive seeking permission to enter the premises to conduct an inspection to determine if the building is considered a dangerous building.
Katherine MacPherson has offered land she owns on Ingraham Hill to provide for the possible extension of the existing public sewer line from the end of the south end of Cottage Avenue to the north end of Knowlton Avenue.
At the Aug. 20 annual town meeting, Owls Head residents gave the board permission to enter into an agreement with MacPherson to accept the easement deed.
The town in return would have the property surveyed and pay the connection fee to Rockland for two services to connect into the proposed Knowlton Avenue pump station and to raise up to $6,000 for the survey work and legal services.
"This is just about the survey," Board Chairman Richard Carver said. "We're not doing the whole job."
In other business before the board, selectmen voted 3-0 to write a letter to the owner of the property at 511 Ash Point Road asking permission to enter the premises and conduct an inspection. The letter would give the owner five days to respond.
The town is considering the dwelling, a mobile home, to be classified as a possible dangerous building, located on a three-sided, 40,000-square-foot lot backing up to the water. No one lives in the building now. The trailer is on a slab or blocking and has been unoccupied for years, according to the town office records.
In August, neighbors of the property attended a meeting and asked the board to authorize the code officer to take action.
Selectmen consulted the Maine Municipal Association on the issue of dangerous buildings.
"Over the years, windows and doors have been boarded up, but also just as often the broken windows have been exposed," Carver wrote in an email to the MMA.
Richard Flewelling of MMA's Legal Services Department replied that the definition of a dangerous building is for the selectmen to determine, based on the evidence. The board may seek a determination from the Maine Superior Court, he said.
One reason for not removing the trailer has been the lot size itself, which is a non-conforming size. Selectmen said the owner's concern is that removing the building would remove the footprint so that another building could not be put in its place.
The board has decided that the next step should be to get the owner's permission to go on the property for an inspection.
In other business Nov. 5, the board gave the go-ahead to Harbormaster Jeff LaBrozzi to look into costs related to repairing the docks at the town harbor.
"The big float is still in the water," said LaBrozzi.
Eric Davis of the American Lighthouse Foundation said the foundation would like to move its offices into the building next to the Owls Head Lighthouse for use year-round. The move would require getting a license for use of the house and tower from its owner, the U.S. Coast Guard, Davis said.
Code Enforcement Officer Scott Bickford said the matter might be given to the planning board for approval.
The board also gave permission to the Mussel Ridge Historical Society to borrow folding tables owned by the town for the society's crafters' fair at the Owls Head Transportation Museum on Saturday, Nov. 17.
Courier Publications reporter George Chappell can be reached by phone at 207-594-4401, ext. 117, or by email at firstname.lastname@example.com.


text:
Well, I listed two consequences of learning GVS. You are nitpicking one of the consequences. But the first consequence helps anyone. One need to go beyond dictionaries to predict pronunciations; that's where GVS helps. Sure, my advice is helpful to a few; just because it is not helpful to some group, it doesn't mean that it is not helpful.
To the OP,
check this post:
The naturalness of British vowels | speech talk
So, we are left with no other choices between these two extremes! Not many believe in that hypothesis, though.
For instance, Karl Marldot and Charles-James Bailey came up with a book for English pronunciation, which includes many heuristics from Old, Middle English, etc. So, I don't need to argue further about the importance of whatever I said earlier.
Their book is: Grundzuge der englischen Phonetologie: Allgemeine Systematik
Last edited by raindoctor; 25-Apr-2012 at 19:48.
[QUOTE=raindoctor;877430]Well, I listed two consequences of learning GVS. You are nitpicking one of the consequences. But the first consequence helps anyone. One need to go beyond dictionaries to predict pronunciations; that's where GVS helps. Sure, my advice is helpful to a few; just because it is not helpful to some group, it doesn't mean that it is not helpful.
To the OP,
check this post:
Thanks a lot!! I will have a good look at it. I always find it hard sometimes to pronounce every word clearly. Is it because of insufficient breath or insufficient focus on the tongue? Do the native speakers put a lot of stress on their tongues or just let it move freely? I am paying more attention to how native speakers pause between stops because i have sort of developed a bad habit of skipping the consonants sounds at the end of words and now find it really hard to do it when i don't know what the speech pattern is. Could you give me some advice on that too?
Since you have a fetish for RP, just go to UK and get trained with Geoff Lindsey ( English Speech Services - Home ), a real phonetician, not some TESL/SLP guy. That's how you can jump start your learning. Otherwise, you end up wasting time with all false starts, practice-wise. In the mean time, you can get borrow books on phonetics and phonology from your library and increase your knowledge, so that you can ask right questions.
There are some many accent reduction trainers out there, selling snake oil crap: for instance, there is one in the bay area, who talks about breath while teaching fricatives. She doesn't even mention the word fricative. That may work for someone who wants to change *a bit*, but not for someone like you.
Online forums are good if you have a specific question like "how to pronounce X", etc.
I mean if u move your tongue consciously when you speak or you hardly notice it's moving at all.
I did a free online assessment and the result is really good.
((Hello Ka,
Thanks for your online free assessment recording. I found you have a beautiful and sophisticated British accent, which is perfect for teaching English in Japan. If you wanted to teach an American accent as well as the Queens English, it would entail only replacing a few sounds.
I only caught two slight traces of an Asian accent. You can work on replacing and fixing those sounds. Below is your assessment. Please give me a call, and I will show you how to say those sounds. Of course this was only a short assessment. If you would like the complete phonetic assessment it would take about an hour. This is included in my coaching package, but if you would like only the assessment, its $85.
Its lovely when I see someone who has a goal like yours, to have perfect pronunciation. I wish you all the best! ))
However, when i talk to friends, i never get such positive comments.
Anyway, i took you advice and contacted Geoff Lindsey. Hope to be able to talk to him soon. Thanks for recommending me such a good speech coach to me. There are so many of them and i didn't which to go to. Now i do now. Thanks.


text:
GMC TRUCKS HEAVY HAULING * LIGHTED BILLBOARD AD for A/F and LIONEL TRAINS
Sold for:
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- Sold Date:
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Hello General Motors Truck enthusiasts, collectors, and Lionel 3-rail, O-scale operators . . . Here's a nice addition to your toy train layout or automotive models diorama… an illuminated billboard advertising GMC trucks from the late 1940's… "What it takes for heavy hauling!" This billboard print features a typical, full-color advertisement from the 1940's. The billboard comes fully wired with a steady-on 18-volt bulb and reflector for full-width, back-lit illumination. You can power this from the accessory terminals of your transformer or a battery eliminator. This billboard looks great even without the illumination…on your layout, desk, or in the display cabinet alongside your favorite die-cast toy truck collectibles. This item was custom-designed and manufactured for use with Lionel Trains. (Please see item photos provided below.) You can examine this item at our home in Northwest New Jersey anytime during the auction.
An optional superstructure frame kit is listed separately for these billboards. (See inset above, right.)
Condition & Features - Brand new, out of the box only for photo and bulb test. O-gauge, O-27 size – matches Lionel, MTH, K-Line, Atlas-O, etc. Also OK for American Flyer S-gauge – overall billboard size is 3½" high by 6" wide. Construction is injection molded plastic with detailed lattice... read more


text:
A MIDDLE-aged man was knocked out as trouble flared outside a busy restaurant and wine bar.
The incident happened at 9.30pm last Saturday (February 15) in the entrance to the car park opposite the Blue Spider wine bar and Pepe's Restaurant, in Station Road, Beamish, County Durham.
In all, six people were assaulted by a mixture of men and women who are believed to have been in the restaurant and bar shortly beforehand.
Loading article content
One of the victims, a 52-year-old man, was knocked unconscious and needed hospital treatment. He also suffered severe bruising to his body.
One of his female companions was pushed over and suffered a possible hairline fracture of her knee, and another woman had an injury to her jaw.
Police are now seeking witnesses to the incident.
A spokesman for Durham Constabulary said: "The circumstances are still being investigated but police believe the victims were attacked after they tried to intervene in a verbal argument involving friends of the other group.
"No arrests have been made at this stage.
"Police are also looking to trace a potential witness, a man who is described as elderly and who was standing nearby and may have seen the incident take place."
Any witnesses should call investigating officer Det Con Marco Fantin, based at Chester-le-Street on the police non-emergency number 101.


