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By Matt Rogers
PSDC Fantasy Sports Guru
Second only to the actual pre-draft stock movement of each player, is the ever-churning rumor mill about possible trades. People love to prognosticate about different teams throwing around players, picks and assets to move up or down the draft to get certain guys they need or want. These rumors often range and rage all over the place. Crazed fans throw out ideas in the universe that take hold. Teams use misdirection to try drive up trade value for players they no longer want. Owners and GMs try to push values of certain players up or down to get what they want for a little as possible. With only a week left to the real draft, the rumors are flying fast and furious and things are starting to take hold. Here is a look at the most interesting, or at least the most common, topic of these rumors, Marcus Mariota.
Tampa Bay Buccaneers
First off, it seems a foregone conclusion that the Bucs are taking Jameis Winston at No. 1. There are almost no rumors about anyone trying to acquire the No. 1 pick from them and even less talk about them shopping the pick. I heard very briefly that there was some interest in the Saints trading Drew Brees for the No. 1 pick to take Winston. That was followed quickly by news that Brees threatened to blow up the Superdome and set Bourbon Street on fire if he was traded. I haven't heard anything further on that front. [Read more…]


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The Studio is Open for Business!
Forever an Astronaut is working alongside Squarefruit Labs to offer a fully functional, multi-purpose, studio space conveniently located in the Central West End and adjacent to the TechArtista Coworking Center.
- Fully treated for audio recording
- Loading elevator with easy parking-lot access
- Private parking-lot with secure entrance
- Private lounge treated for audio recording and video viewing
- Full access to TechArtista Co-Working space built into rental
- Staff member on-hand for load-in, load-out, and pre-production needs

subset: commoncrawl


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Forget pulling little April Fools' Day jokes on just your family and co-workers. These days Facebook is quickly becoming the most popular spot to pull pranks. With instant access to an audience of family, friends and co-workers, pulling a prank on Facebook seems the obvious place to have a little April Fools' Day fun. Check out these prank ideas:
This Facebook prank spotted on Reface.com is sure to give your friends a little giggle. Thisinnocent-looking link will actually take friends to their own profile page when clicked:
Make a note to turn off the automatic thumbnail preview of the link that Facebook includes by clicking on the blue X in the upper right-hand corner so you don't spoil the fun when sharing.
Post things like:
A common April Fools' prank on Facebook is to fake a pregnancy, and folks are wising up to this annual joke. If you're looking to post a prank status update this year, check out some of these alternative ideas:
If you have good photo editing skills, you could photoshop a picture of you with a fake injury or even just post a close-up of a broken arm or a leg in a cast (nothing gory please — keep it light).
For a unique spin on this prank, consider posting a photoshopped image of a fake tattoo. This tutorial shows you how to make any digital image into a tattoo on a photo. While this technique is used by artists to give a sneak preview of what a tattoo would look like, it would also make for an excellent April Fools' prank when posted as your profile picture.
If you have a gazillion random online acquaintances -- oops, we mean Facebook "friends" -- pull an easy prank on them by simply changing your birthday to April 1 and watch the birthday wishes come rolling in. Consider giving your family and inner crew a heads-up so they don't mistakenly blow your cover early on by publicly calling you out on your prank.
If you know your bestie's account information, take a cue from prankster Nicole Richie, who in 2010 hacked into Kim Kardashian's Twitter account and posted silly messages. Keep the postings clean and lighthearted so you don't unintentionally turn your BFF into a frenemy, but have fun by posting random messages and pictures. Change someone's relationship status from single to engaged. Change his or her profile picture to one of someone else. Have a little (harmless) fun.
Even Kardashian thought that the prank pulled by Richie was "hands-down the funniest April Fools'!!"
What are some of your favorite April Fools' Day pranks for Facebook? Share in the comment section below!
Best April Fools' Day pranks for kids
April Fools' Day pranks and tricks
April Fools' Day food pranks
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Even though we woke up to rain on Sunday morning, we thought that it would clear in time for us to all head to TopShots Maroochydore. Besides we had got our boys so excited that we had to go – no matter what the day was like!
Luckily for all of us the rain held off for most of our time spent there. Actually some of the rides are based around water so it really didnt matter.
TopShots Maroochydore
Its free to enter TopShots at Maroochydore. All you do is pay for what you want to ride on, and for the mini Golf. I liked the set up – walking through the door it was almost like walking through a disco, with arcade games on one wall and table/seating on the other side. There is also two different courses for Mini Golf – providing 18 holes on each side of Topshots.
Mini Golf
Our boys were keen to try the rides, but at the same time was looking forward to the Mini Golf – so we headed there first. It was so much fun watching them trying to work out how to hit the ball with the least amount of strokes.
All Three Boys trying to work out how to play Mini Golf ~
Nicholas, Cameron and Kyle with Daddy keeping score!
Not sure but I think Kyle might have broken the record for how many hits it takes to get the ball into one hole!!
Kyle kept on hitting the ball ~
and eventually he got it in!
Blaster Boats
Once they had enough of laughing and
trying playing the mini golf we headed to the rides. Cameron jumped onto the Blaster Boats – where he had fun delight in wetting everyone and getting wet. I was trying to take the photos without getting the camera wet – gosh I never realised how good his aims were!!
Cameron on the Blaster Boats
Extreme Trampoline
The big hit for the day was the Extreme Trampoline. All of our boys lined up for this one…and wanted to have another turn. I havent seen a trampoline on its side before, nor one that tall. Kyle (being the monkey) got the hang of that one straight away. Cameron was so funny – he turned around so many times and instead of hitting the mat with his feet he ended up hitting the mat with his bum!
Nicholas and Cameron on the Extreme Trampoline!
Rock Wall
Inside is the Rock Wall. There are three different levels – easy, medium, and hard. Nicholas, Cameron and Kyle had a go together. Nic had the strength to be at the top in no time. Cameron's little arms and legs were shaking so much half way up. Kyle – he got to the middle and then stated that he was scared of hights.
Nicholas, Kyle and Cameron ~
Climbing up the Rock Wall
He has never ever said that before so David and I started laughing. He is normally the first up a tree and is sitting up the top while others are trying to get to the higher branches. I think it was a case of not having a big branch to wrap his arms and legs around that he thought he couldnt climb up higher. Yet he got down, and was straight back up for another try.
Zachery and Cameron on the Rock Wall ~
Zachery reached the top in no time…Cameron did better this time around!
Zachery sat back and watched everyone. Maybe its a teenager thing – but it took a lot of "come on – what you going to go on" before he had a turn of mini golf and then went on the Rock Wall. I have never seen him climb up like that before – but gee was he fast. Once you get to the top you hit a button and the buzzer goes off – he did it in seconds with all three levels. Good to see a smile on his face!
Pool Table
They even have a pool table……which Kyle and Daddy
had a go at trying pretended they knew how to play. It was good because Kyle and Daddy don't get to spend much time one on one having fun – usually one or two of his brothers are with him!
Woody Boys ~ Playing Pool There way!
Yet it was not your normal pool game. I think every rule in the game was broken that day. From picking up the ball and moving it to another spot for better aim, to even putting the balls into the hole with their hands.
There was so many "Near Misses" from Kyle, lots of laughter from me (as I was watching David cheat I couldnt stop laughing) and lots of trying to coach Kyle back away from the Arcade games to the pool table. Yet I saw both of them smiling from ear to ear so I reckon that the game was worth it!
Kyle was keen to try out the water slide, while Cameron and Nicholas went back onto the Blaster Balls.
Kyle loved the Water Slide
Cameron and Zachery had already raced each other up the climbing wall – well at least Cameron tried to race him!
Soon it was time to leave. Our tickets had been used on all of the attractions…Zachery sharing his around because he only went into the Cannon Ball Blaster and Climbed the rock wall.
Canon Ball Blaster
It was a great day out and the best part was being able to see what TopShots Maroochydore had to offer.
While we were there we watched a HUGE Birthday Party. It was massive – not sure how many children were there but I was thinknig what a brilliant place to have a party!
I also noticed how friendly the staff were. They all pitched in and helped each other, even though it was busy and so loud (children laughter and having lots of fun was heard by all!) there was a really great feel amongst the staff members.
It almost felt like a "Family Team" effort. Even one staff member brought out hot chocolate to the staff member that was looking after the Water Slide. They were young staff so it was good to see them taking care of each other – most of them were still at school or studying at Uni.
All in all it was a great day, and if were staying in the Sunshine Coast area we could so easily buy yearly passes as I could see the value in dropping in when ever we wanted!!
About Topshots Maroochydore
Location :-
Corner Maroochydore Road & Allora Drive
Maroochydore, 4558 Queensland Australia (07) 5452-7007
They have a variety of packages available – from unlimited Mini Golf, Combo Pack, Action Pack and Mega Pack.
Depending on your time will depend on what package will suit you and your family. The Mega Pack gives unlimited rides and unlimited mini golf at the price of $110.00 per family.
Opening Hours:-
Mini Golf, Blaster Boats, Cannon Ball Blaster, Extreme Trampoline, Rock Climbing, Water Slide and Arcade Games
Available for party and group Bookings – perfect for work functions, birthday parties, hens party, special occassions and more!
Have You Been To TopShots Maroochydore?
Please Note – Topshots Maroochydore provided our family passes for unlimited Mini Golf and Five rides. All thoughts and opinions are our own. We also have more photos over at our fanpage!


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Custom vanity with mid-century modern charm!/
When I bought my current home, I decided to rip out the renter-destroyed, heavily listing-to-one-side vanity from 1950 and replace it. I wanted something from the same era that reflected my eclectic style, on a DIY budget, and I wanted it in rose gold. No problem. I became obsessed with this idea until it all came together one day with a successful Craigslist ping. Behold the cute:Read More


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Category: Stock Graphic, Objects
Stock Graphic >> Object - Citrus Blends Watercolor Clip Art 239600 by the big lake @ CreativeMarket
File Size: 23.02 MB; Requirements: Adobe CS4+; Layered: Yes; DPI: 300 DPI.
Hand painted watercolor digital clip art perfect for scrapbooking, card making, blogs, graphic design, websites, logos, textures, photo & text overlays, and more! (Click on image to enlarge)
What you get.
- 10 different hand painted watercolor shapes
- Conveniently located in one PSD file
- Each shape has its own transparent layer
- Colors: warm colors (yellow/orange/red/pink)
- 300 dpi
- Varying sizes and dimensions
- High resolution, can be scaled up or down
Keywords: watercolor, clip art, painted, hand painted, abstract, colorful, digital design, branding, blogs, website, elements, citrus, watercolor brush, shapes, orange, yellow, pink, blended watercolors, drippy, summer clip art.


