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Tough Time for Sal
Here today and gone tomorrow. In real life, we all face that possibility.
For professional athletes, it is more of a way of life. Someone is always after your job. Injuries can alter a career.
Sal Fasano is a veteran catcher, a fellow who turns 35 next month. He has a wife and two sons. He arrived here as a free agent last December and became a folk hero with his Fu Manchu mustache and long black hair. He quickly became the first 2006 fan club, Sal's Pals. Early in the season, Fasano sent pizzas to the upper right field stands where Sal's Pals camped out when he played.
The Phillies were his 17th professional team since he broke in in 1993. He seemed to have found a home. Then, he came down with a knee injury on July 2 and placed on the disabled list two days later. Nearly three weeks on the DL and rehab assignments at Clearwater and Reading were in store before he rejoined the Phillies on Friday, the start of a 12-game homestand.
Like all Phillies, he arrived at Citizens Bank Park early in the afternoon on Saturday. There was a 4 o'clock game preceded by Photo Day, in which the players would parade around the field to allow fans to get close up photos. That was scheduled for 2:15 p.m. for 30 minutes.
Sal was still on the DL although eligible to be activated. When he was going to be reinstated, someone had to go and the most likely candidates were catcher Chris Coste and reliever Geoff Geary, both of whom had minor league options.
Around 1:45 p.m., Fasano was called into manager Charlie Manuel's office. Joining Charlie were Pat Gillick and Ruben Amaro. The message was a very difficult one, Sal was being designated for assignment, meaning the Phillies have until July 31 to trade or release him. He wasn't being activated; he was the one to go. Basically, he got caught in a numbers game which happens often in baseball.
Despite a career in which he has been traded, released and signed numerous times, it still came as a shock and disappointment to Sal. He knew it was the business side of baseball but he wasn't happy.
While his teammates prepared for Photo Day, Sal went to his locker and began packing. Wearing a red t-shirt and blue workout shorts, he cleared out his locker: uniforms, belts, undergarments, bats, shoes, catching gloves, batting gloves, a football and elastic knee braces. He stuffed a large duffle bag and three cardboard boxes.
It was a slow process. Once the players came back from Photo Day, one-by-one they shook his hand and hugged him. Several sat down and consoled him. There's a bond among baseball players that those of us who aren't players can't experience. For seven-plus months, they live and go to war on the field together. They become friends for life.
Three lockers away was Coste, the man who made Sal expendable. It was in the same clubhouse after the final spring training game in early April when Coste was angry and emotional after he was told he was going to Scranton. He had never been in the big leagues in 11 years of professional baseball and at age 33, time was running out.
Nearly four months later, there was a similar scene. This time Coste stayed.
Three's a tendency to view professional athletes as special people, people to idolize, people that appears to be non-human. Seeing Sal pack and the affection he received from his former teammates brought the reality that baseball players are human beings, very human.
2 Comments
Great blog about a difficult subject. Leave it to you to look at the peraonal side with so much compassion.
Nice piece, Larry, and I think Sal deserved as much. I'm glad he found a new home – even if he had to shave and cut his hair. As sympathetic as I am toward Sal, though, I gotta say, I am a huge Chris Coste fan. He's gone so much farther than just being a "nice story" for the press. I'm not local, so I can't do this myself. But I'd love to see a Coste fan club at CB Park…maybe The Coasters with a Motown motif? Let's give Coste the true Philly welcome!


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The Fitchburg Library makes sense of all the facts, helping you sort and manage the ever-expanding flood of information. You'll always find the right answer at your library.
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If You Need It, We Can Probably Find ItIn addition to our extensive collections of books, CDs, DVDs, magazines and newspapers at the library, your Fitchburg Library card gives you access to a world of specialized online and educational materials.
Through this web site, you can find and borrow books that are in any library in central Massachusetts. You can find your favorite music, movies, and magazines. You can research your ancestry, or do your schoolwork. You can even go to school here, studying English as a Second Language.
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Recent Advances in Electrical & Electronic Engineering
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UH Hilo to host fourth diversity symposiumUniversity of Hawaiʻi at Hilo
University of Hawaii at Hilo
The University of Hawaiʻi at Hilo hosts a symposium entitled, "Transforming Our Institution(s): Transforming Ourselves," on Monday, April 17 from 8:00 a.m. to 5:00 p. m. in Campus Center 306-307. The symposium will provide a forum to discuss some of the opportunities and challenges that diversity brings. Representatives from Hawaiʻi County organizations, schools and community members are invited to attend.
At 10:00 a.m., there will the keynote presentation by Dr. Jonathan Okamura, professor of ethnic studies at UH Manoa, on transforming the university for the public good.
Born and raised on Maui, Okamura's family originally came to Hawai'i in the 1880s from Japan. After his family moved in 1964, he attended high school and college in California, ultimately completing his Ph.D. at the University of London in 1983. His dissertation concerned post-1965 Filipino immigrant ethnicity in the Kalihi area of Honolulu. Before his post at UH Manoa, Okamura taught anthropology and sociology in Manila in the 1980s. His research has included many subjects on ethnicity and ethnic relations in Hawai'i, Japanese-Americans and Filipino Americans, minority higher education, and cultural minorities in the Philippines. Currently, he teaches courses on Japanese in Hawai'i, Filipinos in Hawaiʻi, ethnic identity, and Asian Americans. Some of his publications include The Illusion of Paradise: Privileging Multiculturalism in Hawaiʻi, The Japanese American Historical Experience in Hawai'i, and Filipino American History, Identity and Community in Hawai'i.
Student presentations at the symposium include "Social and Cultural Influences on Gender Identity" by Psychology graduate student, Laura Acevedo, at 8:30 am. This will be followed by a discussion of panelists from GLO, the campus Gay and Lesbian Organization, on "Transformation through Indigenous Education" by Communication major Marie Kerby. There will be two other student-facilitated panels.
At noon, the UH Hilo Rhetoric Society will discuss pros and cons of the U.S. Secretary of Education commission's "No College Left Behind" initiative in a presentation entitled, "Transforming…More Than Meets the Eye?" At 1:00 p.m., the freshmen students of Dr. Melissa Johnson's University 101 class will conduct an interactive session, "Voices & Experience," designed to increase understanding of multiple ways of learning and knowing.