text:
> Career Resources
> Interviews > Industry Updates > Banking / Finance > Financial Planning / Wealth Management
While challenges remain, opportunities are improving for wealth management services providers
Investor confidence is steadily returning, as reflected by the uptrend in the stock market, and this phenomenon is benefiting the local wealth management sector.
Mason Wu, head of wealth management centre, Wing Lung Bank Ltd, believes the time is ripe for wealth management professionals to rebuild their business amid improving investor sentiment. "The industry now needs quality people who will help reinvigorate activity and bring back investors to this sector," he says.
New dawn
Wing Lung Bank positions its wealth management unit as a reliable financial partner that offers a full range of investment products, including callable deposits, bonds, currency-linked deposits, equity linked deposits, investment funds services and structured products. The diversified product offering helps clients develop an investment portfolio that will best achieve their investment objectives and preferred level of risk exposure.
To further strengthen its wealth management business in Hong Kong, Wing Lung recently launched a Sunflower wealth management centre, the services and products of which are targeted mainly at clients from China.
Sunflower offers a wide range of services including financial planning, investment and securities trading. The establishment of the centre also marks a milestone for Wing Lung's development following its integration last October into China Merchants Bank (CMB).
Mr Wu says Wing Lung now plans to hire more wealth management professionals as it pursues expansion under CMB. "Attracting quality talent is a long-term challenge in the wealth management industry," he says. "Our wealth management centre currently houses 56 staff. We are now looking for passionate, meticulous, client-oriented and disciplined candidates to beef up our team. We favour candidates with solid industry experience and relevant qualifications."
People focus
Wing Lung Bank attaches great importance to a candidate's performance during job interviews. Screening and interviews of candidates are stringent.
"If a particular candidate is invited for interview, it means we already have an interest in that person. Therefore, we expect that candidate to prepare well before coming for the interview," Mr Wu says.
He notes that people interested in becoming wealth management professionals must embrace a positive and client-oriented attitude and, more importantly, show prospective employers a passion for striking a balance between achieving sales goals and clients services with a high level of integrity and dedication. They are also expected to demonstrate integrity in their personal and professional conduct.
"Achieving short-term sales goals will not guarantee long-term success for a wealth manager. Understanding the ethical concepts in wealth management is more important. For instance, a professional needs to know a client's risk tolerance level before presenting investment options," Mr Wu explains.
He adds, "We are our clients' long-term partner and we assist them in building solid and long-term investment portfolios, focused on their unique financial needs and the risk levels that they can tolerate. Ethics, integrity and dedication are crucial components to a successful long-term partnership between wealth managers and customers."
Long-term prospects
Wing Lung provides new recruits with a three-day orientation to prepare them for a career in wealth management. Supervisors guide newcomers in understanding Wing Lung's corporate culture and its services and products.
Aside from on-the-job training, the bank arranges supplementary programmes, including language courses, for both newcomers and existing staff. This is aimed at enabling everyone to meet stringent company and industry standards.
Mr Wu points out that Wing Lung puts a high premium on its staff's long-term career growth. It appraises work performance regularly to ascertain their expectations and needs. Employees are also guided towards a clear route for career development. For instance, a newly-recruited account executive can work his or her way up to the post of account manager, and eventually, to the post of senior account manager.
Outside Wing Lung, other avenues are available for wealth management practitioners to upgrade the level of their professionalism, says Mr Wu. The Hong Kong Institute of Bankers Outstanding Financial Management Planner Awards is one such initiative that rewards excellence in the industry.
Mr Wu, who served as one of the panel judges, says the competition helps wealth management practitioners assess and upgrade their levels of professionalism. He describes the performance of this year's candidates as encouraging. "Most candidates performed very well during the second round presentation. They demonstrated meticulous attention to product details and clients' needs," he explains. "This is particularly important amid the dynamic investment environment in which wealth management service providers are expected to constantly improve the quality of their services and products."
Free Subscription


text:
BALTIMORE (WNEW/AP) — Acting U.S. Veterans Affairs Secretary Sloan Gibson met Tuesday with administrators in Baltimore to strategize on improving lengthy delays for veterans in need of medical help in Maryland, where a recent audit showed the average wait time is 81 days for new patients seeking a primary-care doctor.
During his visit to the VA Medical Center in Baltimore, Gibson said a budget allotment of $500,000 will help ensure timely medical care for veterans in Maryland. It's supposed to help connect veterans awaiting care with outside physicians able to offer prompt treatment. The Maryland VA system is also in the process of hiring five new primary care physicians.
Gibson said Tuesday the wait time for care in Baltimore is "too long," adding that more than 800 veterans with wait times longer than 30 days have been identified in the past three weeks. The majority of them have been contacted and offered appointments with physicians outside the system, Gibson said.
"My priority is getting veterans off the waitlist and into clinics," Gibson said.
Gibson stepped in as acting VA secretary 18 days ago after former Veterans Affairs Secretary Eric Shinseki resigned amid a scandal involving months-long wait times for veterans and fraudulent scheduling practices designed to conceal the delays.
Gibson vowed Tuesday to try and rebuild trust in the VA system.
"I think it's pretty obvious that we've seen a major erosion of that trust," Gibson said. "My commitment to you, my commitment to all of our veterans, my commitment to the American people is, we will work to earn it back."
Gibson also addressed reports of VA staff members being intimidated or facing retaliation for speaking out against misconduct.
"It's against the law to retaliate against whistleblowers," he said. "We're going to obey the law. Period."
Gibson said he has directed every VA center to visit each clinic and "personally engage" with those responsible for scheduling to ensure the appointment logs are accurate.
WNEW Annapolis Bureau Chief Karen Adams contributed to this report. Follow her and WNEW on Twitter.


text:
My Favorite Nonprofits
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Letter received from Peer-Support Client on 12/23/14: "I would like to thank you for having my back today in court. Nobody has... more »
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text:
WASHINGTON (CBSDC) — "InternsROCK!" is an appreciation week for interns in the nation's capital that begins June 8.
The third annual event offers to any intern working in Washington D.C. discounts at participating restaurants, museums, tour companies, music venues and retail stores.
To receive the discounts, participants must present a special InternsROCK! keycard from The Washington Center.
Learn more at the event's website, internsrockdc.com.


text:
The NAUE group is a manufacturer of products for the geosynthetic industry. NAUE offers project specific product development, geotechnical engineering support, and provide solutions to complicated challenges. NAUE geosynthetics are used for different applications such as tunneling, groundwater protection, civil engineering, hydraulic engineering, waterproofing and landfills. Geotextiles are used for Erosion Control, Packing, Drainage, Reinforcement, Separation and Sealing. NAUE's geosynthetics are exported worldwide.
Company websites
www Main site


text:
Blane Klemek column: Precautions can protect birds from later winter disease
Winter is almost over. It's been a long one. Last year at this time we were enjoying one of the warmest Marches on record. In fact, many of the Northland's wetlands and shallow lakes were ice-free by the end of March 2010. I canoed on the little lake behind my house, Lake Assawa, on March 30, the day after ice-out.
But this winter has been a little different than last winter. While the snow and cold came earlier and seems to be hanging with us later this year, I've enjoyed the winter nonetheless. One of this winter's highlights for me has been observing and feeding the huge influx of evening grosbeaks, common redpolls and pine grosbeaks. Indeed, I never get tired of watching these delightful species visiting my backyard feeding stations.
Sadly, I recently picked up a dead pine grosbeak from the ground near one of my feeders. I wondered why it had perished. And while I cannot be certain, the bacterium Salmonella, which is frequently the reason why birds become sick and die in late winter and early spring, especially around feeders, crossed my mind.
A fact sheet that I have about salmonella states that it is a normally occurring bacterium found in the gut of many different species of wild and domestic birds. However, because of limited food sources and concentrations of birds around available food, which is often exacerbated by bad weather, birds experience stress and, as a consequence, become susceptible to the disease.
Symptoms of the disease are easy to identify. Afflicted birds appear lethargic with droopy heads, spread wings, puffed out feathers, and labored breathing. They lose their natural inclination to flee from danger and often allow peoples' and other animals' close approach, thus increasing their likelihood of being killed by cats and other predators or dying from exposure to the elements.
Birds typically stricken are young and old birds, but outbreaks can occur in entire populations, especially when stressors such as major winter storms and the absence of preferred food sources tax the physiological needs of already nutritionally deprived birds.
Surprisingly, salmonellosis isn't a "birds only" disease. Though rare, there have been cases of people contracting the disease through contact with diseased birds, from cleaning and removing contaminated feeders or seed, and from cats that have become diseased.
So, what do we do when we observe sick and dying birds around our wintertime feeders? Or, more importantly, wish to avoid seeing such birds? First, it's important to take measures to insure that our feeding stations do not become sources of infection. This can be accomplished by making certain that the feeders we use to attract birds are clean or cleaned before putting out.
Secondly, be attentive about the condition of your seed. Is it damp? Moldy? How, where, and in what do you store your seed in? If your seed is stored inside the garage or some other out-building that's subject to temperature and humidity fluctuations, then it's vital that you store your seed in a container that is both weather and mouse-proof. Providing clean, dry, and fresh seed is essential to maintaining a healthy environment for your visiting bird friends.
During periods of warm, damp winter weather, birdseed inside feeders and residual seed on the ground becomes excellent sources for molds to grow and flourish from. Contaminated bird droppings are equally dangerous for visiting birds. Thus, keeping your feeders and areas surrounding your feeders clean is essential.
Removing your feeders from time to time and thoroughly sanitizing them with disinfectant is a fundamental practice to adhere to, especially if you feed birds in the winter or have conditions ripe for molds to grow, and if you have observed sick and dying birds. Use water and a 10 percent bleach solution to kill the bacteria.
After your feeders have been sanitized and residual seed has been picked up from below feeders and properly disposed of, you can also reduce the chances of disease transmission by placing your feeders in new locations. Doing so will alter the concentrations of birds - a vital step in controlling the spread of this deadly disease.
Remember, it's important for you to maintain vigilance. Feeders may need to be cleaned and moved at least once a week until signs of the disease diminish. Additionally, if you don't feed birds in the summertime, remove and clean your feeders and put them away until you're ready to hang them back outside for wintertime feeding.
When performing your important birdfeeder and birdseed cleaning chores, it's wise to take precautions to protect yourself from possible contamination, too. Wash your hands with soap and water and wear rubber gloves when handling feeders for cleaning purposes or when picking up dead or sick birds and old seed. And always dispose of used gloves, old seed, and dead birds in a proper place to reduce the risk of spreading the disease.
As already mentioned, Salmonella is present in the digestive systems of many species of wild and domestic birds. Inevitable outbreaks occur during periods of stress usually brought on by harsh weather. But we can help slow the spread of such outbreaks by ensuring that we always provide clean feeders and clean seed for our feathered friends as we get out and enjoy the great outdoors.
Blane Klemek is the Bemidji area assistant wildlife manager, DNR Division of Fish & Wildlife. He can be reached at email@example.com.