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MarkUBiz President Nominated for Top 20 Under 40
MarkUBiz is proud to announce our President and Founder Devin Sizemore's nomination to the Reno Tahoe Young Professionals Network Top 20 Under 40 award. MarkUBiz would like to thank all those nominated and voted on Devin's behalf.
About Top 20 Under 40
The RTYPN and the RGJ sponsor the yearly Top 20 Under 40 competition to recognize young and accomplished leaders under the age of 40. We were notified by the Executive Director of the RTYPN that our President had been nominated, and we were thrilled to see the descriptions a few of our nominators left.
Working For Devin Sizemore
We feel truly spoiled to work alongside Devin Sizemore every day and we are thrilled that his efforts to grow our company have paid off in so many different ways. Devin's leadership and inspiration is indicative of the business development and entrepreneurial spirit alive in the Reno-Tahoe area today.
Growth of MarkUBiz
MarkUBiz is approaching our 2-year anniversary where we will unveil our newly renovated office. Sizemore has grown the company from a small room in his apartment to a two-story building in Sparks where he now houses 6 employees.
Starting as a website development and online marketing company, MarkUBiz has adapted our focus to a full-scale agency to better suit the needs of our clients.
The focus on Client Relations continues to be the heartbeat of MarkUBiz, driving innovation and growth each year.
Come Celebrate With Us
The MarkUBiz team will be spending plenty of time in the community this month as we continue our Client Appreciation month. Please come visit our exhibit at the NCET Expo to find out more about the changes happening in our company.
We will also be hosting our Chamber Ribbon Cutting Ceremony late this month, which will be combined with our Educational Hour. We will have food and dessert at our office so please come join!


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Skip to content
As of 1 January 2010, this information only applies to the state public sector (including most Government Business Enterprises) and local government entities. For further information please refer to Industrial Relations.
Employers are required to pay employees their correct employment entitlements, including rates of pay, leave and allowances. For various reasons, employees do not always receive their correct entitlements.
If an employee believes that they have not been paid correctly, or not received all of their employment entitlements, they can request that SafeWork SA investigate the matter. If you are unsure whether you are under a State Award /Agreement or State Legislation, ring the SafeWork SA Help Centre on 1300 365 255.
Industrial Relations Claim Form
Fill out the Industrial Relations Claim Form if you are/were employed under a state award/agreement or state legislation.
If in doubt, ring the SafeWork SA Help Centre on 1300 365 255 for information or assistance.
When filling in the form, please ensure that you:
Please note: During the course of SafeWork SA's investigation, circumstances may arise which require us to make a copy of this claim available to your employer. Accordingly, you are encouraged to ensure that all statements or allegations made are accurate and truthful.
Industrial Relations Claim FormUpdated 12 March 2014 (PDF 112kb)


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Cup holders Bann and Elks start title defences in Dublin
Banbridge will begin the defence of their Irish Senior Cup with a trip to Dublin to face UCD on October 31.
Mark Tumilty guided his team to the final last season where they beat Cork C of I after extra time to guarantee European hockey and he's keen to see his team clear this year's first hurdle against the students.
Lisnagarvey and Annadale have been paired with Ulster Premier League opposition Civil Service and Belfast Harlequins respectively while Cookstown are one of three teams who were handed byes.
There are six cross-border ties including Instonians against Avoca.
Women's Irish Senior Cup holders Ulster Elks start with a tough trip to Old Alex in Dublin but Pegasus have an easier task against Ulster Premier League side North Down while Ards and Lurgan were two of six teams who receive byes.
Just five Ulster teams have entered the Irish Hockey Trophy while eight have entered the women's equivalent.
Men's Irish Senior Cup 1st round (October 31): Instonians v Avoca, Belfast Harlequins v Annadale, UCD v Banbridge, Newry Olympic v Glenanne, Rathgar v Mossley, Weston v Monkstown, Lisnagarvey v Civil Service, Railway Union v Raphoe, Kilkeel v Cork Harlequins, Corinthian v Cork C of I, North Down v YMCA, Clontarf v Pembroke Wanderers, UCC v Dublin University: Byes: South Antrim, Three Rock, Cookstown
Women's Irish Senior Cup 1st round (October 31): Randalstown v Armagh, Railway Union v Glenanne, Lisnagarvey v Dungannon, Hermes v Greenfields, Ballymoney v Cork C of I, Old Alex v Ulster Elks, Pegasus v North Down, UCC v Belfast Harlequins, UCD v Queen's, Pembroke v Loreto. Byes: Lurgan, Cork Harlequins, Corinthians, Muckross, Trinity, Ards
Men's Irish Hockey Trophy 1st round (October 31): Fingal v Antrim, Portadown v Bandon. Byes: Ashton, Bangor, Campbellians, Kilkenny, Limerick, Queen's
Women's Irish Hockey Trophy 1st round (October 31): Limerick v Ashton, Civil Service v Omagh, Clontarf v Dromore, Naas v NUIG, Ballymena v Catholic Institute, Three Rock Rovers v Portadown, Larne v Bandon, Kilkenny v Galway, Bray v Rainey, YMCA v Waterford, Clonakilty v Rathgar, Avoca v Monkstown. Byes: North Kildare, Genesis, Our Lady's, Banbridge.
Belfast Telegraph
Related Content
- Defender Pamela Glass happy to be back in the fold at Pegasus
- Ireland's call leads to big Bann clash being postponed
- Garvey stutter as Bann fire out derby warning


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Following the two devastating World Wars in the first half of the 20th century, a number of European leaders in the late 1940s became convinced that the only way to establish a lasting peace was to unite the two chief belligerent nations - France and Germany - both economically and politically. In 1950, the French Foreign Minister Robert SCHUMAN proposed an eventual union of all Europe, the first step of which would be the integration of the coal and steel industries of Western Europe. The following year the European Coal and Steel Community (ECSC) was set up when six members, Belgium, France, West Germany, Italy, Luxembourg, and the Netherlands, signed the Treaty of Paris. The ECSC was so successful that within a few years the decision was made to integrate other parts of the countries' economies. In 1957, the Treaties of Rome created the European Economic Community (EEC) and the European Atomic Energy Community (Euratom), and the six member states undertook to eliminate trade barriers among themselves by forming a common market. In 1967, the institutions of all three communities were formally merged into the European Community (EC), creating a single Commission, a single Council of Ministers, and the European Parliament.
Britain at first declined to be a member, largely it said because of its dependence on food at privileged prices from Australia and New Zealand. There was also its links with other countries outside of Europe which at that time were still British colonies. When Britain later tried to join, during the 1960s, the application was twice vetoed by the French president, Charles de Gaulle, because he thought that Britain would be a disruptive member.
In 1973, the first enlargement of the EC took place with the addition of Denmark, Ireland, and the United Kingdom.
This paper describes first describes British entry in European Union and its various aspects of relation with EU. It then describes how Britain has been reluctant in...


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- Please select a date to see the proper prices!
- Meal can be requested on the spot
Best offer
50 € / person / night, no meal
Description of the Accommodation
Rooms, services 42 comfortably furnished rooms are offered by Hotel Al Faro Cervia to guests looking for accommodation in Cervia. You are also welcome at the hotel for a fine local meal in the restaurant. The fans of actively spent leisure time may take the nearby opportunities to play table tennis, rent a bike, play bowling, billiard, minigolf, volleyball, go sailing, surfing and rent a boat. Upon preliminary request airport transfer is provided. The café and the bar have excellent atmosphere for a relaxed evening talk or a personal meeting. In the safe you may secure your valuables. An exact and detailed list of equipment in the rooms and of the services provided by Hotel Al Faro Cervia you will find on the information sheet below, including any applicable additional fees.
Payment In order to finalize the reservation you may be required to provide credit card guarantee or advance payment by credit card, depending on the chosen room, date and price.
Arrival, opening hours The earliest check-in time is 07:00, the latest check-out time is 10:00. The personnel is at your service in Italian and English languages.
Hotel Al Faro Cervia rooms Rooms
- Please select a date to see the proper prices!
Accommodation services
Relaxation: Table-tennis, Billiard, Minigolf, Bowling, Bike rental at the accommodation
Volleyball facility nearby, Sailing nearby, Surfing nearby, Boat rental nearby
Default services: Pet friendly (5 €/night), Garden, Bar, Cafe, Elevator, Safe deposit box
Airport transfer
Own restaurant
Hairdryer, Desk in the room


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Can I use Apple TV in my hotel room?
- Asked by Leonhard H
1 Answer from the Community
Depends, if you can plug your Apple TV into the tv in your room and if you can connect it to wifi.
It really depends on the tv that the hotel has provided because sometimes they will not let you have access to change the input to the TV.
- Answered by Aidan M from Inver Grove Heights
- Jul 5, 2013


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Hi Everyone!
My husband and I will be visiting the Washington, D.C. area for the first time this weekend and am hoping some of you will be able to suggest some places to eat during our visit since we are completely out of our element. Budget friendly would be nice, but not completely necessary. We will be staying in the Dupont Cirlce area near P street. We would also like to hear any suggestions on where to go grab a beer after dinner...we are in our late 20's and don't feel like doing the whole "club" scene...Thanks!


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The sgt_kiasfrogman.zip file you have requested: Skins / Players / Axis Frogman - 1.13mb is not available. Perhaps try browsing all files for the game Medal of Honor and upload any files you want to share or are missing. This is the only information we could locate:
A very nice frogman (scuba diver) skin which i believe was unfinished by EA but was finished by Sgt KIAVery nice skin, a nice change to the game, recommend the downloadDaniel_2005
We recommend you return to the download list and browse the links from there. If the problem persists, contact us with the details.


