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The Evil Rich Began Acting Rationally
So, about that big sell off on Wall Street after the election…
It turns out there were a lot of selfish, rich capitalist pigs who decided to take their chips off the table rather than gamble on dodging the proverbial soaking that the American electorate voted to commence.
President Obama ran on a promise to raise taxes on annual incomes more than $250,000. And people who understand wealth, asset management, and investment protection see the writing on the wall:
Fearing an increase in capital gains and dividend taxes, many of the rich are unloading stocks, businesses and homes before the end of the year.
Wealth advisors say that with capital-gains taxes potentially going to 25 percent from 15 percent, and other possible increases in the dividend tax, estate tax and other taxes, many clients are selling now to save millions in taxes.
Democrats are now saying they'll be okay with allowing all of the Bush-era tax cuts expire, and then go back and try for new replacement cuts.
Higher income households can expect to see an additional 5% tax hike on their healthcare benefits and changes in itemized deductions. So, someone living off investments would see their federal tax burden hit about 25% of their annual income. This, obviously, does not count any non-investment income, state income taxes, and property taxes.
Also, the expiration of the Bush tax cuts would mean taxes on dividends would triple (from 15% to 43%).
Bottom line: It's just not going to be as profitable to take risks as it was. The payoffs will be curtailed, so the more-riskier investments will be abandoned.
The federal government will also stake a majority claim on all estates worth more $1 million. So, a family farm with assets valued at one million dollars would have to pay $550,000 in death taxes.
Talk about creating generational poverty.
Experts are also expecting small business owners to sell off their companies before the New Year, in order to get the maximum return on their investments. In a down economy, I'm sure this will mean some great deals for big business looking to consolidate holdings and eliminate small competitors.
Talk about benefiting the big corporations.
There are also reports that businesses (like the parent company of Olive Garden and Longhorn restaurants) are moving employees to part-time status to avoid paying for health benefits. Other companies are shedding employees in order to stay under the 50-employee cap after which businesses must offer benefits. Still other companies are considering abolishing benefits altogether, instead paying the federal fine (which costs less than the benefits).
This was, of course, predictable and entirely predicted. But when people put faith in a government to give them everything at no cost, there is little room for logic.
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Noosa Beach
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text:
Release Date: 2008 |
Album Rating: 4.0I know this is a short review, I tried to keep it as simple as possible. This is only my second review so don't be too harsh. This Message Edited On 04.06.09
It's undeniable she has a good voice? I can't hear it for a wall of effects and gay production.
She's quite possibly the most annoying thing on the planet.
Album Rating: 4.0"She's quite possibly the most annoying thing on the planet."
No, I'm pretty sure i've seen worse. But Maybe the opener was a bit of a strech
Album Rating: 3.5gay production
Digging: Alvvays - Antisocialites
Album Rating: 3.0A pretty average pop album, although some songs are extremely catchy. I wish they would stop playing just dance, which is an album low for me.
very good album
lol benzum
not rly
hey benzum try and be more of a fuck ass who has little idea wtf they're talking about idk
hey benzum deep dicking lol
your opinion sux
best thread evers
I have to agree with Benzum. It's deliberately packaged and commercial to a degree I hardly recall seeing before. Her UNIQUESTYLE is simply stupid, and it's music for shallow morons who don't understand music and have no interest in talent/originality/emotion. Atop that, it's too annoying to be a good pop album - the production and effects being just 2 of the 'quirks' (read: deliberately and demographically targeted modifications) that piss me off the most.
She's also not fit.
There is nothing about this music that appeals to me at all.
The way I see it, this is monotone, prewritten music for people for key demographic
that nobody in their right mind over the age of 12 should ever consider listen to.
this is horrible
Album Rating: 4.5 | Sound Offlol Benzum
Can't read his poker face
Album Rating: 4.0arguuuments!
Just like to point out that using modern pop music as a benchmark for musical quality would make everything 5/5.
We're discussing the album maaaate.
Last I checked this was a music discussion site. Zomg.This Message Edited On 04.07.09
Benzum.... From downtown! Is it the shoes?
Review is good, gaga is not. Paparazzi sounds like a Mariah Carey, but worse. If that's possible.
Album Rating: 4.5 | Sound OffYou're an idiot.
Bands: A B C D E F G H I J K L M N O P Q R S T U V W X Y Z


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Well, I got a little to confident after doing some simpler block of the month blocks. Now I have started a scrappy Civil War Tribute quilt. The first block came out 18 inches instead of 18.5 inches. Good thing it was all scraps of fabric. I love the inside of the block and all the points are ok so I am going to use the block somewhere else and do it again.
Does anyone who has made these blocks have any hints or suggestions to make it easier?


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LONE WOLF, Okla. — The ongoing drought that's lowered the water level at Lake Altus-Lugert in southwestern Oklahoma by about 20 feet has also reduced the number of vacationers, but officials at Quartz Mountain State Park say the water and fish in the lake remain safe.
"Those conditions have really affected park and lodge revenues," park director Terry Mosley told The Lawton-Constitution. "For us, you can take your pick of the situations affecting us — low water, fish kill, drought and extremely hot conditions. But we still had a very good crowd on Memorial Day weekend and looking for a good crowd on July 4.
"For today's recreational user, the water is safe," he said. "And our boat ramps are still functional."
The latest U.S. Drought Monitor report, released Thursday, shows that the region remains in severe to extreme drought, although rain has improved conditions in adjacent areas to moderate drought in recent weeks.
Mosley said the golden algae that has appeared at the lake and resulted in the deaths of fish is only harmful to fish and other gilled animals. He said the algae forms because of cold weather during spring cold snaps that bring late freezes to the area, and concentrations of salt. He said the lake is being restocked.
"We actually had good fishing with some catfish and crappies stocked in the lake," he said.
One family that comes to the park to camp annually said that the water conditions haven't deterred them from visiting again this year.
"Every year we have a family reunion here," said Connie Sanchez of Amarillo. "We've come here every year for the past 50 years."
Sanchez said the annual reunion attracts family from Oklahoma, Texas, Iowa and Montana. Although she and other family members were "saddened" by the low water level, which detracts from the park's beauty, she has no regrets about coming back.
"Even if there was no water, we'd still be coming here," she said.


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Ten Years of Effort Have Failed to Reduce Violence in Israel's Schools
The Education Ministry has failed to deal with the problem of violence in the schools, the State Comptroller's Report said. Over the years, numerous professional committees have been appointed to study this problem, but most of their recommendations were never implemented.
"Over the past decade, the education system worked to reduce incidents of violence and improve the educational climate in schools. That goal was not achieved," the report stated.
Between 1996 and 2006, the frequency of violence - physical, social and sexual - at educational facilities remained virtually unchanged.
"During those years, about a third of students were victims of harassment or bullying on school property," the report said.
Several committees were established over that decade to review the problem, but their recommendations were ignored. Moreover, "the ministry does not have a body devoted exclusively to dealing with bullying and violence."
"The theoretical approach of the ministry's psychological counseling service is that the key to lowering the violence level depends on the nature of a school's atmosphere and climate," the report continued. "However, the ministry did not examine alternatives to that approach, despite the research data in its possession, which indicate no change in the bullying trend."
The ministry has no data on enforcement of regulations concerning school violence, and has not set up an efficient enforcement system. "The district inspectors, whose responsibility this is, are not doing their jobs properly in this regard."
Ministry regulations do not give teachers tools for enforcing discipline, making it hard for them to break up schoolyard fights and identify victims of violence and sexual assault. The comptroller found that teachers also refrain from defending pupils against bullying by classmates because they are afraid of lawsuits by pupils and parents.
Furthermore, teacher training programs do not prepare the future teachers to deal with school violence.
The Education Ministry said it is working to implement some of the report's recommendations. Reducing school violence is a mainstay of its activity, it added, and to this end, it runs a program at 800 schools designed to create "a safe climate."
On another education front, the comptroller found, the ministry is not keeping a proper eye on ultra-Orthodox schools designated "recognized but unofficial." The ministry has funding for only a few inspectors for these schools, and even some of these positions remain unfilled.
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Where: Escondido
What: The 31,000-square-foot H. Johnson building at 131 S. Broadway, and a half-acre lot at Juniper Street and Grand Avenue.
Cost: Undetermined for the H. Johnson building and $675,000 for the Juniper and Grand lot.
Pros: Control downtown redevelopment, with hopes of partnering with a developer or leasing the properties.
Cons: No money in the coffers, except for future income from the redevelopment agency.
The city of Escondido is hoping to buy key downtown properties so it can control redevelopment and diversify its revenue, now heavily dependent on sales tax income.
There's a catch, though: Escondido's coffers are practically empty because of continuing budget deficits that required the repeated use of reserves.
The two properties being considered are the 31,000-square-foot H. Johnson building, a former furniture store on South Broadway near Grand Avenue, and a half-acre vacant lot at Juniper Street and Grand Avenue. Grand Avenue is the business artery of downtown.
The City Council's goal is to partner with developers to build mixed-use, residential-commercial projects or a parking garage, or lease the properties. Either way, the council hopes to use them to generate steady income that could help Escondido wean itself off sales tax revenue, which has plummeted in the recession.
Since Escondido has no cash on hand, it could issue revenue bonds based on future tax-increment income from the downtown redevelopment area, Councilman Dick Daniels suggested.
Last month, the council discussed the two properties in a closed-door meeting. Jo Ann Case, the city's economic development director and real estate agent, said afterward that the council didn't make a decision, but asked for further studies.
She declined to reveal what the city would be willing to pay for the huge H. Johnson building, but Tom Crowley, the commercial broker who represents the owner, said it is selling for $4.5 million.
The half-acre lot, which a broker said was once used as a gas station, is for sale at $675,000. It's used occasionally as a staging, parking or band area for special events.
The H. Johnson building is no stranger to council discussions. It was built in 1952 and leased to Sears, Roebuck and Co., and when Sears moved to the mall, H. Johnson Furniture moved in. The store finally moved out in 2007 because the owner wanted to sell the building.
Two years ago, Escondido tried to buy that building and two lots across the street for $4 million, but that didn't happen because the money had to be used to fill budget gaps. Several developers subsequently tried to open a restaurant or a market there, but none of the ideas panned out, and the building has remained vacant.
"This is the right time to buy. It's a critical investment," Mayor Lori Holt Pfeiler said. "We might like to do something like San Marcos."
That city is a landlord and owns 1.7 million square feet of leasable space, including the Creekside Marketplace mall, City Hall and its public safety center.
The properties will generate $8.4 million in rent this fiscal year, 2009-10, accounting for 14 percent of the city's $61 million general fund budget, San Marcos city spokeswoman Jenny Peterson said.
That steady stream of income helped San Marcos achieve a balanced budget this fiscal year, at a time when most municipalities in the region are struggling with deficits, Peterson said.
Owning property may be a good idea for San Marcos, but it doesn't pencil out for Escondido, said Chuck Smiar, a real estate broker who lives just outside Escondido's city limits and has been following its politics. He's a past president of the North San Diego County Association of Realtors.
"I understand the theory behind it," Smiar said. "Where are they going to get the money? They can use bonds, but it is a tax — somebody's going to pay it.
"They keep spending money they don't have. It's not prudent."
Smiar also criticized the idea of a parking lot, saying that it wouldn't bring enough income to justify the cost of purchase and construction. Escondido's downtown simply isn't vibrant enough to support a garage year-round, he said.
"The only time they can fill it is Friday night, when they have (the hot-rod event) Cruisin' Grand," Smiar said.
Pfeiler disagreed, saying that a lot of people in and outside Escondido are interested in living in a downtown environment and are looking for a place that isn't as busy as San Diego's.
"When the market was busier, and condos were building, lots of people were talking about living downtown. They were excited about it," she said.
Escondido's attempt to rejuvenate its downtown began two decades ago, when the city tried to attract a developer to build a full-service hotel there. City leaders thought back then that hotel-room tax and tourism dollars would diversify the city's income. As enthusiasm for the idea built, the council committed $19 million toward the hotel, money that hotel opponents called a developer subsidy.
But the developer couldn't obtain a loan, and last year the council withdrew its offer. The developer later revived the project, asking for $12 million in city money. However, by then the council was in the throes of its latest budget crisis, and soon decided to use the hotel money to cover expenses.
Now without a hotel, the city faced another blow. Several mixed-use developments downtown have stalled because of the real estate and credit market crash. This year, Escondido projected an unprecedented $10.5 million gap, primarily because of declining sales tax income, in its $72.9 million general fund, which has to be reconciled within several months before the fiscal year ends June 30.
Council members decided to work harder to find new sources of revenue.
"We want income that's immune from economic vagaries," Daniels said. "We're using properties in the most effective way to promote the viability of downtown. If not, the properties will be picked up by owners who will underutilize them."Copyright © 2017, The San Diego Union-Tribune