Faculty presenters include Kalani Makekau-Whittaker, the associate director of Kipuka, the UH Hilo Native Hawaiian Student Center, who will speak on "Transforming UH Hilo Beyond the Student Body" at 9:30 a.m. At 3 p.m., Dr. Catherine Becker, associate professor and department of communication chair, will present her research on "Healing on Hawaiʻi Island: How the Values and Practices of Native Hawaiian and Holistic Practitioners Transform." This session will be followed with dialogue with Kumu Mahealani Kuamo'o-Henry from Puna on "Transformation Through Ho'oponopono Ke Ala."
A 4 p.m. dialog session completes the day, facilitated by Dr. Gay Barfield, Hilo psychotherapist. Barfield, a long-time colleague of the influential therapist Carl Rogers, is a funding director of the Carl Rogers Institute for Peace.
This year's symposium is sponsored by Kipuka, Mu Pi (the UH Hilo Chapter of the Lambda Pi Eta National Communication Association Honors Society), Department of Communication, National Student Exchange and Chancellor's Committee on Diversity.
The event is free and parking will be available for $3.00 at the UH Hilo main entrance on Kawili Street.


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The angel faces east, overlooking the old cemetery. There are more elegant monuments in this place, but I love the austerity of the wings.
The angel faces east, overlooking the old cemetery. There are more elegant monuments in this place, but I love the austerity of the wings.
Musings on my year in India, navigating the classroom, & everything in between
Celebrating gardens, photography and a creative life
You can have it all. Just believe in your dreams.
adventures of empty nesting, music loving, forty-something undergrad
"Sometimes a person needs a story more than food to stay alive." Barry Lopez
An exploration of writing and reading
by Patti Bender
All the latest news, ideas, and opinions from Denver's Independent Literary Center: lighthousewriters.org
Fiction, Creative Nonfiction, News, and Thoughts
Where Eco Meets Life
Celebrating literary fiction and memoirs by women
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Melanie Marttila, BA, MA, Dreamsinger, Ink Alchemist, and Learning Mutt.
finding poetry
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This Moroccan-theme jewel situated in the midst of the trendy Melrose strip provides an atmosphere that takes you away from your everyday reality. This dual bar and restaurant sports two floors of Moroccan flair. Dangling metallic stars, leafy tropical plants and two trickling waterfalls create dimly lit intimacy in multiple lounges, topped only by the patio's candlelit bungalows. Electronica beats provide background for friendly conversation, romantic dates and the weekend's busy, easygoing singles scene.
Mediterranean-inspired fare like Moroccan "cigars" (spicy ground beef wrapped in phyllo), chicken satay with peanut sauce, and lobster tail served with coconut-curry asparagus round out the vibe. Bungalow Club dishes up entrees such as a center-cut pork chop, lamb chop and a delicious filet mignon; they've even added some sushi, thrusting a caterpillar and spicy tuna roll into the mix.
Add to that a few fruit-infused mojitos and a full range of exotic martinis, such as the almost-blasphemous chocolate martini, and you're starting to experience the Bungalow Club in its element. As you huddle together in any one of the outdoor bungalows (the jewels of the property filled with sexy soundtracks), each diner can experience sublime centerpieces that give off the feeling of dining in a private fort.
Special tip for the lazy: The Bungalow Club hosts pajama parties on weekends for brunch, so if you show up in your PJs any time between 10AM and 4PM, they might just reward you with a free round of mimosas.
Bungalow Club
7174 Melrose Ave
Los Angeles, CA 90046
(323) 964-9494
Cross Street: Formosa Avenue


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It was a banner night for the Brandeis men's basketball team's two senior captains, as both Ben Bartoldus (Hillsborough, N.H./Proctor Acad. (N.H.)) and Derek Retos (No. Attleboro, Mass./Brimmer and May School) etched their names in the Judges' record book. Bartoldus became the 31st player in Brandeis history to tally 1,000-career points, while Retos tied the school record in career 3-pointers.
Unfortunately for the Judges, those accomplishments came in a loss, as Brandeis fell at home to No. 4 Washington University in St. Louis, 95-82. The Judges fall to 11-10 overall, 3-7 in University Athletic Association (UAA) play. The Bears are 19-2 overall, 10-0 in conference.
Bartoldus entered the game with 979 career points, needing just 21 to reach the milestone. He got exactly that, finishing 8-of-10 from the field including a pair of 3-pointers. The senior guard got off to a scorching start, scoring 10 points in the first seven minutes, and had 14 by halftime. His 999th and 1000th points came on a strong drive to the basket with 5:26 left in the game.
Retos needed two 3-pointers to tie Steve Harrington '92 for the most treys in Brandeis history. The sharpshooter hit his first of the game with 7:40 left in the first half but had to wait until the last basket of the game to hit his record-tying 209th longball.
The Judges got off to a strong start, controlling a small lead over the Bears for most of the first half. A layup by junior Ishmael Kalilou (Windsor, Conn./Taft School) stretched Brandeis' lead to 22-15, and Retos' first 3-pointer put Brandeis ahead, 25-20. But WashU quickly battled back, tying the game at 27. The Bears took the lead for good on a pair of free throws with 4:17 left, closing the first half on a 17-7 run to take a 48-38 lead into the break.
Bartoldus had 14 points for the Judges in the first half, while the Bears' trio of Alan Aboona (Wheeling, Ill./St. Viator), Chris Klimek (Inverness, Ill./William Fremd) and Matt Palucki (Park Ridge, Ill./Maine South) combined for 41 of their teams 48 points.
Brandeis battled back early in the second half, getting as close as seven on two separate occasions. Unfortunately, the Judges could get no closer, and at 60-53, WashU went on a 12-0 run to balloon its advantage to 19. The run was led by Palucki, who scored 12 points on 5-of-5 shooting over a five-minute span. The Judges never got closer than 12 the rest of the way.
Brandeis shot 51.8% from the field, including 12-for-24 from downtown and 12-for-13 from the charity stripe. However, WashU shot a season-best 60.9% from the field and 60% from behind the 3-point line. Palucky led the way, pouring in a career-high 32 points on 11-16 shooting. Aboona scored a season high 30 as the senior finished 6-of-7 from deep and 10-of-10 at the line. Klimek finished with 17.