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|Home | About | Journals | Submit | Contact Us | Français
Dilated cardiomyopathy (DCM) is a major cause of morbidity and mortality. Two genes have been identified for the X-linked forms (dystrophin and tafazzin), whereas three other genes (actin, lamin A/C, and desmin) cause autosomal dominant DCM; seven other loci for autosomal dominant DCM have been mapped but the genes have not been identified. Hypothesizing that DCM is a disease of the cytoskeleton and sarcolemma, we have focused on candidate genes whose products are found in these structures. Here we report the screening of the human δ-sarcoglycan gene, a member of the dystrophin-associated protein complex, by single-stranded DNA conformation polymorphism analysis and by DNA sequencing in patients with DCM. Mutations affecting the secondary structure were identified in one family and two sporadic cases, whereas immunofluorescence analysis of myocardium from one of these patients demonstrated significant reduction in δ-sarcoglycan staining. No skeletal muscle disease occurred in any of these patients. These data suggest that δ-sarcoglycan is a disease-causing gene responsible for familial and idiopathic DCM and lend support to our "final common pathway" hypothesis that DCM is a cytoskeletalopathy.
Dilated cardiomyopathy (DCM) is a primary heart muscle disease characterized by left ventricular dilation and systolic dysfunction, with secondary diastolic dysfunction and occasionally associated right ventricular disease (1). This disorder has an incidence of 3.5–8.5/100,000 population per year and a prevalence of approximately 36/100,000 population (2, 3), which appears to be on the rise. In addition, DCM is the most common reason for heart failure and for cardiac transplantation in the US, with an estimated cost of $10 billion to $40 billion yearly (4).
The underlying causes of DCM are heterogeneous (5, 6), including myocarditis, drug toxicity (adriamycin), and ischemia-induced, metabolic, mitochondrial, and genetic abnormalities. A genetic cause of DCM is identified in approximately 30% of cases (7–9), with autosomal dominant inheritance being the most common (6). X-linked, autosomal recessive, and mitochondrial inheritance have also been reported, albeit less frequently (10).
In the past several years, the genetic basis of DCM has been sought, resulting in the identification of multiple genetic loci and five genes causing DCM to date. For X-linked DCM, two genes have been identified, including tafazzin (G4.5) in cases of the infantile-onset DCM (Barth syndrome) (11, 12) and isolated left ventricular noncompaction (13, 14), and dystrophin in later-onset X-linked cardiomyopathy (XLCM) (15–17). In the more common autosomal dominant DCM, five loci have been mapped for pure DCM (1q32 [ref. 18], 2q31 [ref. 19], 9q13-q22 [ref. 20], 10q21-q23 [ref. 21], and 15q14 [ref. 22]), and four loci have been mapped in families with DCM and associated with conduction disease (1p1-1q21 [ref. 23], 2q14-q22 [ref. 24], 2q35 [ref. 25], 3p25-p22 [ref. 26], and 6q23 [ref. 27]). Thus far, only the gene on chromosome 15q14 encoding cardiac actin (22), the gene on chromosome 2q35 encoding desmin (25), and the gene on chromosome 1p1-1q21 encoding lamin A/C (28) have been identified and mutations characterized.
We have proposed a "final common pathway" hypothesis (29, 30), which states that hereditary cardiovascular diseases with similar phenotypes and genetic heterogeneity will occur due to abnormalities in genes encoding proteins of similar function or genes encoding proteins participating in a common pathway cascade. In the case of DCM, we have proposed that mutations affect elements of the cell cytoarchitecture, based around the cytoskeleton (i.e., a cytoskeletalopathy) and sarcolemma, but also including elements that interact with the cytoskeleton including dystrophin, the dystrophin-associated glycoprotein complex (DAG; i.e., the sarcoglycans and dystroglycans), and intermediate filaments. Other final common pathways for specific cardiac phenotypes include the sarcomere in hypertrophic cardiomyopathy (31) and ion channels in cardiac rhythm disorders, such as long QT syndromes and Brugada syndrome (32).
Animal models of cardiomyopathy have also been described, including the BIO14.6 hypertrophic cardiomyopathy and the TO-2 DCM hamsters (33, 34), which are both due to mutations in the δ-sarcoglycan gene (35–37). These animals also exhibit histological features of muscular dystrophy (38). Mutations in this gene in humans cause autosomal recessive limb-girdle muscular dystrophy, LGMD2F (39), a disorder in which skeletal muscle disease can vary from mild (i.e., ambulatory beyond 15 years, similar to Becker muscular dystrophy [BMD]) to severe (i.e., similar to Duchenne muscular dystrophy [DMD] with early requirement of a wheelchair), and cardiac involvement has been documented in some patients (40). In addition, other LGMD2 disorders (LGMD2C, 2D, 2E) are caused by sarcoglycan mutations (γ-, α-, and β-sarcoglycan, respectively), suggesting that some LGMD phenotypes are sarcoglycanopathies. LGMDs may also include cardiac involvement associated with skeletal myopathy (41).
For these reasons, we have begun to analyze patients with DCM for mutations in genes encoding these proteins. In this report, we describe the identification of mutations in the δ-sarcoglycan gene in familial and sporadic cases of pure DCM. This extends the spectrum of phenotypes seen with sarcoglycanopathies, now adding pure DCM to the potential clinical presentation.
All patients were evaluated by physical examination (particularly focused in the cardiac and neuromuscular systems), chest radiography, electrocardiography, and echocardiography. The left ventricular size and function was evaluated off M-mode and two-dimensional echocardiographic images as described previously (17–19). Cardiac catheterization, angiography and endomyocardial biopsy was performed in some patients based on clinical indication. After informed consent, blood for lymphoblastoid cell line immortalization and DNA extraction was obtained, as described previously (17, 18, 21).
Two hundred unrelated and unaffected individuals (100 male, 100 female), as determined by history, physical examination, and echocardiography, were analyzed. After written informed consent, blood for lymphoblastoid cell line immortalization and DNA extraction was obtained.
A human BAC DNA PCR pool library (Research Genetics, Huntsville, Alabama, USA) was screened by PCR using primers designed to amplify each of the exons containing the coding region. PCR was performed in a 10-μL reaction containing 1.5 mM MgCl2, 10 pmol of each primer, 0.5 U Taq DNA polymerase (Life Technologies Inc., Rockville, Maryland, USA), using a Stratagene Robocyler (La Jolla, California, USA). After a 5-minute denaturation step at 94°C, 35 rounds of amplification (94°C for 30 seconds, 54–60°C for 30 seconds, and 72°C for 20 seconds) were performed. This was followed by a 72°C incubation for 2 minutes.
The exons of δ-sarcoglycan were subcloned into the vector pZero (Invitrogen, Carlsbad, California, USA). Clones were identified by whole cell PCR (20 μL reaction) and sequenced using an ABI373 (Perkin-Elmer Applied Biosystems, Foster City, California, USA) and Big Dye Terminator chemistry, according to the manufacturer's instructions.
Mutation analysis was performed using a modification of the method of Orita et al. (42). PCR primers were designed to amplify across the entire human δ-sarcoglycan gene in an exon-by-exon manner using the primers in Table Table1.1. Radioactive PCR was performed with 100 ng genomic DNA in a 10 μL reaction containing 1.5 mM MgCl2, 10 pmol of each primer, 0.05 μCi [α-32P] dCTP (Amersham Life Sciences Inc., Arlington Heights, Illinois, USA), 0.5 U Taq DNA polymerase, and 30 rounds of amplification (92°C for 30 seconds, Y°C for 30 seconds, 72°C for 30 seconds), where Y represents the annealing temperature shown in Table Table1.1. After PCR amplification, the samples were denatured and then electrophoresed for 24 hours in a denaturing 10% polyacrylamide:bisacrylamide (50:1; Bio-Rad Laboratories Inc., Hercules, California, USA) gel with and without 12% glycerol, at 8 W in a 4°C cold room. Bands were visualized by exposure of the dried gels to Kodak BioMax MS-1 film (Eastman Kodak Co., Rochester, New York, USA).
Normal and aberrant single-strand conformational polymorphism (SSCP) conformers were cut directly from dried gels, eluted in 100 μL of distilled water (65°C for 30 minutes), and then reamplified. After purification using Qiaquick columns (QIAGEN Inc., Valencia, California, USA), PCR products were sequenced, as already described here. Protein secondary structure predictions were performed using the Garnier-Osguthorpe-Robson algorithm (43) with the Wisconsin Package (version 10.0), Genetics Computer Group (Madison, Wisconsin, USA).
Frozen myocardial sections (5-μm) were cut from the left and right ventricles. Unfixed sections were stained, using anti–α-, anti–β-, anti–γ-, and anti–δ-sarcoglycan antibodies, as well as antidystrophin (COOH-terminal antibody; Novocastra, Newcastle, United Kingdom). Each primary antibody was diluted 1:10 in PBS (pH 7.2) containing 5% BSA and then added to the sections; these were incubated for 30 minutes at room temperature. The slides were washed three times in 0.1X PBS (pH 7.2) at room temperature. The sections were then incubated with secondary antibody (FITC-conjugated anti-mouse; Novocastra), diluted 1:400 in PBS (pH 7.2) containing 5% BSA, for 15 minutes at room temperature. The slides were washed three times in 0.1X PBS (pH 7.2) and mounted with Cytoseal 280 mounting medium (Stephens Scientific, Riverdale, New Jersey, USA) before observation.
One family with familial DCM (FDCM no. 1100) was identified by history, physical examination, and echocardiography. All affected individuals were symptomatic with evidence of congestive heart failure at young age (Table (Table2).2). Neuromuscular examination was normal in all individuals, including muscle bulk and strength, reflexes, and gait. All affected individuals remained athletic until their onset of heart failure or sudden death. Echocardiographically, all affected individuals had severely dilated left ventricular chambers (with Z scores > 4) and moderate to severe systolic dysfunction (ejection fractions < 35%). None of the clinically unaffected members of the family had abnormal echocardiograms. Cardiac transplantation was necessary in the 21-year-old son (III:7) of the proband (II:5) as seen in the pedigree (Figure (Figure1).1). Before transplant, cardiac catheterization with angiography was performed. The coronary arteries were normal on selective angiography. Gross and histopathologic examination of the explanted heart demonstrated features of classic DCM, including increased heart weight, left ventricular dilatation, histopathologic evidence of myocyte hypertrophy, and moderate fibrosis. No evidence of ischemia was noted, and no inclusions were seen. The coronary arteries were normal by inspection and histologically. Creatine kinase (CK) was mildly elevated in this patient (Table (Table2),2), with the muscle isoform (CK-MM) entirely responsible for the elevation. No other affected members of the family had CK levels analyzed before death, and the unaffected members (II:2, II:3, III:3, III:4, and III:5) had normal levels. Autopsy specimens for deceased individuals were pathologically similar to those found in the explant of patient III:7, and the coronary arteries were normal in all cases.
Fifty patients ranging in age from 3 days to 18 years (mean, 9.5 years) with clinically apparent DCM presenting with heart failure and echocardiograms diagnostic for DCM were identified. Cardiac catheterization, angiography and endomyocardial biopsy was performed in 17 patients, and inflammatory infiltrate consistent with borderline (n = 4) or active (n = 2) myocarditis using the Dallas criteria was found in 35% of these individuals. The remaining patients were negative for inflammatory infiltrates. Coronary angiography was normal in all cases. In eight patients, cardiac transplantation was performed, whereas five patients died prematurely and without transplantation. Coronary arteries were normal in all cases. CK levels were also normal in these individuals (Table (Table22).
The cDNA sequence published by Nigro et al. (44) (GenBank accession no. X95191) and by Jung et al. (45). (GenBank accession no. U58331) identified alternative sequences at the 3′ end of the mRNA in expressed sequence tags (ESTs) identified in muscle (44) or in placenta (45). Subsequently, we refer to these spliced forms as the muscle (M) and placental (P) isoforms, respectively, although both are expressed in the heart (data not shown).
Screening of a human BAC library identified five BACs encoding the exons of δ-sarcoglycan. BACs 523E7 and 417E23 encoded exons 2 and 3; BACs 555B9 and 557H6 encoded exons 4, 5, 6, and 7; and BAC 212M24 encoded exons 8 and 9. Subcloning of these BACs into plasmid vectors, followed by DNA sequence analysis, produced the sequences of the exon-intron boundaries, and primers complementary to intron sequences were synthesized for SSCP analysis (Table (Table1).1). Primers were designed to amplify across each of the exons including exon 9 of both the muscle isoform (D-Sarc9mF and D-Sarc9mR; Table Table1)1) (44) and the placental isoform (D-Sarc9pF and D-Sarc9pR: Table Table1)1) (45). Nigro et al. (44) reported the locations of seven introns within the coding region of human δ-sarcoglycan mRNA. We identified an eighth intron located within the 5′ UTR. The location of this intron within the 5′ UTR suggests that the initiation codon is located within exon 2, as occurs in the hamster.
SSCP was performed using the primers designed to amplify across the δ-sarcoglycan gene. In family FDCM no. 1100, three affected individuals were identified with abnormal SSCP conformers (Figure (Figure2).2). None of the unaffected members of the family and none of the 200 control individuals had this abnormal conformer. DNA sequence analysis identified a single nucleotide change, 451T→G in exon 6, which changes the amino acid at codon 151 from serine to alanine (S151A). This change from a polar to nonpolar amino acid is significant and is predicted to alter the secondary structure of δ-sarcoglycan, enabling an extended α-helix. Computer modeling of this portion of the protein (43) supports secondary structural changes (data not shown) as well, but functional studies are required to confirm the effect of these mutations.
SSCP analysis of the fifty sporadic cases of DCM identified four patients with abnormal conformers. In two patients, a 3-bp deletion (either 710–712delAGA or 711–713delGAA) of δ-sarcoglycan exon 9p was identified (Figure (Figure3)3) that deletes a codon encoding the amino acid lysine at position 238 (ΔK238); screening 200 control individuals, as well as the phenotypically normal parents of these children, did not identify the same abnormality. The deletion of lysine 238 is predicted to result in a change in the secondary structure in which the folding of the protein is disrupted, consistent with a disease-causing mutation. In addition, two other patients had abnormal conformers that, upon sequencing, appear to be polymorphisms. In one case, a 290G→A transition in exon 4, which changes the arginine at codon 97 to glutamine (R97Q), was identified. This 290G→A transition was previously reported to be a polymorphism (45). In another patient, a T→A transversion within intron 4, 38 nucleotides from the intron 4–exon 5 boundary, was found. One of 200 controls was identified with the identical change, most likely representing a polymorphism, especially considering the distance from the intron-exon boundary. However, in an attempt to document whether this caused a change in the splicing of the mRNA, RNA was isolated from lymphoblastoid cell lines (from the patient and from a control) and subjected to RT-PCR using primers designed to amplify this region. However, amplification was unsuccessful, probably due to limited illegitimate transcription of δ-sarcoglycan in lymphoblasts.
Tissue from the explanted heart of one of the patients with the ΔK238 deletion was available for immunohistochemical analysis. Frozen sections of right and left ventricle were stained with antibodies against α-, β-, γ-, and δ-sarcoglycan, or the COOH-terminus of dystrophin. In parallel, myocardial sections from the explanted heart of a patient with congenital heart disease (i.e., control patient) were stained for comparison. Although the staining of dystrophin and α-, β- (data not shown), and γ-sarcoglycan (Figure (Figure4)4) was indistinguishable between the control and affected patient samples, the staining for δ-sarcoglycan was significantly reduced in the patient with the ΔK238 mutation (Figure (Figure4).4). Interestingly the δ-sarcoglycan antibody is NH2-terminal specific whereas the mutation is COOH-terminal, suggesting this mutation leads to a significant change in δ-sarcoglycan structure.
Although the pathophysiology of DCM is well known (5), the underlying genetic mechanism for this disorder has remained unclear. Whether the disease results from inflammation, autoimmune, or genetic causes has been speculated upon for decades (46) but a unifying mechanism has not been proved. During the past several years, however, a variety of clues to the underlying cause of DCM, as well as the underlying basis for other inherited cardiovascular diseases, have emerged. This has led us to speculate on the existence of a final common pathway of cardiovascular disease in which specific phenotypes result from mutations in families of proteins essential for specific functions. For instance, the basis for hypertrophic cardiomyopathy (HCM), a primary heart muscle disease in which ventricular wall thickening (hypertrophy) and diastolic dysfunction occur, has been demonstrated to be due to mutations in genes encoding sarcomeric proteins such as β-myosin heavy chain, α-tropomyosin, cardiac troponin T, cardiac troponin I, myosin binding protein-C, essential and regulatory myosin light chains (reviewed in ref. 31), and cardiac actin (47). In addition, the inherited long QT syndromes (LQTS) have been shown to be due to mutations in genes encoding ion channels, such as the potassium channel genes KVLQT1, KCNE1, and HERG, KCNE2, and the cardiac sodium channel gene SCN5A (reviewed in ref. 32). Owing to the consistent protein classes found to be mutated in phenotypically similar patients (i.e., the final common pathways of sarcomeric proteins in HCM; ion channels in LQTS), we used this final common pathway hypothesis (29, 30, 48) to speculate that similar protein types would be mutated in DCM as well.
Five genes have been previously identified and characterized in cases of familial DCM. In Barth syndrome, the gene G4.5, which encodes a novel protein family called tafazzins, is mutated (11–14). Although well characterized at the molecular level, to our knowledge the function of the encoded protein is not currently known. However, the gene responsible for XLCM, dystrophin, is well defined (15–17). This gene, which also causes Duchenne (DMD) and Becker (BMD) muscular dystrophy when mutated (49), encodes a large (427-kDa) cytoskeletal protein that resides at the inner face of the sarcolemma, colocalizing with β-spectrin and vinculin. Dystrophin protein is thought to assume a rod-shaped structure with an actin-binding domain at the NH2-terminus. The COOH-terminal domain is associated with a large transmembrane glycoprotein complex, the DAG, which is thought to mechanically stabilize the plasma membrane of muscle cells as well as serving a cell signaling role. This complex is formed by the dystroglycan subcomplex (α-dystroglycan and β-dystroglycan), sarcoglycan subcomplex (α-, β-, γ-, and δ-sarcoglycan), caveolin-3, syntrophin, dystrobrevin, and sarcospan and serves as a link between cytoplasmic actin, the membrane, and the extracellular matrix of muscle via laminin-α2 (50, 51). Mutations in dystrophin, the DAG subcomplexes, or laminin result in a wide spectrum of skeletal myopathy and/or cardiomyopathy in humans and animal models such as the mouse or hamster (30–36, 52).
The third mutant gene thus far identified, cardiac actin, has been identified as the gene responsible for the chromosome 15q14-linked autosomal dominant FDCM (22). This gene encodes a member of the thin filament of the sarcomeric unit. When mutated near the dystrophin-binding site, DCM occurs. However, when mutations near the sarcomeric end of actin occur, a HCM phenotype develops (46). The likely reason that this mutant gene causes a DCM phenotype is that the link between dystrophin and actin is disrupted, thereby disassociating the actin cytoskeleton from the muscle membrane and extracellular matrix, leading to cellular degeneration and necrosis. Recently, mutations in α-actin were shown to cause the skeletal muscle disorders actin myopathy and nemaline myopathy as well (53).
The other two genes identified in FDCM are desmin (2q35) (ref. 25) and lamin A/C (1p1-1q21) (ref. 28), both of which are thought to cause abnormalities of structural support when mutated, as well. Interestingly, these genes have both been shown to be associated with skeletal myopathy and, in some cases, with conduction system disease (28, 54, 55). The identification of mutations in δ-sarcoglycan, another member of the cytoskeleton/sarcolemmal structural support, further supports our final common pathway hypothesis (29, 30, 48). Furthermore, mutations in this gene have previously been shown to cause either dilated or hypertrophic cardiomyopathies in the hamster and mouse, providing support that this gene, which maps to chromosome 5q33-34 in humans (42), is disease-causing in the patients described in this report.
LGMDs are a group of disorders that are characterized by progressive muscle weakness affecting both upper and lower limbs. They mainly have autosomal recessive inheritance, elevated CK, and are due to mutations in sarcoglycans, including LGMD2C (γ-sarcoglycan), LGMD2D (α-sarcoglycan), LGMD2E (β-sarcoglycan), and LGMD2F (δ-sarcoglycan). LGMD2F was initially reported by Nigro et al. (56) in four Brazilian families, and all affected members had a frameshift mutation in exon 7 (Δ656C) that resulted in premature truncation of the translatable δ-sarcoglycan protein. These patients had severe DMD-like disease. Duggan et al. (57) and Moreira et al. (40) identified homozygous mutations (W30X and R165X nonsense mutations, and E262K missense mutation, respectively) in δ-sarcoglycan in patients with DMD-like disease as well. In the case of the family studied by Moreira et al., the electrocardiogram was consistent with left ventricular hypertrophy, but no other cardiac information (i.e., echocardiogram) was reported.
Thus, LGMD associated with sarcoglycan mutations appears to be inherited as a recessive disease. However, in the patients with DCM described in this report, we propose that dominant negative mutations in δ-sarcoglycan result in absent skeletal myopathy in the face of late-onset DCM. These mutations are similar to those described in LGMD2F, except that they are heterozygous. Although heterozygotes within LGMD2F families have not been described to be affected, it is possible that cardiac evaluation overlooked cardiac pathology or the cardiac dysfunction had not become apparent at the time of evaluation, given that DCM is, in many instances, age dependent. In DMD and BMD, disorders of dystrophin, female carriers commonly develop cardiomyopathy but usually do so later in life than the affected males. Further, as cardiac disease is now appearing to be common in most (if not all) skeletal myopathies, it is not surprising that δ-sarcoglycan mutations could have wide clinical phenotypic heterogeneity. Melacini et al. (41) reported DCM to be relatively common in sarcoglycanopathies (about 30%), although they did not find DCM with δ-sarcoglycan mutations in the LGMD patients with DCM studied.
Interestingly Nigro et al. (44) identified a dominant missense mutation (N211Y) in δ-sarcoglycan in a family with mild proximal myopathy and mild CK elevations (threefold). Four autosomal dominant forms of LGMD have also been described (LGMD1A-D). To our knowledge, only genes for LGMD1B, which is associated with atrioventricular conduction disturbances, and LGMD1C have been identified, namely, lamin A/C (58) and caveolin-3 (59), respectively. It is possible that mutations in different domains of δ-sarcoglycan result in either a cardiac or skeletal muscle phenotype, similar to that described for dystrophin (15–17, 49). Similarly, these differences could account for the modes of inheritance (i.e., autosomal recessive or autosomal dominant).
Multiple animal models with sarcoglycan deficiency have been produced or are naturally occurring, including the cardiomyopathic hamster due to deletion of exons 1 and 2 of δ-sarcoglycan (35). Hack et al. (60) generated a γ-sarcoglycan–deficient mouse that developed progressive muscular dystrophy, pronounced cardiac muscle degeneration, and reduced survival. These mice also had reduced levels of β- and δ-sarcoglycan staining of muscle (with normal dystrophin, dystroglycan, and laminin-α2) and elevated CK at baseline (suggesting CK release occurs by mechanisms other than mechanical injury) and with exercise. Coral-Vazquez et al. (61) studied mice deficient in α-sarcoglycan and δ-sarcoglycan and demonstrated that only δ-sarcoglycan null mice developed cardiomyopathy, with focal areas of necrosis by 3 months of age; death occurred by 6 months of age typically. Coronary artery abnormalities, particularly constriction with pre- and poststenotic dilation and reduction in lumen size, were noted. This has been supported in studies in humans (62), but no coronary artery disease has been found in any of the patients described here. Coronary angiography and echocardiography (transthoracic and in some cases transesophageal) identified normal coronary arteries in all patients with δ-sarcoglycan mutations, and no evidence of ischemia was found in the myocardium. Histologically and by gross evaluation, the coronary arteries were normal in the explanted hearts of the transplanted sporadic and familial cases. Araishi et al. (63) studied β-sarcoglycan–deficient mice, which exhibited progressive muscular dystrophy, muscular hypertrophy, severe elevations in CK (about 100 times higher than in wild type), and cardiac fibrosis. Immunohistochemical staining demonstrated α-, β-, γ-, and δ-sarcoglycan and sarcospan to be absent in the sarcolemma, whereas laminin-α2, α- and β-dystroglycan, and dystrophin were normal. In one patient with a ΔK238 deletion, no reduction in α-, β-, or γ-sarcoglycan or dystrophin, was noted.
In conclusion, the description of mutations in δ-sarcoglycan in patients with DCM provides further support for the concept that the final common pathway for DCM is the cytoarchitecture, comprising the cytoskeleton, sarcolemma, and interacting components. In addition, the fact that mutations in δ-sarcoglycan and dystrophin, as well as mutations in G4.5, can also result in skeletal myopathy, suggests that patients with DCM should be carefully evaluated for skeletal muscle weakness and that neurologists caring for patients with skeletal myopathies should be cognizant of the potential for associated cardiomyopathies in their patients.
We thank P. Sen of the Child Health Research Center, Baylor College of Medicine, for the DNA sequence analysis. K. Bowles is a Howard Hughes Medical Institute predoctoral fellow. This work was supported by the Abercrombie Cardiology Fund of Texas Children's Hospital (N.E. Bowles), Texas Children's Hospital Foundation Chair in Pediatric Cardiac Research (J.A. Towbin) and NIH grants from the National Heart, Lung, and Blood Institute (J.A. Towbin).
PubMed Central Canada is a service of the Canadian Institutes of Health Research (CIHR) working in partnership with the National Research Council's national science library in cooperation with the National Center for Biotechnology Information at the U.S. National Library of Medicine(NCBI/NLM). It includes content provided to the PubMed Central International archive by participating publishers.