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Wallace wins recall after hardest pick
Irish rugby coach Declan Kidney admitted that the decision to omit Gordon D'Arcy from his panel of 22 for Sunday's Croke Park test match with Australia was one of the most difficult he has ever had to make.
"You don't like leaving a fella like Gordon out. That's not an easy or a nice thing to have to do," said Kidney.
"But you pick what you believe to be the best team to do a particular job against particular opponents on a particular day and that's what I have done."
The beneficiary of Kidney's difficult decision is Ulster captain Paddy Wallace, who has been chosen to partner Brian O'Driscoll in midfield.
Kidney refused to elaborate on his thinking in choosing Wallace ahead of D'Arcy.
"They're different players with different types of things to offer. Last season Paddy was unlucky to miss out with injuries," was as far as he was prepared to go.
The other Ulster starter is blindside Stephen Ferris, whose back row colleagues are Munster flanker David Wallace and Leinster No. 8 Jamie Heaslip. That's a breakaway unit featuring three Lions.
Other than inside centre, the position around which there had been debate was loose head prop, with Ulster's Tom Court and Leinster's Cian Healy in contention for the number one jersey left vacant as a result of Marcus Horan's as yet undefined health problems.
In this instance the young Clontarf front row player got the nod for what will be his international debut at senior level.
It is a decision which Court accepted with good grace.
"I can't begrudge Cian his cap; he has been playing really well – and consistently," the Australian-turned-Irishman said. "Good luck to him, and I mean that.
"But if I get on, hopefully I'll take my chance. I'm ready for it. I'm up for this."
Elsewhere, it is pretty much as expected, with the vast experience of hooker Jerry Flannery and tight head John Hayes counting for more than the fact they have had precious little match-time to date this season.
With Kidney famed for having said that he would select on current form, it was surprising to hear him admit that, on this occasion, it had not necessarily been the case.
"You look at the opposition and you try to weigh up how best to beat them," he said. "That was our thinking in choosing the side we have chosen to face Australia."
The locks are Munster and Lions comrades-in-arms, Donncha O'Callaghan and Paul O'Connell.
It's a Munster half-back pairing, too with Tomas O'Leary partnering Ronan O'Gara who is coming under increasing pressure to hold on to his outside-half's jersey.
Leinster's Jonny Sexton will be on the bench on Sunday, in which case there is a very good chance that he will start against Fiji six days later.
It's an all-Lions back three, too, with Rob Kearney, Tommy Bowe and Luke Fitzgerald wearing numbers 15, 14 and 11 respectively.
Once again O'Driscoll captains the side in what, including Lions matches, will be his 100th Test outing.
But the skipper was keen to point out that he plays in a team "with leaders throughout it".
There can be no disputing that, with Munster ace O'Connell having captained the 2009 Lions as well as leading his province, and O'Driscoll's midfield colleague Wallace this term's Ulster skipper.
Ireland squad v Australia, Sunday November 15 at Croke Park (3.00pm): R Kearney (Leinster); T Bowe (Ospreys), B O'Driscoll (capt) (Leinster), P Wallace (Ulster), L Fitzgerald (Leinster); R O'Gara (Munster), T O'Leary (Munster); C Healy (Leinster), J Flannery (Munster), J Hayes (Munster); D O'Callaghan (Munster), P O'Connell (Munster); S Ferris (Ulster), D Wallace (Munster), J Heaslip (Leinster).
Replacements: S Cronin (Connacht), T Court (Ulster), L Cullen (Leinster), D Leamy (Munster), E Reddan (Leinster), J Sexton (Leinster), K Earls (Munster).
Belfast Telegraph