WashU extended its winning streak to 14 games and wrapped up at least a share of the UAA title.
Brandeis seniors Alex Stoyle (Goffstown, N.H./Tilton School), Ruben Kanya (Ottawa, Ontario/Bridgton Acad. (Maine)) and Gabriel Moton (St. Petersburg, Fla./St. Petersburg) each scored 10 points to join Bartoldus in double figures. All three finished 2-for-3 from behind the arc. Moton also dished out a game-high six assists.
The Judges host the University of Chicago on Sunday at noon. The Bears travel to NYU to take on the Violets in a game that will be held at 11 a.m.


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Apple Orchard Pork Roast
Total TimePrep: 25 min. Bake: 1-1/4 hours + standing
Makes8 servings (1 cup sauce)
- 1 boneless whole pork loin roast (3 to 4 pounds)
- 1 garlic clove, peeled and halved
- 1 teaspoon salt
- 1/2 teaspoon pepper
- 6 fresh sage leaves
- 3 fresh rosemary sprigs
- 3 fresh thyme sprigs
- 3 large tart apples, cut into wedges
- 2 medium onions, cut into chunks
- 4 garlic cloves, thinly sliced
- 1/4 cup butter, cubed
- 1-2/3 cups sparkling apple cider, divided
- 1 tablespoon soy sauce
- 1/4 cup sour cream
- Preheat oven to 350°. Place roast in a shallow roasting pan; rub with garlic halves and sprinkle with salt and pepper. Top with herbs. Arrange apples, onions and sliced garlic around roast; dot with butter. Combine 1 cup cider and soy sauce; pour over top.
- Bake, uncovered, 1-1/4 to 1-1/2 hours or until meat reaches desired doneness (for medium-rare, a thermometer should read 145°; medium, 160°), basting occasionally with pan juices. Remove the roast, apples and onions to a serving platter; keep warm. Let stand 10 minutes before slicing.
- Meanwhile, skim fat from pan juices; transfer juices to a small saucepan. Add remaining cider. Bring to a boil. Remove from heat; whisk in sour cream until smooth. Serve with pork.
Nutrition Facts1 each: 359 calories, 15g fat (7g saturated fat), 105mg cholesterol, 506mg sodium, 21g carbohydrate (16g sugars, 3g fiber), 34g protein.
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Oct 30, 2016
My family loves this recipe!! They ask for it often!! My son is studying in Rome right now and he requested this meal for when he gets home in December, the same with my son in Honolulu!!The only changes I make to recipe is to increase the amount of sauce/gravy. I do this my using an entire bottle of sparkling cider and the appropriate amount of soy sauce.
Nov 14, 2012
If I make this again, I'll make a few adjustments. I ended up with a crowd for dinner and had very little leftover, so apparently it was good! Unlike other reviewers, I thought the herbs were an appropriate amount. I could not find "sparkling apple cider", so I used apple juice. I think this led to a sauce that was too thin and didn't hold up well, so I would try harder to find that or substitute cider rather than juice. I didn't save any of the sauce for leftovers, and the pork got dry when we tried to eat it the next day. It seemed to be too many apples along the side, I cut that back - I ran out of room in the pan anyway! No one really wanted those anyway. I loved the amount of garlic. Smells delicious! Served with fresh applesauce (which was better than the apples roasted with the pork), roasted sweet potatoes, and green beans for a great company dinner night!
Nov 12, 2011
I cut the sage, thyme and and salt by 1/2. The cooking time for a 3 1/2 Lb. Pork roast turned out to be over two hours (meat thermometer used). This was well worth the extra time. Everyone had seconds and commented that this was the most flavorfulpork roast that they had ever had. I will make this again soon.
Nov 1, 2011
Had some people over when I made this recipe, was hoping to have some for leftovers the next day but they ate it ALL!!! Love this recipe! Perfect for fall!!
Oct 29, 2011
THis was a awesome quick and Easy dish!! The whole family loved it!!
Oct 4, 2011
This dish is amazing! I love the soft apples and onion combo to go with it and the sace tastes delicious! Definitely going to be using this recipe ALOT!
Oct 4, 2011
Oct 4, 2011
Wow! So good and so beautiful. It was moist and flavorful. The fresh herbs made it amazing. This is a winner!!
Sep 20, 2011
This is a great recipe! The pork was very tender and flavorful! I would definitely try this again.


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Being a parent today seems to require a hyper-vigilance to make sure your child is protected from unhealthy — sometimes even toxic chemicals — in their toys, clothing, eating utensils, furniture, household items, and more. Between lead-based paint, PVC and phthalates in toys, bisphenol A (BPA) in water bottles, flame retardant in pajamas and recently cadmium — a carcinogen — in McDonald's Shrek glasses, there's a lot to keep moms and dads on their toes.
The question becomes: What is the best way to keep your child safe? How can a parent know that something they (or a friend or relative) buy for their little one isn't going to cause them harm? Even if you make your own toys, buy them handmade by an artisan or buy supplies for your children to make their own simple toys, how can you know that the materials are all safe?
The fact is there is not enough being done in the United States to protect anyone, but especially children, from harmful chemicals.
According to the CNN article Toxic chemicals finding their way into the womb, "The EWG [Environmental Working Group] study found an average of 232 chemicals in the cord blood of 10 babies born late last year."
They are chemicals found in a wide array of common household products — a list that is as long as it is familiar — shampoos and conditioners, cosmetics, plastics, shower curtains, mattresses, electronics like computers and cell phones, among others.
"For 80 percent of the common chemicals in everyday use in this country we know almost nothing about whether or not they can damage the brains of children, the immune system, the reproductive system, and the other developing organs," said Dr. Phil Landrigan, a pediatrician and director of the Children's Environmental Health Center at Mount Sinai School of Medicine. "It's really a terrible mess we've gotten ourselves into."
Environmental attorney and mother Patti Goldman believes, "When it comes to protecting our kids from toxic chemicals, parents need a system that meets us halfway. We need to shift the burden from families to the companies who are manufacturing and distributing the chemicals used in these products."
The potentially good news is that new legislation called the Safe Chemicals Act of 2010 was recently introduced by Senator Frank Lautenberg (D-NJ) on April 15. This new act amends the 1976 Toxic Substances Control Act and would "require manufacturers to prove the safety of chemicals before they are marketed. Of particular concern are carcinogens, to which the public remains dangerously exposed and uninformed."
