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You can save 432 Pounds per month on your phone calls to Kuwait! Instead of paying 100.5 pence per minute to BT, with CheapCalls.co.uk you can make cheap calls to Kuwait for just 1 pence per minute plus your phone provider's access charge.
No subscription or signup is needed! To start saving on your calls, simply dial our access number in front of an Kuwaiti phone number. That's all!
Saving Tip: Program access numbers 0843 926 1300 and 0843 212 2000 in front of the phone numbers of your relatives in Kuwait! Follow the instructions of our handy guide!
Saving Example: If you call each week 2 hours to an Kuwaiti landline. Calculate your savings with our savvy cost calculator!


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Search Instructions
Searching for Test Names Only
To search for test name information only, please enter a test name in the form. Test names will be queried for a match. Use this search method if you feel you know the test you want but are unsure of the exact name. This search method searches names, not individual test contents.
The search currently is case insensitive, and a simple search and compound search will be performed (if you enter more than one word, the search will try to find the exact pattern, rather than searching each word indepedently - if no match is initially found, each individual word will be queried independently for a match). The entire list of laboratory tests is available for viewing. The Manual is generally organized by the name of the analyte rather than specimen type, e.g., "Sodium", not "Serum Sodium". Antibodies should generally be sought under the name of the Antigen, e.g., "Toxoplasma", not "Anti-Toxoplasma". Infectious disease testing should be searched under the causitive organism name rather than disease name. It may be necessary to look for key parts of the name to find an appropriate cross-reference to the listing.
Due to the constant updates to individual test entries, bookmarking individual tests is discouraged. If you do bookmark an individual test, and the link is broken in the future, you may have to perform the search again to locate the individual test entry. For example, if the test name changes from "Sodium" to "Sodium (Na)", the previous bookmark will need to be updated.
Using an Advanced Boolean Search Engine
This search option gives you maximum capability and flexibility to search the content of the entire Laboratory Manual: test contents, lab manual web page contents, or a complete combination of the two. You may make your request as simple or as complex as you desire, according to the syntax set out below. Form your search as a query, using a combination of text or phrases, eg., urea, "urea blood", as well as operators, eg., +, AND. To make a search, enter your query into the form and choose the scope of documents to be searched. A pull down list shows the scope of documents against which the query is made. You may choose to search the contents of tests only, the contents of the lab manual web pages only, or the complete collection of test and web page contents.
Your query results will be returned to you in the form of a structured list of links to your chosen set of searched documents. The results will be sorted according to a weighted boost parameter, by which the search engine scores the closeness of this document as a match to your query. A small sample of document text will be returned to you, with the query terms highlighted. Should you desire more information from that document, a link is provided for your convenience.
Query syntax:
- To search for a word, just put that word into the Search box.
- To search for a phrase, surround the phrase in "double quotes", such as "blood proteins".
- Use the + (MUST_HAVE) and - (MUST_NOT_HAVE) operators, just as in Google query syntax, to indicate required and forbidden terms, respectively.
- Enclose a combination of text and operators in parentheses.
- Use any combination of boolean operators, quoted text, parenthetical text.
The following constructs are recognized:
- Boolean operators 'AND', 'OR', and 'AND NOT'.
- Prepended + plus and - minus, indicating that the test or web page content should be either required (MUST_HAVE) or forbidden (MUST_NOT_HAVE) the query term -- be it a single word, a phrase, or a parenthetical group.
- If neither a + nor a - is prepended, the default meaning is SHOULD.
- Logical groups, delimited by parentheses, (+urea +blood) AND NOT (urine).
- Phrases, delimited by double quotes.
- Default logical connector has two possible values: 'AND' and 'OR'. The default is 'OR', which means: return documents which match any of the query terms.
The search engine boost factor is formed using the following schema:
- Documents containing all the search terms are good
- Matches on rare words are better than for common words
- Long documents are not as good as short ones
- Documents which mention the search terms many times are good
- About Us
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subset: commoncrawl


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Sell your property with Exclusive Algarve Villas, The REAL estate agency for luxury properties in the Algarve.
Exclusive Algarve Villas is a real estate agency based in the Algarve which has won, for 3 years in a row, the award for Best Real Estate Agency Portugal by the International Property Awards. Being recognized by property professionals in the industry for our website, personalized service, 24-7 availability and no-pressure approach has carried us into our 10th year of operation.
We have offices in Lagoa and Vilamoura to serve those looking to buy a luxury villa in the Western Algarve and the Golden Triangle area in Central Algarve. Our Algarve real estate agency brokers in luxury ocean front villas, sea view villas, modern contemporary style villas, luxury beach and sea view penthouses, ocean front and frontline apartments, townhouses and villas, golf course villas, luxurious apartments in Lagos & Vilamoura marina. Our main work areas in the Algarve are: Lagos, Lagoa, Albufeira, Vilamoura, Almancil, Vale do Lobo, Quinta do Lago, Loule
Our property professionals are knowledgeable and can assist you easily through the process of buying a holiday home or permanent home in the Algarve. We have good connections with local professionals such as architects, builders, lawyers, banks, and accountancy firms etc to guide you through the whole purchasing process of becoming a proud owner of a villa under the Portuguese sun and enjoy the best that life has to offer.
Our real estate company has a wide range of prestige property in the Algarve for sale, from luxury golf villas & townhouses, beach front villas, sea view homes, luxury penthouses, resort holiday homes and large permanent residencies throughout the Algarve.
Exclusive Algarve Villas consists of a team of property professionals who have all been in the Algarve, and active in luxury real estate sales for many years. With our multi lingual team, you can communicate with us in English, French, Spanish, Dutch, German and Portuguese - whichever you prefer. We have great local knowledge and experience of which you as a client can benefit from.
The Algarve in Southern Portugal is a popular destination, not just for tourism but also to purchase a second holiday home in the sun or to find your permanent residency. The all year climate is perfect for those wanting to enjoy the relaxed lifestyle, wander on the stunning beaches and enjoy a round of golf on one of the courses dotted around the Algarve.
The Algarve is also a place where you can easily adapt to the culture and language. Because of the great influence from England, Germany, France, Belgium and Dutch, local businesses and residents are fluent in various languages.
For the luxury property buyers the Algarve real estate market has much to offer. Currently the 'golden visa buyers' and the 'non habitual residents' are taking advantage of favorable tax regimes offered by Portuguese government.
24 / 7
Lagoa (Carvoeiro) Office
Rua Ernesto Cabrita - Edificio Vales Loja A
8400-387 Lagoa - Algarve
Head Office
Avenida Tivoli, Corpo B, Bloco 3, R/C Esquerdo
8125-410 Vilamoura - Algarve
Call Us
Phone: +351 289 321 276


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Things To Do :: Community Calendar
The Walkerton Business Improvement Area welcomes community members to post events here! Please ensure your event takes place within Brockton, is non-profit in nature or a fundraiser for a recognized charity, and is open to the general public.
All posted events are subject to approval. We reserve the right to remove any event from the calendar at any time, without notice.
Thursday, February 22, 2018 10:30am - 12:00pm
Location: Walkerton Community Centre 290 Durham St. W Walkerton
Get Fit for Active Living will engage, educate and provide fitness opportunities for the older adult. Fitness opportunities include an exercise class, a number of individual fitness equipment, learn how to play pickleball and carpet bowling.
Contact: Brockton Parks and Recreation
Phone: 519-881-0625
Email: firstname.lastname@example.com
Website: http://www.brockton.ca


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Welcome Returning Students
Academic Year 2018/2019
Financial Aid Priority Deadline is March 30, 2018
As you prepare for another year in college, you are reminded that applying for financial assistance is a yearly process. Each spring the aid application materials must be completed and submitted by the College's processing deadlines in order for your aid eligibility to be determined for the next academic year.
We are excited about having you back at Skidmore College and look forward to assisting you with the financial aid process. Please select the appropriate category below to learn about the documents you need to complete, along with their deadlines.
Students who enrolled at Skidmore College with Skidmore College grant aid and do not fall in one of the categories below.
Students admitted to Skidmore College through Skidmore College's Higher Education Opportunity Program (HEOP) or the Academic Opportunity Program (AOP). International AOP students should review information for International Students.
Students who are enrolled at Skidmore College with Skidmore Grant who are not U.S. Citizens nor have U.S. Permanent Residency Status.
Students who enrolled at Skidmore College without Skidmore College grant aid normally are first eligible to receive such aid, if need is demonstrated, in their junior year.
Skidmore College participates in the Federal Direct Loan program. If you borrow a Federal Direct Student Loan or a Federal Direct PLUS loan your funding will come directly from the Federal government.


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Important Information & Inn Policies
Room Rates: Rates shown are for one or two people per room. These rates do not include state and local taxes. For rooms that can accommodate more than two guests, $25 plus tax is charged for each additional guest. Rates include a full, 3 course irresistible breakfast served from 8:00 – 9:00 a.m. Rates are subject to change at any time before a reservation is confirmed.
Taxes: By law, the Adobe Rose Inn is required to collect state and local taxes for all room revenue. The current tax rate is 12.05% plus $4 per night.
Information Security: We take precautions to protect your information. When you submit sensitive information via the website, your information is protected both online and offline. Wherever we collect sensitive information such as credit card data, that information is encrypted and transmitted to us in a secure way. You can verify this by looking for the McAfee Secure Logo next to the Credit Card Information Request or looking for "https" at the beginning of the address of the web page.
While we use encryption to protect sensitive information transmitted online, we also protect your information offline. Only three employees who need the information to perform a specific job such as processing reservations, are granted access to personally identifiable information. The computers/servers in which we store personally identifiable information are kept in a secure environment.
If you feel that we are not abiding by this privacy policy, please contact us immediately via telephone at 520-318-4644 or via email at email@example.com.
CHECK-IN TIME: Rooms are available for check-in from 4:00 p.m. to 6:00 p.m. If this time is not convenient, please let us know and we'll make alternative arrangements.
CHECK-OUT TIME: Unless prior arrangements have been made, guests must check-out before 11:00 a.m.
DEPOSIT FOR CONFIRMED RESERVATIONS: When multiple rooms are booked or during major events such as Gem Show, Homecoming, Parents Weekend, and Graduation, a 50% deposit of the total room charges may be required.
CANCELLATION POLICY: Rather than increase our overall pricing to compensate for losses due to cancellations, the following cancellation policy has been instituted.
Guests are responsible for payment of all nights reserved with a confirmed reservation. For cancellations received within 14 days of your scheduled arrival date, the first night amount of your scheduled reservation becomes non-refundable. Payment for the remaining reservation amount will be charged as well but will be refunded on your next visit. We will make every effort to resell the cancelled rooms. If we are successful, we will not charge you for the re-sold rooms. If you shorten your scheduled stay within 14-days of your scheduled arrival or after you've checked-in, you will be responsible for the cost of your original reservation, unless we can resell the room(s). No-shows will be charged for the full amount of the reservation.
MAXIMUM OCCUPANTS PER ROOM: Adobe Rose Inn rooms are designed to comfortably accommodate 2 guests per room. However, limited accommodations for 3 guests are available in the Atanacia Room, with a roll-away bed, and our Casita, by converting our sofa to a twin-sized bed. Our Santa Rita Suite can accommodate 4 guests by converting the sofa to a full-sized bed. There is an extra nightly charge of $25 plus tax per night for each additional guest.
PAYMENT OPTIONS: We gladly accept American Express, Visa, MasterCard, Discover, Traveler's Cheques, Money Orders, Personal Checks, and Cash.
NON-SMOKING POLICY: For the comfort of others, smoking is not permitted anywhere on the premises. This includes all patios and balconies.
PET POLICY: Pets of all types are strictly prohibited, inside or outside the Inn including the parking areas.
GUESTS WITH CHILDREN: Children aged 10 and over are welcome as guests. The Adobe Rose Inn is not equipped to accommodate small children, especially with regard to our other guests and the presence of our pool and spa. In specific instances, the Adobe Rose Inn may waive this restriction with prior approval. Factors that we consider include maturity of the child, availability of parents to watch the children at all times, and the guest rooms available.