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Sphingosine 1-phosphate (S1P) is a biologically active lysophospholipid that serves as a key regulator of cellular differentiation and survival. Immune stimuli increase S1P synthesis and secretion by mast cells and platelets, implicating this molecule in tissue responses to injury and inflammation. Binding of S1P to Gi protein-coupled receptors activates phosphatidylinositol 3-kinase and Akt in a variety of tissues. To elucidate the mechanisms by which S1P enhances adult cardiac myocyte survival during hypoxia, we used a mouse cell culture system in which S1P1 receptors were observed to transduce signals from exogenous S1P, an S1P1 receptor antibody with agonist properties, and the pharmacological agents FTY720 and SEW2871. S1P1 receptor mRNA and protein were abundantly expressed by adult mouse cardiac myocytes. S1P-S1P1 receptor axis enhancement of myocyte survival during hypoxia was abolished by phosphatidylinositol 3-kinase inhibition. S1P1 receptor function was closely associated with activation of Akt, inactivation of GSK-3β, and reduction of cytochrome c release from heart mitochondria. These observations highlight the importance of S1P1 receptors on ventricular myocytes as mediators of inducible resistance against cellular injury during severe hypoxic stress.
- heart
- lysophospholipids
- ischemia
- cardioprotection
- mitochondria
sphingosine 1-phosphate (S1P) is a biologically active lysophospholipid that serves as a regulator of cell differentiation and survival (8, 33, 38, 66). S1P is produced by mast cells, platelets, cardiac myocytes, and other cell types in de novo biosynthetic pathways and by metabolism of the plasma membrane phospholipid sphingomyelin (8). Secreted S1P is present in extracellular fluids at nanomolar to micromolar concentrations bound by albumin and plasma lipoproteins (1, 51). Immune stimuli increase S1P synthesis and secretion, implicating the molecule in injury responses and inflammation (5, 13, 15, 51, 53).
Although S1P exerts intracellular effects, functions triggered by extracellular binding to plasma membrane G protein-coupled receptors (GPCRs) designated as S1P1, S1P2, S1P3, S1P4, and S1P5 are better understood. For example, Windh et al. (68) used both insect and mammalian heterologous expression systems to confirm that S1P1 activated only Gi family members. In contrast, S1P2 and S1P3 were coupled with Gi, Gq, and G13 (68). Signaling pathways involving S1P1 and S1P3, Gi subunits, phosphatidylinositol 3-kinase (PI3K), and Akt mediate the protective actions of S1P in a range of tissues (49).
Lecour et al. (34) used an ex vivo rat heart protocol to demonstrate that extracellular S1P administered at physiological concentrations reduced infarction during subsequent myocardial ischemia-reperfusion. S1P treatment mimicked cardioprotection conferred by ischemic preconditioning (34). Those investigators did not identify cardiac cell types or signaling pathways required for S1P-mediated protective effects. S1P1, S1P2, and S1P3 receptors are expressed by cardiac myocytes and fibroblasts and coronary artery endothelial and smooth muscle cells (1, 7, 49). S1P modulation of ion homeostasis and contraction (6, 18, 23, 32, 37, 39, 45, 55, 61, 70) may influence myocyte resistance to injury.
Our laboratory previously examined effects of S1P pretreatment on ex vivo mouse hearts subjected to ischemia-reperfusion (26). Physiological concentrations (10 nmol/l) of extracellular S1P infused before ischemia reduced infarction by one-half and augmented myocardial contractile recovery during reperfusion by several-fold. Treatment of hearts with ganglioside GM-1 (10 nmol/l), which increases intracellular concentrations of S1P through its activation of sphingosine kinase (7), stimulated equivalent protection against ischemia-reperfusion injury. Interestingly, GM-1 treatment was not protective in protein kinase Cε (PKCε) null hearts, leading us to postulate that PKCε is a critical modulator of sphingosine kinase activity and intracellular S1P production in intact myocardium (26).
In studies of cardioprotective signaling stimulated by ischemic preconditioning (IPC), we determined that IPC increased sphingosine kinase localization to tissue membrane fractions, elevated intracellular S1P concentrations, and reduced infarction size during ischemia-reperfusion (24). IPC also triggered sphingosine kinase translocation to tissue membrane fractions in PKCε null hearts but did not alter enzymatic activity or decrease infarction size, again suggesting functional interactions between PKCε and sphingosine kinase. We employed a pharmacological inhibitor, dimethylsphingosine (DMS), to show that sphingosine kinase function was necessary for the cardioprotective effects of IPC (24). However, inhibitory effects of DMS on PKC (52) confounded data interpretation.
Findings from these previous investigations suggested autocrine and paracrine roles for S1P in constitutive and inducible cardioprotective mechanisms. However, available data did not distinguish cardiac cell types, membrane receptors, and signaling pathways required for S1P-mediated resistance to heart tissue injury. Accordingly, we adapted an adult mouse cardiac myocyte culture model for in vitro hypoxia studies to focus on a key component of stress associated with interruptions in coronary blood flow. This culture model allowed us to measure effects of S1P on cardiac myocyte viability during hypoxic stress and activation of intracellular signaling from plasma membrane to mitochondria.
We developed a monoclonal antibody termed 4B5.2 that binds specifically to mouse and human S1P1 receptors (14). 4B5.2 monoclonal antibody also functions as an S1P1 receptor agonist, as demonstrated by its ability to mimic the suppressive effects of S1P treatment on T cell receptor-stimulated γ-interferon release by mouse CD4 T cells (14). We employed SEW2871 as an alternative selective agonist for S1P1 receptors; it has been shown to recapitulate the actions of S1P on this receptor subtype for all signaling pathways tested (27). We employed VPC23019, lead compound from the series of S1P analogs synthesized by Davis et al. (11), as a competitive antagonist at S1P1 receptors. These agents were used to address the following key questions. 1) Are S1P1 receptors expressed by mouse cardiac myocytes? 2) Does S1P1 receptor activation enhance the viability of adult cardiac myocytes subjected to hypoxia? 3) Are the protective effects of S1P1 receptor activation mediated at least in part by Gi subunits, PI3K, and Akt?
S1P, wortmannin, LY294002, and pertussis toxin were purchased from Biomol International (Plymouth Meeting, PA). VPC23019 was purchased from Avanti Polar Lipids (Alabaster, AL). FTY720 and SEW2871 were purchased from Calbiochem (San Diego, CA). Primary antibodies directed against cytochrome c and the phosphorylated and total endogenous forms of Akt and glycogen synthase kinase-3β (GSK-3β) were purchased from Cell Signaling Technology (Danvers, MA). S1P1 polyclonal antibody for Western blotting was purchased from Abcam (Cambridge, MA). S1P1 monoclonal antibody used for all in vitro experimental protocols was derived in the Goetzl laboratory at University of California, San Francisco, as published previously (14).
Male C57Bl/6 mice (20–25 g) were purchased from Charles River Laboratories (Hollister, CA). Animals were fed standard rodent chow and water ad libitum. All studies were approved by the Institutional Animal Care and Use Committee of the San Francisco Veterans Affairs Medical Center. All protocols conformed to the National Research Council's Guide for the Care and Use of Laboratory Animals.
Adult mouse cardiac myocyte culture protocol.
Ventricular myocytes were cultured with a modification of the method described by Zhou et al. (72). Mice were anti-coagulated with heparin (50 units ip) and euthanized with pentobarbital sodium (200 mg/kg ip). Hearts were excised and cannulated via the aorta for retrograde perfusion for 2 min with Ca2+-free isolation buffer containing (in mmol/l) NaCl 120, KCl 5.4, MgSO4 1.2, NaH2PO4 1.2, glucose 5.6, NaHCO3 4.6, HEPES 10, taurine 5, 2,3-butanedione monoxime (BDM) 10. Hearts were subsequently perfused for 9 min with the same isolation buffer containing 50 μmol/l CaCl2 and 1.5 mg/ml collagenase II (Worthington, Lakewood, NJ). Digested hearts were quickly removed from the perfusion apparatus. Atrial tissue and major vascular structures were trimmed away with scissors and discarded. Ventricles were teased apart with forceps, pipetted in collagenase II buffer, filtered through a cell dissociation sieve, and centrifuged at 40 g for 1 min. Cardiac myocyte pellets were serially resuspended in isolation buffers supplemented with 100, 250, 500, and 1,200 μmol/l CaCl2. The final Ca2+-resistant myocyte pellets were resuspended in minimal essential medium (MEM) containing HBSS, 10 μg/ml penicillin, 1.5 μmol/l vitamin B12, 2.5% bovine calf serum, and 10 mmol/l BDM.
Isolated cardiac myocytes were plated for 1 h on 35- and 60-mm tissue culture dishes coated with 10 μg/ml laminin. After an initial attachment period, myocytes were incubated overnight at 37°C in a humidified atmosphere of 1% CO2 and air with serum-free plating medium supplemented with 1 mmol/l BDM. This concentration of BDM is lower than concentrations shown by other laboratories to inhibit L-type Ca 2+ channel function (2), activate ryanodine receptors (59), inhibit transient outward K+ current (69), or disrupt gap junction communication (62) in cardiac myocytes. Nevertheless, all cells were incubated with BDM-free medium for 2 h before experimentation to reverse any residual effects of the agent. This cell culture protocol routinely yielded >90% cardiac myocytes at 50 cells/mm2; 80% of myocytes were rod shaped and viable at pH 7.2 for 48 h. All experiments were performed on the morning after cardiac myocyte isolation.
Cardiac fibroblasts were obtained from the 40 g supernatant of the ventricular cell suspension described above. Fibroblasts were pelleted at 500 g for 10 min, washed to remove collagenase, and resuspended in MEM supplemented with 10% fetal bovine serum and antibiotics (100 U/ml penicillin and streptomycin). Following 30 min of plating on culture dishes, weakly attached cells (cardiac myocytes, endothelial cells, smooth muscle cells, leukocytes, and erythrocytes) were rinsed free and discarded. Adherent fibroblasts (>95% by immunophenotyping for vimentin) were incubated overnight under the same conditions described above for cardiac myocytes. Cardiac fibroblasts were harvested for quantitative PCR analysis without passaging on the day after isolation.
Quantitative real-time PCR.
Total RNA was isolated from primary cultures of cardiac myocytes and fibroblasts using TRIzol (Life Technologies, Grand Island, NY), treated with DNase I, and amplified quantitatively in 50-ng replicates using TaqMan primers and probes for mouse S1P receptors and a constitutive standard, GAPDH (Integrated DNA Technology, Coralville, IA). Analyses were conducted with the Prism 7700 Sequence Detection System and recommended optimal reagents and conditions, generating interanalysis coefficients of variation <4% (PE Applied Biosystems, Foster City, CA). Values for each unknown were determined by standard threshold cycle methods with GAPDH as reference sequence and calibration curves derived from known RNA amounts (16).
Hypoxia experimental protocol.
On the morning after isolation, cardiac myocytes were incubated for 2 h in normoxic experimental medium consisting of serum-free, glucose-free MEM with HBSS that did not contain BDM. Cells were subsequently treated with pharmacological agonists and antagonists under normoxic conditions as indicated. For studies requiring inhibition of Gi-mediated signaling, cells were incubated with pertussis toxin at a final concentration of 100 ng/ml for 16 h before experiments (22). After treatment, myocytes were rinsed and incubated in fresh normoxic or hypoxic medium. Normoxic experimental medium was equilibrated overnight in water-jacketed incubators (Forma Scientific, Marietta, OH) under a humidified atmosphere of 1% CO2 and air. Hypoxic medium was preequilibrated in Bactron I anaerobic chambers (Sheldon Manufacturing, Cornelius, OR) under a humidified atmosphere of 1% CO2 and 99% N2. Hypoxic treatment groups were placed into the anaerobic chamber for 5 h at 37°C. Normoxic groups were placed into a water-jacketed incubator at 37°C during the same period.
Measurement of cell viability.
Cardiac myocyte viability was measured by staining of cells in tissue culture dishes for 10 min at room temperature with Trypan blue solution (Sigma Chemical, St. Louis, MO) diluted to a final concentration of 0.04% (wt/vol). Myocytes were visualized at ×100 magnification by bright-field microscopy. The numbers of viable (unstained) and nonviable (blue stained) cardiac myocytes in 10 random microscopic fields were recorded, with at least 300 cells counted for each dish. Percent survival was defined as the number of unstained myocytes counted for each hypoxic treatment dish divided by the number of unstained myocytes counted for each corresponding normoxic control dish, a calculation that accounted for the detachment and loss of nonviable cells during the hypoxia experimental protocols. In preliminary studies, we demonstrated that measurements of cardiac myocyte survival derived with the Trypan blue exclusion assay correlated with other cell viability measurements published by our laboratory (17, 30, 31).
Western blot analysis.
Lysates prepared from cultured cardiac myocytes and HTC4 rat hepatoma cells retrovirally transduced to express high levels of human S1P GPCRs were subjected to SDS-PAGE and transferred to nitrocellulose membranes as described (17, 26). Proteins of interest were detected with selective primary antibodies (see Materials), appropriate secondary antibodies conjugated with horseradish peroxidase, and enhanced chemiluminescence reagents (Amersham, Piscataway, NJ). Reactivity was quantitated by densitometry.
Statistical analysis.
All results are reported as means ± SE. Comparisons between groups were made by one-way analysis of variance (ANOVA). Post hoc analysis was performed using the Student-Newman-Keuls test. P < 0.05 was considered significant.
S1P1 mRNA and protein are abundantly expressed by mouse ventricular myocytes.
We performed quantitative real-time PCR assays on total RNA extracted from primary cultures of mouse ventricular myocytes and fibroblasts to measure relative expression of lysophospholipid receptors between these two cell types. As shown in Fig. 1A, S1P1 mRNA was the most abundant species, with a 10-fold greater expression in myocytes compared with fibroblasts isolated from the same heart. S1P3 mRNA was the next most abundant species, with myocyte expression approximately one-half that observed for S1P1 mRNA. Interestingly, S1P2 mRNA and type 1 lysophosphatidic acid receptor (LPA1) mRNA were more abundant in fibroblasts vs. myocytes. Other lysophospholipid GPCR mRNAs were minimally expressed.
In Western blot analyses of lysates prepared from myocytes and ventricular tissue, antibodies specific for S1P1 protein detected a single band at the predicted molecular mass of 43 kDa (Fig. 1B). Western blot analyses of lysates from HTC4 rat hepatoma cells retrovirally transduced to express a high level of human S1P1 also generated an immunoreactive band at the same molecular mass. The commercial antibody did not react with lysates of HTC4 cells expressing human S1P2 or S1P3 receptors (Fig. 1B).
S1P and S1P1 monoclonal antibody enhance heart myocyte viability during hypoxia.
In preliminary work, we adapted the adult mouse cardiac myocyte culture protocol that was originally described by Zhou et al. (72) for our investigation of severe hypoxia. As shown in Fig. 2A, this modified protocol consistently yielded >90% cardiac myocytes at 50 cells/mm2. Approximately 80% of ventricular myocytes were rod shaped at pH 7.2 for 48 h. Cell viability quantitated with Trypan blue exclusion assays correlated closely with viability measurements previously published by our laboratory (17, 30, 31, 56).
As shown in Fig. 2B, incubation in hypoxic experimental medium for 5 h decreased myocyte viability by 40% compared with normoxic controls. In contrast, pretreatment with S1P (100 nmol/l) preserved cell viability after severe hypoxia. Pretreatment with S1P1 monoclonal antibody mimicked cytoprotection stimulated by S1P administration. Effects of simultaneous treatment with S1P and S1P1 antibody were no different from the effects of either agent given alone (data not shown). Wortmannin, an inhibitor of PI3K activity (3), did not alter cell viability during hypoxia (Fig. 2B). However, PI3K inhibition consistently blocked cytoprotection induced by S1P and S1P1 monoclonal antibody administration.
Additional experimental evidence further supported the importance of S1P1 receptor activation for enhancement of mouse ventricular myocyte viability during hypoxia. For the studies summarized in Fig. 2C, we used the S1P analog VPC23019 at 100 nmol/l as a competitive antagonist of S1P1 receptors. Davis et al. (11) demonstrated that this concentration of VPC23019 had no significant effect on S1P3 receptor activation with a broken cell assay that measured S1P-induced binding of γ-35S-GTP to membranes of HEK293T cells transfected with S1P3 receptor, Gi2α, Gβ1, and Gγ2 plasmid DNA. They also determined that this concentration of VPC23019 did not disrupt specific binding of radiolabeled S1P to S1P3 receptors in membranes from the same cell transfectants.
We used the immunomodulator FTY720 as an activator of S1P GPCRs that does not differentiate among four S1P receptor subtypes (5). FTY720 is phosphorylated by sphingosine kinase, and the resultant phosphate ester (FTY720-P) is an agonist of nanomolar potency for S1P1, S1P3, S1P4, and S1P5 receptors. We used SEW2871 as a selective agonist for S1P1 receptors, as it is shown to recapitulate the actions of S1P on this receptor subtype in all signaling pathways examined (27). SEW2871 does not activate S1P2, S1P3, S1P4, or S1P5 receptors at micromolar concentrations (53).
As indicated in Fig. 2C, incubation with hypoxic medium for 5 h reduced ventricular myocyte viability by 45% compared with normoxic controls. In contrast, pretreatment with either S1P or FTY720 (1 nmol/l) under normoxic conditions preserved viability during subsequent hypoxia. Selective inhibition of S1P1 receptors by VPC23019 blocked the cytoprotective effects of S1P and FTY720. As predicted, treatment with S1P1 receptor agonist SEW2871 (1 μmol/l) preserved cardiac myocyte viability during hypoxic stress. Importantly, S1P1 receptor inhibition abolished cytoprotection triggered by SEW2871.
S1P and S1P1 monoclonal antibody increase Akt activation in ventricular myocytes.
Our findings of 1) abundant expression of S1P1 in cardiac myocytes and 2) inhibition of S1P effects on viability during hypoxia by wortmannin led us to test the hypothesis that S1P stimulates cardioprotective signaling involving S1P1, Gi complexes, PI3K, and Akt. As shown in Fig. 3, A and B, treatment of myocytes with S1P or S1P1 antibody for 20 min doubled phosphorylation of Akt at serine-473. In parallel studies, we observed that S1P and S1P1 antibody also doubled Akt phosphorylation at threonine-308 (data not shown).
As indicated in Fig. 3C, S1P1 receptor inhibition prevented phosphorylation of Akt at serine-473 in response to either S1P or S1P1 receptor monoclonal antibody stimulation. Inhibition of Gi-mediated signaling by an overnight incubation of myocytes with pertussis toxin abolished Akt activation caused by S1P or S1P1 receptor antibody (Fig. 3, A and B). Decreased PI3K function following administration of the competitive inhibitor LY294002 (20 μmol/l) or the irreversible inhibitor wortmannin (100 nmol/l) also blocked Akt activation.
We tested the hypothesis that cardioprotective signaling persists throughout hypoxia by harvesting myocytes for Western blot analysis after 60-min normoxic incubations with either S1P or S1P1 antibody followed by 5-h incubations under hypoxic conditions. As shown in Fig. 4, A and B, hypoxia alone caused a robust increase in Akt phosphorylation compared with normoxic controls. S1P or S1P1 antibody treatment stimulated additional Akt phosphorylation. Interestingly, wortmannin prevented Akt activation in response to hypoxia alone and to treatment with S1P or S1P1 monoclonal antibody (Fig. 4, A and B).
S1P inactivates GSK-3β and reduces cytochrome c release from heart mitochondria.
Juhaszova et al. (29) determined that the beneficial effects of Akt activation on myocyte viability during hypoxia-reoxygenation were caused in large part by phosphorylation and inactivation of GSK-3β. In the present study, we determined that S1P or S1P1 antibody treatment increased GSK-3β phosphorylation (Fig. 4C). Conversely, inhibition of PI3K prevented GSK-3β inactivation following S1P or S1P1 antibody administration (Fig. 4C). S1P1 receptor inhibition with VPC23019 also blocked GSK-3β inactivation (not shown).
GSK-3β inactivation has been shown to preserve mitochondrial function under stress conditions by disrupting translocation of BH3 domain-containing proteins, enhancing the outer membrane stabilizing effects of MCL-1, and inhibiting permeability transition pore opening (4, 10, 40, 43, 60, 65). In the present study, the findings of S1P-induced and S1P1 antibody-induced GSK-3β phosphorylation (Fig. 4C) prompted us to test the hypothesis that S1P1 receptor signaling increases heart cell survival during hypoxia at least in part by preserving mitochondrial membrane integrity. As indicated in Fig. 4D, we measured release of cytochrome c into myocyte cytosolic fractions as one marker of mitochondrial injury. S1P or S1P1 antibody pretreatment substantially reduced cytochrome c release during subsequent hypoxia, a cytoprotective action that was abolished by wortmannin.
The present study generated three principal findings that advance understanding of S1P actions on cardiac myocytes subjected to hypoxic stress. First, S1P1 receptors are abundantly expressed by adult mouse ventricular myocytes. Second, S1P is protective during hypoxia through mechanisms that require S1P1 receptor activation. Finally, PI3K is a key mediator of S1P-S1P1 receptor axis enhancement of myocyte viability, possibly via modulation of Akt activity, GSK-3β activity, and mitochondrial membrane integrity.
The existence of S1P1 receptors on cardiac myocytes has been controversial. Using subtype-selective antibodies against S1P1 and S1P3 receptors for immunofluorescence staining, Forrest et al. (13) determined that S1P1 protein was undetectable on myocytes in adult rat and mouse heart sections. S1P1 antibody stained vascular endothelial cells, identified by double labeling with a platelet-endothelial cell adhesion molecule antibody. In contrast, S1P3 receptor antibody stained cardiac myocytes without labeling vascular endothelial cells (13). Those investigators proposed that S1P1 receptor activity on endothelial cells determines S1P effects on blood pressure regulation, whereas S1P3 receptor activity on cardiac myocytes might be responsible for S1P effects on heart rate.
Other investigations of S1P1 receptor expression in cardiovascular tissue generated conflicting data. For example, Robert et al. (50) used polyclonal antibodies against an S1P1 receptor domain displaying high homology across different mammalian species to establish that the receptor subtype was present in neonatal rat heart homogenates and membranes prepared from cultured neonatal cardiac myocytes. In subsequent studies, Mazurais et al. (41) used the same antibodies to demonstrate that S1P1 receptors were localized on human ventricular myocytes in addition to coronary artery endothelial cells. Concurrent experiments based on Northern blot, in situ hybridization, and Western blot analyses confirmed immunohistochemical localization of human S1P1 receptors (41).
Findings reported by Nakajima et al. (44) strongly support S1P1 receptor localization and function on neonatal and adult cardiac myocytes. Using neonatal cells, investigators identified an S1P1 receptor isoform by RT-PCR with 100% homology to rat brain sequences. Quantitative RT-PCR analysis demonstrated sevenfold higher expression of S1P1 receptor mRNA in myocytes vs. fibroblasts from the same neonatal rat heart (44). Antibodies against the extracellular domain of S1P1 receptors labeled the plasma membranes of neonatal cardiac myocytes and sarcolemma of adult rat cardiac papillary muscles. Importantly, transfection of neonatal myocytes with antisense vector reduced both S1P1 receptor expression and S1P modulation of cellular calcium transients (44).
Zhang et al. (71) cloned a mouse homolog of the S1P1 receptor gene and observed abundant expression of S1P1 receptor mRNA in adult C57BL/6J hearts by Northern blot analysis. Liu et al. (38) disrupted the S1P1 gene by inserting a LacZ-neo cassette into the open reading frame. Although S1P1 receptor null mice died in utero from bleeding, β-galactosidase activity was prominent in embryonic cardiac myocytes and endothelial cells (38). Thus results from the present study and a growing consensus in the published literature favor S1P1 receptor expression by cardiac myocytes throughout development.
S1P is widely recognized as a modulator of T cell and B cell trafficking between the systemic circulation and lymphoid organs (15, 16, 51, 53). Therefore, the effects of S1P treatment on immune responses can be difficult to distinguish from more direct actions on ventricular myocytes during in vivo cardiac ischemia-reperfusion. Similarly, effects of S1P on myocardial contractile function and viability in ex vivo perfusion protocols result from the combined activation of S1P receptor subtypes expressed by mixed populations of heart cells. Although we recognize the limitations of all in vitro experimental systems, our group established cardiac myocyte culture models as powerful and complementary tools for elucidation of cardioprotective signaling mechanisms that are operative during hypoxia (17, 30, 31, 56). Independent groups validated the utility of adult mouse cardiac myocyte cultures for studies of intracellular signaling and genetic physiology (19, 21, 72).
After interruptions in coronary blood flow, myocardial injury is caused in large part by the oxidative stress of reperfusion. However, severe ischemia alone has been shown to produce substantial tissue damage. For example, Borutaite et al. (4) demonstrated that global ischemia without reperfusion stimulated cytochrome c release from mitochondria, respiratory chain complex dysfunction, and ventricular myocyte apoptosis in isolated rat hearts. Similarly, Lesnefsky et al. (35) found that reactive oxygen species generated by respiratory chain complex III in ischemic rabbit hearts depleted mitochondrial cardiolipin, triggering cytochrome crelease and cytochrome oxidase dysfunction. Our investigation measured cardiac myocyte viability during hypoxia and highlights interactions between the endogenous cytoprotective molecule S1P and one major component of ischemia.
As depicted schematically in Fig. 5, our findings strongly support S1P-S1P1 receptor axis enhancement of adult mouse cardiac myocyte survival during hypoxia. We showed that the S1P1 receptor antagonist VPC23019 blocked protection generated by pretreatment with S1P itself or the synthetic compound FTY720 (Fig. 2C), whereas the S1P1 receptor-activating antibody 4B5.2 and the S1P1 receptor agonist SEW2871 conferred equivalent resistance to hypoxia-induced myocyte death (Fig. 2, B and C). Although these data are compelling, it is important to consider that different S1P receptor subtypes may mediate protection against other components of tissue stress triggered by ischemia-reperfusion. Theilmeier et al. (57) demonstrated that S1P pretreatment decreased infarction size in mice subjected to 30-min coronary artery ligation followed by 24-h reperfusion. Those investigators found that cardioprotection could be mimicked by induction of leukopenia with hydroxyurea and abolished by targeted disruption of the S1P3 receptor gene (57). Means et al. (42) showed that simultaneous loss of S1P2 and S1P3 receptor signaling in S1P2,3 double-knockout hearts increased infarction size and decreased Akt phosphorylation compared with wild-type hearts. Those investigators postulated that S1P generated during in vivo ischemia-reperfusion stimulated cardioprotection through S1P3 receptor-mediated activation of endothelial nitric oxide synthase in endothelial cells or through S1P2- and S1P3 receptor-mediated activation of Akt in cardiac myocytes (42).
We demonstrated that S1P-S1P1 receptor axis enhancement of ventricular myocyte viability was accompanied by increased Akt phosphorylation, whereas inhibition of PI3K with wortmannin blocked inducible cytoprotection and Akt activation (Figs. 2B and 3B). Akt is widely recognized as a molecular target of PI3K signaling and a key mediator of resistance to apoptotic and necrotic cell death (10, 28, 29, 46, 60). Interestingly, hypoxia alone significantly increased Akt phosphorylation in ventricular myocytes compared with normoxic controls (Fig. 4, A and B). Mechanisms responsible for hypoxia-induced Akt activation in tumor cells and nonmalignant cells are the focus of intense investigation. Pelicano et al. (48) showed that severe hypoxia caused NADH accumulation in human colon cancer cells and in human malignant glioma cells, which led to inactivation of the redox-sensitive phosphatase PTEN and increased Akt phosphorylation at serine-473.
Li et al. (36) observed that hypoxia triggered phosphorylation and nuclear translocation of mammalian target of rapamycin (mTOR) in rat aortic endothelial cells and in mouse embryonic fibroblasts followed by mTOR-dependent Akt phosphorylation at serine-473, validating work by other groups that identified mTOR as a cellular oxygen sensor (9, 54).
In our experiments, hypoxia-induced Akt activation did not increase myocyte viability during stress. However, S1P1 receptor activation increased Akt phosphorylation above values measured after hypoxia alone (Fig. 4, A and B), a response that correlated with increased cell survival (Fig. 2B). These results suggest that signaling through the S1P-S1P1 receptor axis augmented Akt activity above the threshold necessary for protection against hypoxia-induced cell death. An alternative interpretation is that S1P1 receptor activation of PI3K signaling stimulated cardioprotection through molecular targets other than Akt, such as protein kinase C and p70S6-kinase (17, 25, 26, 28, 46, 49, 58). Future studies can test the relative importance of downstream effector molecules using pharmacological and genetic approaches beyond the scope of the present investigation.
Ion channels constitute an important category of proteins regulated by S1P that may contribute to resistance against hypoxic injury. In studies focused on hypoxia and cell electrophysiology, Henry et al. (20) enveloped isolated adult rat ventricular myocytes in mineral oil droplets saturated with nitrogen gas. The investigators found that simulated ischemia produced both inhibition and activation of distinct inward rectifier K+ currents. Diaz et al. (12) later determined that isolated adult rabbit ventricular myocytes could be preconditioned, thereby enhancing cell viability during simulated ischemia-reperfusion. The investigators showed that pharmacological inhibition of inward rectifier K+ current (IK1) and knockdown of IK1 channel subunits Kir2.1 and Kir2.2 were equally effective in blocking preconditioning-induced cardioprotection. Ochi et al. (45) demonstrated that S1P activated the G protein-gated inward rectifier K+ current IK(S-1-P) in guinea pig atrial myocytes carried by the same channel proteins as those activated by acetylcholine.
Importantly, MacDonnell et al. (39) found that S1P had no significant effect on IK1 in adult rat ventricular myocytes. Their data suggest that IK(S-1-P) activation is unlikely to be a major component of S1P-mediated cardioprotection in mouse ventricular myocytes. However, S1P treatment was shown to reduce inward sodium current (INa) and to increase stimulus currents required to elicit action potentials (39). Intracellular Na+ accumulation during ischemia facilitates cardiac injury by causing cytosolic and mitochondrial Ca2+ overload, whereas agents that block sarcolemmal Na+ entry are cardioprotective (64, 67). We look forward to experiments designed to test the hypothesis that S1P enhances myocyte viability during hypoxia through INa inhibition.
In summary, we used a mouse cardiac myocyte culture model to study mechanisms responsible for protection against hypoxia-induced cell death. We determined that S1P1 receptors were abundantly expressed by adult ventricular myocytes and necessary for S1P-mediated cardioprotection. S1P-S1P1 receptor axis enhancement of cell viability during hypoxia required PI3K activity and was associated with Akt activation, GSK-3β inactivation, and reduced cytochrome c release from mitochondria. Our data advance understanding of S1P1 receptors as mediators of resistance to hypoxic injury in cardiac myocytes and may have broader implications for the prevention of ischemic heart disease.
This work was funded by grant no. R01-AA-11135 from the National Institute on Alcohol Abuse and Alcoholism; a research project award from the Alcoholic Beverage Medical Research Foundation; program project grant no. P01-HL-068738 from the National Heart, Lung, and Blood Institute; and the Research Service of the Department of Veterans Affairs.
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
- Copyright © 2007 by the American Physiological Society