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Fri 10th Dec 2010 12:00pmBundoran Surf Co's Bundoran - The Peak Surf Report
10th December 2010 @ 10am Tullan is 2 to3 foot and onshore. Warmer than it has been but not great. Tomorrow looks better. High tide: 08:29 3.9m Low tide: 14:46, 1.1m 3 Day Forecast (to 13th December 2010) The weekend is looking good. New swell on the way and by Sat should be 3-4 foot and clean at most reefs in Bundoran with light winds. Probably a bit big for Tullan so check Rossnowlagh or Streedagh for a beach surf. Smaller on Sun but still 2-3 foot and clean at Tullan.
View the Bundoran - The Peak Surf Report and Forecast. Bundoran Surf Co's Reports have received a total of 858495 views.
This report has received 436 views since 10/12/10.


text:
gd is a library for creating and reading PNG, JPEG, GIF, WBMP, and XPM images. It has many features and can be used in scripts (e.g. PHP, Perl, Ruby, Lua, and Python) for dynamic image generation. PHP users should note that PHP 4.3.x includes its own distribution of gd, which is currently the best choice for PHP applications.
|Software Development Libraries
Release Notes: This release fixes reported bugs and glitches.
Release Notes: Most PHP libgd enhancements and functions were merged. Only symbols which should be exported are now exported. SONAME was bumped to 3.
Release Notes: Minor issues in the copy and PNG functions and a possible crash in the WBMP read have been fixed.
Release Notes: This release introduces a number of fixes for bugs and security issues. Thread safety of the GIF read and the Freetype functions have been improved. VMS build scripts have been added.
Release Notes: Various new issues have been discovered and fixed since the last release candidate. A regression in the arc function has been fixed.
A Fluent OpenStack client API for Java.
A TWiki appliance that is easy to use and lightweight.