"America's system for regulating industrial chemicals is broken," said Senator Lautenberg. "Parents are afraid because hundreds of untested chemicals are found in their children's bodies. EPA does not have the tools to act on dangerous chemicals and the chemical industry has asked for stronger laws so that their customers are assured their products are safe. My 'Safe Chemicals Act' will breathe new life into a long-dead statute by empowering EPA to get tough on toxic chemicals. Chemical safety reform is not a Democratic or Republican issue, it is a common-sense issue and I look forward to building bipartisan support for this measure."
In the meantime, what is a parent to do?
- You can start by checking out the U.S. Consumer Product Safety Commission Toy Hazard Recalls list to see if any of your children's toys have been recalled.
- Vote with your dollars. Buy toys from manufacturers or artisans you feel you can trust.
- Stay current on what's going on in the movement to protect children from harmful chemicals by reading Healthy Child Healthy World
- Check the Environmental Working Group's Cosmetic Database to find out what personal care products – shampoo, soap, lotion, sunscreen, toothpaste, diaper cream, etc. – are safest for children
- Watch the EWG's video "10 Americans"
- Visit Safer Chemicals Healthier Families – A nationwide effort to pass smart federal policies that protect us from toxic chemicals.
- Take Action! by reading about the Safe Chemicals Act and send emails to your representatives and senators, email Congress, and don't forget to tell your friends about the act and ask them to take action as well!
Cross-posted on BlogHer
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Your doctor will ask about your symptoms. A physical examination will be done. The doctor will often be able to make a diagnosis based on your symptoms and the physical exam.
Infectious Disease Society of America (IDSA) base the diagnosis of acute sinusitis on the presence of certain symptoms. Acute sinusitis will have at least 2 of the following major symptoms or one major symptom plus 2 or more minor symptoms:
Major symptoms include:
- Nasal congestion or obstruction
- Facial congestion or fullness
- Facial pain or pressure
- Discharge with pus from nose
- Rear nasal discharge that has pus or is discolored
- Decreased or no ability to smell
- Fever
Minor symptoms include:
- Headache
- Ear pain, pressure, or fullness
- Bad breath
- Dental pain
- Cough
- Fatigue
Your doctor may need to decide if a virus or bacteria caused the sinusitis. Infections caused by bacteria may have the following characteristics:
- Signs or symptoms lasting 10 days or more without any signs of improvement
- Worsening signs or symptoms after a period of improvement
- Severe symptoms such as fever 102°F (39ºC) or more and nasal discharge with pus that lasts 3-4 consecutive days or more
Other tests may be done in certain situation include:
This simple procedure involves shining a bright light (as from a flashlight) over your cheek in a dark room. If no light illuminates certain areas of your face, then it's likely that you have a sinus infection. This test is not very reliable and is not commonly performed.
Nasal Culture
Your doctor might send a sample of your nasal discharge to a laboratory, where it can be tested for the presence of bacteria. Accurate evaluation of a nasal culture usually requires that the culture be obtained during nasal endoscopy. If you are healthy and have acute sinusitis, a nasal culture is usually not done.
Sinus X-ray
X-rays of the sinuses are of limited use for diagnosing the presence of acute sinusitis.
CT scan
This type of imaging study can be useful for diagnosing sinusitis, including in those areas not well visualized by sinus x-rays. CT scans are particularly effective for diagnosing chronic sinusitis.
MRI scan
Your doctor may order an MRI scan if complications of sinusitis are suspected.
Sweat Chloride Test
This is a test for cystic fibrosis in children who also have polyps and/or chronic sinus infections.
Blood Tests for Immune Function
Your doctor may request these tests if you have recurrent or chronic sinusitis.
Sinus Puncture
If there's some confusion about your diagnosis, your doctor may choose to send you to a specialist to have a sinus puncture performed. This involves using a needle to remove a bit of fluid from within your sinuses. This fluid will then be sent to a lab to identify the infecting bacteria and to determine the most effective type of antibiotic for treatment.
Nasal Endoscopy
This procedure uses a slim, flexible tube with a fiberoptic light at the end (endoscope). It is inserted into your nose. Your doctor can inspect the mucosa of the nose and the openings of the sinuses. If indicated, he can also take samples or biopsies through the endoscope for lab examination to look for fungus, tumor, or other uncommon cause of your sinusitis.