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Archive for February, 2009
Today's mermaid
Big Daddy: No capes!
We're doing the Big Daddy Regatta two weeks from now. Like the Great Pumpkin race, it is a themed event, and this year the theme is superhero costumes. My crew Edward is thinking of wearing a costume. I'm trying to warn him off capes, for reasons amply illustrated below:
Today's (real live) mermaid followup
Nadya Vessey, in her element.
Way back in the early day's of Never Sea Land, I posted a news story about double amputee Nadya Vessey's quest to swim with artificial mermaid tail. That post is one of the most popular at NSL, accounting for over a third of all traffic and generating 823 comments to date. Now we are glad to see that her dream is a reality!
Effects shop fulfills amputee's mermaid dream
Good: double amputee gets prosthetic legs so she can walk. Better: double amputee gets realistic-looking mermaid tail so she can swim. Awesome: it's developed and built by Weta, the special-effects company that did work for the "Lord of the Rings" movies, as well as "King Kong" and "The Chronicles of Narnia" series.
Nadya Vessey's legs were amputated below the knee when she was a child due to illness. At one point, reports Stuff, a child asked her what happened to her legs and she told him she was a mermaid. The idea stuck with her, so she wrote to Weta Workshop in Wellington, New Zealand, two years ago asking for a mermaid tail. To her surprise, they said they'd do it.
Now she has a fully functional mermaid tail with an attached suit, making her look practically just like a real mermaid (if, you know, mermaids were real).
Links: full story, video on YouTube
Thanks to Marina for the find.
Today's mermaid
Olson 34 pic of the day
photo © www.norcalsailing.com
Fellow Olson 34 owner Brian Boschma (Red Sky) graciously invited me to crew for the Corinthian Midwinters. I had a great time and made some new friends. This shot is from Saturday; Sunday's race was in the pouring rain. Good times! Read all about it at norcalsailing.com.
Creating a mermaid
How to.
Today's mermaid
David Crosby's Mayan
For only $1M you can own David Crosby's 1947 59′ Alden centerboard schooner Mayan, currently lying Santa Barbara. In a recent interview, the current owner said "I started sailing when I was 11, and so I've been sailing 54 years. … I wrote many songs on this boat. Down in that main cabin there, I wrote 'Wooden Ships,' I wrote 'Page 43.' I wrote 'Carry Me.' "
As beautiful below as above, and quick on the water, she would be a delight to own and sail, although one knowledgeable source estimates she would take $4000/mo to keep in prime condition.
Thanks to S/A for the find.
I don't like Mondays
Marine critters that keep us safe (?)
Some of the nation's most sophisticated military submarines are based in the chilly waters of Puget Sound, an inlet of islands, peninsulas and harbors that is worryingly vulnerable to terrorist attack from a furtive diver or brazen suicide swimmer.
But the Navy's plan to use a squadron of highly trained dolphins and sea lions to patrol and protect the submarine fleet is running into opposition from those who fear the glacier-fed waters of the sound are too frigid for warm-water dolphins.
Full story, via Navagear
Sam Davies Roxy Redux
Nice recap video for those undergoing VG withdrawal.
Mini Transat 6.50 USA670 — the deal of a lifetime
Mini Transat Boat (USA-670) MAY 2007
Big discount – great opportunity for any of you recession-proof Anarchists. The boat is in good condition and is quite well equipped. Brand new bottom job finished in October '08 and only in the water for 3 months. Just completed the Lauderdale to Key West Race with decent results given the conditions. Please see website for complete equipment list, info about the boat and photos. $46,000
This is an incredble deal on a turn-key, completely tricked out Zero. I often think (while working on the head in my boat) that I might have better off with this very boat.
End of an era
It is with profound sadness that NSL reports on the departure of part-owner and master mixologist Martin Cate from the best bar in the universe, Alameda's Forbidden Island. Watch the video above, and remember if you can. If you missed the glory that was FI under Martin's management, then know it was truly a Golden Age.
Vendée globe 2008/2009 : Arrivée de Samantha Davies Skipper Roxy
Just in time for Valentine's Day…
Samantha Davies, GBR, (Roxy) crossed the finishing line at 00hrs 41mins 01 secs as the third competitor to complete this epic sixth edition of the Vendée Globe solo non stop around the world race and return to Les Sables d'Olonne.
Ironically Davies will have to wait two days and two hours (50 hours) to see whether she hang on to third place in this sixth Vendée Globe as the final result will depend on Marc Guillemot's finishing time.
Guillemot was given a time compensation for standing by the badly injured skipper Yann Elies who was rescued from his Open 60 Generali on 20th December.
95 days 4 hours 39 mins 01 sec WITH redress: Roxy crossed the finish in the midst of a dark February night, in the small hours of St Valentine's day, having sailed 27 470 actual miles on the water at an average speed of 12.02 knots.
Davies is the first British competitor to complete this edition of the race, which began off Les Sables d'Olonne back on 9th November 2008, and leads home Brian Thompson, GBR (Bahrain Team Pindar) and Dee Caffari, GBR, (Aviva) who are on course to finish in fifth and sixth places respectively. They are likely to finish late Sunday or Monday.
If she is not displaced from third place (if Marc Guillemot does not finish before Monday morning), she will become only the second woman on the podium in the history of the race and the third British sailor after Ellen MacArthur in 2000-2001 and Mike Golding in 2004-2005.
Never set sail on a Friday
'Twas Friday morn when we set sail,
And we had not got far from land,
When the Captain, he spied a lovely mermaid,
With a comb and a glass in her hand.
from The Mermaid, trad.
It's one of the many traditions/superstitions of the sea that it's bad luck to set sail on a Friday. So isn't it doubly so to set sail on a day like today, Friday the 13th?
For voyage planning, NSL provides a list of all the Friday the 13ths for the next 100 years or so:
13 February 2009
13 March 2009
13 November 2009
13 August 2010
13 May 2011
13 January 2012
13 April 2012
13 July 2012
13 September 2013
Continue reading 'Never set sail on a Friday'