text:
Typical Gully
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One of the several gullies that function as ladders for climbers headed for the top. The main risk with these routes are the rattlesnakes, scorpions, and tarantulas that inhabit the cracks in the rocks.
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text:
Muscle performance is influenced by turnover of contractile proteins. Production of new myofibrils and degradation of existing proteins is a delicate balance, which, depending on the condition, can promote muscle growth or loss. Protein synthesis and protein degradation are coordinately regulated by pathways that are influenced by mechanical stress, physical activity, availability of nutrients, and growth factors. Understanding the signaling that regulates muscle mass may provide potential therapeutic targets for the prevention and treatment of muscle wasting in metabolic and neuromuscular diseases.
Skeletal muscle is a plastic organ that adapts its mass to the different pathophysiological conditions by affecting pathways that regulate protein and cellular turnover.
Cell size is determined by a balance between new protein accumulation and degradation of existing proteins. Genetic studies in both drosophila and mammals have shown that pathways controlling protein synthesis and protein breakdown have an important role to determine cell size. The two processes are tightly regulated and interrelated. The first level of connection occurs during protein synthesis when the quality control of the cell degrades proteins that are not correctly folded. At a further level, protein degradation systems determine the half-life of protein and, in muscle, are required to replace sarcomeric proteins as a consequence of changes in muscle activity. Both systems need ATP, and muscle energy level is one of the cellular check points that decide either to promote growth and hypertrophy or activate protein breakdown and atrophy. Importantly, the proteolytic systems can produce alternative energy substrates that are used by the cell to maintain internal homeostasis in conditions of energy stress. Recent findings provide a new view, which considers the growth-promoting pathways and the proteolytic systems coordinately regulated. The following short review will focus mainly on in vivo studies and will be schematically divided into two parts: the first part will describe pathways controlling muscle hypertrophy, and the second part will be focused on signaling involved in muscle atrophy.
Muscle Hypertrophy
The growth of skeletal muscle mass, like the mass of any other tissue, depends on protein turnover and cell turnover (83). Cellular turnover plays a major role during muscle development in embryo. Moreover satellite cell incorporation into the growing fibers takes place during postnatal muscle growth (65) concomitantly with increased protein synthesis. The activation of satellite cells is important for maintaining a constant size of each nuclear domain (quantity of cytoplasm/number of nuclei within that cytoplasm). Unlike young muscle, the contribution of cellular turnover to homeostasis of adult fibers is minor, and its role in hypertrophy has even been recently debated (56, 73). In adult muscle, the physiological conditions promoting muscle growth, therefore, do so mainly by increasing protein synthesis and decreasing protein degradation. However satellite cells are activated in compensatory hypertrophy (65, 85), and addition of new nuclei to the growing fiber seems to be required for extreme hypertrophy. The pathways controlling cellular and protein turnover are different, and their contribution to muscle hypertrophy has to be considered during the interpretation of data resulting from studies with transgenic animals. Loss- and gain-of-function studies in which the transgene is perturbed early during postnatal growth might affect cellular turnover significantly more than protein synthesis. Results could be completely different if the same pathway is acutely perturbed in adult muscle age when the role of protein turnover is dominant (FIGURE 1⇓).
IGF1-AKT signaling and the control of muscle growth
IGF1 is among the best characterized muscle growth-promoting factors. In addition to circulating IGF1, mainly synthesized by the liver under GH control, local production by skeletal muscle of distinct IGF1 splicing products has recently raised considerable interest. A specific IGF1 splicing product is important for load- and stretch-induced adaptations in skeletal muscle (25). Increased IGF1 gene expression has been demonstrated following functional overload induced by elimination of synergistic muscles (55). Muscle-specific overexpression in transgenic mice of an IGF1 isoform locally expressed in skeletal muscle results in muscle hypertrophy (68) and, importantly, the growth of muscle mass matches with a physiological increase of muscle strength. Moreover even acute ectopic expression of IGF1 in adult muscles by electroporation is sufficient to promote muscle hypertrophy (6). Although these results suggest an autocrine/paracrine role for local IGF1 in activity-dependent muscle plasticity, direct evidence for such a role through loss-of-function approaches, such as knockout or knockdown experiments, has not yet been reported.
Akt activation is induced by IGF1 and insulin through the generation of phosphatidylinositol-3,4,5-triphosphates produced by PI3K, which is opposed by the activity of the phosphatase PTEN and SHIP2. Phosphatidylinositol-3,4,5-triphosphates recruit Akt to the plasma membrane by binding to its NH2-terminal pleckstrin homology domain. At the membrane, Akt is phosphorylated on separate residues by at least two distinct kinases, PDK1 and the mTOR-Rictor complex. The role of Akt in muscle growth was first suggested by the finding that an active Ras double mutant (RasV12C40) that selectively activates the Akt pathway through the phosphatidylinositol 3 kinase (PI3K) promotes muscle growth, thus opening new perspectives in the signaling of fiber size (67) (FIGURE 2⇓). This observation was subsequently confirmed by overexpressing a constitutively active form of Akt in adult skeletal muscle (10, 72). Similar results were obtained by the generation of conditional transgenic mice in which Akt is expressed in adult skeletal muscles only after tamoxifen (41) or tetracycline (37) treatment.
In mammals, there are three Akt genes, Akt1 (PKBα), Akt2 (PKBβ), and Akt3 (PKBγ), which appear to have distinct functions. In skeletal muscle, Akt1 and Akt2 are expressed at higher levels compared with Akt3, which is mainly expressed in the brain. Targeted deletion experiments have shown that Akt1-null mice display growth retardation and muscle atrophy, whereas Akt2-null mice suffer from a Type 2 diabetes-like syndrome, and Akt3-null mice have impaired brain development (111).
Exercise in vivo is associated with activation of Akt1 but not Akt2 and Akt3 kinases in contracting muscles (99). Akt activity was increased in the rat plantaris after functional overload induced by elimination of synergistic muscles (10). Subsequent studies both in rats and humans confirmed that Akt activity is increased in response to muscle contractile activity (69, 78–80). Surprisingly, this effect was observed only in the fast EDL but not in the slow soleus muscle (78, 79). The finding that passive stretch of the fast rat EDL muscle can also induce Akt activation has suggested that mechanical tension may be a part of the mechanism by which contraction activates Akt in fast-twitch muscles (79). However, it remains to be established how mechanical stress is converted to Akt activation. Akt activity is also increased in response to hormonal and growth factor stimulation, in particular insulin is known to activate Akt2, whereas IGF1 activates primarily Akt1. Taken together with other observations, these results suggest that Akt1 is a major mediator of skeletal muscle hypertrophy. Although it has been established that Akt plays a crucial role in muscle growth, the downstream targets involved in muscle hypertrophy remain to be defined.
mTOR-S6K and the control of protein synthesis
Two major downstream branches of the Akt pathway, which are relevant to muscle hypertrophy, are the mTOR pathway, which is activated by Akt, and glycogen synthase kinase 3β (GSK3β), which is blocked by AKT; both of them control protein synthesis. A third downstream target of Akt is FoxO pathway, which controls protein degradation and will be discussed below in the atrophy section. GSK3β is inhibited by Akt and in turn blocks the eukaryotic initiation factor 2B (eIF2B), which is involved in protein synthesis. Expression of a dominant negative kinase inactive form of GSK3β induces a dramatic hypertrophy in skeletal myotubes (75). However, it remains to be proven in vivo whether inhibiting the negative action of GSK3β on eIF2B is sufficient to promote muscle growth.
The kinase mTOR (mammalian target of rapamycin) has recently emerged as a key regulator of cell growth that integrates signals from growth factors, nutrients, and energy status to control protein synthesis and other cell functions (32, 97). As the name implies, mTOR is selectively inhibited by rapamycin, a drug used as an immunosuppressant in organ transplantation: rapamycin binds to members of the FK binding protein (FKBP) family and the complex rapamycin/FKBP binds to mTOR and blocks its activity. The role of mTOR in muscle growth was demonstrated by in vivo studies showing that rapamycin blocked overload hypertrophy and regenerating muscle growth (10, 72). Indeed in tetracycline-inducible Akt transgenic mice, rapamycin completely blunts Akt effects on muscle growth (37). The activation of mTOR by Akt is indirect and involves the phosphorylation and inhibition by Akt of tuberous sclerosis 2 (TSC2). TSC2 is a GTPase activating protein (GAP) that functions together with TSC1 to inactivate the small G protein Rheb that in turn activates mTOR in complex with the raptor adapter protein (mTOR-raptor or TORC1). Transgenic mice overexpressing TSC1 specifically in skeletal muscle show a defect in muscle growth (103).
mTOR is part of two multiprotein complexes: mTORC1, which contains raptor and is rapamycin sensitive, is required for signaling to S6K and 4EBP1, whereas mTORC2, which contains rictor, is required for signaling to Akt-FoxO (FIGURE 2⇑). The effect of mTOR on the translation machinery and protein synthesis is mediated by TORC1-dependent phosphorylation of the ribosomal protein S6 kinases (S6K1 and 2) and of 4E-BP1, a repressor of the cap-binding protein eIF4E. S6K1 appears to be an important effector of the Akt pathway, since muscle fibers are smaller in S6K1-null mice, and their hypertrophic response to IGF1 and to activated Akt is blunted (71). However S6K1 knockout mice show no impairment in polysome formation, in protein synthesis, and in protein degradation (60). TORC1 complex also negatively regulates the IGF1 pathway via S6K1 (4, 100). Thus the two mTOR complexes, mTORC1 and mTORC2, may have opposite effects on Akt activity: TORC1 negatively regulates IGF1 signaling, whereas TORC2 enhances AKT activity (FIGURE 2⇑). An additional factor that complicates the pathway is that long-term rapamycin treatment in vitro can inhibit not only TORC1 but also the mTORC2 complex and thus potentially affect, in some cell types, the Akt-FoxO signaling. This raises the possibility that, under certain circumstances, rapamycin may induce transcriptional regulation not through a direct effect, e.g., by blocking mTOR phosphorylation of downstream targets, but through an indirect transcriptional effect by inhibiting Akt and thus derepressing FoxO. It is therefore suggested that FoxO activity/localization should always be monitored in studies involving rapamycin treatment (44).
Myostatin and the cellular turnover
Myostatin, a member of the TGF-β family, is expressed and secreted predominantly by skeletal muscle and functions as a negative regulator of muscle growth. Mutations of the myostatin gene lead to a hypertrophic phenotype in mice, sheep, and cattle, and a loss-of-function mutation in the human myostatin gene was also found to induce increased muscle mass (14, 47, 59, 87). The increase in muscle mass is a consequence of hyperplasia, which is an increase in cell number, and hypertrophy, which is an increase in cell size. The hyperplasia suggests an activation of muscle stem cells, and, in fact, the myostatin pathway influences Pax 7, MyoD, and myogenin expression inhibiting satellite cell activation and differentiation (36, 57, 58). Only a few studies explore the effect of myostatin inhibition in adult muscle. Treating 24-wk-old mice with an anti-myostatin antibody for 5 wk induces a 12% increase in muscle mass (109). Furthermore, when tamoxifen-inducible Cre recombinase removes the floxed myostatin gene in 4-mo-old mice, muscle mass increases 25% during the next 3 mo (108). However, despite the effect on muscle mass, the specific muscle force has not been measured in these two studies. Overexpression of follistatin, an inhibitor of myostatin (47), promotes a great increase in muscle size. Interestingly, mice resulting from follistatin transgenic and myostatin knockout mice show tremendous increases in muscle mass supporting the concept that other myostatin-like molecules are present and relevant for muscle growth (46). There are few studies and conflicting results on the effect of exercise on myostatin gene expression in skeletal muscle (15). Furthermore, the increase of muscle mass of myostatin-null mice does not correlate with an increase in muscle force (7). Ultrastructural observations reveal an accumulation of tubular aggregates in type IIB fibers. This evidence is also supported by the decrease in specific force generation of hypertrophic ski transgenic mice (12). Ski negatively regulates Smad phosphorylation, thereby inhibiting signaling of TGF-β-like factors, such as myostatin. These findings contrast with muscle-specific overexpression of insulin-like growth factor 1, where fiber hypertrophy is accompanied by increased maximum force generation and maintained specific force levels. Myostatin binds to activin receptor IIB (48), a type II TGF-β receptor, and muscle hypertrophy is induced in transgenic mice expressing a truncated and inactive activin receptor (ActRIIB) (47). The downstream targets of the myostatin pathway and their role in protein synthesis as well as protein degradation (see below) are still to be determined. However, myostatin inhibition is benefical for maintaining muscle mass in animal models of Duchenne muscular dystrophy in which the contribution of satellite cells to rounds of regeneration is important (61, 102).
Beta adrenergic and mechanical sensors
Among the hormonal responses increased by exercise, the acute elevations in catecholamines are especially interesting with respect to changes in muscle phenotype. Beta-agonists such as clenbuterol, acting through β2-adrenoreceptors, are known to cause muscle hypertrophy and a slow-to-fast fiber-type switch. Interestingly, some effects of catecholamines could be mediated by local production of IGF-I and IGF-II by skeletal muscle (8, 90). Indeed the growth effect of beta-agonists is, at least partially, mediated by AKT-mTOR pathway since rapamycin almost completely blunted the hypertrophic effects of clenbuterol (40). Activation of beta receptors is known to also increase intracellular cAMP levels and activates protein kinase A (PKA), which may also activate the AKT pathway, and the transcription factor CREB; however, this pathway has not been explored in contracting muscle.
An attractive emerging concept in muscle biology is that signals dependent on muscle activity, and specifically on mechanical load, may arise in the sarcomere, the basic unit of the contractile machinery of striated muscles, and from there transmitted to the nucleus to affect gene expression (43). The giant elastic protein titin, which spans half the sarcomere extending from the Z disk to the M band and interacts with a large number of muscle proteins, provides an exciting example of a sarcomeric activity-dependent signaling complex (signalosome) (42). A unique property of titin is the presence in the M-band region of a serine/threonine kinase domain that can be induced to acquire an open active conformation by stretch and contraction (28). In active muscle cells, the titin kinase domain (TK) is linked through two zinc-finger scaffolding proteins, nbr1 and p62, to a member of the muscle-specific RING-finger proteins, MURF2 (43). In the absence of mechanical activity, the signalosome is dissociated, and MURF2 translocates to the nucleus where it can interact with the serum response transcription factor SRF, leading to nuclear export of SRF and loss of SRF-dependent gene expression. This pathway may thus control muscle growth because SRF is know to regulate muscle gene expression, and conditional deletion of the SRF gene causes severe skeletal muscle hypoplasia during the perinatal period (51). SRF regulates muscle gene expression by binding serum response elements (SRE) in target genes and seems to integrate different growth promoting pathways: for example, SRF is a target of Akt signaling in Hela cells (107) and can recruit the androgen receptor to muscle gene promoters (101). The titin kinase-SRF pathway described above is probably just one of several links between the sarcomere and the nucleus that are only now beginning to emerge (43).
Muscle Atrophy
Atrophy is a decrease in cell size mainly caused by loss of organelles, cytoplasm, and proteins. This concept is important when a genetic approach is used to dissect the contribution of certain pathways to muscle loss. As mentioned above, the mass of a tissue is controlled by cellular turnover and protein turnover (FIGURES 1⇑ AND 2⇑). Genetic modifications that interfere with embryonic and postnatal growth result in smaller muscles in adults. This reduction in muscle size is caused by failure/inhibition of growth and not by a real atrophy process. Keeping in mind the above definition, another important concept is that protein turnover is dominant over cellular turnover during acute phases of muscle wasting when sarcomeric proteins are rapidly lost such as during fasting, disuse, and denervation. Evidence that blocking satellite cells is sufficient to trigger muscle atrophy in adult muscle has never been determined. Furthermore, myonuclei are normally reduced during muscle atrophy to keep rather constant the size of the nuclear domain (16, 22). Thus the current understanding suggests that inhibiting cellular turnover would not influence protein breakdown and muscle weakness and would not affect nuclear domain maintenance, but it might be important for the replacement of damaged myofibers or myonuclei. The importance of cellular turnover for long-term muscle atrophy, e.g., long-term denervation, has yet to be addressed.
Atrophy: an active process that requires transcriptional regulation
A major contribution in understanding muscle atrophy comes from the pioneering studies on gene expression profiling performed independently by groups of Goldberg and Glass (9, 26). The idea to compare gene expression in different models of muscle atrophy leads to the identification of a subset of genes that are commonly up- or downregulated in atrophying muscle. Since all the diseases used for the experiments of microarray (i.e., diabetes, cancer cachexia, chronic renal failure, fasting, and denervation) have muscle atrophy in common, the commonly up or down genes are believed to regulate the loss of muscle components and are called atrophy-related genes or atrogenes (76). Together, these findings indicate that muscle atrophy is an active process controlled by specific signaling pathways and transcriptional programs. Furthermore, the two most induced genes are two novel muscle-specific ubiquitin ligases, atrogin-1/MAFbx and MuRF1, that are upregulated in different models of muscle atrophy and are responsible for the increased protein degradation through the ubiquitin-proteasome system (9, 26). In fact, knockout mice for either atrogin-1/MAFbx or MuRF1 are partially resistant to denervation atrophy (9). Importantly, recent findings suggest that myosin heavy chains are ubiquitinated and degraded by MuRF1 (13, 23). Thus, up to now, these two genes are actually the best markers for muscle atrophy and could be considered as master genes for muscle wasting. However, several other genes among the atrophy-related genes are of potential interest, including genes coding for lysosomal protease, transcription factors, regulators of protein synthesis, and enzymes of metabolic pathways, but their particular role in muscle wasting has to be defined in the next future.
IGF1-AKT-FoxO signaling
A subsequent crucial step was the identification of the signaling pathways that regulate the expression of the two muscle-specific ubiquitin ligases. Previous studies have shown that IGF1/insulin signaling, while promoting muscle growth, is able to suppress protein breakdown (77). Furthermore, IGF1 transgenic mice are resistant to muscle atrophy induced either by angiotensin treatment or in a mouse model of cardiac cachexia (88, 91), and local IGF1 injection is sufficient to block disuse atrophy (93). In these models of muscle loss, IGF1 completely suppressed the induction of the two critical ubiquitin-ligases. Further data supporting the role of this pathway in regulating muscle atrophy come from experiments of Akt transfection in adult mice. Electroporation of constitutively active Akt in adult myofibers completely blocked muscle atrophy induced by denervation (10). These findings are important to elaborate the various contributions of the different signaling pathways during muscle atrophy. The upregulation of atrogin-1/MAFbx and MuRF1 is normally blocked by Akt functioning through negative regulation of the FoxO family of transcription factors (49, 82, 93). The FoxO family in skeletal muscle is comprised of three isoforms: FoxO1, FoxO3, and FoxO4. Akt phosphorylates FoxOs, promoting the export of FoxOs from the nucleus to the cytoplasm. As predicted, the reduction in the activity of the Akt pathway observed in different models of muscle atrophy results in decreased levels of phosphorylated FoxO in the cytoplasm and a marked increase of nuclear FoxO protein. The translocation and activity of FoxO members is required for the upregulation of atrogin-1/MAFbx and MuRF1, and FoxO3 was found to be sufficient to promote atrogin-1/MAFbx expression and muscle atrophy when transfected in skeletal muscles in vivo (82). Accordingly, FoxO1 transgenic mice showed markedly reduced muscle mass and fiber atrophy, further supporting the notion that FoxO is sufficient to promote muscle loss (39, 92) (FIGURE 2⇑). On the other hand, the knockdown of FoxO expression by RNAi is able to block the upregulation of atrogin-1/MAFbx expression during atrophy and muscle loss (52, 82). Cross talk between protein breakdown and protein synthesis is not limited only to AKT but also involves FoxO. Activation of FoxO upregulates 4EBP1 and downregulates both RAPTOR and mTOR (92). Thus, when AKT in active protein breakdown is suppressed but when FoxO is induced, protein synthesis is further suppressed. This is not trivial since FoxO activity is regulated by different posttranslational modifications, which include phosphorylation, acetylation, and mono- and polyubiquitination (34) (FIGURE 3⇓). Most of these regulatory mechanisms are AKT independent and may play a role in muscle atrophy induced by oxidative or energy stress (see below).
Inflammatory cytokines and NF-κB signaling
The NF-κB transcription factors, which play a major role as mediators of immunity and inflammation, are also expressed in skeletal muscle and appear to mediate the effect of inflammatory cytokines, in particular TNF-α, on muscle wasting and cachexia. In the inactive state, NF-κB is sequestered in the cytoplasm by a family of inhibitory proteins called IκB. In response to TNF-α, the IκB kinase (IKK) complex phosphorylates IκB, resulting in its ubiquitination and proteasomal degradation; this leads to nuclear translocation of NF-κB and activation of NF-κB-mediated gene transcription. Muscle-specific overexpression of IKKβ in transgenic mice leads to severe muscle wasting mediated, at least in part, by the ubiquitin-ligase MuRF1, but not by atrogin-1/MAFbx (11) (FIGURE 2⇑). On the other hand, although muscle-specific inhibition of NF-κB by transgenic expression of a constitutively active IκB mutant leads to no overt phenotype, denervation atrophy is substantially reduced (38). Muscle atrophy induced by hindlimb unloading is likewise reduced in mice with a knockout of the p105/p50 NF-κB1 gene (35). However, TNF-α and pro-inflammatory cytokines also cause insulin resistance and suppression of the IGF1 pathway (17, 19, 33). Therefore, AKT phosphorylation should always be considered and explored when the NF-κB pathway is perturbed, since AKT inhibition can substantially contribute to muscle atrophy. This concept is supported by results obtained with conditional knockout mice for IKKβ, which are resistant to muscle atrophy but show hyperphosphorylation of AKT (66). Thus the amount by which muscle atrophy is reduced by IKKβ ablation and the degree to which it is AKT dependent is unclear. The cross talk between the two pathways is nevertheless important, and future studies should establish the contribution of IKK-NF-κB pathways versus AKT-FoxO pathways in relation to muscle atrophy. Interestingly, modulation of IKK-NF-κB pathway seems to affect cellular turnover in mdx mice (2).
Myostatin and the enigma of the downstream targets
Despite the hypertrophic effect of myostatin inhibition, the opposite situation of myostatin activation and its role in triggering muscle atrophy is not obvious. The first report that sustains this notion described a severe atrophy when CHO cells, engineered to express myostatin, were injected in skeletal muscles (113). The atrophy in these mice was so severe that some animals died. However, these findings were not confirmed by transgenic mice. Expressing myostatin specifically in skeletal muscles leads to only 20% of atrophy in males and no phenotype in females (74). Electroporation experiments show that myostatin expression in adult muscle induces a degree of atrophy comparable to that observed in transgenic mice (21). These findings suggest that CHO cells substantially contribute to muscle atrophy by secreting some cachectic factors and that the myostatin pathway is synergistic with other pathways. No report clearly shows whether myostatin is sufficient to trigger atrogenes expression and protein breakdown in vivo. However, in muscle cell culture, myostatin is reported to upregulate the critical atrophy-related ubiquitin ligases, and interestingly the mechanism of such regulation is FoxO dependent (58). In fact, myostatin treatment blocks the IGF1-PI3K-AKT pathway and activates FoxO1, allowing the increased expression of atrogin-1. This cross talk between the two pathways does not require NF-κB, whose inhibition does not prevent upregulation of atrogin-1 (58). Similarly, in cardiac cells, myostatin abrogates phenylephrine hypertrophic effects through inhibition of AKT (64). A further level of complexity is that myostatin expression is controlled by FoxO1, supporting the notion that the myostatin pathway is synergistic to AKT-FoxO signaling (5). However, despite the evidence of cross talk between AKT and TGF-β pathways, it is still unclear whether Smads, the transcription factors downstream of TGF-β signaling, are mediating some of the myostatin effects in muscle. Furthermore, Smads can recognize the DNA sequence CAGAC, but their affinity seems too low to support unassisted binding to DNA. In addition, if their affinity for the simple sequence were higher, Smads would decorate the entire chromosome. Therefore, activated Smad proteins must associate with different DNA-binding cofactors for the recognition and regulation of specific target genes (54). Interesting members of the forkhead box O family (FoxO1, FoxO3, and FoxO4) play such a role (27). To further confuse the role of Samds during muscle wasting is the presence of TGIF, an inhibitor of Smads, among the upregulated atrophy-related genes (76). Thus the mystery of why an inhibitor of Smads is activated early, before muscle loss becomes evident, must be addressed. Dissecting the roles of Smads and identifying the co-factors that mediate Smad transcriptional activity in adult muscle are intriguing questions that require attention in the coming years.
Rediscovering lysosomes under a new light: autophagy-mediated protein breakdown
Lysosomes are the cellular system charged with the removal of organelles and protein aggregates. Indeed, autophagy is constitutively active in skeletal muscle, as shown by the accumulation of autophagosomes seen in human myopathies caused by a genetic deficiency of lysosomal proteins, e.g., Pompe's and Danon's disease, or by pharmacological inhibition of lysosomal function, as in chloroquine myopathy (89). Different studies have shown that cathepsin-L, a lysosomal protease, is upregulated in different models of muscle wasting (18, 45). The role of cathepsin-L induction is still unclear, but recent evidence suggests that the autophagy-lysosome system is activated during atrophy. Mizushima et al. (62) generated transgenic mice expressing LC3 fused with GFP. LC3 is the mammalian homolog of Atg8 gene and is critical for membrane commitment and growth to engulf organelles, cytoplasm, glycogen, and protein aggregates. Morphological analyses documented the activation of the autophagy system during fasting in skeletal muscle (62). Indeed, muscle cell culture confirmed that the autophagy-lysosome system is the major proteolytic pathway implicated in nutrient-dependent proteolysis (63). Further experiments lend insight into the signaling pathways involved and identified an mTOR-independent but PI3KIII-beclin-dependent control of the autophagic system in myotubes (96). Furthermore, electron microscopic and biochemical studies have shown that autophagy is activated also in denervation atrophy (24, 86). However, denervation-induced atrophy shows a slower pace of autophagy when compared with fasting-mediated atrophy. This effect is mediated by Runx1, which is upregulated during denervation and is required to preserve muscle mass. Lack of Runx1 resulted in myofibrillar disorganization and excessive autophagy in denervated muscles (105). Runx1 knockout mice show double- or multimembrane vacuoles, which enclose mitochondria and membranes. This finding indicates that excessive autophagy is promoting severe wasting during denervation and needs to be reduced by Runx1. We have recently shown that the autophagy-lysosome and ubiquitin-proteasome systems are coordinately regulated during muscle wasting (53, 112). In fact, some critical autophagy-related genes are among the atrogenes and are under FoxO3 control. Expression of FoxO3 is sufficient and required to activate lysosomal-dependent protein breakdown in cell culture and in vivo. Interestingly, the role of mTOR signaling for the regulation of autophagy is irrelevant in skeletal muscles. However, the contribution of the autophagy-lysosome and ubiquitin-proteasome systems to organelle remodeling, protein breakdown, and, finally, muscle atrophy remains to be investigated.
Mitochondrial homeostasis and energy balance: the metabolic control of cell size
Several metabolic adaptations occur in atrophying muscles. In many forms of muscle wasting, expression of a variety of genes for enzymes important in glycolysis and oxidative phosphorylation are suppressed coordinately (45). Indeed, we have recently shown that PGC-1α, the master regulatory gene for mitochondria biogenesis, is downregulated in different models of muscle wasting. Furthermore, when the levels of PGC-1α are maintained, either by use of transgenic mice or by transfecting adult muscle fibers, muscles are protected from the atrophy induced by denervation, fasting, or expression of FoxO3 (81). Treatment with statins induces FoxO-mediated atrogin-1 activation and related muscle alterations. In cell culture and in zebrafish, statins cause muscle atrophy, disorganization of myofibrils, and mitochondrial dysfunction (31). These changes are completely aborted by either the deletion of atrogin-1 or by PGC-1α overexpression. These results may explain why oxidative fibers tend to be resistant to atrophy compared with glycolytic fibers and suggest that metabolic changes are crucial for muscle atrophy (50). Among the different energy-dependent pathways, AMPK acts as the cellular sensor of energy balance. Indeed, stressing energy in muscle cell culture either by oligomycin treatment or by replacing glucose with 2-deoxyglucose triggers myotube atrophy (4). Interestingly, increased levels of AMP, activation of AMPK, lipid consumption, and smaller muscles have all been observed in S6K1 and S6K2 knockout mice. Importantly, AMPK inhibition rescues skeletal muscle growth in these mice, confirming that S6K1/2 deletion alters energy balance (4) and suggesting that AMPK activity is a key factor for myofiber size. Interestingly, these mice show normal methionine incorporation and polysomal profiles as well as autophagy and upregulation of atrogin-1/MAFbx and MuRF1 (60). Altogether, these findings confirm that a metabolic program controls cell size, but the molecular mechanisms of such control remain to be understood. Very recent findings describe a connection between AMPK and FoxO3. AMPK phosphorylates several AKT-independent sites of FoxO3, stimulating its transcriptional activity on target genes (29, 30). Indeed, treating muscle cell culture with AICAR, an activator of AMPK, causes an increase of protein breakdown and atrogin-1/MAFbx expression via the FoxO family (70). The physiological relevance of such important control over protein breakdown and muscle atrophy in vivo remains to be explored.
Within the myofiber, mitochondria are crucial in regulating metabolism and might be a potential source of catabolic signals. Insulin resistance and diabetes have been reported to trigger caspase3-mediated actin cleavage, which would release myofibrils from the sarcomere for subsequent degradation via the proteasome (20). Caspase3 activation is mediated by Bax, which disrupts the mitochondrial external membrane, causing cytochrome-c release and apoptosome formation (49). Furthermore, inhibition of caspases by XIAP overexpression protects adult skeletal muscle from atrophy in an animal model of diabetes (106). However, the contribution of caspases to muscle atrophy should be further investigated using loss of function approaches.
Mechanical sensor of inactivity
The dystrophin glycoprotein complex (DGC) anchors the muscle cytoskeleton to the cell membrane via dystrophin and its binding partners. This complex is important for correct transduction of myosin movements on actin to the extracellular matrix. Indeed, lack of dystrophin exacerbates mechanical stress on the myofiber plasma membrane, causing muscle damage and degeneration. This classical view considers a purely structural function of DGC proteins. However, an attractive role of dystrophin in transduction of mechanical signals to the nucleus has recently been proposed. In fact, dystrophin is lost from the cell membrane under atrophic conditions, causing a loss of continuity between the cell membrane of the myofiber and the extracellular matrix (1). This decreased interaction between membrane and matrix is required for muscle loss since forced dystrophin expression in transgenic mice counteracts both cachexia-induced muscle wasting and upregulation of atrogin-1/MAFbx and MuRF1. Further support for the DGC acting as a mechanical sensor has recently been published. Neuronal NOS (nNOS) is normally bound to the DGC, but when the DGC is disrupted, as occurs in dystrophic muscle, its localization is disturbed and it is no longer at the sarcolemma. A similar nNOS dysregulation has recently been described during disuse-induced muscle atrophy. Free nNOS dislocates to the cytoplasm where it enhances FoxO3-mediated transcription and upregulation of atrogin-1 and MuRF1(95). Interestingly, the NF-κB pathway is not involved in nNOS-mediated muscle atrophy (95). Since nNOS generates NO, an important player in protein nitrosylation and in reactive oxygene species generation, the role of oxidative stress in muscle atrophy is an important aspect to be analyzed in future studies.
Glucocorticoids-induced muscle atrophy
Glucocorticoids are elevated in many pathological conditions associated with muscle loss. Moreover glucocorticoid treatment induces atrogin-1 and MuRF1 expression and muscle wasting both in cell culture and in vivo (10, 13, 77, 82, 84). Importantly, adrenalectomy or treatment with a glucocorticoid receptor antagonist (RU-486) attenuates muscle loss in some diseases (84). However, the mechanisms of glucocorticoid-mediated muscle atrophy are unclear. In fact, none of the atrophy-related genes have been found to be directly regulated by glucocorticoids, and no glucocorticoid response elements on atrogenes promoters have been identified as critical for their expression (45). Thus most of the glucocorticoid effects are indirect, mainly affecting pathways previously described to be crucial for muscle growth or loss. Glucocorticoids are reported to decrease IGF1 production and increase myostatin secretion. Other effects like downregulation of the anabolic transcription factor ATF4, activation of p300/HAT, or upregulation of REDD1, an inhibitor of mTOR signaling, are described, but no obvious mechanism can explain the direct involvement of corticosteroids in regulation of atrophy-related genes (3, 84, 104, 110). Even less clear is the recent description of dexamethaspone-dependent MyoD and Id1 degradation by NH2-terminal ubiquitination pathway, especially if we consider that MyoD is described to be an atrogin-1 substrate (94, 98). How MyoD loss can contribute to weakness and muscle protein breakdown is unclear. Loss and gain of function experiments on glucocorticoid receptor should be performed to address the direct role of this pathway in muscle loss.
Over the last few years, the mechanisms controlling muscle loss have attracted the attention of the scientific community due to their relevance in various fields of study such as ageing, prognosis of many diseases, quality of life, and sports medicine. From the recent findings, a new scenario emerges that considers the size of the myofiber and muscle performance a result of not a single pathway but of a network of signaling (FIGURES 2⇑ AND 4⇓). Intriguingly, the different pathways cross talk and modulate one another at different levels, coordinating protein synthesis and degradation simultaneously. Findings of the last few years offer new and exciting perspectives to the field and introduce a series of new stimulating questions to the community, setting the base for future studies, which should enable us to identify new therapeutic targets and drugs.
The critical reading of Kenneth Dyar is gratefully acknowledged. I apologize to colleagues whose studies were not cited owing to space limitations.
Our work is supported by grants from ASI (OSMA project), Telethon-Italy (TCP04009), and Compagnia San Paolo.
- © 2008 Int. Union Physiol. Sci./Am. Physiol. Soc.