text:
"Ethan, what is this?" Sarah held up the small blue box. I smiled, turning from my now-closed locker to look at her.
"Just a gift." My cheeks grew hot, and I ducked my head, hoping she didn't notice. She gave me a look, but opened the box anyway.
I tilted my head up just enough to see her face. It was one of hurt, anger, and a touch of…hunger.
"A compact mirror? Ethan, is this some sort of sick joke, because it's not funny!" Her fangs flared out, tears sprouting in her eyes. For a second, I felt bad, but I reminded myself what I had done.
"No, Sarah, please just open it." Sarah looked at me, a single tear slid down her cheek. A look of doubt in her eyes, she slowly opened the mirror. At the exact moment she caught a glimpse of the mirror, it fell from her hands, and a gasp escaped from her mouth in shock
"E-Ethan, I can see myself in this!" She cried out, wrapping her arms around me tightly. I smiled, hugging her back.
"Yeah, Benny made it for me." I murmured, looking down ever so slightly.
"That is the nicest thing anyone has ever done for me! Thank you so much, I'll treasure it forever." She pecked me on the cheek, and I blushed even harder. Sarah picked the compact mirror up from the floor and buried it in her back-pack. She turned back to me, and with a dark blush on her face, she pecked me again, on the lips.
"Thank you Ethan, really." She turned away. "I love you." She muttered before rushing away to her next class.
I stood, shocked, touching the spot where her lips had been only seconds ago. "I love you too." I said softly, even though nobody was listening.