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The Royal Crescent Hotel & Spa
Hotel and restaurant in town.
United Kingdom, Bath
Unique in the world:
"The hotel eludes sophistication and charm and provides the ideal historic city centre retreat."Jonathan Stapleton, Maître de Maison, presents his property:
Located in the centre of arguably the world's finest crescent in the World Heritage site of Bath, the Royal Crescent Hotel & Spa is a destination in its own right. Combining period architecture and luxury furnishings alongside modern day technologies, the hotel eludes sophistication and charm and provides the ideal historic city centre retreat. Behind the Georgian façade lie peaceful gardens with rose beds and lavender-lined paths, tranquillity spa and elegant, award-winning dining in The Dower House Restaurant offering diners a modern take on traditional British cuisine. A world away from the hustle and bustle of daily life, visitors from around the globe are invited to discover all the delights that the Royal Crescent Hotel & Spa has to offer.
- Car Park
- Garage
- Valet
- Children welcome
- Terrace
- Lift / Elevator
- Indoor
- Canoeing/kayaking
- Golf 9 holes
- Golf
Are you in possession of a CRÉATION Gift Certificate or Box?Call:+44 (0)1225 82 33 33
The Royal Crescent Hotel & Spa
16 Royal Crescent
BA1 2LS Bath
United Kingdom
Email: firstname.lastname@example.com
of a Creation ?
75002 Paris, France
+33 (0)18.104.22.168.00
Ouverture les lundis 4, 11 & 18 décembre
Ouverture les dimanches 10, 17 & 24 décembre
Nocturne jusqu'à 20h les jeudis 14 & 21 décembre