text:
LISBON (Reuters) - Portugal's government hopes to announce next week how it plans to drag the economy out of a deep recession without compromising budget goals agreed under its international bailout, the prime minister said on Friday.
Pedro Passos Coelho was speaking in a parliamentary debate a day after his administration approved new spending cuts to put the budget agreed with the European Union and International Monetary Fund back on track after the country's constitutional court rejected parts of this year's plan.
"Now that we are more confident on the path of budget consolidation, we have to bet on everything that promotes growth," he told parliament. "The government decided to hold an extraordinary cabinet meeting on Tuesday to approve a strategy of growth and industrial development."
The premier's plan reflects recent concerns among European policymakers about how far budget cuts aimed at containing the region's debt crisis have damaged economic growth.
EU Economic and Monetary Affairs Commissioner Olli Rehn told Reuters earlier the euro zone will slow its budgetary belt-tightening to help reinvigorate the economy.
Such a change in tack could at least simplify the acceptance in Brussels of Lisbon's potential tax incentives for companies making new productive investment. The government has said it was considering such incentives, but stopped short of outlining specific terms saying those had to be coordinated with Brussels.
A growth strategy is also aimed at trying to win back a broad political consensus for the bailout after the main opposition Socialists refused to back any more austerity.
The coalition government has a comfortable majority in parliament, but Lisbon's lenders want broader support to give the reforms a better chance of long-term success.
Still, Passos Coelho reiterated that the country had to scrupulously meet its budget tightening goals set out under the bailout in order to end the rescue programme as planned by mid-2014 and be able to rely on debt market financing.
"It is vital for Portugal to succeed in this process to secure market financing. Portugal does not want a second assistance programme," Passos Coelho said.
Portugal's European Union and IMF lenders last month eased Lisbon's budget goals, but it still has to slash the deficit to 5.5 percent this year from 6.4 percent last year, then to 4 percent in 2014 and 2.5 percent in 2015.
The government has already imposed the largest tax hikes in living memory from January, adding to other tax rises and spending cuts introduced since the mid-2011 bailout. Consumer demand and investment has collapsed, causing the deepest recession in Portugal since the 1970s.
The economy is expected to shrink 2.3 percent this year after last year's 3.2 percent slump before returning to meagre growth in 2014.
Despite the economic pain and growing protest, Lisbon's borrowing costs have dropped since the start of 2013, suggesting investors believe the European Union will make the bailout work.
Writing by Andrei Khalip; Editing by Ruth Pitchford