text:
Triiodothyronine activates lactate oxidation without impairing fatty acid oxidation and improves weaning from extracorporeal membrane oxygenation
Background: Extracorporeal membrane oxygenation (ECMO) provides a rescue for children with severe cardiac failure. We previously showed that triiodothyronine (T3) improves cardiac function by modulating pyruvate oxidation during weaning. This study was focused on fatty acid (FA) metabolism modulated by T3 for weaning from ECMO after cardiac injury. Methods: Nineteen immature piglets (9.1-15.3 kg) were separated into 3 groups with ECMO (6.5 hours) and wean: normal circulation (Group-C);transient coronary occlusion (10 minutes) followed by ECMO (Group-IR); and IR with T3 supplementation (Group-IR-T3). 13-Carbon labeled lactate, medium-chain and long-chain FAs were infused as oxidative substrates. Substrate fractional contribution to the citric acid cycle (FC) was analyzed by 13-Carbon nuclear magnetic resonance. Results: ECMO depressed circulating T3 levels to 40% baseline at 4 hours and were restored in Group-IR-T3. Group-IR decreased cardiac power, which was not fully restorable and 2 pigs were lost because of weaning failure. Group-IR also depressed FC-lactate, while the excellent contractile function and energy efficiency in Group-IR-T3 occurred along with a marked FC-lactate increase and [ATP]/[ADP] without either decreasing FC-FAs or elevating myocardial oxygen consumption over Group-C or -IR. Conclusions: T3 releases inhibition of lactate oxidation following ischemia-reperfusion injury without impairing FA oxidation. These findings indicate that T3more »
- Publication Date:
- OSTI Identifier:
- 1188923
- Report Number(s):
48162; 600306000
- DOE Contract Number:
- Resource Type:
- Journal Article
- Resource Relation:
- Journal Name: Circulation Journal, 78(12):2867-2875
- Research Org:
- Pacific Northwest National Laboratory (PNNL), Richland, WA (US), Environmental Molecular Sciences Laboratory (EMSL)
- Sponsoring Org:
- Country of Publication:
- United States
- Language:
- English
- Subject:
- ECMO; Myocardial metabolism; Pediatric; Environmental Molecular Sciences Laboratory