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Korean cooking forum topics
Home › Forums › Recipe requests › Yang Nyum Tong Dak Recipe?
This topic contains 5 replies, has 3 voices, and was last updated by Maangchi 5 years, 7 months ago.
Firstly, fantastic site you have!
and secondly, i've been on the net for the last few hours looking for a recipe for Yang nyum tong dak, especially the sauce. I found a few but judging from the ingredients they don't seem right.
Any help would be appreciated! Thanks!
Yang nyum tong dak is on my list of recipe videos to make. I will post it later!
Thanks alot!
Please, please, please make Yang nyum tong dak video! It is the best fried chicken ever!
haha, yangnyum tongdak, sure! Thank you!
Yangnyeom tongdak recipe! https://www.maangchi.com/recipe/yangnyeom-tongdak
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Mead made speedily
Lost Cause Meadery noteworthy for reduced fermentation period
Ian Anderson 4 p.m., Nov. 19
Oh, cars, both a blessing and a curse. Joyous wonders to behold. When in good running condition, all is right in our world. Sheer nirvana.
Like our spouses or families we can take cars for granted, while expecting nothing but perfection and ultimate performance back. Yet, it's somehow acceptable for us to forget about washes, tune-ups, oil changes, brakes and tire rotations. If our cars disappoint us, we show our faithful vehicles instant hostility. The car is now somehow to blame for everything going wrong in our lives. Not unlike how we tend to find fault with our loved ones, when stubbing a toe, the computer goes down, someone cuts you off on the freeway, or you just had a crappy day at work.
I'm here to tell you about how my car makes me feel. When she is down, I miss her. It doesn't matter that I'm still driving a car. I miss MY CAR. I can read her. The quirky little sounds she makes. The feel of the steering, the brakes, or her acceleration. The way the engine purrs, or coughs like a cat with a hair ball, depending on the day or how well she's been maintained.
Sometimes my car is a teacher. Whether I need to slow down to enjoy life, or that life in general is just coming at me too fast, somehow she knows it. I'll get a flat tire, need gas, or deciding I need to stay put, she just stops; forcing me to slow down, whether I choose to or not. To be honest it works. I may get upset initially and then decide …what's the point? Nothing will change if I get upset.
Then a funny thing begins to happen…..I'll live in the moment. I'll sing, write, or take a moment to call a friend who may be having, "One of those days too."
There has also been more than one occasion where my car may have saved my life, or kept me from being stranded in the middle of nowhere.
Two weeks ago, I was headed to work and was running twenty minutes ahead of schedule. The check engine light came on and I checked the codes and reset them with a portable diagnostic computer. The code was nothing urgent, just a loose gas cap, so I headed to work. It only took about five minutes to take care of the situation. Thankfully I was delayed. When I entered the 15 Fwy, south, off Via Rancho Pkwy, in Escondido, traffic was at a standstill. I called work to alert them of the situation, there had been a five car accident. One car was facing the wrong way (north), two went head on into the center divider and resembled crushed beer cans. The last two cars were blocking the number one and two lanes.
I called 511 to find out the driving times and possible secondary incidents, to see just how late I might be. The obnoxious voice on 511 alerted me as to when the accident occurred. If I had not been delayed those few minutes to stop and check the engine code, I could have been in that same accident, or in the immediate aftermath. See how my car protects me?
In 1991, we bought a used Volvo 240DL. A beautiful blue color, with low mileage. The car ran like a champ. I was two months pregnant and we were going to drive to Los Angeles to see my mother-in-law. Those of you who remember will know, in 1991 the 15 Fwy, North from Escondido until you got to Colton, was desolate. You couldn't see a gas station or structure of any kind from the road. This was pre-cell phone and there weren't any call boxes yet.
If you broke down you'd pretty much be stranded in the middle of no where. We washed the car and then stopped at a 7-11 for gas. The Volvo, (Old Blue, as we lovingly referred to her), had an engine that ran so smooth, you couldn't hear it when it idled. I paid for a full tank of gas and two Slurpees, jumped in the car and she wouldn't start. The timing belt broke.
My husband is a glass half empty kind of guy and was not happy in the least. I myself am a glass half full kind of gal and I began to explain how blessed we were. Explaining to my frustrated spouse, that at least we were only about two miles from home, instead of being stranded in the middle of God's left Egypt somewhere. Being pregnant, I was grateful we were still close to home, safe and the belt hadn't broken, as we were driving 65 miles an hour with a car behind us.
We had Old Blue for 10 years. She had her quirks, but ran strong, even when we donated her to charity. I like to think she's still out there somewhere protecting a teen age driver.
Blue was replaced by a 2001 Dodge Grand Caravan. We got her when she was new and only had 54 miles on the odometer. This car has been great. We've taken her to Yosemite and the Grand Canyon on vacation, as well as Yellowstone National Park. She has hauled around a plethora of Girl Scouts, band equipment, FFA members, band members, girls varsity basketball team, as well as, the varsity shot put and discus throwers for Escondido High and my dogs.
She has been my think tank, a place I go at lunch to read or write. When I've traveled solo, there are times when she is my motel on wheels. Popping out the seats to create a sleeping area, taking cat naps at rest areas, in an effort to stay refreshed for the long drive ahead.
Another time my car saved me from being stranded was earlier this year. My daughter had come home from college for Christmas break and I was going to take her back to Flagstaff, Arizona on Saturday January 9th. Her friends called a few days before and asked her to carpool back with them. She agreed. She decided I didn't need the physical stress on my body, the car and it would save a lot of gas money. The day before we would have left, the engine went out while I was driving to work. If that had not happened, we might have broken down in the middle of the desert with no cell phone service. It was a mixed bag of blessings. We were also in the process of moving, and found ourselves without my trusty steed.
Three months later she had an engine transplant, and an a/c-ectomy. All was right in my world again. I hadn't had an a/c in three years and was in heaven.
Just before Mother's day, my check engine light came on. I would be driving to Flagstaff in two days to get my daughter and all her belongings from school and went to my mechanic to have it checked out. When I arrived, the check engine light was just a loose gas cap, but my radiator was flowing like the mighty Mississippi. They ordered a radiator and my car was delivered to me the next day.
See how my car was looking out for me? Or is it possible divine intervention is working through her? Either way I feel blessed.
It's interesting how people love their cars. I know i do... But it always makes me feel rather materialistic and shallow to express such strong emotions for metal... I should just change my wording.
Driving a car, especially, my car, after awhile always feels so gooood. Like putting on a pair of old, grungy, pajamas after they have just come out of the dryer.
Amen to that. I totally miss my car when she's down. Just like having a spouse or close relationship, you know all the little quirks that are uniquely theirs. If you read my Automotive Karma, you'll know I was without her for awhile. boo hiss. thanks for the comments


text: Am Sonntag, 18. Januar 2009 17:22 schrieb Sebastian Sylvan: > Is there some sort of bundle that you can use to install cabal-install > easily? Because it looks to me like I'd have to spend the better part of an > evening manually downloading and installing the gazillion of dependencies > it has, which is far too much work when I just wanted to spend ten minutes > playing with some package... > Wait, 'gazillion of dependencies'? If you have the extralibs bundle built, there are only three dependencies to take care of - a recent Cabal library - HTTP - zlib Of course, downloading and building them manually may take half an hour or so, but it's time well spent, cabal-install makes playing around for ten minutes with some other package so much easier. And of course, as has already been mentioned, there's now a bootstrap.sh included which takes care of the above dependencies for you.


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What is Project Unity?
Created in the Spring of 2007, Project Unity is a civic and social forum for Skidmore's students of color, students of various sexual orientations and gender identities and expressions, international students, and their allies. The goal of the program is to promote the creation of an inter-group alliance and, in turn, help form a clear, strong and unified voice for all "minority" students at Skidmore College. Project Unity also aims to address students' snes of campus-belonging by establishing a supportive "home-base" at the College. For more informaion, please email firstname.lastname@example.com.
Project Unity meets every Wednesday at 8:00pm in the Intercultural Center.