Revision Information
- Reviewer: David L. Horn, MD, FACP
- Review Date: 09/2018 -
- Update Date: 09/17/2014 -


text: Langkawi Imagine 99 islands enshrouded in romantic legends with an endless to-do list, from water sports to eco-tourism activities. Sheltered from major storms by the peninsula on one side and Sumatra on the other, Langkawi has world class attractions available throughout the year. So yes, there's more to the island than just shopping, although the island's duty free status is a huge draw by its own. Top 5 Must Do's Duty Free Shopping It's time to train your arms because you are going to need them to carry bags full of chocolates, cigarettes and liquor. With sales tax out of the way, Langkawi is a shopping wonderland for all! Hunt for bargains at duty-free shops at Langkawi Parade shopping mall, and in Kuah, Pantai Cenang, Pantai Kok, Pantai Tengah and Padang Matsirat. Panorama Langkawi SkyCab & SkyBridge Ever wondered what eagles see as they soar above the island? You might not have the ability to fly but you can certainly have a bird's eye view by taking the cable car. On the way up to the top of Mount Mat Cincang, you will be treated to a fantastic view of the lush vegetation below. End your day with sunset-viewing from the suspended SkyBridge -- perfection! Langkawi Geopark To see rocks would be boring, but to see rocks that existed and formed even way before the dinosaurs roamed the earth is definitely something else! Here at the very first geopark in Southeast Asia is where you'll find the true rock star in the geology department. Unleash the explorer in you and marvel at karst landscapes, sea stacks, fine caves and other geological formations at Mat Cincang Cambrian Geopark Forest, Kilim Karst Geoforest Park and Dayang Bunting Marble Geoforest. Pulau Payar Marine Park Only an hour's boat ride from the main island is a well-preserved and uninhabited marine park. Its sparkling jade waters will make you want to just jump in and be one with the ocean. Swim, snorkel and dive among the reefs accompanied by your new finned friends. Don't fancy getting wet? Opt for the underwater observation chamber instead! Beaches There are enough beaches in Langkawi to entertain all types of tourists. Cenang Beach is the most popular sandy stretch with various resorts and water sports facilities. Looking for a relaxing quiet time? Tengah Beach is the way to go, whilst those with deep pockets can splurge at Kok Beach and Tanjung Rhu. To and from Langkawi airport Transportation To Duration Fare Taxi Cenang Beach / Kuah Jetty 10 – 25 mins Around MYR 24 Kok Beach 10 – 15 mins Around MYR 28 Tanjung Rhu 25 – 30 mins Around MYR 35 Datai Bay 30 – 40 mins Around MYR 50 Your awesome getaway awaits you right here! Book now Quick Facts CurrencyMalaysian Ringgit (MYR)Electricity 220-240V 50 Hz LanguageBahasa Malaysia, English, Chinese, TamilTime zone UTC +8Tel code +60 4Religion Islam, Christianity, Hinduism, Buddhism Want to read more? Download FREE Awesome Malaysia Guide now! Weather Apr - Oct Rainy season - Heavy rainfall 22 °C - 33 °CPrepare your umbrella, but don't worry as the fun doesn't stop despite the showers. Nov- Mar Dry season - Warm and dry23 °C - 34 °CTime to come out and get soaked! Make sunblock your best friend. View how you can fly in with our interactive map! Map it out Check out these other destinations! Australia Gold Coast Melbourne Sydney Cambodia Siem Reap China Changsha Hangzhou Kunming Shanghai Wuhan Xi'An Hong Kong Hong Kong India Kochi Indonesia Bali Bandung Jakarta Solo Yogyakarta Japan Osaka Tokyo Malaysia Kota Kinabalu Kuala Lumpur Kuching Langkawi Miri Penang Myanmar Mandalay Nepal Kathmandu Singapore Singapore South Korea Busan Taiwan Taipei Thailand Bangkok Chiang Mai Krabi Phuket Surat Thani Vietnam Hanoi Ho Chi Minh City


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How Close Are We to Solving the Puzzle? Review of the Alopecia Areata Research Workshop
-David Norris, M.D. University of Colorado Health Sciences Center Denver, CO
Speakers at the Fourth Research Workshop on Alopecia Areata have clearly presented the state of current knowledge in three fundamental areas of research in alopecia areata : genetics, immunology, and targets, triggers and controls. The final speakers have reviewed what we know about the treatment of alopecia areata and what are the prospects for new treatment modalities in the future. It is clear that the research enterprise related to hair biology and alopecia areata in particular is now firmly established and expanding into important areas of fundamental biology including stem cell research and sophisticated studies of epidermal differentiation and morphogenesis. It is evident that the mechanism of hair follicle dysfunction in alopecia areata is immunological, controlled by activated T cells. Whether this response is truly autoimmune mains to be firmly established, but there are strong indications that self antigens, including melanocyte antigens are the key targets. Susceptibility to alopecia areata is likely to be genetically determined. Linkage to genes controlling the immune response is strongest in patients with severe AT and AU, and it is likely that AA is a polygenic complex trait, with distinct genetic linkages determining specific gene subsets. Our understanding of the mechanisms through which the cycling hair follicle is damaged and dysfunctional in AA have been thoroughly reviewed in this conference. "How close are we to solving the puzzle?" In spite of the progress reported here, we have a long way to completely understand the mechanisms of disease and to identify AA-specific targets for treatment. On the other hand, we may be very close to providing better treatment approaches for AA. Treatments proven to be effective in other autoimmune skin diseases can be used in AA in "proof of concept" trials which will both verify mechanisms of disease and provide practical approaches for treatment of this important disease.
Since alopecia areata is likely to be a complex genetic trait, understanding of the complexities of polygenic interactions is necessary to understand how genetic analysis of AA should proceed. Fred Nijhout from Duke University presented an elegant perspective on complex genetic interactions, using models developed in Drosophila to study the nature of robustness and genetic mechanisms. Complex traits don't follow Mendel's laws, the correlations are often not linear and that there are complex networks of interaction that can be mathematically modeled. But even within these networks there may be flat planes of response in which there is linearity. The effect of individual genes in such models depends entirely on context. The summation of properties law states that the sum of the squares of the effects of all genes in a pathway is one; identification of a gene with a major effect means that the effects of other genes in the pathway may be low. For example, if we identify an immune response gene that is necessary for the development of alopecia areata, then the other genes in the pathway may be rather minor in their importance and only some of them may be necessary for expression of disease. Certain genes may determine which subsets of disease such as AA or AU or AT may occur. The importance of context is clear in the hair follicle, where cross talk among different cell populations control the cycling of the follicle. This point was made repeatedly in many of the presentations here , especially in the elegant presentation by Elaine Fuchs on the control of epidermal and follicular differentiation.
Richard Kalish presented a summary of data that he and Amos Gilhar have produced over the past 10 years, demonstrating that AA is an autoimmune disease mediated by T lymphocytes in which autoantiogens are necessary to activate T cells that produce the disease. The model that they used is a SCID mouse (deficient in the ability to respond to human skin grafts) engrafted with hair bearing human skin. Leukocytes from AA patients are stimulated in vitro with hair follicle antigens and injected into these engrafted mice., producing immunologic hair loss similar to that seen in AA. Similar SCID mouse models have been effectively used to study autoimmune skin disease in psoriasis and photosensitive lupus, but the Gilhar/Kalish model is a particularly useful and robust model. Using this model they have shown that cells from AA patients, activated by hair follicle antigens, can transfer AA. In this Adoptive transfer model, both CD4 and CD8 T cells are necessary for maximal effect even though CD8 cells are sufficient to induce hair loss. They have more recently shown that the requirement for hair follicle antigens to stimulate T cells in this transfer model can be replaced by follicular melanocytes. This provides evidence that follicular melanocytes may be the targets for activated T cells in AA, as originally proposed by Tobin and Bystryn. It is interesting that control of certain melanocytic peptides are linked to immune response (MHC) loci, providing another possible point of control of AA by the MHC.