text:
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Aunt Issy
New Member
Date Joined Jun 2008
Total Posts : 7
Posted 6/17/2008 8:04 AM (GMT -7)
Hello everyone. I'm a newbie here. I had a question for everyone and wondered if I could get some advice. I was diagnosed with IBS at the age of 17. At the age of 28 I had some tests done and the doctors confirmed the cause of my IBS to be overgrowth of bacteria in my small bowel. I have chronic diarreaha and it pretty much controls my life. I have tried treatments, but nothing really works. Recently, I found out I am pregnant. I am only about
3-4 weeks along now. For the last week and a half my problems with diarreaha are worse than ever!!! I go to the bathroom anywhere around 6-12 times a day and it's always diarreaha. I called my OBGYN and they aren't too concerned about
it. A friend of mine, who is a nurse, says it may be a surge in hormones causing these problems. I always noticed before right when I was to start my period my IBS would go nuts. Anyways, I wondered if anyone has experienced this same problem when they were pregnant. I am going crazy!!! I feel like my life just isn't in my control. I stay at home all the time and am afraid to go anywhere. I am even uncomfortable in my home sometimes because we only have one bathroom here and when my husband is home I am afraid he will be using it when I need it. Anyways, I hope someone can offer me some advice. I am tired of all this! Thanks for listening.
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Veteran Member
Date Joined Apr 2005
Total Posts : 3269
Posted 6/17/2008 8:16 AM (GMT -7)
Hi Aunt Issy,
Welcome to HealingWell!
I can't really help you here, as I have never been pregnant. I just wanted to wish you a warm welcome and to say HANG IN THERE. I've seen a few moms come through here that have said their IBS got worse, and some say it got better when they were pregnant. Like your nurse friend mentioned, it's all hormonal. Maybe, just maybe, you'll get past the dreaded 3 month mark, do a total 180, and feel even better than before.
Hopefully someone else will come along who has actually been pregnant...
Take care and good luck!
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Veteran Member
Date Joined Jun 2005
Total Posts : 2976
Posted 6/17/2008 8:17 AM (GMT -7)
I haven't been pregnant, but yes, there's definitely a hormonal link! Some women on here have gotten normal (!!!) while pregnant, only to go back to the same old thing after the baby, but then some are like you and get worse. While your doctor may not be concerned with your D right now, she should be if you continue to have it. Make her check your vitamin and mineral levels regularly so that you can make sure that you and the baby are getting everything you need. Pregnancy is depleting enough of those things, but D will make it worse.
What sort of treatments did you have for your bad bacteria problem?
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Lady Frog
Regular Member
Date Joined Feb 2008
Total Posts : 139
Posted 6/17/2008 8:22 AM (GMT -7)
My pregnancy didn't pan out due to complications but I had the same thing happen. At about
3 weeks my IBS went bonkers. I swear every hour on the hour I was in the bathroom. When I called my OB/GYN they didn't seem to care either. In fact when I asked if there was anything they could do to help( between my morning sickness that started at the same time and my IBS I couldn't eat anything and could barely drink 16oz of fluid a day) they said they would not do anything that might hurt the baby. Yeah and mom losing 10 lbs in two weeks is good for the baby. Everything thing I have read though is that your IBS will go nuts for the first trimester, ease up in the second and in the third start going nuts again but not as bad. Personally when hubby and I try again in fall I have a new doctor that listens and he has already said that if I'm near as bad as when I finally saw him this time, he's not going to do anything that might hurt the little one but wants to try different ways to help me control my IBS. The big thing was dehydration and I don't want that to happen to you. Please keep your fluid intake up for both yourself and the little guy. Eat what ever strikes your fancy. I was told it wasn't so much what you eat but just that you do. I ate nothing but bagels and applesauce for a month. I'm sick of them now but I'd eat them again in a heartbeat if that's what my tummy wanted. Good luck with the little one.
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Aunt Issy
New Member
Date Joined Jun 2008
Total Posts : 7
Posted 6/17/2008 8:22 AM (GMT -7)
Hi Keriamon. My gastro dr. would put me on a coarse of anti-biotics for my IBS. It never worked very long. A week or two at the most. Getting an appointment with her right now is very hard. Doesn't seem to matter how much trouble I am having. I will also keep in contact with my OBGYN about
the diarreaha. Thanks for your advice and also thanks to 7Lil for the nice words.
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Aunt Issy
New Member
Date Joined Jun 2008
Total Posts : 7
Posted 6/17/2008 8:27 AM (GMT -7)
Lady Frog,
It is nice to hear from someone who knows what I am going through right now. Thanks for the advice. I am trying to take extra good care of myself right now because a year ago yesterday I miscarried with the first pregnancy. I really paranoid about
everything right now and this IBS doesn't make it any easier! I just want a healthy baby. I don't think I can go through that pain again. Anyways, thanks again. I appreciate it.
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Veteran Member
Date Joined Jun 2005
Total Posts : 2976
Posted 6/17/2008 8:38 AM (GMT -7)
Bad bacteria is EXTREMELY hard to eradicate. Based on what others on here have gone through, it seems to take a strong antibiotic for weeks, even months, to clear some of it up. I have read about
someone being on Cipro, I think it was, for like 6 months! Some antibiotics are better at clearing out the guts than others; not all will work well. Also, did anyone put you onto probiotics? That's good bacteria. You really have to have the combination to have any hope of it sticking. If you put the good bacteria in there after you have wiped your guts clean, they will take up residence and keep the bad stuff pushed out. If you wipe it clean and leave it empty, though, it's easy for a few hidden bad bacteria, or some you pick up, to get in that nice empty space and breed and spread worse than kudzu. They'll take over again.
Might be something you talk to your doctor about
trying again after the baby.
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Veteran Member
Date Joined Apr 2005
Total Posts : 3269
Posted 6/17/2008 9:19 AM (GMT -7)
As Keri mentioned before, make sure your doc does blood work. When I was at my worst (D like 6-10 times a day) my Folic Acid and B12 were extremely low. My doc told me that if I wanted to get pregnant I had to make sure both those levels were in the normal range.
Again, as Keri suggested, probiotics are essential to a healthy gut flora. In order to push out the bad bacteria, it is extremely important to replenish the good bacteria.
Wishing you well...
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Veteran Member
Date Joined Jul 2007
Total Posts : 1956
Posted 6/17/2008 9:31 AM (GMT -7)
Hi there. My IBS-like symptoms have been brought on by having part of my colon removed (rectal cancer) and/or my gall bladder out, 9 years ago. While I've never been officially diagnosed with IBS-D, my symptoms mimic so many of you here and I've been able to find wonderful support on this forum. So please stick around! Warmest congratulations on your pregnancy!
I'm 53 now so my periods are hit or miss, usually 3 months apart. But when I was regular, I noticed loose bm's, long before my IBS issues started. Someone once told me that our periods are nature's way of cleaning us out (bowels too). I could almost predict when I would start because the loose bm's would come. I noticed this connection as far back as my 20s. Many women here on this site have mentioned IBS flares before their periods start.
What I would suggest is eating foods that firm up your stool. Just tackle this increase in D, with a low residue diet (what I still follow, 9 years now). I would concentrate on foods such as bananas, mashed potatoes, applesauce, white bread/bagels/english muffins, chicken, turkey, fish, plain or vanilla flavored yogurt. I would also avoid foods or beverages that increase D - whole wheat products, fresh produce such as berries, pineapple, baby lettuce greens, hot tea, coffee, caffeine, carbonated beverages, etc. Try this for a 24 to 48 hour period and keep a food journal. See if you notice an improvement. If so, ask your OB if you could go on a low residue diet while pregnant or at least for this transitional stage (your GI tract getting used to hormonal surges).
I hope you feel better.....hang in there. You found the right place to vent, etc.
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Veteran Member
Date Joined Jun 2005
Total Posts : 2976
Posted 6/17/2008 1:03 PM (GMT -7)
Ooo, dehydrated banana chips will constipate anyone in a heartbeat. Doesn't take too many to do in a regular person. I have been known to eat them just because I was having a long-running spell of my stools being too loose, or I'm getting ready to take a trip. I think they should be an in-car snack for anyone with D!
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Regular Member
Date Joined Jun 2008
Total Posts : 416
Posted 6/17/2008 1:11 PM (GMT -7)
Aunt Issy,
I found that during my pregnancy my IBS went away. I'm sorry that's not the case for you. And I'm sorry about
your misscarriage. I had one of those too. Very very heartbreaking. I will keep you in my prayers. May God bless you and your baby.
"There is hope for every man, a solid place where we can stand, in this dry in weary land, there is hope for every man... Jesus is hope for every man" -Casting Crowns
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Aunt Issy
New Member
Date Joined Jun 2008
Total Posts : 7
Posted 6/18/2008 7:44 AM (GMT -7)
Thank you all for the advice. I really appreciate it. I am so glad I found a place where I can share what is going on and have people have the same problems. Today hasn't been too bad so far. I'm hoping the symptoms calm down some. Before I got pregnant I always had IBS problems, but never this much. My biggest concern is going places. I always have to make sure there is a bathroom I can use whenever I need it. I called my OBGYN again yesterday and she told me as long as I keep myself hydrated I should be fine, but if the symptoms get worse I should call them back. They suggest I call my Gastro dr. I did, but they didn't seem to have any advice for me. I was so frustrated and angry at them. I am considering changing Gastro drs. It feels like no one cares. I am going crazy here. Every twinge of pain I get I think the worse. I guess that was from miscarrying last year. I am afraid the same thing will happen again. My hubby said that last time I was pregnant, my IBS didn't flare up much so maybe it flaring up this time is actually a good sign. I laughed at that, but who knows....maybe it is! Maybe I have to suffer some to get some happiness. Oh well, I am going on and on and on here!!! I just need to vent some I guess. Thanks all for listening and caring.
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Rooms, services Take a few-days trip to Germany and enjoy the hospitality of Gutshaus Kubbelkow Bergen auf Rügen. The guests of the hotel may stay in eight nicely furnished, comfortable rooms in Bergen auf Rügen. In case you ever feel like eating in, you may taste delicious local dishes in the restaurant of the hotel. For guests arriving by car parking possibility is available nearby. Refreshing wellness services will be available to you on the spot, <a/an> steam room will also be at your disposal. Car rental service and organized city tours can also help you discover all important attractions nearby. If you wish to spend your leisure time actively, you may also take the nearby opportunities to play table tennis, rent a bike, play bowling, billiard, minigolf, go water skiing, play volleyball, go diving, sailing, surfing and rent a boat. The bar is an ideal location for a personal meeting and a relaxing evening talk. In the safe your valuables can be the safely secured. If you have a suitable portable device, you can connect to the Internet via a wireless network (WiFi) available at the hotel. The exact list of services available at Gutshaus Kubbelkow Bergen auf Rügen (including those for an extra fee) and the exact list of equipment in a room can be found on the information sheet below.
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Persian wedding videography – Neda&Saj // Florence – Italy
We got a wonderful experience in last July in Tuscany with the persian wedding of Neda&Saj. Three intensive days spent with them. The rehearsal dinner at Four Season in Florence, the wedding day at Castello di Vincigliata and the brunch at Obica, famous pizza restaurant in Florence. Lot of fun people, party, tradition, speeches, sweet moments surrounded by the Tuscan hills. Here we go!!
Videography by – Matteo Castelluccia&Michela Santilli
Wedding Planner – Supertuscanweddingplanner
Photography – Lisa Poggi


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I jumped on the OTS (off-the-shoulder) bandwagon because I thought this blouse would be a nice addition to my Spring/Summer wardrobe. Since the elastic sits around your shoulders, you can adjust the height based on the amount of shoulder cleavage you want to expose. Since I'm an OTS novice, I aired on the conservative side. But if you are younger, far more adventurous and perhaps after a tequila shot… or five, I guess this blouse could also make a nice skirt.
DL1961 Jeans
Sole Society heels (similar)
Gucci purse


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Storybook Land
6415 Black Horse Pike (Routes 40 / 322)
Egg Harbor Township, NJ 08234
Park Phone: (609) 641-7847
Office Phone: (609) 646-0103 (Ext. 5)
Office Fax: (609) 646-4533
|Early Ticket Sale coming soon!
|Tickets $19.99 + tax each – Good for 1 visit.
Online tickets are sold throughout the season at a discounted rate of $23.50 + tax.
Regular admission at the ticket window is $26.50 + tax.
|April 8, 9, 14, 15, 16
|The Easter Bunny hops in for his annual visit!
(check operating schedule for hours)
|April 15, 16
|Easter Egg Hunt!
Join Mr. & Mrs. Bunny for an Easter Egg Hunt Ongoing from Noon - 4:00PM. This event is especially designed for small children.
|Sunday, July 9
|20th Annual Classic Car Show
Classic car owners will show their cars from 11:00AM - 4:00PM.
|Saturday, July 15
|Happy 62nd Birthday to Storybook Land!!
Anniversary Parade, Character meet & greets, and more!
Noon - 4:00PM.
|Saturday, July 22
|Christmas in July!
Santa and Mrs. Claus spend the day at Storybook Land from Noon - 4:00PM.
|Saturday, July 29
|Pirate Adventure Day
Back by popularrr demand!
Meet and greet with characters from noon - 4:00PM and go on a treasure hunt!
Pirate costumes "arrr" welcomed!
|Saturday, August 5
|Princess Tea Party!
Meet and Greet with your favorite Storybook Princesses from Noon - 3:00PM.
Wear your best Princess costume!
|Happy October Fun!
Thursdays, Fridays, Saturdays, Sundays and Columbus Day from October 1 - October 26.
Climb aboard the Happy Hayride, pick and decorate a pumpkin, and find your way through Elmer's Hay-Mazin' Maze!
Combine all this with festive decorations, exciting rides, and our classic Storybook attractions, and you have a fun filled day for the whole family! No pumpkin decorating on October 27, 28, and 29.
|October 27, 28, 29
|Trick-Or-Treat Weekend
11:00 - 5:00
Kids receive a FREE Trick-or-Treat Bag with paid admission and collect treats at over 20 different stations!
Don't forget to wear your costumes!
These kid-friendly events are all the fun without the fright!
|Saturday, November 11
(Rain Date: Sunday, November 12)
Christmas Fantasy with Lights Parade Santa's Grand Arrival! 4:30PM
Join us on this very special evening as we welcome Mr. & Mrs. Claus to Storybook Land and see all of your favorite Storybook characters on beautifully decorated floats!
The parade concludes with the lighting on the park by Santa Claus himself!
|November 11 - December 30
(Closed 11/24, 12/24, 12/25)
Christmas Fantasy With Lights - A South Jersey Tradition for over 25 years!
Come experience holiday magic right before your eyes! Be here by 5:00PM when Santa Claus appears in his chimney, waves his magic wand, and lights the park with over one million lights for the holiday season!
All of our rides, attractions, and snack bars are open!
(Santa is in his home and lights the park until December 23.)
|December 1, December 8 and December 15
Toys for Tots Toy Drop
Receive 1 free hot chocolate and 1 free small popcorn for every toy donated.
|*All events subject to change without notice. Check operating schedule. No group reservations.
|Please visit our Fall & Christmas Events page for information about our special Fall / Christmas events!