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The cheap oak bedroom furniture
in this room is modern but it is easily associated with a completely different case style. For homes with large family heirlooms including cabinets, armoires, and more, simply pair with a lightweight, small modern part.
In this midcentury and modern day space, there are cheap oak bedroom furniture
and a modern coffee stand. Add in your personal modern style in lounger selection and selecting a couple of pieces while adding heirlooms in other parts of the area. This kind of living area is also an example of a space that incorporates several types of wood.
This kind of cheap oak bedroom furniture
set for a child's room features a modern chest, desk, and bed. Any set of cheap oak bedroom furniture
can also including shelving for exhibiting your child's favorite bits. With a little little of creativity, anything special to your child can be used as well.


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Hate Crowds? Shop On Wednesday This Week.
Experts say the lightest crowds of the season will be found this Wednesday, December 4th. If you hate crowds, that's the day to shop!
The Black Friday crowds have dispersed, but it's still expected to be a busy holiday shopping season overall, and the stores will be crowded all the way until Christmas.
How was your Black Friday shopping experience? I went to the big Door Buster sale at Walmart Thursday night at 6, and it was a big fat fail for me! Here's why I didn't do well:
My big mistake was failing to plan ahead. I went to the store thinking I'd grab a few DVDs and a Blu Ray player, but missed the detail that the Blu Ray player I wanted was going on sale at 8pm, not 6pm. Whoops! So I worked my way through the elbow-room-only crowd only to find a store employee guarding the stack of Blu Ray players and turning away shoppers who had jumped the gun. And I couldn't find the DVDs on sale in the huge crowd and I could barely move, so I left! I happened to be up at 1am, so I went back at that point and there were two Blu Ray players left. So I lucked out by waiting and going later.
If you don't like crowds, there are a few days next week that are supposed to have light traffic in stores. Next Monday, Tuesday, and Friday are expected to be just semi-crowded, and among the least-crowded days of the season. The Saturday before Christmas will see the heaviest traffic.
Today of course, is Cyber Monday, but I hear many of the sales from the big stores will run all week. Happy shopping!


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McCain urges Obama to resolve sequestration
Sen. John McCain, a top Republican on the Senate Armed Services Committee, is calling on President Barack Obama to provide leadership to end the standoff over sequestration and the looming budget cuts for the Pentagon.
"What I would like to see is the president call the [party] leaders over to the White House and say, 'Look, we've got to solve this problem,'" McCain said on "Fox News Sunday." "All he does is go out and make speeches."
Tens of billions of dollars of spending cuts under sequestration will kick in on March 1 unless Obama and Congress act to prevent them. And Defense Secretary Leon Panetta and other Pentagon leaders have warned those cuts could seriously harm U.S. national security.
"Republicans and Democrats are responsible for this new 'cliff,' and I'll take responsibility for it for the Republicans. But we've got to avoid it, we've got t\o stop it," McCain added. "The president is the same one that during the campaign said, 'It's not going to happen.' He just dismissed it."
"The world is very dangerous," McCain said. "The men and women in the military deserve better than what we're giving them."
McCain opposes broader tax increases or rate changes to offset the defense cuts under sequestration, but added that he was open to "some revenue closers, maybe so."


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Greene Strip Clubs
Looking for some of the best Greene strip clubs?. We list popular Greene Gentlemen's Club in our directory. If you have problems finding a Greene strip club, please use our exclusive zip code search. Enter any zip code in the Greene area or search by club name, state, county or city, click the search button and voila a list of Greene strip clubs.
Go luck dear friends, it is time to visit your favorite Greene local club, please relax and have fun!.


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This is just a poem. If you dont have the same feeling towards this element/weather or if you thought of a different one please by all means post it here.
The rushing cold touches my skin lightly, not asking for permission, but as if to tease you to come into it arms. The warmth holds promise of sleep and rest but the cold of the rainfall holds a silent whisper of things that go beyond the taste of the sweetest fruit, the smell of a flower hidden away from all eyes but the smell has drove men to the edge of the earth. Raindrops swirl and dance a dance of forgotten love, of new love found, of a childs first smile in this world, and the smile of a person whose age and time have come and soon are to past. Glistening like emeralds on the grass and sparkling like the rarest rubies on the petals of the red rose, like tears of a bride when she realizes this is her time and the tears of the groom when the beauty of his soon to be wife overwhelms him to the point of a heart ache. Silence so thick it puts frosting of all kinds to shame. The wind, oh the wind, so gentle, the sun's sleepy eyelids so careful and fragile, looking out to the mountains tops and the sea bottomless heart. I close my eyes, catching the rain on my eyelashes one by one, feel it tremble with my breath.Open my eyes slowly, the drops sliding over my slow and quiet grin, so calm and meaningless, yet neon tinting my world into the clouds and oblivion.


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Elon Musk is going to space if it kills him (or, more likely, bankrupts him).
The Tesla founder launched SpaceX nine years ago with the goal of lowering the cost of space travel by creating an efficient, reusable rocket.
The company currently has 1,500 employees and is inching closer.
Air & Space has an excellent profile of the company and the founder in the January 2012 issue.
One of the details jumped out:
They don't even file patents, Musk says, because "we try not to provide a recipe by which China can copy us and we find our inventions coming right back at us."


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Putnam appeared in all 50 games, making 49 starts, during her senior season ... named to All-Big West Second Team for her play at second base ... set new career highs with .294 batting average, 40 hits, two triples, 34 RBIs, 64 total bases, 19 walks and 11 stolen bases ... tied career highs with eight doubles and four home runs ... lead team with .471 slugging percentage and nine sac bunts in addition to triples, home runs, RBIs, total bases and stolen bases ... improved her batting average every season at CSUN and led Matadors in sac bunts all four years of her career ... sported .963 fielding percentage with 129 put-outs and 106 assists in 244 chances at second base ... ranked among Big West Conference top 10 in slugging percentage, RBIs, stolen bases, sac bunts and ... had career-high four hits against Cal Poly on Apr. 18, missing the cycle by only a home run ... drove in career-high four RBIs on three different occasions ... batted team-high .316 in 21 conference games and led CSUN in hits, doubles, triples, home runs, RBIs, total bases, slugging percentage, walks, on-base percentage and stolen bases during conference season.
Putnam was one of two Matadors to play in and start all 47 games during her junior season ... set new career highs in batting average (.279), runs (23), hits (36), doubles (7), home runs (4) and total bases (55) ... batting average was 50 points higher than her career average entering the season ... only Matador to hit two home runs in a game, smacking a pair against Pacific on Mar. 29 ... led all Big West Conference second basemen in extra-base hits (11) and fielding percentage (.977) ... scored a career-high three runs against Cal State Bakersfield on Mar. 22 ... had a career-high three hits on three different occasions: vs. North Dakota on Mar. 7, vs. Cal State Bakersfield on Mar. 22 and vs. UC Santa Barbara on Apr. 12 ... drove in two RBIs on four different occasions ... led CSUN in sacrifice hits for third-straight season, finishing year with 11 sac bunts and one sacrifice fly ... tied a career high with six stolen bases ... finished second on the team with a .426 slugging percentage and third with .343 on-base percentage.
Putnam played in all 47 games for the Matadors, starting 46 ... finished with three home runs, 16 RBIs and a .243 batting average ... recorded 10 sacrifice hits, the second-most on the team ... finished second on the team with six steals in 10 attempts ... walked 18 times during season, second-highest on the team ... finished eighth on the team with 26 hits and her 15 runs was good tied her for sixth on the squad ... registered four multi-RBI games, three multi-hit games and two multi-run games ... went 2-for-3 with three RBIs and a home run against UC Riverside on Apr. 28 ... belted a home run against Florida State on Mar. 15, finishing the game with two runs and two RBIs ... drove in two runs and scored two more against Cal Poly on Apr. 14 ... hit first home run of the season against Oregon on Feb. 10 ... recorded first career triple against Canisius on Mar. 13 ... finished with 85 assists, second most on the team and finished with a fielding percentage of .948.
Putnam started all 40 games she appeared in during her freshman season ... hit .204 with one home run, 12 runs batted in and a team-leading 12 sacrifice hits ... also scored 13 runs and had four doubles ... hit .261 (12-for-46) during Big West play with nine RBI and seven runs scored ... posted five multiple-hit games and three multiple-RBI contests ... went 2-for-3 with two runs scored and two walks in her first collegiate game against New Mexico on Feb. 10 ... hit her first home run, a two-run shot, against Fresno State on Feb. 12 ... had two hits and two runs scored in each of the three games at UC Riverside (Apr. 29-30), finishing the weekend 6-for-12 (.500) with six runs scored, four runs batted in and two doubles ... also had a two-hit, two-run contest against Southern Utah (Feb. 23) ... drove in a pair in wins over UC Santa Barbara (Apr. 22) and UC Riverside (Apr. 29) ... laid down two sacrifice bunts in a game twice, against Southern Utah and Cal Poly (Apr. 14) ... stole both her bases at the Aztec Classic on Mar. 4 against Loyola Marymount and Oregon.
Justin-Siena High School
Putnam played three sports at Justin-Siena High School in Napa, Calif. ... earned four letters in softball, three in basketball and one in volleyball ... earned All-Marin County League and all-county honors all four seasons in softball ... was also named Most Valuable Player as a junior and senior ... received all-county accolades twice and all-league honors as a senior in basketball ... graduated in 2005 with a 3.0 grade point average.
Born on March 3, 1987 in Berkeley, Calif. ... parents are Nia and Mike Putnam ... has one sister, Taylor and one brother, Athan ... engaged to A.J. Vera ... favorites include the San Francisco Giants, actress Sarah Jessica Parker, actor Gerard Butler and the movies "Mulan" and "It's a Wonderful Life" ... enjoys spending time with loved ones, watching movies and reading when she has time to relax ... names Anne Frank as the person from history she would most like to meet ... says the best advice she has ever received is to "believe in yourself" ... majoring in child andadolescentdevelopment.