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Health savings account participation, and contributions, is continuing to grow at a record pace, according to new analysis.
Roughly 70 percent of workers with a health reimbursement account or a health savings account said their employers contributed to the account in 2012, continuing a steady increase since 2009, according to research released Wednesday by the Employee Benefits Institute.
Employer contributions of $200−$499 increased from 14 percent to 22 percent between 2009 and 2011, while employers that contributed $1,000 or more increased from 24 percent to 28 percent. Among workers with family coverage, employer contribution levels were unchanged between 2010 and 2012, with 63 percent contributing $1,000 or more.
Forty-two percent of employees said they contributed at least $1,500 to an HSA last year, while just 15 percent said they made no contribution, the institute found.
EBRI Director Paul Fronstein said the growing contributions may be due in part to the strengthening economy. There was a slight drop in the accounts during the recent recession, as average account balances leveled off in 2008 and 2009, and fell slightly in 2010. But they have been picking back up in 2011 and 2012.
According to the EBRI's research, 11.6 million adults ages 21–64 (or 7 percent of the population) were enrolled in a plan with an HRA or HSA. An additional 7 million reported that they were covered by an HSA-eligible plan but had not opened such an account. Thus, overall, 18.6 million adults ages 21–64 with private insurance, representing 15.4 percent of that market, were either in a CDHP or an HSA-eligible plan but had not opened the account that would be used to fund covered expenses. When their children were counted, 25.2 million individuals with private insurance, representing 14.6 percent of the market, were either in a CDHP or an HSA-eligible plan.
These individual health accounts are a central element in so-called "consumer-driven" health plans, which first began to appear in the work place about 12 years ago. They are designed to give individuals more control over funds allocated for health care services, thereby causing health plan participants to spend the money more responsibly. But the Patient Protection and Affordable Care Act includes some new restrictions on HSAs, as they can no longer be used to buy over-the-counter drugs unless a doctor writes a prescription.