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Beyond developing her own writing, Leila loves enriching her musicianship by immersing herself in the works of others. Her diverse repertoire spans several hundreds of songs, ranging from pop, folk, soul, and rock music, to jazz standards, film/television soundtracks, and classics in English, Arabic, French, and Spanish. Her perfect pitch allows her to easily learn tunes for any occasion and setting, including weddings, proposals, corporate functions, private parties, restaurants, and hotel/resort lounges (where she enjoys taking requests from guests on the spot). Leila has a weekly residency at Calamigos Guest Ranch in Malibu, and also regularly performs at The Victorian and Basement Tavern in Santa Monica, the Montage Hotel in Laguna Beach, Grilliant Restaurant in Culver City, and most recently, the Four Seasons in Beverly Hills.
She is also making a name for herself in the Lebanese-American community, sharing her cultural pride through her performances at festivals, conventions, charity dinners, regional gatherings, red carpet events, and more.
To view Leila's cover repertoire, please click here.
To hire Leila for an event, please contact her here.


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5 Young Life Camp Timber Wolf Lake(MI) & Feed The Fire(IN):
I could rap like everyone else, you know, say some fun stuff and then get out the way. But honestly thats really not how God made me, Its not the passion He's given me. I rap and speak because I enjoy seeing people have "aha" moments and truly become who God made them to be. I was given this opportunity as a teen and It changed my life, so its always a joy when I get invited to speak or rap at teen events.
One particular weekend I found myself booked to speak at a Young life camp for the Michigan area Young Life groups and Feed the Fire Youth Conference in Elkhart, IN. It was one of the most powerful weekends of my year. Of course I was exhausted from all the driving(we nearly put in 6 hours a day) but it was worth it to see the teens responding and getting to encourage their leaders.
4 Interview With DJ Wadeo: I've listened to DJ Wadeo for years, we even met in DC back in 06 but he forgot me.lol This year I had an amazing oppurtinty to do an interview with him on his nationally syndicated radio show. We talked Heroes Never Die, my spiritual and Cleveland up bringing, and life in Chicago. Wadeo has over 3 million listens to date and puts out quality work. This was definitely a resume moment for me, plus he's a good brother from Ohio:D
3 Released Heroes Never Die: This was the hardest project for me to released in my 11 year short career. Between running out of financial means to finish it, not reaching our Indiegogo campaign goal, and business investments that didn't go well I sat on release day emotionally and spiritually tired. I had 5 additional tracks for this project that we weren't even able to release. I'm confident that my next one won't be as exhausting. I have developed tougher skin and been given the capacity to ask questions I won't have prior to this experience. https://youtu.be/w5RHPlvOINA
Along with the downs of HND there were many good things that happened. I got to work with my good friend Alex Hitchens to begin crafting my authentic sound, and my brother in law Adam Amezaga, Insomniac Studios, and Miller Street Studios provided me a polished mix and mastered project. Honestly, I don't know how far this project will go, but I do know it was a labor of love from my indiegogo supporters, faithful partners, Wife, and Jesus.
2 The Cavs Won:
I remember in 6th grade when I went to a CAVS game with my math teacher, CJ Rice. The Cavs were following their late 90's trend of being awful and possibly losing, but that wasn't what I remembered. I remember receiving a Mark Price jersey button as they retired his number in to the rafters. Moments like those allowed me to love a home team as terrible as mine.
Halfway though high school that was not the case because one of my fellow Ohioans was drafted to the Cavs. We got Lebron James! We had some good years and the Cavs became a good team, but like any sports moment for a Cleveland fan it all came crashing down when he left. Now a days it almost seems like that never happened because Believeland got its long awaited championship after 52 years of anticipation. For a kid from a depressed town this lifted my spirits even if it was only a game. I felt like I was watching the story of my life unfold on a hardwood floor. We were down 3-1 and no team had ever comeback from that end of an NBA match up. But we did it and that's a moment that I will never forget.
1 Stepped Off The Boat: This year I turned 30 and with that I began to think even deeper about how I'm made and why I'm made that way. After much thought and prayer(for years) I decided to leave my familiar job of seven years and become a full time artist and speaker. Since I was a boy I have loved to draw cartoon characters and pen poems, but at 19 when I started rapping all my other artistic passions took a backseat. I could freestyle for hours and most of all I loved creatively telling people about God's love for them. I loved it so much that I began to think it must be wrong. This was to fun to be a God thing. Then soon after I began to settle and tell myself that I had to keep my artistic expression a hobby and keep a real job(which was legit for a season) because that will honor the Lord more.
The one thing I had neglected in this rationale of thought was the reality that making music is hard work! Its a lot of thinking, planning, reading the dictionary, and creatively sharing in a way that is memorable. Show planning can be a wholenother(thats slang for another) beast! The sales, budget, personnel, venue coordination, promotion, hoping, an
d expecting but never being for certain about your turn out. Then I said "Yep, thats a job!" And I began to put away comments like "Your a selfish missionary" and "No one is going to pay for that."
So my number one is dedicated to all the people who encouraged me to step out in faith and be who I was uniquely crafted to be. I am thankful for your words of encouragement, and much need critiques. I'm a better man for it all be
cause I know who I am and I won't waste another 30 years not taking the risk the Lord has called me to.


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I Love Cats and Dragons
Personal Stories, Advice, and Support 2 People
Friend Asking For MoneyThere is just this friend. who i haven't spoke in months. He is obviously my best friend(Weird right..) So i thought of messaging him and woahhllaa I did. Well yeah he was like "Yeah I guess so, I will see" I was like mothef*** He walked on to me at school and he was like hey...
Hammit 18-21, M 0 Oct 5, 2011


text: Search Results Use the search box below to revise your search, or start a new search. Studies (7) Variables Publications Your query returned 7 studies. Series results are grouped under the most relevant study. Ungroup series results to view all results. Sort by: Title A-Z Released/Updated Time Period Most Cited in ICPSR Bib. 1. Effects of Prior Record in Sentencing Research in a Large Northeastern City, 1968-1979: [United States] (ICPSR 8929) Welch, Susan; Spohn, Cassia 2. National Opinion Survey of Crime and Justice, 1995 (ICPSR 6720) Flanagan, Timothy J.; Longmire, Dennis R. 3. National Supported Work Evaluation Study, 1975-1979: Public Use Files (ICPSR 7865) Manpower Demonstration Research Corporation 4. New York Drug Law Evaluation Project, 1973 (ICPSR 7656) Association of the Bar of the City of New York; Drug Abuse Council, Inc. 5. Race and Drug Arrests: Specific Deterrence and Collateral Consequences, 1997-2009 (ICPSR 34313) Mitchell, Ojmarrh 6. Recidivism Among Convicted Drunk Drivers: Minnesota, 1982 (ICPSR 8601) Minnesota Criminal Justice System Driving While Intoxicated Task Force 7. Sentencing in Eight United States District Courts, 1973-1978 (ICPSR 8622) Forst, Brian; Rhodes, William