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The recent competitive successes of a bilateral, transtibial amputee sprint runner who races with modern running prostheses has triggered an international controversy regarding the relative function provided by his artificial limbs. Here, we conducted three tests of functional similarity between this amputee sprinter and competitive male runners with intact limbs: the metabolic cost of running, sprinting endurance, and running mechanics. Metabolic and mechanical data, respectively, were acquired via indirect calorimetry and ground reaction force measurements during constant-speed, level treadmill running. First, we found that the mean gross metabolic cost of transport of our amputee sprint subject (174.9 ml O2·kg−1·km−1; speeds: 2.5–4.1 m/s) was only 3.8% lower than mean values for intact-limb elite distance runners and 6.7% lower than for subelite distance runners but 17% lower than for intact-limb 400-m specialists [210.6 (SD 13.2) ml O2·kg−1·km−1]. Second, the speeds that our amputee sprinter maintained for six all-out, constant-speed trials to failure (speeds: 6.6–10.8 m/s; durations: 2–90 s) were within 2.2 (SD 0.6)% of those predicted for intact-limb sprinters. Third, at sprinting speeds of 8.0, 9.0, and 10.0 m/s, our amputee subject had longer foot-ground contact times [+14.7 (SD 4.2)%], shorter aerial [−26.4 (SD 9.9)%] and swing times [−15.2 (SD 6.9)%], and lower stance-averaged vertical forces [−19.3 (SD 3.1)%] than intact-limb sprinters [top speeds = 10.8 vs. 10.8 (SD 0.6) m/s]. We conclude that running on modern, lower-limb sprinting prostheses appears to be physiologically similar but mechanically different from running with intact limbs.
- prosthetics
- running economy
- sprinting
- running
- fatigue
- locomotion
- biomechanics
- Copyright © 2009 the American Physiological Society


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New York Dermatologist Dr. Steven Victor Offers the Dermal Filler Xeomin®
Dr. Victor explains the many advantages of the anti-aging treatment, Xeomin®
December 23, 2013 (Newswire.com) - Over time, many people will experience the noticeable signs of aging, including wrinkles, and frown lines. When store-bought wrinkle or anti-aging creams no longer work, it may be time to consider an injectable dermal filler to rejuvenate skin, and restore a more youthful appearance. FDA-approved Xeomin® (sometimes known as "the X-Factor") is one treatment which can help restore a patient's appearance.
Dr. Steven Victor, of Victor Dermatology and Rejuvenation, says that Xeomin® is quite effective for temporarily improving the appearance of visible facial lines, folds, and wrinkles on the forehead, under the eyes, and on the neck. He explains that Xeomin®, which is still fairly new in the United States, contains botulinum toxin A, which is the same active ingredient found in BOTOX® Cosmetic.
According to Dr. Victor, Xeomin® essentially performs many of the same functions as BOTOX®. It is injected into a targeted area of muscle, and helps smooth out wrinkles, and frown lines. It also reduces activities in the facial muscles which contribute to the appearance of facial wrinkles. However, Dr. Victor adds, that Xeomin® is a "purer" form of BOTOX®, since it contains none of the additives found in BOTOX®. Xeomin® is also extremely helpful in alleviating severe neck pains.
Dr. Victor says that Xeomin® should only be injected by a trained doctor familiar with the product. He adds that injections can be done in more than one area at a time. The injection will take only a few minutes, although it may take up to a week for the results to become noticeable. Like with similar treatments, the effects of a Xeomin® injection are temporary, lasting about 3 to 6 months. Dr. Victor strongly advises warns patients against receiving injections of Xeomin® from more than one medical professional at a time. Some possible side-effects associated with Xeomin® include redness, swelling, or itching, though these side-effects are temporary, Dr. Victor adds.
Dr. Victor says that, while Xeomin® is a safe, non-invasive way of treating wrinkles and frown lines, the treatment is not for everyone. Patients who have severe allergies, or who have previously had an allergic reaction to Dysport® or BOTOX®, should not be injected with Xeomin®. Those with serious health issues, such as heart disease, are also not considered good candidates for the treatment.
Dr. Victor works closely with each of his patients, ensuring that they receive the best care possible, both before and after treatment. If you are interested in learning more about Xeomin®, you may reach Dr. Victor by phone at 212.249.3050, or by visiting http://www.victordermatologyandrejuvenation.com
About Dr. Victor
Dermatologist Dr. Steven Victor is dedicated to the pursuit of pioneering, perfecting and delivering the most effective anti-aging treatments in existence today.
Over the past 30 years his reputation has brought in numerous worldwide celebrities, TV personalities and models who have sought out his rejuvenating treatments.
Upon graduation from New York Medical College, Dr. Victor established his New York City practice, Victor Dermatology and Rejuvenation. Through the practice, Dr. Victor developed a reputation for creating safe, modern and minimally invasive treatments and pioneered both the "lunchtime peel" and mesotherapy. He continues to offer innovative cosmetic and rejuvenation treatments from injectables, lasers and peels to LaserSculpt -a laser assisted type of Liposuction which melts fat via a tiny laser that goes under the skin and also provides tightening and toning, unlike traditional liposuction. Most recently and most notably, Dr. Victor has developed a state-of-the-art laboratory and a patented, proprietary technology for the efficient and reproducible separation of stromal vascular fraction cells (branded IntelliCell™) containing Mesenchymal Stem Cells. The stromal vascular fraction is then used autologously, (donor and recipient are the same) by a physician to restore function by enabling the body to repair, replace, and regenerate damaged, aging or diseased cells, tissue and organs. Dr. Victor offers his patients this therapy to attenuate a multitude of the skin's signs of aging including firming and volume filling.
He has held teaching appointments at New York University, New York Medical College, Beth Israel Medical Center and Lenox Hill Hospital and was the consulting dermatologist to Elizabeth Arden and Clarins. While earning his bachelor's degree, he assisted the Orentreich Foundation for the Advancement of Science, working on Buf-Puf, Clinique and Head & Shoulders.
He is also the co-author of Ageless Beauty, A Dermatologist's Secrets to Looking Younger without Surgery, published in 2003.
Categories: Exercise and Physical Fitness
Tags: cosmetic dermatologist New York , Dermatologist Manhattan


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Edit Article
wikiHow to Deal With a 7 10 Split in Bowling
The 7-10 is the most notorious shot in bowling. Even professional bowlers only achieve the spare 0.7% of the time with this split.[1] Practicing the right technique can make your attempts much more consistent, but remember that there is a great deal of luck even in the best situation. Unless you're having fun practicing trick shots, you may be better off practicing your general technique. After all, every time you score a strike, that's one split you don't have to deal with.
1Decide whether to go for one pin or two. You probably came here to learn how to hit both pins at once, but even pro bowlers have an extremely low chance to achieve this on a 7-10 split. If picking up one point leaves you in a competitive position, just take it rather than risk scoring no points at all. Follow the instructions below to attempt a spare only when you need a "Hail Mary" to get you back in the game.
- Going for one pin gets even better when you are following a strike, since the single ball will count double.
2Position yourself eight boards from the center. Most right-handed amateur bowlers stand at around the 30th board, feet aligned with the leftmost dot and ball aligned with the large dot at board 30. When you have a 7-10 split, move left to board 38, and aim at the 10 pin. If you are a left-handed player, you would instead move eight boards right (to board 22) and aim at the 7 pin.
- This article counts the boards from right to left. Don't get confused if you are used to the left-handed counting system, which counts from left to right.
- If you do not normally stand at board 30, you can move eight boards from your usual starting point instead. However, for this shot, it may be easier to stand where the average person would, on board 38 or 22.
3Aim for the center arrow. Aiming for an arrow is much easier than aiming for a pin. Now that you are eight boards to the side of the center, you should be able to aim through the center arrow in order to hit the opposite pin.
- If you moved eight boards from your usual starting position, instead aim for the arrow you would normally use to hit the center of the pins.
4Bowl hard. Swing your arm in a long pendulum so the ball releases with a great deal of force. Your goal is to impart enough force into the target pin that it bounces off the kickback, then back to the other pin.
5Spin the ball. Spin allows you to hook the ball, curving the path it travels along. You are more likely to score the spare if you can curve the ball into the side of the pin, slamming it against the nearest side wall.
- If you add a significant hook to the ball, you may want to stand even closer to the edge of the lane.
- Instead of hitting the pin against the kickback, some bowlers prefer to strike the pin on the gutter side, sending it onto the equipment at the center of the pit, then at the opposite pin. In this case, you should put an extreme amount of spin on the ball, and aim for the closer pin (7 for lefties, 10 for righties).
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- 7-10 splits usually happen when the ball hits the first pin head on. Practice hitting the pocket to minimize the chance of ending up in this situation.
- Pay attention to how the pins behave throughout the game. Whether from manufacture differences or wear, some pins ricochet with more force than usual. You're more likely to score the spare on 7-10 splits with these pins.


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Monday, 03 January 2011 08:28
HTC 4G model to be announced at CES?
First Verizon LTE handset to be announced
Wednesday, 22 December 2010 09:42
Palm to show off new Pad at CES
To be called the PalmPad product family
Wednesday, 15 December 2010 10:16
Windows 8 to be shown at CES?
Rumor mill in overdrive once again
Wednesday, 15 December 2010 10:07
Microsoft to take on iPad at CES
Will unveil a number of new tablets
Wednesday, 24 November 2010 11:42
Nintendo to exhibit at CES
First return since 1994


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A 2-out hit for the pitcher, and Babe Borne homers to give Atlanta a 2-1 lead.
A 2-out hit for the pitcher, and Babe Borne homers to give Atlanta a 2-1 lead.
"The players make the manager, it's never the other way." - Sparky Anderson
Board Moderators may, at their discretion and judgment, delete and/or edit any messages that violate any of the following guidelines: 1. Explicit references to alleged illegal or unlawful acts. 2. Graphic sexual descriptions. 3. Racial or ethnic slurs. 4. Use of edgy language (including masked profanity). 5. Direct personal attacks, flames, fights, trolling, baiting, name-calling, general nuisance, excessive player criticism or anything along those lines. 6. Posting spam. 7. Each person may have only one user account. It is fine to be critical here - that's what this board is for. But let's not beat a subject or a player to death, please.