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|Spicy harissa (top left), pomegranate tahini with smoked paprika, and beet and za'atar relish
Harissa, a smoky and spicy Tunisian hot sauce made from a base of roasted peppers. While it's great as a dip, it also goes very well as a condiment for grilled meat or fish, stir fried vegetables, or even on top of scrambled eggs.
Pomegranate Tahini, combines sesame tahini with Greek yogurt, the tang of lemons, and a hint of pomegranate sweetness.
Beet & Za'atar relish, roasted beets and the popular Middle Eastern spice mix combine with Greek yogurt for a sweet and savory relish.
All of these spreads are easy to make in a food processor or blender. Get the za'atar and pomegranate molasses online (click the links) or visit your local Middle Eastern market. Serve with toasted pita.
Beet & Za'atar Relish5 medium-sized beets
3/4 cup Greek yogurt
1 1/2 tablespoons pomegranate molasses
2 1/2 tablespoons extra virgin olive oil
1 1/2 tablespoons plus more to taste za'atar
1. Follow our method of roasting beets: preheat oven to 400 degrees. Trim beets and wash them thoroughly. Then dry slightly but while still damp wrap individually in tin foil. Put in the oven for around 45 minutes until a sharp knife easily penetrates the center of the beets.
2. Meanwhile, make the other spreads!
3. When the beets are done, cool, and remove the skins. You can use paper towels if you don't want your hands to become red with beet juice. Puree the beets with the other ingredients.
4. Serve, topped with more za'atar.
Harissa3 red peppers
1 small can diced tomatoes
2 medium red onions
3 Thai chilis
4 cloves garlic
1 1/2 teaspoons cumin
1 1/2 tablespoons ground coriander
1 cup parsley
2 tablespoons tomato paste
1 tablespoon smoked paprika
Juice from 3 lemons
2 tablespoons extra virgin olive oil
1. Grill or broil the red peppers until they are black and charred. Allow to cool slightly and, if you'd like, remove the skins, by rubbing the peppers with paper towels.
2. Puree all of the ingredients in a large food processor or blender, adding a generous amount of salt and pepper.
3. Serve, topped with chopped parsley.
Pomegranate Tahini3/4 cup tahini
2 cloves garlic
1/2 cupparsley, mint, or a combination of the two
2/3 cup Greek Yogurt
1/4 cup lemon juice plus grated zest of 1 lemon
1 teaspoon pomegranate molasses
About 3/4 cup water
1. Mince the garlic cloves and roughly chop the herbs.
2. In a large mixing bowl, add the tahini, garlic, herbs, yogurt, lemon juice and zest, pomegranate molasses, and some salt and pepper. Stir well as you slowly add the water. You want to end up with a thick but pourable consistency, similar to honey. Stop adding the water when you reach the desired consistency.
3. Serve, topped with smoked paprika.
Total time: 1 hour 15 minutes for all three spreads.
Makes a lot of each, enjoy the leftovers!


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Former Litchfield County state attorney Frank Maco said the statute of limitations on accusations by Allen's adopted daughter Dylan Farrow ran out at least 15 years ago.
The now retired prosecutor said he did not have enough evidence to prosecute Allen back in 1993.
It came after Dylan Farrow, in an open letter published in The New York Times on Saturday, claimed Allen sexually assaulted her when she was seven after he and actress Mia Farrow adopted her.
The message to columnist Nicholas Kristof detailed the alleged 1992 incident.
She said she was motivated to speak out because of Hollywood's continued embrace of Allen, who has always maintained his innocence.
She wrote: "That he got away with what he did to me haunted me as I grew up. I was stricken with guilt that I had allowed him to be near other little girls."
In the letter, Farrow said Allen led her to a "dim, closet-like attic" at their Connecticut home before sexually assaulting her.
She added: "For as long as I could remember, my father had been doing things to me that I didn't like.
"These things happened so often, so routinely, so skillfully hidden from a mother that would have protected me had she known, that I thought it was normal."
She also mentioned Hollywood actors who have starred in Allen's films.
"What if it had been your child, Cate Blanchett? Louis CK? Alec Baldwin?" she said in the letter.
"What if it had been you, Emma Stone? Or you, Scarlett Johansson? You knew me when I was a little girl, Diane Keaton. Have you forgotten me?"
In response to the letter, Blue Jasmine star Blanchett reportedly said: "It's obviously been a long and painful situation for the family and I hope they find some resolution and peace."
Allen was investigated on child molestation claims over the alleged 1992 incident, but prosecutors chose not to charge him.
The New York Times said Allen declined to comment.
The 1992 allegation came shortly after Allen became involved with Mia Farrow's adopted daughter, Soon-Yi Previn.
Allen was not the adoptive father of Previn, who was 19 at the time.
The pair married in 1997 and have two adopted daughters.
The letter comes not long after Allen was given a lifetime achievement award at the Golden Globes.
Mia Farrow and her son with Allen, Ronan Farrow, both took to Twitter to criticise Allen getting the honour in January.
When the director's tribute began to start, the actress, who had been tweeting throughout the show, stopped and said on the microblogging site: "Time to grab some ice cream & switch over to #GIRLS."
Ronan was more explicit, saying on Twitter: "Missed the Woody Allen tribute - did they put the part where a woman publicly confirmed he molested her at age 7 before or after Annie Hall?"
:: Watch Sky News live on television, on Sky channel 501, Virgin Media channel 602, Freeview channel 82 and Freesat channel 202.


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Sunday, March 31, 2013
Twas a great weekend...full of family, fun, food and faith. Easter is one of my absolute favorite holidays. So full of joy and hope, you can't help but feel happy and loved. I'll admit, it DID feel not so Eastery, what with the 83 feet of snow on the ground and the temps hovering just at freezing, but it was still great, nonetheless!
And so now I sit, wanting to show you some fun photos of our weekend, but too lazy to drag my butt out of my comfy bed to get my camera, so I'll do it tomorrow. M'kay?
Goodnight, my friends...and God bless!
3 comments:
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Yes, snow kind of steals the springy-feel that Easter usually has. Blessings to you and your family. I'm looking forward to the Easter photos!ReplyDelete
Easter is a wonderful time...I love it! And I love Springtime! (We woke up to sleet this morning and that seemed a bit weird...but I know sunny days are just around the corner!)ReplyDelete
Can't wait to see your pictures!
I love comments! And, I welcome your thoughts that aren't in agreement with mine...as long as they are respectful!