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by Brian DeCandia, sports information graduate assistant
MILLEDGEVILLE, Ga. – The Georgia College men's cross country team put three on the All-Peach Belt Conference (PBC) Academic Team as announced by the conference Thursday.
The three positions lead the all-academic team with UNC Pembroke's two being the next.
Junior Daniel Horseman (Cohutta, Ga.) owns the teams best GPA with a 3.72 in pre-outdoor education. Senior Erik Ottoson (Suwanee, Ga.) is the only senior on the squad for Georgia College with a 3.33 GPA in management and sophomore Nick Widener (Newnan, Ga.) completes the list for the Bobcats achieving a 3.45 GPA in pre-mass communication.
To be eligible for the all-academic team, a student-athlete must participate in at least half of his/her team's events and be either a starter or significant contributor, achieved a 3.30 cumulative grade point average (on a 4.0 scale) and completed at least one full academic year at his or her current institution.
The Bobcats are back in action Nov. 6 at 9 a.m. at the Peach Belt Conference (PBC) Championships in Evans, Ga.
The Georgia College Department of Athletics, back-to-back winners of the PBC Commissioner's Cup, sponsors 10 varsity athletic programs at the NCAA Division II level. As a Division II program, Bobcat Athletics prides itself on balancing the life of the student-athlete, evidenced by the teams' multiple appearances in post-season competition as well as documented academic success and community-service involvement. Sign up at www.twitter.com/GCSUBobcats and www.facebook.com/gcbobcats for up-to-the-minute reports, and visit www.GCBobcats.com for more information, and to nominate your favorite former Bobcats and Colonials to the GC Athletics Hall of Fame.


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In an effort to reduce pedestrian and bicycle fatalities involving newly-arrived Hispanic immigrants, NHTSA has made available these traffic safety materials in Spanish (e.g., posters, brochures, radio announcements, et al) for use by local, State, and national traffic safety advocates in our combined effort to educate these newly-arrived individuals on pedestrian and bicycle safety in the United States.
When Hispanic immigrants arrive here, they often rely on bicycles and/or walking as their primary means of transportation. However, they often are not familiar with our traffic signs, signals, and practices. Their language barrier may also affect their ability to understand how to safely travel. For these reasons, they are at a higher risk of being involved in pedestrian and/or bicycle crashes. Hispanic adult men, in particular, may be at an even higher risk.