Jerry Niederkorn provided some new perspectives on how certain locations in the body, such as the eye, might have very unique immunologic environments, a concept developed by his mentor Wayne Streilein. The eye is a unique structure characterized by "immune privilege", the resistance to induction of acquired immunity in that site. This resistance to immune response is based on a number of mechanisms: lack of lymphatic drainage, anterior chamber immune deviation, immunosuppressive effects of the aqueous humor itself , Low MHC expression, low expression of Langerhans cells or antigen presenting cells, and inhibition of natural killer cells. Dr. Niederkorn proposed the idea that immune privilege in the hair follicle is to also protect the key structures of the hair follicle such stem cells in the bulb from immune destruction.
Ralf Paus is the father of father of the concept of immune privilege in the hair follicle. MHC Class I molecules are not expressed in the hair matrix, in the dermal papilla or in the outer root closest to the bulb. Class I MHC molecules are necessary in initiate immune responses in which endogenous antigens are presented to activate CD8 T lymphocytes.
Interferon gamma generated by activated T lymphocytes and natural killer cells can up regulate Class I expression. In the hair follicle, such expression may be inhibited locally by growth factors such as a-MSH, TGF-B and IGF-1, acting in this instance as immune-modulating molecules. But it's inhibited locally he proposes by a number of growth factors acting through the receptors, who in this sense act as immuno-modulating chemicals.
It may be that the purpose of immune privilege in the hair follicle is indeed to protect the stem cells in the hair follicle. I propose an alternative explanation: that the lack of MHC Class I expression in the lower regions of the hair follicle is intended to protect the hair follicle from induction of auto-immunity during regression of the catagen follicle. In regression of the catagen follicle, the epithelial cells and melanocytes of the matrix, and the epithelial cells of the root sheaths nearest the hair bulb the root sheaths, all undergo apoptosis. Apoptotic fragments of the cells are available for ingestion by cells locally. If those cells had Class I expression could internalize those antigens, present them on the surface in the context of Class I that would induce an immune response against self-antigens. The hair follicle is unique in that it repeatedly undergoes cycles of cell death and then regrowth, repeatedly leaving apoptotic materials within the dermis. The differentiating epidermis, on the other hand, disposes of apoptotic corneocytes by desquamation.
In this context, Ralf Paus proposes an "Immune privilege collapse model" to explain the development of autoimmunity in alopecia areata. In this model, infections, bacterial super antigens, or follicular damage trigger release of gamma interferon, which induces expression of Class I MHC on follicular cells leading to induction of CD8 positive cytotoxic cells, and also induction of Cass II MHC molecules leading to induction of CD4 help, and then to downstream autoimmune phenomenon and then downstream from all this there's a spread of the immune response with antibody, macrophagus, expression of Fas ligand, apoptosis and damage to follicular cells. Is there a genetic predisposition to the breakdown of immune privilege in alopecia areata? I believe that is clearly one area of hair biology research that requires additional funding.
David Duggan provided a clear review of how gene arrays might be applied in general to the study of gene expression in cancer and inflammatory diseases. Several speakers presented their work on the application of micro array technology to the study of alopecia areata in human and animal models. I was impressed with Jerry Shapiro's studies using micro array and proteomic analysis to look at gene and protein expression patterns in the rat alopecia areata model in response to therapy. Another important approach is that reported by John Sundberg, using induction of AA in the C3H/HEJ mice to study those genes that are turned on in the induction of AA. In both of these approaches, micro array changes are studied in the context of turning-on or turning off AA. Initial studies by Sinha of micro array analysis in human AA have shown predictable changes in keratins and in cytokines. David Duggan made a case for application of micro array technology to human AA, but we should be wary in the experimental approach employed. I would favor using micro arrays as they have been applied in animal models of AA, looking at experimental situations where AA is turned on or off, i.e. at AA in transition, not just in established disease.
C3H /HEJ mice develop spontaneous alopecia areata-like disease in about 20%, and will predictably develop multiple sites of alopecia if one grafts involved skin onto un-involved mice. This allows the development of large populations of alopecia mice with active progressing disease, which is an ideal model for gene and protein expression studies. Using micro array analysis, Sundberg found decrease in genes controlling pigment and hair proteins early on, which is just what one would expect. As the hair follicles are involuting, he found increases in gamma interferon and in antigen presenting cells, and later on induction of antibodies of multiple specificities. The changes in antigen-presenting cells may be an important determinant of the development of autoimmunity. This animal model, which has the capacity for induction of disease by grafting of alopecia skin grafts, may be the perfect model for the study of the breakdown of immune privilege in alopecia, and for the study of T cell responses in alopecia areata.
Epitope spreading is the expansion of the specificities of an immune response with time, characterized by the spreading of the immune response to recognize more epitopes on the same protein or to epitopes similar to the one that initiated the immune response. An epitope is a small polypeptide fragment recognized by antibody or T cell receptor. The C3H/HEJ animal model is the place to begin looking for epitope spreading, for T cell receptor repertoire, for specific receptors and what antigens they recognize, using the inducible aspect of the model to study early and later immune responses in this model. The genetic associations in this animal model show strong linkage to chromosome 17: DQB1, DRB1, TNF and LT and to chromosome 9: CD3 NCAM. These are clearly regions that control the immune response, and provide some idea of the genetic loci that will be identified in human alopecia areata.
Madeleine Duvic presented an update on the National Alopecia Areata Registry. This Registry will provide the means for collection of data on disease subsets and natural history of disease. In addition, we will focus on collection of multiplex families and sib pairs. These will be important in the study of genetic linkages in AA, AT and AU.
The power of genetic approaches was addressed by Angela Christiano. She reported on the results of study of 5 large multiplex families with AA, using some families that are not enrolled in the registry. Her initial results show significant linkages at four sites: Chromosome10, 6, 16, 18. So we're starting down the road of finding the genes responsible for alopecia areata.
Elaine Fuchs discussed the WNT signaling pathway and how it controls cell proliferation, transcription and adhesion and attachment. WNT signaling is important in stem cell development, in hair follicle determination, and in committing hair matrix cells to formation of hair keratins. The details of how such signaling pathways link cell attachment, proliferation and differentiation will provide fundamental understanding of the molecular control of hair follicle development and cycling. In the context of alopecia areata, such knowledge may make it possible to maintain hair follicle growth even in the face of immune attacks in alopecia areata.