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Winning start for Bilbao
Athletic Bilbao began life at the San Mames Barria stadium on the right note with a hard fought 3-2 victory over Celta Vigo.
Last Updated: 16/09/13 11:35pm
Athletic Bilbao began life at the San Mames Barria stadium on the right note by opening the new arena with a hard fought victory over Celta Vigo.
Celta striker Charles Dias opened the scoring in the first half, but his effort was quickly cancelled out by Mikel San Jose. Andoni Iraola put the hosts in front on 61 minutes and Benat Etxebarria looked to have made sure of the victory eight minutes later, although Santi Mina made for an exciting finish by pulling one back for Celta with 12 minutes remaining.
Athletic went out keen to make their mark on this historic occasion and took the initiative, enjoying 60 per cent of the possession over the 90 minutes, while Luis Enrique's side played on the counterattack.
Iraola had two chances to score within the first three minutes, the first a volley which was comfortably saved by Celta goalkeeper Yoel Rodriguez, the second a miscued attempt at the far post following a cross from Markel Susaeta.
Ander Herrera, playing his first match since his move to Manchester United on transfer deadline day fell through, then shaved the far post, as he tried to take full advantage of a slip from Andres Fontas.
Athletic thought they could have had a penalty when a free-kick by Benat struck the arm of Rafinha Alcantara, but the referee deemed it accidental. A minute later, the visitors took the lead thanks to an error from Erik Moran, who misplaced a pass just over the halfway line, and Celta's Rafinha took advantage of Athletic's high defensive line to race through alone, before squaring to Charles. The Brazilian kept a cool head to slot into the bottom corner, giving his side the lead and himself a place in the history books, the first player to score at the stadium.
Athletic reacted well to going behind and were level within four minutes. Benat sent a cross into the danger zone, which San Jose rose to meet but missed, but pounced on a mishit clearance by Hugo Mallo to shoot into the bottom corner.
At the other end Nolito could have given Celta the lead again, but his shot was easy for Iago Herrerin to gather.
The 25-year-old almost got his team in big trouble when he fumbled the ball at the feet of Augusto Fernandez, but the danger was cleared immediately.
The goalkeeper was then punished for his indecision, as he brought down Nolito in the area, and received a booking, while Celta were awarded a penalty. To Herrerin's relief, Charles sent the spot-kick over the bar and bouncing off the wall behind the goal where the final stand of the stadium is being constructed.
Charles had an opportunity to compensate for his miss four minutes before half time, with just Herrerin to beat, but put the ball wide as he tried to lift it over the goalkeeper.
Athletic took the lead just after the hour mark thanks to a superb interchange between Iraola and Iker Muniain. The fullback chipped a pass towards the forward on the edge of the box, Muniain controlled, waited and then returned the ball with a deft back heel into Iraola's path, and the 31-year-old put his shot away into the bottom corner.
Benat, who ran the show from midfield then got on the scoresheet, beating the offside trap to race down the right wing towards goal, turning a Celta defender and then shooting into the opposite corner with his left foot.
Herrerin then had another nightmare, failing to catch a straightforward cross, and substitute Mina gratefully headed in.
However, the home side did not become consumed by nerves towards the end of the game, and comfortably saw out the final 12 minutes.
They could have even scored again, Ibai Gomez missing a glaring chance in the closing stages, trying to bundle the ball home from three yards out following a knock down from Oscar de Marcos, and Fontas cleared it off the line.
Athletic moved up to fifth place in the Primera Division table thanks to the win, which was their third victory of the season, while Celta suffered their first defeat of the campaign and slipped down to eighth.


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New tools to help Buyers through challenging times
Happy fall, everyone. Hope you all had a fabulous summer, once it finally showed up. Market conditions over the last few months have changed dramatically over the beginning of the year. We are still seeing multiple over full price bids on many homes, but only those that fall into one of two categories – (a) properties that are absolutely cream-puff homes, in great condition, properly staged and priced right, and (b) properties of normal desirability that are properly priced reflective of the current market conditions. When either of those two stars align, the result can be incredibly dramatic – and often shocking to Buyers new to the market who had thought that with all they had heard about the so-called "Buyers' market" they could walk in and buy any home they wanted for 80 cents on the dollar. The key, as I always tell my Sellers, is to spend the extra time and money getting the home into picture perfect condition, before the first Buyer ever walks through the door. To help with this, I've put together a nice team of people who can handle painting, carpet, handyman repairs, plumbing – basically anything we could possibly need. They're trained to approach every job from the standpoint of finding the most cost efficient means of getting things ready for the market, while always ensuring a high quality job. Most importantly, since they work for me so often, they actually show up … which puts them light years ahead of many others. If you're in that line of work, and want to be considered for our team, please e-mail me at steve@stevelevine. com and we can chat about it.
Okay, so I wanted to let you loyal readers of mine know first about a HOT NEW PROGRAM that we're going to be rolling out in the next few weeks. This should prove to be a benefit to Sellers and Buyers alike, and may help take some of the pressure off your shoulders in these challenging economic times. I'm talking about being one of the only agents in Massachusetts to be able to offer "Job Loss Insurance" (JLI) to home Buyers who are working with me on a purchase. This JLI policy will provide the peace of mind that all Buyers need, in times when employment is so incredibly volatile – and will kick in and pay your mortgage should you become involuntarily unemployed. Now don't get me wrong … if your company just announced a round of layoffs, you really shouldn't be buying a house until things stabilize. That said, if things on the job front are looking okay, this type of benefit may be just what you need to provide a little peace of mind to allow you to take advantage of this great time to buy. JLI policies can be paid for by either the Buyer, as a safety net to make them feel good, or could be purchased by a Seller to make their home stand out above the crowd. They will come in a variety of different benefit packages, based on how long they will pay the mortgage, when they will kick in following a severance, and the level of mortgage that they will pay. How's that for a bit of "value added service" for our Buyers and Sellers?
If you're interested in learning more about the program, send me an e-mail and I'll forward you a package of information just as soon as we finalize the various package options that will be available.
The year 2009 is also seeing a strong resurgence in the use of Home Warranty programs, both purchased by Buyers, for their own benefit, and being offered by Sellers as an incentive for purchasers to consider their home. These policies were big in the late 1990s and then seemed to disappear off the radar screen until recently. Everyone I know who has purchased one of these policies over the years has sworn by it and told me that they've gotten their money's worth time and time again. They are unbelievably inexpensive and cover a wide array of different home repairs that may come up during the first year of home ownership. At times when money is tight, having someone else pick up the tab for a repair is a huge benefit. We're going to be offering a selection of these policies from the most respected home warranty provider for our Buyers and Sellers starting Oct. 1.
Lastly, but perhaps the most importantly, what we're going to be working heavily on in the month of October is putting together packages with local portfolio lenders in our community, to bypass some of the draconian policies being implemented by the national lenders, which have made it incredibly difficult for Buyers in Worcester County in the >$400K range, with less than 20 percent down. Our intent is to develop a more consistent plan of action with a local lender who is willing to work with loans that "make sense" in the community – and make homeownership a real possibility for Buyers who've been getting shut out over the last six months. If you're operating in the Middlesex/Worcester County marketplace, and willing to issue loans that truly make sense, let's meet and see if we can work together to make the dream of home ownership a reality for deserving families right here in our area.
Steve Levine is President of Steve Levine Inc. and an agent for REMAX First Choice. He's been recognized as the #1 REMAX Agent in New England, and one of the Top 100 agents in the world since 1999. He can be reached on the web at his website, www. stevelevine.com, by e-mail at firstname.lastname@example.com, or by phone at 508-735-HOME (4663).
Short URL: http://www.communityadvocate.com/?p=5692


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Im thinking of getting a quadcopter for filming and general messing about. Do any of them have a follow function - so you can set it to follow you at say 20 or 30 feet away and just follow you? Does such a thing exist?
Bike Forum
Quadcopters - follow function?
The CIA probably do, it would explain the buzzing sounds I keep hearing.
Most I've seen are operated by someone, there would be a few issues with trees and power lines for a blind follow.
smogmonster » Im thinking of getting a quadcopter for filming and general messing about. Do any of them have a follow function - so you can set it to follow you at say 20 or 30 feet away and just follow you? Does such a thing exist?Yes
Unsympathetic OH: "So what you're saying is that you want to buy a really expensive remote control helicopter to go with your really expensive video camera to make videos of yourself riding one of your really expensive bikes?"
You: "Yes, it will look really cool, be lots of fun, and I can afford it."
Unsympathetic OH: "What, so this is going to make all the difference to those boring videos of you riding slowly on some flat path and sometimes getting a foot into the air? You don't even bother taking the camera out with you anymore because you said it takes too long to film from different angles."
You: "Yes, but this will make all the difference, it's going to look so pro, like a movie."
Unsympathetic OH: "We're still talking about you riding your bike here?"
You: "Yes, I just want it ok, it's cool!"
Unsympathetic OH: "Your definition of cool is VERY different to mine. When are you going give up all these toys? They're all a bit geeky rather than cool."
You: "I'm going for a ride! And I've already bought it anyway."
Conceptually, that was a lot shorter in my head! I'd love one, but it is serious boys toys territory.
Bear in mind the limited battery life once you start hanging cameras and gimbals underneath. My DJI Phantom with GoPro manages about six or seven minutes (more if you fly gently).
Mikrokopters will do this - but the limited flight time (15-20 mins) and cost mean it's probably not all that practical for bike riding.
There was a company launching one specifically for road cycling, dunno how far they got with that.
And that Iris is only follow the thing wearing a
GPS antenna and one of our 3DR telemetry/control radios.
Could you achieve the same thing by tying a kite to your seatpost?
And watch out for trees. The aerial footage of Southampton Bike Park is shorter than planned because the guy flying it was following the bikes using the goggles to see through the camera and failed to see the branches the bikes rode under.
People flying using POV cameras and not direct line of sight, or autonomous flying in public with no pilot ready to take control- naughty naughty.
I do wonder whenever I see drone footage a) if the person did it legally and b) when we'll first see someone prosecuted (say you film something mucking around, then sell the footage later - not currently legal)
IA » People flying using POV cameras and not direct line of sight, or autonomous flying in public with no pilot ready to take control- naughty naughty.
Indeed - but I don't think most of the owners of quadcopters actually have any idea about the law on this, let alone have any insurance.
I think this is the big reason I built a bunch of Mikrokopters a few years ago, and it's died off completely - not many people want to go through the whole CAA approval thing.
I did some flying around Peckham a few years ago - that was pretty dodgy.
They did have a second guy spotting but didn't quite get the words out quick enough.
WorldClassAccident » They did have a second guy spotting but didn't quite get the words out quick enough.
Which doesn't make it legal. The pilot in charge is supposed to have normal direct visual contact (if you want to fly FPV you're supposed to be on a buddy box).
I had similar thoughts about a quadrocopter/ gopro combo, then I figured that something similar could possibly be achieved (in true Heath Robinson style) with a small helium balloon.
Helium balloons - long string and a gimble.
- tie string to bike , float go pro on gimble below the balloon and go ride.....
A company providing one of these 'copters for this very function was recently on kick starter. Looked very very good and they smashed their target a zillions times. Think they got near a million dollars when they were looking for something like 35 grand.... It was called Pocket Drone.
D'oh! Just spotted HandyAndys post above....
Oh God I've seen the future. The sky black with personal drones like Philip Pullman's daemons.
Aaaaghh. Runs away screaming and hides head under pillow.
I thought these things were pretty much illegal to fly in the U.S. ??
I know for flying comercially in the UK you need a licence, wonder how many bike film companies actually have this, especially given every new MTB film seems to have a quadcopter segment?
I thought these things were pretty much illegal to fly in the U.S. ??
Overturned last week, but subject to appeal:
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