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Sickle-cell disease
|Sickle-cell disease
|Classification and external resources
Figure (A) shows normal red blood cells flowing freely through veins. The inset shows a cross section of a normal red blood cell with normal haemoglobin. Figure B shows abnormal, sickled red blood cells log jamming, sticking and accumulating at the branching point in a vein. The inset image shows a cross-section of a sickle cell with long polymerized HbS strands stretching and distorting the cell shape.
|med/2126 oph/490 ped/2096 emerg/26 emerg/406
Sickle-cell disease (SCD), or sickle-cell anaemia (SCA) or sometimes drepanocytosis, is a hereditary blood disorder, characterized by an abnormality in the oxygen-carrying haemoglobin molecule in red blood cells. This leads to a propensity for the cells to assume an abnormal, rigid, sickle-like shape under certain circumstances. Sickle-cell disease is associated with a number of acute and chronic health problems, such as severe infections, attacks of severe pain ("sickle-cell crisis"), and stroke, and there is an increased risk of death. Sickle-cell disease occurs when a person inherits two abnormal copies of the haemoglobin gene, one from each parent. Several subtypes exist, depending on the exact mutation in each haemoglobin gene. A person with a single abnormal copy does not experience symptoms and is said to have sickle-cell trait.
The complications of sickle-cell disease can be prevented to a large extent with vaccination, preventative antibiotics, blood transfusion, and the drug hydroxyurea/hydroxycarbamide. A small proportion requires a transplant of bone marrow cells.
Almost 300,000 children are born with a form of sickle-cell disease every year, mostly in sub-Saharan Africa, but also in other countries such as the West Indies and South Asia, and in people of African origin elsewhere in the world. The condition was first described in the medical literature by the American physician James B. Herrick in 1910, and in the 1940s and 1950s contributions by Nobel prize-winner Linus Pauling made it the first disease where the exact genetic and molecular defect was elucidated.
- 1 Signs and symptoms
- 2 Genetics
- 3 Pathophysiology
- 4 Diagnosis
- 5 Management
- 6 Prognosis
- 7 Epidemiology
- 8 History
- 9 Research
- 10 See also
- 11 References
- 12 Further reading
- 13 External links
Signs and symptoms
Sickle-cell disease may lead to various acute and chronic complications, several of which have a high mortality rate.[1]
Sickle-cell crisis
The terms "sickle-cell crisis" or "sickling crisis" may be used to describe several independent acute conditions occurring in patients with SCD. SCD results in anemia and crises that could be of many types including the vaso-occlusive crisis, aplastic crisis, sequestration crisis, haemolytic crisis, and others. Most episodes of sickle-cell crises last between five and seven days.[2] "Although infection, dehydration, and acidosis (all of which favor sickling) can act as triggers, in most instances, no predisposing cause is identified."[3]
Vaso-occlusive crisis
The [4] or lungs are considered an emergency and treated with red-blood cell transfusions. Incentive spirometry, a technique to encourage deep breathing to minimise the development of atelectasis, is recommended.[5]
Splenic sequestration crisis
Because of its narrow vessels and function in clearing defective red blood cells, the [7][8] preventive antibiotics and vaccinations are recommended for those with such asplenia.
Splenic sequestration crises are acute, painful enlargements of the spleen, caused by intrasplenic trapping of red cells and resulting in a precipitous fall in hemoglobin levels with the potential for hypovolemic shock. Sequestration crises are considered an emergency. If not treated, patients may die within 1–2 hours due to circulatory failure. Management is supportive, sometimes with blood transfusion. These crises are transient, they continue for 3–4 hours and may last for one day.[9]
Acute chest syndrome
Acute chest syndrome (ACS) is defined by new pulmonary infiltrate with a manifestation of pulmonary symptoms such as tachypnea and dyspnea.[10] It is the second-most common complication and it accounts for about 25% of deaths in patients with SCD, majority of cases present with vaso-occlusive crises then they develop ACS.[10][11] Nevertheless, about 80% of patients have vaso-occlusive crises during ACS.
Aplastic crisis
Aplastic crises are acute worsenings of the patient's baseline anaemia, producing pallor, tachycardia, and fatigue. This crisis is normally triggered by parvovirus B19, which directly affects production of red blood cells by invading the red cell precursors and multiplying in and destroying them.[12] Parvovirus infection nearly completely prevents red blood cell production for two to three days. In normal individuals, this is of little consequence, but the shortened red cell life of SCD patients results in an abrupt, life-threatening situation. Reticulocyte counts drop dramatically during the disease (causing reticulocytopenia), and the rapid turnover of red cells leads to the drop in haemoglobin. This crisis takes 4 days to one week to disappear. Most patients can be managed supportively; some need blood transfusion.[13]
Haemolytic crisis
Haemolytic crises are acute accelerated drops in haemoglobin level. The red blood cells break down at a faster rate. This is particularly common in patients with coexistent G6PD deficiency.[14] Management is supportive, sometimes with blood transfusions.[5]
One of the earliest clinical manifestations is dactylitis, presenting as early as six months of age, and may occur in children with sickle-cell trait.[15] The crisis can last up to a month.[16] Another recognised type of sickle crisis, acute chest syndrome, is characterised by fever, chest pain, difficulty breathing, and pulmonary infiltrate on a chest X-ray. Given that pneumonia and sickling in the lung can both produce these symptoms, the patient is treated for both conditions.[17] It can be triggered by painful crisis, respiratory infection, bone-marrow embolisation, or possibly by atelectasis, opiate administration, or surgery.
Sickle-cell anaemia can lead to various complications, including:
- Increased risk of severe bacterial infections due to loss of functioning spleen tissue (and comparable to the risk of Streptococcus pneumoniae and Haemophilus influenzae. Daily penicillin prophylaxis is the most commonly used treatment during childhood, with some haematologists continuing treatment indefinitely. Patients benefit today from routine vaccination for S. pneumoniae.[18]
- Stroke, which can result from a progressive narrowing of blood vessels, prevents oxygen from reaching the brain. Cerebral infarction occurs in children and cerebral haemorrhage in adults.
- Silent stroke causes no immediate symptoms, but is associated with damage to the brain. Silent stroke is probably five times as common as symptomatic stroke. About 10–15% of children with SCD suffer strokes, with silent strokes predominating in the younger patients.[19][20]
- Cholelithiasis (gallstones) and cholecystitis may result from excessive bilirubin production and precipitation due to prolonged haemolysis.
- Avascular necrosis (aseptic bone necrosis) of the hip and other major joints may occur as a result of ischaemia.[21]
- Decreased immune reactions due to hyposplenism (malfunctioning of the spleen)[22]
- Priapism and infarction of the penis[23]
- Osteomyelitis (bacterial bone infection), the most common cause of osteomyelitis in SCD is Salmonella (especially the atypical serotypes Salmonella typhimurium, Salmonella enteritidis, Salmonella choleraesuis and Salmonella paratyphi B), followed by Staphylococcus aureus and Gram-negative enteric bacilli perhaps because intravascular sickling of the bowel leads to patchy ischaemic infarction.[24]
- Opioid tolerance can occur as a normal, physiologic response to the therapeutic use of opiates. Addiction to opiates occurs no more commonly among individuals with sickle-cell disease than among other individuals treated with opiates for other reasons.
- Acute papillary necrosis in the kidneys
- Leg ulcers[25]
- In eyes, background retinopathy, proliferative retinopathy, vitreous haemorrhages, and retinal detachments can result in blindness.[26] Regular annual eye checks are recommended.
- During pregnancy, intrauterine growth retardation, spontaneous abortion, and pre-eclampsia
- Chronic pain: Even in the absence of acute vaso-occlusive pain, many patients have unreported chronic pain.[27]
- Pulmonary hypertension (increased pressure on the pulmonary artery) can lead to strain on the right ventricle and a risk of heart failure; typical symptoms are shortness of breath, decreased exercise tolerance, and episodes of syncope.[28]
- Chronic renal failure due to sickle-cell nephropathy manifests itself with hypertension, protein loss in the urine, loss of red blood cells in urine and worsened anaemia. If it progresses to end-stage renal failure, it carries a poor prognosis.[29]
Normally, humans have haemoglobin A, which consists of two alpha and two beta chains, haemoglobin A2, which consists of two alpha and two delta chains, and haemoglobin F, consisting of two alpha and two gamma chains in their bodies. Of these, haemoglobin F dominates until about 6 weeks of age then A dominates throughout life.
Sickle-cell conditions have an autosomal recessive pattern of inheritance from parents. The types of haemoglobin a person makes in the red blood cells depend on what haemoglobin genes are inherited from her or his parents. If one parent has sickle-cell anaemia and the other has sickle-cell trait, then the child has a 50% chance of having sickle-cell disease and a 50% chance of having sickle-cell trait. When both parents have sickle-cell trait, a child has a 25% chance of sickle-cell disease, 25% will not carry any sickle-cell alleles, and 50% will have the heterozygous condition.
Sickle-cell gene mutation probably arose spontaneously in different geographic areas, as suggested by restriction endonuclease analysis. These variants are known as Cameroon, Senegal, Benin, Bantu, and Saudi-Asian. Their clinical importance is because some are associated with higher HbF levels, e.g., Senegal and Saudi-Asian variants, and tend to have milder disease.[30]
In people heterozygous for HgbS (carriers of sickling haemoglobin), the polymerisation problems are minor, because the normal allele is able to produce over 50% of the haemoglobin. In people homozygous for HgbS, the presence of long-chain polymers of HbS distort the shape of the red blood cell from a smooth doughnut-like shape to ragged and full of spikes, making it fragile and susceptible to breaking within capillaries. Carriers have symptoms only if they are deprived of oxygen (for example, while climbing a mountain) or while severely dehydrated. The sickle-cell disease occurs when the sixth amino acid, glutamic acid, is replaced by valine to change its structure and function; as such, sickle-cell anemia is also known as E6V. Valine is hydrophobic, causing the haemoglobin to collapse on itself occasionally. The structure is not changed otherwise. When enough haemoglobin collapses on itself the red blood cells become sickle-shaped.
The gene defect is a known mutation of a single nucleotide (see single-nucleotide polymorphism - SNP) (A to T) of the β-globin gene, which results in glutamic acid being substituted by valine at position 6. Haemoglobin S with this mutation is referred to as HbS, as opposed to the normal adult HbA. The genetic disorder is due to the mutation of a single nucleotide, from a CTC to CAC codon on the coding strand, which is transcribed from the template strand into a GUG codon. This is normally a benign mutation, causing no apparent effects on the secondary, tertiary, or quaternary structures of haemoglobin in conditions of normal oxygen concentration. What it does allow for, under conditions of low oxygen concentration, is the polymerization of the HbS itself. The deoxy form of haemoglobin exposes a hydrophobic patch on the protein between the E and F helices. The hydrophobic residues of the valine at position 6 of the beta chain in haemoglobin are able to associate with the hydrophobic patch, causing haemoglobin S molecules to aggregate and form fibrous precipitates.
The allele responsible for sickle-cell anaemia can be found on the short arm of chromosome 11, more specifically 11p15. A person who receives the defective gene from both father and mother develops the disease; a person who receives one defective and one healthy allele remains healthy, but can pass on the disease and is known as a carrier or heterozygote. Heterozygotes are still able to contract malaria, but their symptoms are generally less severe.[31]
Due to the adaptive advantage of the heterozygote, the disease is still prevalent, especially among people with recent ancestry in malaria-stricken areas, such as Africa, the Mediterranean, India, and the Middle East.[32] Malaria was historically endemic to southern Europe, but it was declared eradicated in the mid-20th century, with the exception of rare sporadic cases.[33]
The malaria parasite has a complex lifecycle and spends part of it in red blood cells. In a carrier, the presence of the malaria parasite causes the red blood cells with defective haemoglobin to rupture prematurely, making the Plasmodium parasite unable to reproduce. Further, the polymerization of Hb affects the ability of the parasite to digest Hb in the first place. Therefore, in areas where malaria is a problem, people's chances of survival actually increase if they carry sickle-cell trait (selection for the heterozygote).
In the USA, with no endemic malaria, the prevalence of sickle-cell anaemia among blacks is lower (about 0.25%) than in West Africa (about 4.0%) and is falling. Without endemic malaria, the sickle-cell mutation is purely disadvantageous and will tend to be selected out of the affected population by natural selection. However, the African American community of the USA is known to be the result of significant admixture between several African and non-African ethnic groups, and also represents the descendants of survivors of slavery and the slave trade. Thus, a lower degree of endogamy and, particularly, abnormally high health-selective pressure through slavery may be the most plausible explanations for the lower prevalence of sickle-cell anaemia (and, possibly, other genetic diseases) among African Americans compared to sub-Saharan Africans. Another factor limiting the spread of sickle-cell genes in North America is the absence of cultural proclivities to polygamy, which allows affected males to continue to seek unaffected children with multiple partners.[34]
The loss of red blood cell elasticity is central to the pathophysiology of sickle-cell disease. Normal red blood cells are quite elastic, which allows the cells to deform to pass through capillaries. In sickle-cell disease, low-oxygen tension promotes red blood cell sickling and repeated episodes of sickling damage the cell membrane and decrease the cell's elasticity. These cells fail to return to normal shape when normal oxygen tension is restored. As a consequence, these rigid blood cells are unable to deform as they pass through narrow capillaries, leading to vessel occlusion and ischaemia.
The actual anaemia of the illness is caused by haemolysis, the destruction of the red cells, because of their shape. Although the bone marrow attempts to compensate by creating new red cells, it does not match the rate of destruction.[35] Healthy red blood cells typically function for 90–120 days, but sickled cells only last 10–20 days.[36]
In HbSS, the complete blood count reveals haemoglobin levels in the range of 6–8 g/dl with a high reticulocyte count (as the bone marrow compensates for the destruction of sickled cells by producing more red blood cells). In other forms of sickle-cell disease, Hb levels tend to be higher. A blood film may show features of hyposplenism (target cells and Howell-Jolly bodies).
Sickling of the red blood cells, on a blood film, can be induced by the addition of sodium metabisulfite. The presence of sickle haemoglobin can also be demonstrated with the "sickle solubility test". A mixture of haemoglobin S (Hb S) in a reducing solution (such as sodium dithionite) gives a turbid appearance, whereas normal Hb gives a clear solution.
Abnormal haemoglobin forms can be detected on haemoglobin electrophoresis, a form of gel electrophoresis on which the various types of haemoglobin move at varying speeds. Sickle-cell haemoglobin (HgbS) and haemoglobin C with sickling (HgbSC)—the two most common forms—can be identified from there. The diagnosis can be confirmed with high-performance liquid chromatography. Genetic testing is rarely performed, as other investigations are highly specific for HbS and HbC.[37]
An acute sickle-cell crisis is often precipitated by infection. Therefore, a urinalysis to detect an occult urinary tract infection, and chest X-ray to look for occult pneumonia, should be routinely performed.[38]
People who are known carriers of the disease often undergo genetic counseling before they have a child. A test to see if an unborn child has the disease takes either a blood sample from the fetus or a sample of amniotic fluid. Since taking a blood sample from a fetus has greater risks, the latter test is usually used. Neonatal screening provides not only a method of early detection for individuals with sickle-cell disease, but also allows for identification of the groups of people that carry the sickle cell trait.[39]
Folic acid and penicillin
Children born with sickle-cell disease will undergo close observation by the pediatrician and will require management by a haematologist to assure they remain healthy. These patients will take a 1 mg dose of folic acid daily for life. From birth to five years of age, they will also have to take penicillin daily due to the immature immune system that makes them more prone to early childhood illnesses.
Malaria chemoprophylaxis
The protective effect of sickle-cell trait does not apply to people with sickle cell disease; in fact, they are more vulnerable to malaria, since the most common cause of painful crises in malarial countries is infection with malaria. It has therefore been recommended that people with sickle-cell disease living in malarial countries should receive anti-malarial chemoprophylaxis for life.[40]
Vaso-occlusive crises
Most people with sickle-cell disease have intensely painful episodes called vaso-occlusive crises. The frequency, severity, and duration of these crises, however, vary tremendously. Painful crises are treated symptomatically with analgesics; pain management requires opioid administration at regular intervals until the crisis has settled. For milder crises, a subgroup of patients manage on NSAIDs (such as diclofenac or naproxen). For more severe crises, most patients require inpatient management for intravenous opioids; patient-controlled analgesia (PCA) devices are commonly used in this setting. Diphenhydramine is also an effective agent that is frequently prescribed by doctors in order to help control any itching associated with the use of opioids.
Acute chest crisis
Management is similar to vaso-occlusive crisis, with the addition of antibiotics (usually a quinolone or macrolide, since cell wall-deficient ["atypical"] bacteria are thought to contribute to the syndrome),[41] oxygen supplementation for hypoxia, and close observation. Should the pulmonary infiltrate worsen or the oxygen requirements increase, simple blood transfusion or exchange transfusion is indicated. The latter involves the exchange of a significant portion of the patients red cell mass for normal red cells, which decreases the percent of haemoglobin S in the patient's blood.
The first approved drug for the causative treatment of sickle-cell anaemia, hydroxyurea, was shown to decrease the number and severity of attacks in a study in 1995 (Charache et al.)[42] and shown to possibly increase survival time in a study in 2003 (Steinberg et al.).[43] This is achieved, in part, by reactivating fetal haemoglobin production in place of the haemoglobin S that causes sickle-cell anaemia. Hydroxyurea had previously been used as a chemotherapy agent, and there is some concern that long-term use may be harmful, but this risk has been shown to be either absent or very small and it is likely that the benefits outweigh the risks.[44]
Transfusion therapy
Blood transfusions are often used in the management of sickle-cell disease in acute cases and to prevent complications by decreasing the number of red blood cells (RBC) that can sickle by adding normal red blood cells.[45] In children prophylactic chronic red blood cell (RBC) transfusion therapy has been shown to be efficacious to a certain extent in reducing the risk of first stroke or silent stroke when transcranial Doppler (TCD) ultrasonography shows abnormal increased cerebral blood flow velocities. In those who have sustained a prior stroke event it also reduces the risk of recurrent stroke and additional silent strokes.[46][47]
Bone marrow transplants
Bone marrow transplants have proven to be effective in children. Bone marrow transplants are the only known cure for SCD.[48] However, bone marrow transplants are difficult to obtain because of the specific HLA typing necessary. Ideally, a twin family member (syngeneic) or close relative (allogeneic) would donate the bone marrow necessary for transplantation.
About 90% of patients survive to age 20, and close to 50% survive beyond the fifth decade.[49] In 2001, according to one study performed in Jamaica, the estimated mean survival for sickle-cell patients was 53 years old for men and 58 years old for women with homozygous SCD.[50]
The highest frequency of sickle cell disease is found in tropical regions, particularly sub-Saharan Africa, India and the Middle-East.[51] Migration of substantial populations from these high prevalence areas to low prevalence countries in Europe has dramatically increased in recent decades and in some European countries sickle-cell disease has now overtaken more familiar genetic conditions such as haemophilia and cystic fibrosis.[52] In 2010, there were about 29,000 deaths attributed to sickle-cell disease globally.[53]
Sickle-cell disease occurs more commonly among people whose ancestors lived in tropical and sub-tropical sub-Saharan regions where malaria is or was common. Where malaria is common, carrying a single sickle-cell allele (trait) confers a selective advantage—in other words, being a heterozygote is advantageous. Specifically, humans with one of the two alleles of sickle-cell disease show less severe symptoms when infected with malaria.[54]
Three quarters of sickle-cell cases occur in Africa. A recent WHO report estimated that around 2% of newborns in Nigeria were affected by sickle cell anaemia, giving a total of 150,000 affected children born every year in Nigeria alone. The carrier frequency ranges between 10% and 40% across equatorial Africa, decreasing to 1–2% on the north African coast and <1% in South Africa.[55] There have been studies in Africa that show a significant decrease in infant mortality rate, ages 2–16 months, because of the sickle-cell trait. This happened in areas that were known to be predominant areas of malarial cases.[56]
United States
The prevalence of the disease in the United States is approximately 1 in 5,000, mostly affecting Americans of Sub-Saharan African descent, according to the National Institutes of Health.[57] In the United States, about 1 out of 500 African-American children and 1 in every 36,000 Hispanic-American children born will have sickle-cell anaemia.[58] It is estimated that sickle-cell disease affects 90,000 Americans.[59] Most infants with SCD born in the United States are now identified by routine neonatal screening. Forty-four states along with the District of Columbia, Puerto Rico and the Virgin Islands currently provide universal neonatal screening for SCD.[60][61] Sickle cell trait occurs among about 1:12 African-Americans and 1:100 Hispanic-Americans.[62] It is estimated that 2.5 million Americans are heterozygous carriers for the sickle-cell trait.[63]
As a result of population growth in African-Caribbean regions of overseas France and immigration from North and sub-Saharan Africa to mainland France, sickle-cell disease has become a major health problem in France.[64] SCD has become the most common genetic disease in the country, with an overall birth prevalence of 1/2,415 in mainland France, ahead of phenylketonuria (1/10,862), congenital hypothyroidism (1/3,132), congenital adrenal hyperplasia (1/19,008) and cystic fibrosis (1/5,014) for the same reference period. In 2010, 31.5% of all newborns in mainland France (253,466 out of 805,958) were screened for SCD (this percentage was 19% in 2000). 341 newborns with SCD and 8,744 heterozygous carriers were found representing 1.1% of all newborns in mainland France. The Paris metropolitan district (Île-de-France) is the region that accounts for the largest number of newborns screened for SCD (60% in 2010). The second largest number of at-risk is in Provence-Alpes-Côte d'Azur at nearly 43.2% and the lowest number is in Brittany at 5.5%.[65][66]
United Kingdom
In the United Kingdom, all babies receive a blood test to screen for this condition.[67]
Middle East
In Saudi Arabia about 4.2% of the population carry the sickle-cell trait and 0.26% have sickle-cell disease. The highest prevalence is in the Eastern province where approximately 17% of the population carry the gene and 1.2% have sickle-cell disease.[68] In 2005 in Saudi Arabia a mandatory pre-marital test including HB electrophoresis was launched and aimed to decrease the incidence of SCD and thalassemia.[69]
Sickle-cell disease is common in many parts of India, where the prevalence has ranged from 9.4 to 22.2% in endemic areas.[70]
Caribbean Islands
In Jamaica, 10% of the population carries the sickle-cell gene, making it the most prevalent genetic disorder in the country.[71]
The first modern report of sickle-cell disease may have been in 1846, where the autopsy of an executed runaway slave was discussed; the key findings was the absence of the spleen.[72][73] There were also reports amongst African slaves in the dentistry. He died of pneumonia in 1916 and is buried in the Catholic cemetery at Sauteurs in the north of Grenada.[75][76] Shortly after the report by Herrick, several other cases appeared in the medical literature. In the description by Verne Mason in 1922, the name "sickle cell anemia" is first used.[76][77] Childhood problems related to sickle cells disease were not reported until the 1930s, despite the fact that this cannot have been uncommon in African-American populations.[73]
The Memphis physician Lemuel Diggs, a prolific researcher into sickle cell disease, first introduced the distinction between sickle cell disease and trait in 1933, although it took until 1949 until the genetic characteristics were elucidated by James V. Neel and E.A. Beet.[76] 1949 was the year when Linus Pauling described the unusual chemical behaviour of haemoglobin S, and attributed this to an abnormality in the molecule itself.[76][78] The actual molecular change in HbS was described in the late 1950s BY Vernon Ingram.[79] The late 1940s and early 1950s saw further understanding in the link between malaria and sickle cell disease. In 1954, the introduction of haemoglobin electrophoresis allowed the discovery of particular subtypes, such as HbSC disease.[76]
Large scale natural history studies and further intervention studies were introduced in the 1970s and 1980s, leading to the more widespread use of prophylaxis against pneumococcal infections amongst other interventions. The 1990s saw the development of hydroxycarbamide, and reports of cure through bone marrow transplantation appeared in 2007.[76]
Gene therapy
No trials of gene therapy for sickle-cell disease were found in a systematic review published in October 2014.[80]
See also
- ^ Yawn, BP; Buchanan, GR; Afenyi-Annan, AN; Ballas, SK; Hassell, KL; James, AH; Jordan, L; Lanzkron, SM; Lottenberg, R; Savage, WJ; Tanabe, PJ; Ware, RE; Murad, MH; Goldsmith, JC; Ortiz, E; Fulwood, R; Horton, A; John-Sowah, J (Sep 10, 2014). "Management of sickle cell disease: summary of the 2014 evidence-based report by expert panel members.". JAMA 312 (10): 1033–48.
- ^ "BestBets: How long should an average sickle cell crisis last?". Retrieved 2010-11-27.
- ^ Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson; Aster, Jon (2009-05-28). Robbins and Cotran Pathologic Basis of Disease, Professional Edition: Expert Consult - Online (Robbins Pathology) (Kindle Locations 33498-33499). Elsevier Health. Kindle Edition.
- ^ Olujohungbe A, Burnett AL (2013). "How I manage priapism due to sickle cell disease". British Journal of Haematology 160 (6): 754–65.
- ^ a b Glassberg J (August 2011). "Evidence-based management of sickle cell disease in the emergency department". Emergency Medicine Practice 13 (8): 1–20; quiz 20.
- ^ Anie KA, Green J (2012). Anie, Kofi A, ed. "Psychological therapies for sickle cell disease and pain". Cochrane Database of Systematic Reviews (Online) 2: CD001916.
- ^ Pearson HA (Aug 1977). "Sickle cell anemia and severe infections due to encapsulated bacteria" (Free full text). J Infect Dis. 136 Suppl: S25–30.
- ^ Wong WY, Powars DR, Chan L, Hiti A, Johnson C, Overturf G (Mar 1992). "Polysaccharide encapsulated bacterial infection in sickle cell anaemia: a thirty year epidemiologic experience". Am J Hematol 39 (3): 176–82.
- ^ Khatib R, Rabah R, Sarnaik SA (January 2009). "The spleen in the sickling disorders: an update". Pediatric Radiology 39 (1): 17–22.
- ^ a b Dessap AM, Leon R, Habibi A, Nzouakou R, Roudot-Thoraval F, Adnot S, Godeau B, Galacteros F, Brun-Buisson C, Brochard L, Maitre B (2008). "Pulmonary hypertension and cor pulmonale during severe acute chest syndrome in sickle cell disease". Am. J. Respir. Crit. Care Med. 177 (6): 646–53.
- ^ Paul RN, Castro OL, Aggarwal A, Oneal PA (2011). "Acute chest syndrome: sickle cell disease". Eur. J. Haematol. 87 (3): 191–207.
- ^ Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson; Aster, Jon (2009-05-28). Robbins and Cotran Pathologic Basis of Disease, Professional Edition: Expert Consult - Online (Robbins Pathology) (Kindle Location 33329). Elsevier Health. Kindle Edition.
- ^ Slavov SN, Kashima S, Pinto AC, Covas DT (August 2011). "Human parvovirus B19: general considerations and impact on patients with sickle-cell disease and thalassemia and on blood transfusions". FEMS Immunology and Medical Microbiology 62 (3): 247–62.
- ^ Balgir RS (March 2012). "Community expansion and gene geography of sickle cell trait and G6PD deficiency, and natural selection against malaria: experience from tribal land of India". Cardiovascular & Hematological Agents in Medicinal Chemistry 10 (1): 3–13.
- ^ Jadavji T, Prober CG (April 1985). "Dactylitis in a child with sickle cell trait". Can Med Assoc J 132 (7): 814–5.
- ^ http://www.ejbjs.org/cgi/content/abstract/58/8/1161
- ^ Miller ST (May 2011). "How I treat acute chest syndrome in children with sickle cell disease". Blood 117 (20): 5297–305.
- ^ Kavanagh PL, Sprinz PG, Vinci SR, Bauchner H, Wang CJ (2011). "Management of children with sickle cell disease: a comprehensive review of the literature". Pediatrics 128 (6): e1552–74.
- ^ Adams RJ, Ohene-Frempong K, Wang W (2001). "Sickle cell and the brain". Hematology Am Soc Hematol Educ Program 2001 (1): 31–46.
- ^ Adams RJ (November 2007). "Big strokes in small persons". Arch. Neurol. 64 (11): 1567–74.
- ^ Martí-Carvajal A, Dunlop R, Agreda-Perez L (Oct 2004). Martí-Carvajal, Arturo J, ed. "Treatment for avascular necrosis of bone in people with sickle cell disease". Cochrane database of systematic reviews (Online) (4): CD004344.
- ^ Kenny MW, George AJ, Stuart J (July 1980). "Platelet hyperactivity in sickle-cell disease: a consequence of hyposplenism".
- ^ Chrouser KL, Ajiboye OB, Oyetunji TA, Chang DC (April 2011). "Priapism in the United States: the changing role of sickle cell disease".
- ^ Almeida A, Roberts I (May 2005). "Bone involvement in sickle cell disease". Br. J. Haematol. 129 (4): 482–90.
- ^ Rudge FW (1991). "Hyperbaric oxygen therapy in the treatment of sickle cell leg ulcers".
- ^ Elagouz M, Jyothi S, Gupta B, Sivaprasad S (July 2010). "Sickle cell disease and the eye: old and new concepts".
- ^ Smith WR, Penberthy LT, Bovbjerg VE, McClish DK, Roberts JD, Dahman B, Aisiku IP, Levenson JL, Roseff SD (Jan 2008). "Daily assessment of pain in adults with sickle cell disease". Annals of Internal Medicine 148 (2): 94–101.
- ^ Gladwin MT, Sachdev V, Jison ML, Shizukuda Y, Plehn JF, Minter K, Brown B, Coles WA, Nichols JS, Ernst I, Hunter LA, Blackwelder WC, Schechter AN, Rodgers GP, Castro O, Ognibene FP (February 2004). "Pulmonary hypertension as a risk factor for death in patients with sickle cell disease". N. Engl. J. Med. 350 (9): 886–95.
- ^ Powars DR, Elliott-Mills DD, Chan L, Niland J, Hiti AL, Opas LM, Johnson C (Oct 1991). "Chronic renal failure in sickle cell disease: risk factors, clinical course, and mortality". Annals of Internal Medicine 115 (8): 614–20.
- ^ Green NS, Fabry ME, Kaptue-Noche L, Nagel RL (Oct 1993). "Senegal haplotype is associated with higher HbF than Benin and Cameroon haplotypes in African children with sickle cell anemia". Am. J. Hematol. 44 (2): 145–6.
- ^ Allison AC (October 2009). "Genetic control of resistance to human malaria". Current Opinion in Immunology 21 (5): 499–505.
- ^ Kwiatkowski DP (Aug 2005). "How Malaria Has Affected the Human Genome and What Human Genetics Can Teach Us about Malaria". Am. J. Hum. Genet. 77 (2): 171–92.
- ^ Ponçon N, Toty C, L'Ambert G, Le Goff G, Brengues C, Schaffner F, Fontenille D (2007). "Biology and dynamics of potential malaria vectors in Southern France". Malar. J. 6: 18.
- ^ Lesi FE, Bassey EE (July 1972). "Family study in sickle cell disease in Nigeria". J Biosoc Sci 4 (3): 307–13.
- ^ "How Does Sickle Cell Cause Disease?". Retrieved 2010-11-27.
- ^ "Sickle Cell Anemia: eMedicine Emergency Medicine". Retrieved 2010-11-27.
- ^ Clarke GM, Higgins TN (August 2000). "Laboratory investigation of hemoglobinopathies and thalassemias: review and update". Clin. Chem. 46 (8 Pt 2): 1284–90.
- ^ "BestBets: Does routine urinalysis and chest radiography detect occult bacterial infection in sickle cell patients presenting to the accident and emergency department with painful crisis?". Retrieved 2010-11-27.
- ^ Lee, C., Davies, S.,& Dezatoux, C. (2000). Neonatal Screening for sickle cell disease. The Cochrane Collaboration. John Wiley & Sons, Ltd.
- ^ Oniyangi O, Omari AA (2006). Oniyangi, Oluseyi, ed. "Malaria chemoprophylaxis in sickle cell disease". Cochrane Database of Systematic Reviews 13 (4): CD003489.
- ^ Aldrich TK, Nagel RL. (1998). "Pulmonary Complications of Sickle Cell Disease.". In Reynolds HY, Bone RC, Dantzker DR, George RB, Matthay RA. Pulmonary and Critical Care Medicine (6th ed.). St. Louis: Mosby. pp. 1–10.
- ^ Charache S, Terrin ML, Moore RD, Dover GJ, Barton FB, Eckert SV, McMahon RP, Bonds DR (May 1995). "Effect of hydroxyurea on the frequency of painful crises in sickle cell anemia. Investigators of the Multicenter Study of Hydroxyurea in Sickle Cell Anemia". N. Engl. J. Med. 332 (20): 1317–22.
- ^ Steinberg MH, Barton F, Castro O, Pegelow CH, Ballas SK, Kutlar A, Orringer E, Bellevue R, Olivieri N, Eckman J, Varma M, Ramirez G, Adler B, Smith W, Carlos T, Ataga K, DeCastro L, Bigelow C, Saunthararajah Y, Telfer M, Vichinsky E, Claster S, Shurin S, Bridges K, Waclawiw M, Bonds D, Terrin M (April 2003). "Effect of hydroxyurea on mortality and morbidity in adult sickle cell anemia: risks and benefits up to 9 years of treatment". JAMA 289 (13): 1645–51.
- ^ Platt OS (Mar 2008). "Hydroxyurea for the treatment of sickle cell anemia". N. Engl. J. Med. 358 (13): 1362–9.
- ^ Drasar E, Igbineweka N, Vasavda N, Free M, Awogbade M, Allman M, Mijovic A, Thein SL (March 2011). "Blood transfusion usage among adults with sickle cell disease - a single institution experience over ten years". Br. J. Haematol. 152 (6): 766–70.
- ^ Gyang E, Yeom K, Hoppe C, Partap S, Jeng M (January 2011). "Effect of chronic red cell transfusion therapy on vasculopathies and silent infarcts in patients with sickle cell disease". Am. J. Hematol. 86 (1): 104–6.
- ^ Mirre E, Brousse V, Berteloot L, Lambot-Juhan K, Verlhac S, Boulat C, Dumont MD, Lenoir G, de Montalembert M (March 2010). "Feasibility and efficacy of chronic transfusion for stroke prevention in children with sickle cell disease". Eur. J. Haematol. 84 (3): 259–65.
- ^ Walters MC, Patience M, Leisenring W, Eckman JR, Scott JP, Mentzer WC, Davies SC, Ohene-Frempong K, Bernaudin F, Matthews DC, Storb R, Sullivan KM (August 1996). "Bone marrow transplantation for sickle cell disease". N. Engl. J. Med. 335 (6): 369–76.
- ^ Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson; Aster, Jon (2009-05-28). Robbins and Cotran Pathologic Basis of Disease, Professional Edition: Expert Consult - Online (Robbins Pathology) (Kindle Locations 33530-33531). Elsevier Health. Kindle Edition.
- ^ Wierenga KJ, Hambleton IR, Lewis NA (2001). "Survival estimates for patients with homozygous sickle-cell disease in Jamaica: A clinic-based population study". Lancet 357 (9257): 680–683.
- ^ Weatherall DJ, Clegg JB (2001). "Inherited haemoglobin disorders: an increasing global health problem". Bull. World Health Organ. 79 (8): 704–12.
- ^ Roberts I, de Montalembert M (July 2007). "Sickle cell disease as a paradigm of immigration hematology: new challenges for hematologists in Europe". Haematologica 92 (7): 865–71.
- ^ Lozano R, Naghavi M, Foreman K, Lim S, Shibuya K, Aboyans V, Abraham J, Adair T, Aggarwal R, et al. (Dec 15, 2012). "Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010". Lancet 380 (9859): 2095–128.
- ^ Wellems TE, Hayton K, Fairhurst RM (September 2009). "The impact of malaria parasitism: from corpuscles to communities". J. Clin. Invest. 119 (9): 2496–505.
- ^ WHO. "Sickle-cell anaemia - Report by the Secretariat" (PDF). Retrieved 2010-11-27.
- ^ Aidoo, Michael, Dianne J Terlouw, Margarette S Kolczak, Peter D McElroy, Feiko O ter Kuile, Simon Kariuki, Bernard L Nahlen, Altaf A Lal, and Venkatachalam Udhayakumar. "Protective Effects of the Sickle-cell Gene Against Malaria Morbidity and Mortality." The Lancet. 359.9314 (2002): 1311-1312.
- ^ National Heart, Lung and Blood Institute. "Sickle cell anemia, key points". Retrieved 2010-11-27.
- ^ "September is Sickle Cell Awareness Month". CDC. Retrieved 6 February 2011.
- ^ "Sickle Cell Disease: Data & Statistics".
- ^ American Academy of Pediatrics Section on Hematology/Oncology Committee on Genetics (2002). "Health Supervision for Children with Sickle Cell Disease". Pediatrics 109 (3): 526–535.
- ^ Pass KA, Lane PA, Fernhoff PM, Hinton CF, Panny SR, Parks JS, Pelias MZ, Rhead WJ, Ross SI, Wethers DL, Elsas LJ (2000). "US newborn screening system guidelines II: follow-up of children, diagnosis, management, and evaluation". J Pediatr 137 (37): S1–S46.
- ^ "Sickle Cell Disease and Your Baby". March of Dimes®. February 2008. Retrieved 11 November 2014.
- ^ Cinnchinsky EP, Mahoney DH, Landlaw SA (29 November 2011). "Uptodate: Sickle Cell Trait". Retrieved 8 November 2011.
- ^ Bardakdjian J, Wajcman H (September 2004). "[Epidemiology of sickle cell anemia]". Rev Prat (in French) 54 (14): 1531–3.
- ^ Bardakdjian-Michau J, Bahuau M, Hurtrel D, Godart C, Riou J, Mathis M, Goossens M, Badens C, Ducrocq R, Elion J, Perini JM (January 2009). "Neonatal screening for sickle cell disease in France". J. Clin. Pathol. 62 (1): 31–3.
- ^ Le dépistage néonatal de la drépanocytose en France. Numéro thématique. La drépanocytose en France : des données épidémiologiques pour améliorer la prise en charge, Bardakdjian-Michau J, INVS, July 2012
- ^ http://www.nhs.uk/conditions/sickle-cell-anaemia/Pages/Introduction.aspx
- ^ Jastaniah W (2011). "Epidemiology of sickle cell disease in Saudi Arabia". Annals of Saudi Medicine 31 (3): 289–93.
- ^ Memish ZA, Saeedi MY (2011). "Six-year outcome of the national premarital screening and genetic counseling program for sickle cell disease and β-thalassemia in Saudi Arabia". Annals of Saudi Medicine 31 (3): 229–35.
- ^ Awasthy N, Aggarwal KC, Goyal PC, Prasad MS, Saluja S, Sharma M (2008). "Sickle cell disease: Experience of a tertiary care center in a nonendemic area". Annals of Tropical Medicine and Public Health 1 (1): 1–4.
- ^ Asnani MR, McCaw-Binns AM, Reid ME (2011). "Excess Risk of Maternal Death from Sickle Cell Disease in Jamaica: 1998–2007". PLoS ONE 6 (10): e26281.
- ^ Lebby R (1846). "Case of absence of the spleen". Southern J of Med Pharmacol 1: 481–3.
- ^ a b c Ballas, SK; Gupta, K; Adams-Graves, P (Nov 1, 2012). "Sickle cell pain: a critical reappraisal.". Blood 120 (18): 3647–56.
- ^ Herrick JB (1910). "Peculiar elongated and sickle-shaped red blood corpuscles in a case of severe anemia". Arch. Intern. Med. 6 (5): 517–521.
- ^ a b Savitt TL, Goldberg MF (Jan 1989). "Herrick's 1910 case report of sickle cell anemia. The rest of the story". JAMA 261 (2): 266–71.
- ^ a b c d e f Serjeant, GR (Dec 2010). "One hundred years of sickle cell disease.". British journal of haematology 151 (5): 425–9.
- ^ Mason VR (1922). "Sickle cell anemia". JAMA 79 (14): 1318–1320.
- ^ Pauling L, Itano HA, Singer SJ, Wells IC (1949). "Sickle cell anemia, a molecular disease". Science 110 (2865): 543–548.
- ^
- ^ Olowoyeye, A (October 2015). "Gene therapy for sickle cell disease". Cochrane Database of Systematic Reviews (10).
Further reading
Library resources about
Sickle-cell disease
- Brown, Robert T., ed. (2006). Comprehensive handbook of childhood cancer and sickle cell disease: a biopsychosocial approach. Oxford University Press.
- Hill, Shirley A. (2003). Managing Sickle Cell Disease in Low-Income Families. Temple University Press.
- Serjeant, Graham R. & Beryl E. (2001). Sickle Cell Disease. Oxford University Press.
- Tapper, Melbourne (1999). In the blood: sickle cell anemia and the politics of race. University of Pennsylvania Press.
External links
- Sickle cell at DMOZ
- Sickle Cell Anaemia OER Project
- Use British English from November 2010
- Articles with contributors link
- Articles to be expanded from October 2014
- All articles to be expanded
- CS1 French-language sources (fr)
- Commons category without a link on Wikidata
- Articles with DMOZ links
- Autosomal recessive disorders
- Chronic pain syndromes
- Hereditary hemolytic anemias
- Health in Africa
- Hematopathology
- Disorders of globin and globulin proteins