Another crucial signaling pathway controlling hair follicle development is the hedgehog signaling pathway, discussed by Andrzej Dlugoz. Sonic hedgehog is required for hair follicle growth but not differentiation, and mutations in this pathway produce basal cell carcinoma. Downstream mutations in this pathway stop hair follicle regression and induce tumors like BCC. We are developing fundamental understanding of control of the development and cycling of hair follicles involving multiple signaling elements and growth factors: WNT and hedgehog pathway, Keratinocyte Growth Factor, Fibroblast Growth Factor V, NOGGIN.
It is clear that neuropeptides are involved in controlling the immune response in psoriasis and atopic dermatitis. Vladimir Botchkarev has proposed that neurotropins may control CD8 lymphocyte populations in alopecia areata. His evidence is compelling that neurotropins are present in the hair follicles in AA lesions, and that neurotropins can kill peripheral blood CD8 positive T cells from AA patients. Do neurotropins eliminate CD8 suppressors intended to terminate the immune response? David Whiting has shown us that T cells are eliminated from lesions of long-established AA. Are neurotropins the mechanism for lymphocyte disappearance? We need new studies to determine what stimulates T lymphocytes in AA, and what makes them disappear in long-standing lesions.
Kevin McElwee presented additional work showing how valuable the C3H/HEJ mice model can be. Grafting involved skin from one animal to syngeneic mice without alopecia leads to the progressive development of AA. If these induced mice, there are complex immunologic changes: inflammatory infiltrates consisting of CD4> CD8 lymphocytes, macrophage and B cells; local increases in cytokines IL-12, IL-6> IL10, IL-4; all T cell subsets including T regulatory cells: and hair follicle changes requiring Fas and FasL. The specific role of T cell cytokines in inducing apoptosis in the follicle in AA will be an area of active investigation.
Desmond Tobin has continued and persisted in his quest to identify antibodies in different alopecia areata models – human, mouse, horse, chicken, and others. In human AA there are high titer antibodies to hair follicle antigen, sometimes as high as 1 to 10,000. In the rat model they precede hair loss. If you grow melanocytes from hair follicles these antibodies bind to them and the binding can be nuclear, cytoplasmic and membrane. In multiple animal models there are also antibodies to keratin or trichohyalin. Effective treatment of alopecia areata decrease the antibody levels and I think it's further evidence for a complex immune response in alopecia areata. These antibodies can also be used as tools to determine immunologic specificity in AA: the antibodies can be easily sampled and one can measure antibody specificities more easily than with T cells, and I believe this is going to be a useful way to look at epitope spreading and maturation of the immune response in alopecia areata. It has been recently shown that immunotherpy in melanoma treatment can induce both regression of melanoma and vitiligo. The melanocyte destruction in these areas of alopecia appears to be mediated by autoantibodies, reawakening our interest in antibody destruction of melanocytes.
Jerry Shapiro showed that one can use modern gene expression techniques in animal models to determine the mechanism of action of some established treatment approaches: topical anthralin and nitrogen mustard. Anthralin induced hair regrowth in the rat alopecia model, along with decreases in gamma interferon, and in thymosin and JNK signaling. Topical nitrogen mustard also decreased gamma interferon, and increased IGF-1. These studies validate gamma interferon as an important mediate in AA, and suggest that other signaling pathways may be necessary for reemergence of new hair follicles.
Jonathan Vogel presented an interesting view of the future and how gene creams or solutions, or injecting DNA can be used to modify skin function and may directed to treat hair disorders such as AA. Even better, hair follicles may be removed, transduced ex vivo and then transplanted to alopecia areata patches. Will gene therapy make AA a surgical disease?
Amy McMichael and Vera Price presented view on the use of new modern immunomodulators developed in psoriasis and now available to test in alopecia areata.
These therapies fall into 4 major categories: killing activated T cells, inhibiting T cell activation, inducing immune deviation, and inhibiting key cytokines. The prototype drug for killing activated T cells is Ontak, a fusion protein containing a toxin and anti-IL-2R antibody. Drugs that block T cell activation interfere with macrophage/T cell interactions by binging the TCR or secondary adhesion and signaling pairs. Immune deviation drugs switch the T cell response from TH1 to TH2. Drugs that inhibit cytokines interfere with cytokines such as TNF-a, or their receptors (Enbrel and Remicaide). Another important approach in development is interference with leukocyte trafficking through binding important adhesion structures such as ICAM-1 and selectins.
The presentations at this Fourth International Alopecia Areata Workshop have taught us about the current state of knowledge in research on AA and hair biology, and on related topics in cutaneous biology. I think that it's also important to ask what we can learn from others who have studied cutaneous autoimmune diseases and how we can apply some of the lessons from these diseases to better understand alopecia areata.
Lupus erythematosus is the prototypical autoimmune disease and there is much to learn from studies in lupus erythematosis. John Harley just presented at the Montagna Symposium on the Biology of Skin the results of 8 years of study of the genetics of lupus erythematosus. He has found is that many of the genetic associations in lupus could only be identified by study of carefully segregated subsets of disease based on organ involvement, autoantibody specificity, and clinical features [Harley 2002, Kelly 2002]. In implementation of the Alopecia Areata registry, we must take care to collect similar clinical data related to AA subsets.
Vicky Werth has studied the susceptibility to photosensitivity in cutaneous lupus and focusing on polymorphisms in genes associated with immune response and cell death, specifically TNF-a [Werth 2000]. This is a key mediator in inflammation in the skin, and in control of cell death. It is believed that these TNF polymorphisms may be important in the UV-induced cell death that leads to auto antibody production in photosensitive lupus. Polymorphisms in TNF, IL-1 and other MHC associated molecules will be important in studies of alopecia areata biology and genetics.
Landmark work done over the past six or seven years by Livia Casiola Rosen and Anthony Rosen at Hopkins has shown that many autoimmune diseases are produced by autoantibodies which are specific for fragments of self antigens produced during apoptosis, and presented to a defective immune system [Rosen 1999, Rosen 2001]. The prototype of this mechanism in photosensitive lupus, in which UVR-induced apoptosis induces fragments of Ro antigens [Casciola-Rosen 1996]. Apoptosis is the principle mechanism of cell death in the regressing catagen follicle and it may be that these apoptotic cells – hair matrix melanocytes, matrix keratinocytes, and root sheath keratinocytes- are being presented to the immune response and autoimmunity develops in alopecia areata because of genetically determined defects in the immune response. Is the immune response in alopecia areata directed against proteolytic fragments of auto antigens exposed during catagen? Is the principal genetic defect in AA related to how the cells of the hair follicle die during catagen?