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Discussion in 'Strings' started by pe3brain, Aug 11, 2010.
I was wondering whats the best spin string avaible right now?
solinco barb wire followed by solinco tour bite.
others such are pro supex blue gear and alu power spin are also pretty good
I agree exactly with Karophiteblu.
#1 Solinco Barb Wire
#2 Solinco Tour Bite
#3 Pro Supex Blue Gear
I'd rate Forten Thin Blend #4. If you're not afraid to try kevlar, it's 19 gauge and has tremendous bite as well. But for me durability was very poor, maybe 3-4 hours at most.
Listen to this guy/s.
From my experience:
Pro Supex Blue Gear
MSV Hex
Kirsch Spiky Shark
Poly Star Turbo
havent tried tour bite yet but it seems to be good for spin as well
Tour bite 18g, Barb Wire
Spiky Shark
MSV Hex and Hepta Twist
Topspin Max Rotation
All great spin strings.
agree with Tornado.. should of added that to my list.. another string I left out which I think is great for spin is Polyfibre TCS
Yes forgot to add TCS as well
if you are really cheap. gosen polylon ice at like 40lbs
definitely Solinco Tour Bite and barbwire
USRSA rated Tour Bite 17 above 18 for spin.
But, I'm surprised nobody has mentioned Genesis Spin-X. It has many other good qualities about it.
Some folks on here testing Barb Wire are reporting issues with tension maintenance.
18g ashaway kevlar/any soft poly <40lbs
Some of the Solinco guy's are here to promote their stuff.
Unbiased opinion, the ones I have tested are:
Isospeed Pyramid
Signum Pro Tornado
MSV Heptatwist
MSV Focus Hex
I'd say Lux Alu Rough & Spin and Tour Bite 18g...
I am a solinco guy cause i like the stuff! don't hate me!
perhaps u should try their strings first before u post things like that
lol,you just had 3 threads where you were asking about Solinco strings 2 days ago and now you say you are a solinco guy??
I know you are another one that is here to promote their strings asking about it,creating threads about it and stuff..I wasn't born yesterday boy .
I don't hate you
hahaha look at my older posts sir! I've been i've been using their strings and stringing them up for my players for a while now if you really want to know!
And you are right, I do promote the strings because I like them and I think they're great and my players like them too. I'll keep trying other strings but until i find one thats better than theirs or lux, Ill keep providing my input
Thanks for not hating me maybe we can battle on the court one day
from my experience, here are the top 4 spin strings in order:
1. barb wire
2. tour bite
3. blue gear
4. msv hex
Babolat RPM Blast 17g for sure!
Very mainstream of me, but of the ones I've tried I have to go with Luxilon Alu Spin.
I bought a reel of Babolat Pro Hurricane Tour 16L because I thought it would produce a lot of spin. It's Ok I guess, but what do you guys think of the Pro Hurricane Tour compared to Solinco, Alu rough, Alu power spin, etc.?
Wow committing to buying a reel of a string you've never used, quite a gamble there. Personally I hated Pro Hurricane Tour. I read the reviews on it here at TW and it makes it sound like it's the best string ever so I bought a set to try. I found it to play very stiff, dead & unresponsive. It also added no extra spin whatsoever. I've tried the majority of all the "spin/texture" polys on the market and that was probably one of the ones I liked the least.
On the other hand I found Babolat RPM Blast to be quite decent. I know there are some ppl who purport that RPM is nothing but black Pro Hurricane, but having used both I felt they played totally different. I guess it's remotely possible that simply adding black dye or whatever could change the characteristics of a string. But RPM is softer and more playable, but like Hurricane Tour (and most other hex shaped strings) it didn't do anything for spin.
While we're on black, hex polys, I've also used Pro Signum Tornado, Volkl Cyclone & Black Code. Tornado and Cyclone play identical to me, their names are even almost the same. They're a step behind RPM in comfort and just a little less responsive, but their cost is much more reasonable. Black Code is a pretty middle of the road string to me, doesn't have any stand out characteristics in my book and none of these hex strings seemed to add any more spin. I actually found Red Code to have more bite than Black Code even though it's a standard shaped string. I think it's because Black Code has a coating that makes it more slippery, probably slows notching. Red Code doesn't seem to have this coating and grabs the ball better.
For real spin production I still feel Tour Bite & Barb Wire do the most, with Blue Gear also providing honest spin increase but not on the level of the first two. But I liked Blue Gear's playability better, more pop, more feel.
Oh yeah you also asked about compared to Alu Rough. I like Alu Rough much more than Pro Hurricane Tour, it's better in all areas except maybe durability. Alu Rough is rather pricey as well. I feel that Tour Bite is like a slightly softer version of Alu Rough and with more spin production.
I have tour bite in a racquet now and it delivers. I also am a huge fan of Topspin Cyberflash and Unique Big Hitter.
The other string to look at is Big Ace Micro, it is really good.
Separate names with a comma.


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Scan tools
Why Choose OBDLink® Scan Tools?
OBDLink® products are compatible with the most extensive selection of the leading diagnostic apps and software. Find out why OBDLink® MX Bluetooth, OBDLink® LX Bluetooth, OBDLink® MX Wi-Fi, and OBDLink® SX USB scan tools are the best globally.
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By Carlyclose - / Friday 16 June 2017 00:00 /
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Top comments
By RememberSchlitz | 9
Apparently the schools you obtained your degrees from aren't fashionable.
By RememberSchlitz | 9
Apparently the schools you obtained your degrees from aren't fashionable.
By RichardPencil | 22
You should have omitted your post-graduate degree on your retail applications. They'll think you're just using them to carry on renegade research experiments.
By katluvr | 21
My advice would have been to your your resume for different positions. While it seems that having magnificent qualifications would be a GOOD THING, often it is not. I hope your perfect position with an organization that will appreciate your dedication and knowledge is out there waiting for you. Try networking?
By pupdog | 1
I feel like there's more to this. I work in cosmetics in a big department store and multiple girls work here at Estee Lauder, Clinique, Lancome, whatevs with no degrees or barely any retail/makeup experience. So it may be the way you interview or something. I personally know a couple of the Account Executives who just want to hire hardworking people, degree or not. Good luck tho.
Kaili McCoy | 4
I feel the same, like they are using the qualifications as an excuse for poor interviews skills or something. It's much nicer to say, "we are so sorry, you're over/under qualified" than, "mate, you're really frickking weird". Perhaps the OP should approach each job with a bespoke resume and cover letter for that particular job (which is what they recommend anyway) and leave post grad out of retail work
stormy0307 | 11
There is a difference between the qualifications for selling makeup (basically just requires a pulse) and the qualifications for chemically making makeup. With that degree OP should be going after jobs for manufacturing it, you and your friends (the ones with no degrees or experience) work at the retail side of it.
By stormy0307 | 11
Hopefully you were applying at some corporate lever to work at those company's manufacturing plants with that sort of degree. Otherwise if you got a post grad to work at a retail makeup store at the mall you kinda deserve it.
By heartsofhavoc | 6
I have a masters degree and have applied to over 21positions in the past month. I was almost happy to receive a rejection letter yesterday instead of radio silence. I deeply feel your pain.
SaltyAsFuck | 3
Masters degree in what?
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Your weekly spin around the fall/winter sports at Maryland.
Field hockey
The top-ranked Terps received a bye into the semifinals of the ACC tournament and will play either No. 4 seed Duke or No. 5 Virginia on Friday at 1 p.m. in Newton, Mass. The game will be televised on Comcast SportsNet and streamed at ESPN3.
The championship game is Sunday at 1 p.m., and televised on the same networks.
Maryland beat No. 7 Duke, 5-1, on Saturday to close the regular season at 18-1 and 6-0 in conference play. Anna Dessoye scored twice in the first half and assisted on a goal as well to lead the Terps offensively.
Men's soccer
Seniors Patrick Mullins and Sunny Jane both scored to lift Maryland to a 2-1 win over North Carolina State on Senior Night at Ludwig Field on Friday night. The Terrapins secured a top 4 seed in the ACC tournament and will host a quarterfinal match on Tuesday night at 7 p.m.
Maryland (9-3-5, 6-1-3), ranked fifth nationally by Soccer America, closes out its regular season on Friday night at Virginia Tech.
Women's soccer
Senior Hayley Brock gave visiting Maryland an early lead, but undefeated Virginia bounced back for a 6-1 victory on Sunday in the ACC tournament quarterfinals. The Terrapins (10-10) will find out Monday afternoon if they will receive an at-large bid to the NCAA tournament. The selection show will be streamed live on NCAA.com at 4:30 p.m.
No. 25 Maryland dominated at the Terrapin Duals, defeating Johns Hopkins, Kutztown and Alderson-Broaddus on Sunday. Senior Jimmy Sheptock, ranked third nationally at 184 pounds, won all three of his matches, including two pins, as the Terps scored 129 points and lost just one individual match.
Sheptock defeated No. 6 Jake Swartz of Boise State in the NWCA All-Star Classic, as well, and junior Geoffrey Alexander captured the Clarion Open title.
Becky Yep led Maryland to the finish line at the ACC championships for the second straight year Friday as the Terrapins placed 14th in the women's team standings. Yep finished the six-kilometer course in 22:16.7. She rallied over the course of the final two kilometers to finish 78th in a field of 140.
The Terps defeated Pittsburgh in four sets on Wednesday before falling at Notre Dame on Friday evening. Junior Ashleigh Crutcher tallied 45 kills in eight sets (5.62/s). Her best effort of the season came in the Terps' win over Pitt, as she totaled 24 kills with a .467 hitting percentage. Senior Sarah Harper posted 42 digs (5.25/s). The ACC's leader in digs, Harper needs just 23 digs to tie the all-time Maryland record (1,668).
Terp of the Week
Maryland linebacker Cole Farrand recorded a career-high 23 tackles against Clemson two weekends ago and was named Terp of the Week. Farrand leads the Terps with 67 tackles this season.


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French artist Henri Matisse is widely regarded as one of the most influential artists in the modern art world, with his work spanning everything from fauvism to impressionism. Though best known as a painter, Matisse was skilled in many other forms of art, including sculpture and print-making, and even venturing into architecture and interior design. In his later years, his works became increasingly abstract and modernist, and with the addition of bold, colorful shapes and collages, Henri Matisse can be seen to have one of the most diverse artistic portfolios of the 19th and 20th centuries.
Kashmiri artisans work together in a cottage industry, handcrafting the entire piece from the design, to the wool, to the beautiful chain-stitch embroidery, the finest in the world. No child labor used and the Wall Hangings are made by highly skilled artisans making a living wage. Indulge yourself and pair this Wall Hanging with some of the Contemporary Throw Pillows to add even more richness and color to your home. Enjoy slight imperfections as this wall art is hand-made and no two pieces are exactly alike.
*see related items below
Matisse Wall Hanging is approximately 48″ x 72″. Dry cleaning recommended. The Wall Hanging is 70% wool and 30% cotton with canvas backing and pocket at top for a dowel. (Dowel not included.) Hand embroidered, traditional chain stitching of India. The Kashmir wool thread makes it soft to the touch, and the raised-swirl texture of the embroidery delights the senses. Expect and enjoy slight variations in color and size as wall hangings are hand made.
One Fair Trade, Matisse inspired Leaves Wall Hanging.
For more information on artist inspiration, as well as similar items, check out our Artist Page – Matisse.


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Anytime Apple holds an event it always garners media attention. One of the annual events that's always a focus of attention is Apple's annual World Wide Developer Conference, which is being held June 2-6 in San Francisco this year.
A particular area of focus tends to be Apple's invitations. In the past, there have certainly been hints of future products in the wording or design of the invitation. What struck me about this year's invitation was the similarity the invitation had to TV pixels and how the color gradient reminded me of the REC709 and UHD color gamuts (with some variation, granted).
Whether or not Apple's 2014 WWDC will yield any long-rumored upgrade to the AppleTV or a physical Apple-developed television remains to be seen. However, with Amazon now releasing it's Amazon Fire TV streaming set-top-box yesterday there is mounting pressure on Apple to release an expanded offering that caters to the living room and integrates with the entire iOS and MacOS ecosystem.
Does the WWDC14 invitation give us a hidden glimpse yet again of something Apple's sleeve or am I just reading too much into it? We'll find out more in June. Stay tuned… no pun intended.


text:
The Avengers reassemble in Avengers: Age of Ultron!
Earth's Mightiest Heroes, including Iron Man, Captain America, Thor, The Incredible Hulk, Black Widow and Hawkeye, are put to the ultimate test as the fate of the planet hangs in the balance. As the villainous Ultron emerges, it is up to The Avengers to stop him from enacting his terrible plans, and soon uneasy alliances and unexpected action pave the way for a global adventure.
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