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Rams Shutdown Centenary on Senior Day
Farmingdale State - 19, Centenary College - 8
Farmingdale, N.Y. - The Farmingdale State men's lacrosse team defeated Centenary College, 19-8, in the final home game of the season today. Seniors Mike Maxwell (West Babylon, N.Y./West Babylon), Sean Maxwell (West Babylon, N.Y./West Babylon) and Thomas Weil (St. James, N.Y./Connetquot) played in their last home game for the Rams. Sean Maxwell finished with four goals and two assists and Mike Maxwell scored three goals and had one assist. Weil finished with one assist, five ground balls and two caused turnovers.
Farmingdale State jumped out to an early 5-0 lead after the first period and led 12-2 at the half. The Rams increased the lead to 19-3 in the fourth period and went on to defeat the Cyclones 19-8.
Farmingdale won 23 of 31 faceoffs, with 11 wins by junior midfielder Adam Zuar (Lindenhurst, N.Y./Lindenhurst) and 10 from freshman midfielder Joe Nacarlo (West Babylon, N.Y./West Babylon), who also had a game-high 11 ground balls. Freshman defender Bobby Lazos (Bellmore, N.Y./Holy Trinity) had seven ground balls for the Rams. Freshman attack Erick Thomson (Floral Park, N.Y./Floral Park) finished with three goals and four assists, while sophomore attacks Eddie Rifice (Babylon, N.Y./Babylon) and Peter McManus (Plainview, N.Y./Plainview) each added three goals for Farmingdale State. Junior goaltender Teddy Leone (East Meadow, N.Y./East Meadow) made five saves in the win.
Centenary senior goalie Brian Troilo (Flemington, N.J./Hunterdon Central) made five saves in the loss, while senior attack Travis Roy (Whippany, N.J./Whippany Park) and junior attack Jason Rieg (Chester, N.J./West Morris Central) led the team with three goals each.
The Rams will travel to Mount Saint Vincent for the final regular season game of the season on Saturday, April 25th at 6:00pm.