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Left hand design, ported barrels, fiber optic bead, gloss oil finish, checkered walnut, egnraved low-profile steel receiver, mechanical trigger, Invector-DS chokes
A perfection package for lefties. This is clearly a top Browning gun for a lot of right reasons and one left reason. The left hand palm swell makes it a joy for any lefty, who by no choice of his own, must let the dominant hand and eye prevail. The 725 lets your eye prevail and lets your shooting prevail.
You say you want an evolution? No revolutions found here. But the new Citori 725 is the evolution of John M. Browning's legendary B25 Superposed, now with the modern performance advantage of a Low-Profile receiver. The new 725 receiver is significantly lower than other Citori 12 gauge receivers, yet the 725 shares the renowned durability of generations of Citori over and unders with the same rugged full-width hinge pin and tapered locking bolt design.
Balance is center stage. With a 725, you get the "one with the gun" feeling you want, with the long lasting durability you expect from a Browning over and under. And the features don't stop there. The 725 showcases an all-new Mechanical Trigger (FireLite) that offers unmatched feel and lighter pull weights than ever before. Inflex Technology has also been added to make shooting more comfortable. And the new Invector-DS choke system moves to a new level of performance. Experience the benefits these improvements can do for your shooting with a new Citori 725.
Please Note: This description and product image may represent a general group of products. Please read the item's title and specifications for more specific information about this particular item.
Guns can only be shipped to a location within the USA that holds an FFL (Federal Firearms License) - this can be your local gun shop, pawn shop, sporting goods store, etc. Your local gun dealer will then handle the transfer of the firearm to you.
Please ensure that you have familiarized yourself with the process before placing a firearm order. Please note that you must confirm your acceptance of all of these policies to place a firearm order:
0 items


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I for one
welcome our jellified overlords.
Sorry, had to be done.
Boffins have fashioned an artificial bio-engineered jellyfish from rat cells that could one day fix up badly damaged human heart tissue. Researchers from Harvard and Caltech working towards building an artificial human heart cobbled together some silicon and some living rat heart cells to make a jellyfish that can pump through …
welcome our jellified overlords.
Sorry, had to be done.
this bit's required apparently.
I like to think it is short for "your welcome will ensure your survival when the day of the jellipocalypse arrives"
In the hillside?
what could possibly go wrong?
I have visions of the legendary "The Thing" being remade...as a documentary.
I'm curious as to how it escaped the usual 'blobomination' tag.
The chicken^Wrat heart was kept alive
in a special solution
thub thub. thub thub.
The XXXXXXXL orange shirt with the initials F.A. on it.
Skrill from Earth: Final Conflict?
"They then dropped Medusoid into a container of saltwater and shocked it into swimming just like the real thing."
Please, please tell me the researchers then clasped their hands together and shouted: "It's alive!", before laughing maniacally.
I do love it when we get to read about the more fun research that is going on around the globe. There are plenty of future practical applications for this sort of tech, but for now, it is just great to know that someone somewhere is being given the budget to make stuff like this work!
Don't worry the..
..brigade will attempt to squash this idea before it goes an further. And if they don't win, the bible bashers will be along right behind them. The kill joys.
But will you still be saying that when the Special Projects Bureau push the envelope??
<< because that's what it might look like!
I mean I'm not even a scientist and I've seen it.
A movie called "The Jelly Rat" doesn't inspire much fear
"In Deep Water, nobody can eat their cheese"
Not to detract from the efforts of these boffins, but weren't we on the verge of growing artificial hearts and or creating pigs with hearts that could be transplanted in to humans years ago? Did all these tacks dead end or were they sunk by the aforementioned killjoy brigades?
"weren't we on the verge of growing artificial hearts and or creating pigs with hearts that could be transplanted in to humans years ago?"
So all the promising pigs disappeared - and then these Rattus Cnidaria suddenly appear ?
Coincidence ?
or does it PROVE that the creationists were right all along?
It'll be a cold, cold day in hell before any of those twats are proven right.
The pun and irony of that statement was intended.
It looks like our favourite hack is confused between silicon and silicone. Let's hope the boffins know the difference.
Given the lack of popularity of plastic surgery in Switzerland and the lack of mating opportunities being buried in an underground tunnel 12hrs a day with other boffins entails...I doubt it.
No.... This doesn't sound like the start to an apocalypse movie at all...
Jellyfish rats come make a clone
Jellyfish rats make bodily parts
With jellyfish, rat and silicone
Jellyfish rats make a jellyfish heart
—will never be practical until they can be made unbreakable.
—The Great and Powerful Oz
You were all thinking it, I jsut said it.
Some amazing stuff over the horizon though.
"I left my jellyfish/rat in San Franciso" sung by Frank (ratpack) Sinatra
and the list goes on . . .
but I hope not.
that the Necronimicon's prophecies were mis-interpreted, the rise of Great Cthulhu from sunken R'Lieh was actually a reference to the rise of the escaped hyper intelligent ratctopus from the depths.
Even death has died.
Hopefully he will eat me first.
...on my part, but what would stop your hyper-intelligent jellyfish-rat heart from getting bored one day, ripping free from where it was implanted inside your chest, and swimming around your delicious, juicy, oozing internal organs and stinging you to death from the inside...?


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Change is good. It allows you to reflect on the past, reassess the present, and plan for a brighter future. Sometimes it's just what you need to live a more fulfilling existence.
While SURFER Magazine has been steering a prosperous course under the direction of Editor, Chris Mauro, for the better part of a decade, Mauro's decision to make a change in his life has afforded the same opportunity to SURFER. And we'll all be darned if it didn't walk through the door at about 6′ 2″ with shaggy hair and a smile in the form of Joel Patterson.
With his new office all set up as of yesterday morning, Patterson represents the fresh face that will guide the magazine into its 50th anniversary year. He will be the one directing the stories, deciding what's important, and delivering the feeling of surfing into your homes each month.
It's only fitting we get to know him a little better. I mean, who is Joel Patterson, really? We conducted an interview to get you better acquainted. We think you'll approve; we're all pretty psyched.
Here's to a long and fruitful relationship.
Tell us a little bit about yourself. Where did you grow up?
I grew up surfing and skateboarding in Newport Beach, California down the street from Quiksilver, Billabong, and the rest of the surf industry. I got a bachelor's in history from Chapman University. Worked as an Editor at TransWorld Skateboarding magazine from 1994 to 2000 then switched seats and was the Editor in Chief of TransWorld Surf magazine from 2000 to 2006. From the summer of 2007 to just a couple months ago, I was the Editor in Chief of Surfline's Water magazine, but when I heard the editor's job at Surfer was being vacated by Chris Mauro, I knew it was my one opportunity to run the bible of our sport.
Tell us about any moments in your career that may have led you towards working at SURFER Magazine?
At TransWorld we used to sit around discussing story ideas for upcoming issues, and every time I'd suggest something I was passionate about someone would scowl, "This isn't SURFER Magazine, Joel."
What direction can we expect SURFER Magazine to go under your guidance?
I'm interested in telling the complete story of surfing. Not just which young kids rip, and also not just how many points Kelly needs to clinch his next world title. I want to give surfers the tools to truly maximize their surfing experience; I want to help them travel better; I want to make sure their next board is a magic one; I want to clue them in to people who are doing cutting edge stuff; I want to assist them in picking a Fantasy SURFER team that blows away all their friends'; I want to tell them the wild stories of the surfers who came before them, and I want them to land an air. It's a big task, but then, this isn't a nine-to-five job.
What is your first order of business as Editor?
Planning. Serious planning.
Name one feature that has yet to be written, that MUST be written as soon as possible.
Yeah, right. I'm not giving Evan Slater any head starts.
In your opinion, what is the most exciting thing happening in surfing today?
See above. But generally speaking, I love surfers who expand their consciousness. I'm most drawn to the surfers who take the roads less traveled.
How do you think the Internet has changed the way surfers digest media, and how is SURFER going to evolve to accommodate those changes?
The internet has had a similar effect on surfers that it's had on mainstream society, and the media companies that will thrive in the modern environment will understand that different stories will work better in different formats. That's Media 101 stuff. We need to do a better job covering the newsy stories (swells, the WCT, the "save Trestles" movement), and we also need to use the Web to tell more complete stories.
Your favorite personal moment in surfing:
Every time I roll up to a right point on a head-high swell.
Top 5 favorite bands:
It changes a lot, but lately I've been loving TV On The Radio, old Beach Boys, Radiohead, Ratatat, MGMT.
Favorite Quote:
I love this quote from the 5th Century philosopher named Boethius: "It's my belief that history is a wheel. 'Inconsistency is my very essence,' says the wheel. 'Rise up on my spokes if you like, but don't complain when you are cast back down into the depths.' Good times pass away, but then so do the bad. Mutability is our tragedy, but it is also our hope. The worst of times, like the best, are always passing away."
Anything else you'd like to say in your official introduction to the SurferMag.com Online Community?
If you're a surfer, this magazine belongs to you. I consider myself a custodian of a pretty awe-inspiring tradition, and I'm going to work very hard to include our readers' voices in the stories we tell, the surfers we profile, and the topics we address. But that concept only works if you participate.


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My Nonprofit Reviews
Review for Neses Ninos Estudiando El Salvador, Bellevue, WA, USA
Our trip to El Salvador with Ricardo and Joy was amazing. The NESES students were an inspiration to all of us. NESES has given them the financial and emotional support which has helped them believe in themselves and their future in El Salvador. With persistence and sacrifice they are achieving their goal of a university education.
These young people exhibit such determination in the face of sometimes nearly impossible circumstances but carry on with smiles and hope. Thanks NESES and all its supporters.
More Feedback
I've personally experienced the results of this organization in...
Raul is determined to be an English professor; Hugo is a natural leader who, while attending university, has established a drug and violence-free youth group in his home town of Armenia pursuing arts and music; Joanna is in her 5th year of university, graduating in English while working part time. She is a shining light; Tomasa works full time, attends university classes each evening in accounting, and cares for two elderly women.
If I had to make changes to this organization, I would...
I can't think of any changes I would make to NESES. I do wish more people could find out about what a difference the organization is making to so many Salvadoran children.
Was your donation impactful?
How likely is it that you would recommend that a friend donate to this group?
How likely are you to donate to this group again?
Why did you make your donation at this time?
We made our largest donation before we traveled to El Salvador with Ricardo and Joy. We were able to see the country and experience the actual students who had taken the NESES study tour as teenagers. We hope more students will benefit from NESES and become outstanding citizens as those we met.
What would you tell others about this organization?
The work is being done. Ricardo, as a Salvadoran national, is a real inspiration to these former orphans. They look up to him and he is a patient mentor. This organization should be a model for other grassroots organizations. We, also, like the fact that the money we donated was double matched.
When was your last experience with this nonprofit?