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Tuesday, 2 February 2010
He Is Too Good And Fair For Death And Me: Whom I Myself Embrace, To Set Him Free.
25 comments:
- tom sullivan said...
You write of an ego revealed to be a mere construct. As you see it, what is ego constructed of?
- 5 February 2010 at 15:29
- No One In Particular said...
Hi Tom. Nothing. Absolutely nothing. There's nothing to constuct it with! Or else sugar and spice and everything nice, in my case, and I suppose snakes and snails and puppy-dog's tails in your case; I always thought it was a bit hard on male energy, that bit of folklore.
- 5 February 2010 at 23:37
- ain_mc said...
Hello, thanks for the blog,and art, I used ti listnen to Old Man look at my life, now I am living it. A grandad/onenese. CHEERS.
- 7 February 2010 at 16:04
- Fernando Rozas said...
'Me' doesn't exist. Only thoughts, 'me'-thoughts.
And thoughts are of the same substance of Awareness.
There are NO Awareness AND thoughts. There is ONLY Awareness AS thoughts. And Awareness is 'nothing, absolutely nothing'.
There is nothing outside of Awareness.
Hi, Suzanne, sorry, no pude evitar la tentación de 'meter la cuchara'.
- 7 February 2010 at 16:41
- No One In Particular said...
Hey Fernando, you shove your oar in anytime you want!
- 7 February 2010 at 18:35
- No One In Particular said...
Hi ain-mc, living it is always happening. We just occasionally label it something else!
- 7 February 2010 at 18:36
- Jenya said...
hi suzanne :)
I am just wondering how thoughts arise and sometimes we wish to change our thoughts and start thinking more positively...but what is doing that?! what decides to change the thoughts? It is like the intelligence energy somehow shows itself through the mind? I know this is only another concept but is does seem this way, no?
- 7 February 2010 at 21:56
- No One In Particular said...
Hi Jenya, the content of the thought, and how it's interpreted, matters not at all. What arises, arises.
- 7 February 2010 at 22:11
- Bernard said...
I noticed some changes, with aging and experiences, acceptance of life-as-it-is becomes very natural, tiny little moments and details are so much enjoyed, delightful.
Planning the future is a very serious matter, hence the useless anguish.One can't help it. But the search for freedom seems to be quite a special mission for the ego,
its ultimate ambition : disappear ! :-) What a relief ! Even better than disappearing : noticing it has never been ! And yet appearing on and on. What an immense joyful joke !
PS : Most of yours videos have also disappeared... :-(
- 8 February 2010 at 14:48
- No One In Particular said...
Hi Bernard, there indeed seems to be the story unfolding of ease with age, and less attachment with experience. That really doesn't have anything to do with direct presence, but it's fascinating!
Not sure what you mean about videos disappearing...oh well, they were never there anyway!
- 8 February 2010 at 15:00
- Bernard said...
Probably a temporary problem with my browser.
It's OK now and I watched the Marx Brothers :-)
Direct presence is the snow falling outside the window
although it has nothing to do with anything.
Direct presence is our dreams and nostalgy of it
and we do not notice.
It is the silence, and that's why we do not hear it.
It is our swift thought, and that's why we do not catch it.
- 9 February 2010 at 09:58
- Peter bunzl said...
Hi Suzanne,
Found this blog through never not here.
I loved your interviews on that site.
Also found out about Tony Parsons meetings here.
So thanks
PS I love that you put fun you tube clips on your site
Do you know this film? The Monk and the Fish...
- 9 February 2010 at 11:36
- Barry said...
Thanks for this clear teaching, Suzanne - and especially for the Marx Bros. clip!
I suspect each of us exercises the "sanity clause" whenever life gets to be "too much" - which, as you make so clear, is just the ego's refusal to take responsibility for the mess it has created.
- 9 February 2010 at 20:50
- Bob Seal said...
You mean there ain't no Santa Claus!
Who's drinking the glass of wine and eating the cake I leave for him then?
Luv your playfulness Suzanne.
- 10 February 2010 at 04:51
- No One In Particular said...
Hi Bernard, pretty pretty!
- 10 February 2010 at 07:30
- No One In Particular said...
Hi Peter, thanks for Monk and Fish link. Fun - there is no point, but that comes close! That and bearing un-fun.
- 10 February 2010 at 07:31
- No One In Particular said...
Hey Barry, your mind can interpret it any way it likes. Define "mess"!
- 10 February 2010 at 07:32
- No One In Particular said...
Hey Bob, it's you eating and drinking those offerings; judging by your picture, your vestigial ego's alter-ego is obviously St. Nick himself!
- 10 February 2010 at 07:33
Hey One Hand Ironing,
Love the post, watched the video and i suppose that every contract is void then haha. This contract was voided long ago, because who is in their right mind?!
<3<3 :)
- 12 February 2010 at 05:49
- No One In Particular said...
Hi liberatedself (Nick),
It's that lovely paradox...nobody, and everybody, is in their right mind.
- 12 February 2010 at 06:28
For whatever reason these fingers always want to write Suzanna!
Anyway, It's a very spunky and lovely paradox indeed. ;)
- 12 February 2010 at 22:29
- Fernando Rozas said...
I VERY much like the picture.
- 13 February 2010 at 02:03
- No One In Particular said...
Hi Nick, yes, paradox can give the mind something to play with...or ignore. And thanks Fernando, comments about the art are always appreciated.
- 13 February 2010 at 07:25
- tom sullivan said...
What IS "happening" is plenty and good enough.
- 13 February 2010 at 16:40
- No One In Particular said...
Hi Tom...a bit too much in fact! Or so it seems from "time" to "time".
- 13 February 2010 at 16:43


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Luke Bryan photo courtesy of Capitol Nashville.
August 6, 2009 — Luke Bryan's passion for singing and songwriting is only rivaled by his passion for hunting and fishing. A passion that has recently landed him a gig as the 2009 honorary chairman for National Hunting and Fishing Day taking place September 26 - a week before his upcoming album release. Past chairmen include actors, entertainers and sports stars like Wade Boggs, Tom Seaver, John Havlicek, Arnold Palmer, Terry Bradshaw and many others.
The National Hunting and Fishing day was initiated by Congress in 1972 with the goal of celebrating responsible hunting and fishing practices. The organization reports that hunting and fishing licenses generate more than $1.75 billion per year which goes towards conservation of fish, wildlife and habitat.
Right now Luke's aim is clearly on getting new music out to his fans. Doin' My Thing, Luke's sophomore release, features his current chart climbing hit "Do I" and will hit stores on October 6.
"I can't wait for my fans to hear my new record," says Bryan. "I have wrapped 3 years of touring, hard work and most importantly meeting fans and I think all of that growth is reflected on this album. Doin' My Thing will make my die hard fans very happy and hopefully will reach out and grab some new fans. I am very proud of the music on this album and can't wait to get it out there!"
For fans that can't wait to get their hands on Luke's new music, it's likely he's playing a concert near you. Lukes playing an average of 3-4 shows a week at fairs and festivals all over the U.S. from now right up to the day his new album hits stores. For a complete list of tour dates check out lukebryan.com.


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7 hours ago
Grant McKenzie
Oh so numbers only matter as you see fit...I comprehend that! Good luck "rain man"!
2 minutes ago
Gosh, you really are dense. I made a complete case for all the numbers, and backed them all up with sound logic. Modern era titles are worth more, the game got competitive. Old titles are worth less. I showed how the early years of any sport have one or two teams winning the lion share of the titles. As I pointed out, when the NBA got tough, the Lakers dug in and competed and the Celtics folded. If good years can add to a team's greatness, bad years can take away from it. Boston missing the playoffs 9 times after Larry Bird retired drags Boston down even further. As I saidi n the opening statements, the Lakers are the greatest franchise and it isn't even close. I challenge, you or anyone to prove my presentation wrong, it can't be done! Thanks for the laughs, you just don't get it.


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HARTSVILLE, S.C. – The Coker women's basketball team blew the roof off the Timberlake-Lawton Gymnasium on Tuesday night defeating the St. Andrews Knights 114-59. Leading the way were four Cobras with double figure points, including Amber Lau's (Mt. Wolfe, Pa.) game and career high 31 points.
The Cobra women hit the gas early, jumping out to an 8-0 lead in the opening minute of play and they never looked back. They took a 51-25 lead into halftime and poured on another 63 points in the second half.
Lau was the leading scorer with 31 points, while Jessica Cohen (Ladsen, S.C.) had a double-double with 20 points and 11 rebounds. But it was Kelley Godbout (Matthews, N.C.) that stole the show with a double-double off the bench of 18 points, 12 rebounds and five assists. Also scoring in double digits was Hailey Yohn (Raleigh, N.C.) with 12 points, all from beyond the arc.
The Cobras had great ball movement throughout the game as 11 of their 13 players registered a basket. They had a combined 32 assists as a team and had 14 total steals.
Brittany Roberts was the Knights leading scorer with 15 points, while Rachel Hewitt added 14 points and Benee Norton had 10.
The Cobras return to the court on Saturday when they host the King College Tornado at 2 p.m. in the Timberlake-Lawton Gymnasium.
McDonald's Player of the Game- Kelley Godbout
Godbout had 18 points, 12 rebounds and five assists.
The McDonald's Player of the Game is presented by the Hartsville McDonald's and is given to the most outstanding performer during each Coker College home athletic event.


text:
USC Upstate took an early 1-0 lead in the first when Brad Wingo scored on a Kyle Bowley base hit to center. The score remained 1-0 in favor of the Spartans until the bottom half of the fourth when Coker scored three runs.
Brantley Bell led of the inning for the Cobras with a double to left center, followed by an RBI double from Nic Fletcher. Next up was Ryan Schaeffer, who grounded into a fielder's choice, that caused Fletcher to be tagged out in a run down between third and home, but Schaeffer was able to advance to second on the play. Ben Davidson came to the plate next for the Cobras and he sent the first pitch he saw soaring over the left field fence for a two-run homer, giving Coker a 3-1 lead.
The Spartans would not be held down for long as they scored four runs in the top on the sixth off an RBI double from Bowley and a two-run homer from Andrew Runion gave the Spartans the lead. USC Upstate would added another run the before the end of the inning, along with two in the seventh, another two in the eighth and another three runs in the ninth, to cruise to a 12-6 victory.
Coker's Jayson Clarke (3-4) took the loss after coming on in relief, giving up six runs, on six hits, with a strike out and a walk in one inning worth of work.
USC Upstate's Dennis McCraney (2-0) earned the win throwing six innings, allowing three runs on four hits, with two strikeouts.
Leading the Coker offense was Fletcher going 2-for-5 with a triple, an RBI and a run scored, while Davidson finished 1-for-4 with a homer run, two RBIs and a run scored.
For the Spartans, Bret Hansen was 3-for-4 with a triple, two RBIs and a two runs scored, while Runion was 2-for-5 with a home run, two RBIs and two runs scored.
Coker's takes the field for their third game in as many days, as they host


text:
|By Admin1 (admin) (adsl-70-240-139-65.dsl.okcyok.swbell.net - 220.127.116.11) on Wednesday, February 08, 2006 - 9:16 am: Edit Post
1981: Paul Gamble served in Sierra Leone in Magbele Ferry beginning in 1981
Returned Peace Corps Volunteer Paul Gamble can be contacted at pauldgamblealexisnexisdcom
Country of Service: Sierra Leone
Training Group: Agriculture
Cities you served in: Magbele Ferry
Arrival Year: 1981
Departure Year: 1983
Work Description: Swamp Development -- Rice
Originally posted: July 31, 2002
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leave a message above where it says "Create New Conversation."
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| The Peace Corps Library
Peace Corps Online is proud to announce that the Peace Corps Library is now available online. With over 30,000 index entries in 500 categories, this is the largest collection of Peace Corps related stories in the world. From Acting to Zucchini, you can use the Main Index to find hundreds of stories about what RPCVs with your same interests or from your Country of Service are doing today.


text: State Employees Trades Council Reaches Tentative Contract Agreement with California State University 8/20/2009 Page Image Image Caption Page Content Union Members to Vote on Furlough Option as Part of Contract State Employees Trades Council Reaches Tentative Agreement with Cal State (August 21, 2009) – The State Employees Trades Council (SETC)-United has reached a tentative agreement with the California State University on a new collective bargaining agreement to run through June 30, 2011. The agreement was reached following recommendations issued by a neutral factfinder. In addition, the SETC-United will hold a vote of its approximately 1,000 members next week on the CSU's proposal to furlough employees two days per month. Almost all of the CSU's 47,000 employees began the furlough process in August, but SETC had previously chosen to opt for layoffs as per its contract. The tentative agreement maintains the current salary scale with no increases, but provides for the option of reopening salary and benefit terms in 2010-2011. SETC-United represents skilled trades such as electricians, plumbers and carpenters who maintain CSU's campus facilities. As part of an overall comprehensive plan to address a $564 million cut to the CSU's general fund support for 2009-10, CSU has implemented two day per month furloughs for employees to cut salary expenditures by $275 million. A furlough is a mandated period of time off without pay. Furloughs differ from salary reductions and pay cuts in that they are temporary and do not affect employment status, or health benefit eligibility or pay rate for retirement benefits. Employees are required not to work on furlough days. ### About the California State University The California State University is the largest system of senior higher education in the country, with 23 campuses, approximately 450,000 students and 46,000 faculty and staff. Since the system was created in 1961, it has awarded nearly 2.5 million degrees, about 90,000 annually. Its mission is to provide high-quality, affordable education to meet the ever-changing needs of the people of California. With its commitment to excellence, diversity and innovation, the CSU is the university system that is working for California. Want to Learn More? Please contact: Public Affairs Department (562) 951-4800 Yes


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PARADISE ISLAND, Bahamas (AP) Russ Smith scored 16 points and No. 2 Louisville overcame a terrible offensive effort for a 51-46 victory over Northern Iowa on Thursday night in the first round of the Battle 4 Atlantis.
The Cardinals had a bad first half, looked as if they straightened things out but then stumbled to the finish.
Louisville (4-0) will face No. 13 Missouri in Friday night's semifinals. The Tigers beat Stanford 78-70.
The Cardinals somehow held a 26-20 halftime lead despite shooting 27.0 percent from the field (10 of 37) and committing 10 turnovers.
They held Northern Iowa (3-1) to one field goal over the opening 10:47 of the second half and that cut Louisville's lead 40-24. It was far from an easy ride to the finish as the Cardinals went 5:12 without scoring and suddenly the Panthers were chipping away.
Jake Koch made two free throws with 2:06 to cut Louisville's lead to 45-44.
Gorgui Dieng scored for the Cardinals and after a missed 3 by Northern Iowa Luke Hancock made one of two free throws for Louisville with 54 seconds left.
Koch made two free throws with 42 seconds left to make it 48-46.
Peyton Siva drove the lane and missed a short shot for Louisville but the ball was tied up and the arrow favored the Cardinals with 6.3 seconds left. On the inbounds pass Wayne Blackshear found Smith who laid it in and was fouled with 5.1 seconds left for the final margin.
Marc Sonnen had 11 points for Northern Iowa and Koch finished with 10. Nate Buss was the man who made the difference for the Panthers scoring eight points in the final 13 minutes - his only playing time of the game. The 6-foot-9 sophomore didn't score as a freshman and had a total of 24 points coming in.
Louisville finished shooting 30.6 percent (19 of 62) while the Panthers hit 34.8 percent (16 of 46).
The Cardinals had a 46-28 rebound advantage including 21-5 on the offensive end.


text:
About Family ASTRO
Spinning off of our successful Project ASTRO™ program, the Astronomical Society of the Pacific developed Family ASTRO to help families, youth groups, after-school clubs, and everyone else learn and enjoy some of the exciting ideas that underpin our understanding of the universe. An important aim of the program is to help parents (and other caregivers) to get more involved in their children's science education, and to spend more time together in active experiments, observations, and discussion.
With funding from the National Science Foundation and the help of astronomers, educators, parents, kids, and game designers, we have put together a series of hands-on activities, thought-provoking discussions, and fun games that allow both children (ages 7 & up) and adults to get involved in some of the key ideas of astronomy. Some are meant for use at special Astronomy Events. Others are for home exploration.
Click here to learn more about the History and Evolution of Family ASTRO. Then use the links below to learn more about how you can get involved in your community:
Family ASTRO Links
For Educators and Astronomers
For Families and Friends
So You Want to Start a Family ASTRO Site?
The Family ASTRO National Network
Family ASTRO Leader Kits (for Educators)
Family ASTRO Astronomy Events
Family ASTRO Take-Home Activities (games and kits)
A Sampling of Hands-On Family ASTRO Activities
Suggested Family ASTRO Event Agendas
Resource Lists and Background Reading
More Tips on Leading Astronomy Events and Working with Families
We gratefully acknowledge the Informal Science Education Division of the National Science Foundation for their generous support of the Family ASTRO program.


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Chroma is a manufacturer that bridges the gap between Japanese tradition and the European design with the type 301 series.
Chroma type 301 cutlery are designed by F.A. Porsche, who worked closely with chef of the decade, Jörg Wörther, in order to develop the final shape of the handle, which is optimized for maximum usability.
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Today, President Obama declared March 4-10, 2012 as National Consumer Protection Week, building on a coordinated effort that encourages consumers nationwide to take full advantage of their consumer rights and make better-informed decisions. The Commerce Department is using this occasion to showcase the efforts of our Internet Policy Task Force, which is leveraging the expertise of several Commerce bureaus that are aimed at ensuring continued innovation in the Internet economy and preserving consumer trust in Internet commerce and online interactions. In particular, the Task Force continues to move forward in our work to promote new efforts that will lead to improved Internet privacy protection and better security for consumers online.
In February, the Obama administration unveiled a "Consumer Privacy Bill of Rights" as part of a comprehensive blueprint to improve consumers' privacy protections and ensure that the Internet remains an engine for innovation and economic growth. The president's report called on the Commerce Department's NTIA to begin convening companies, privacy advocates and other stakeholders to develop and implement enforceable privacy policies based on the Consumer Privacy Bill of Rights.
NTIA is now moving forward and seeking public input on what issues should be addressed through the privacy multistakeholder process and how to structure these discussions so they are open, transparent, and most productive. Today, NTIA issued a formal request for comment (PDF). The comment period will remain open until March 26, 2012.
As NTIA Administrator Lawrence Strickling illustrated last week, we hope to receive meaningful suggestions and input from a range privacy stakeholders. Their continued involvement will be key for the future of consumer protection and we need your help to make it a success.
The report, "Consumer Data Privacy in a Networked World: A Framework for Protecting Privacy and Promoting Innovation in the Global Digital Economy," (PDF) resulted from a comprehensive review of Internet privacy policy and innovation in the Internet economy lead by the Commerce Department's Internet Policy Task Force.
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