Psoriasis provides many possible lessons for those interested in studying alopecia areata. It is a T cell dependent disease, often triggered by infection. What is most unique about psoriasis is that carefully planned clinical trials were used to understand the mechanisms of disease [Gottlieb 1995 , Krueger 2002 ]. The model was simple and direct: employ a highly specific treatment modality that targets a single point in the mechanism you're interested in evaluating. Jim Krueger and Alice Gottlieb used highly selective anti T cell treatments to reverse intractable psoriasis. Those treatments which killed activated T (Ontak, UVR) cells lead to remissions of disease, while those that merely inhibited T cell activation (cyclosporin) produced clinical response but no remission when treatment was discontinued.
In alopecia areata, we must determine if killing T cells will also allow return of normal hair follicle function. If AA is triggered by an infection, will the immune response persist after the infection is gone? If there is epitope spreading, will the disease persist if the activated T cells are killed? Studies using specific anti-T cell treatments are essential in to answer these questions. There are a number of different models that we could use. Drugs that target pathogenic T cells, drugs that inhibit T cell activation, drugs that induce immune deviation towards TH2 cells, and drugs that inhibit cytokines like TNF-a. Killing pathogenic T cells is probably the best treatment because then you can see if you get a remission when the patient is taken off of treatment. Such drugs need to be used in "proof of concept" experiments.
Vitiligo is another autoimmune disease from which we can learn many lessons. Vitiligo is also a complex autoimmune disease characterized by both autoreactive T cells and autoantibodies. In vitiligo, repigmentation of affected skin is a separate process that involves more than just suppressing the immune response. Re-pigmentation of vitiligo is a distinct process different from the process of pigment cell destruction [Norris 1994]. It requires activation of a special population of melanocyte precursors in the outer root sheath [Horikawa 1996]. In alopecia areata, hair cycling returns when immunosupporessive are used, but not in every patient. In the patients that don't respond to the blocking of the immune response do you have to add something else to directly stimulate the hair follicle? Better understanding of follicle cycling and control will provide us the tools to answer this question and perhaps to finds stimuli for anagen growth that overcome the inhibition imposed by the immune response in alopecia area.
This workshop has summarized the significant accomplishments in understanding hair biology and alopecia areata since the first NIAMS-sponsored workshop.
We've established that alopecia areata is a T cell mediated disease, and appears to be autoimmune. In alopecia areata, investigators have identified some of the antigens to which the immune response is directed, which has not yet been accomplished in psoriasis. We've had a tremendous growth in understanding the biology of the follicle and its role as an immune privileged site. We have initial genotyping of immune response associated genes, especially in AT and AU but we're also identifying other genes and we'll continue to do that the larger the patient populations become. We are collecting through the National Alopecia Areata Registry the patient data necessary to understand the natural history and epidemiology of this disease, and are beginning to stratify patients by disease subset, which is necessary for these studies and for the genetic analyses now underway. We have begun to correlate the different stages of pathology of the hair follicle, with disease subset, and with bio-chemical markers of immune disease and also hair follicle response, and with the complex genetic determinants of this alopecia areata and its subsets.
What needs to be done? We must continue to support basic research in hair follicle biology, as the foundation on which understanding of pathophysiology and treatment will be built. We need to support our Alopecia Areata Registry as the basis for fundamental mechanism and treatment trials. We need to strongly support genetic studies if we are to understand diseases mechanism and subsets. We need to fund opportunities to apply new research approaches like gene and protein expression through microarray analysis and proteomics. I strongly believe that we need to aggressively organize proof of concept clinical trials to verify that activated T cells are essential for development of AA and that anti-T cell drugs cause reversal of disease. We have to study the return of hair growth after blocking the immune response to see if additional stimuli. I think it's time for us to take our animal models and develop the appropriate collaborations with fundamental T cell biologists to determine the T cell receptor repertoire in the lesions of AA. What are these cells recognizing? Is it the same, patient to patient? Is there epitope spreading? Does the T cell response cease late in disease? We are indeed close to making major breakthroughs in understanding of the mechanism and treatment of alopecia areata.
I must express sincere appreciation to NIAMS for their support of this entire field over the past 10 years, and I personally and specifically want to thank Alan Moshell, Head of the Skin Program at NIAMS who in so many ways has helped to support the investigators trying to understand alopecia areata and hair biology: through these meetings, through publication of these proceedings in the JID, and through good advice on funding approaches. Of course we also should thank Steve Katz, the Director of NIAMS for his support of the development of this area of research.
- Werth VP, Zhang W, Dortzbach K, Sullivan K. Association of a promoter polymorphism of tumor necrosis factor-alpha with subacute cutaneous lupus erythematosus and distinct photoregulation of transcription. J Invest Dermatol. 2000 115:726-30.
- Rosen A, Casciola-Rosen L: Clearing the way to mechanisms of autoimmunity. Nature Medicine. 2001;7:664-5
- Rosen A, Casciola-Rosen L : Autoantigens as substrates for apoptotic proteases: implications for the pathogenesis of systemic autoimmune disease. [Review] Cell Death & Differentiation. 1999 6:6-12
- Norris DA, Horikawa T, Morelli JG: Melanocyte destruction and repopulation in vitiligo. Pigment Cell Res 7:193-203, 1994.
- Krueger JG. The immunologic basis for the treatment of psoriasis with new biologic agents. J Am Acad Dermatol. 2002 46:1-23. Review.
- Kelly JA, Moser KL, Harley JB. The genetics of systemic lupus erythematosus: putting the pieces together. Genes Immun. 2002 Suppl 1:S71-85.
- Horikawa T, Norris DA, Johnson TW, Zekman T, Dunscomb N, Bennion SD, Jackson RL, Morelli JG: DOPA-negative melanocytes in the outer root sheath of human hair follicles express premelanosomal antigens but not a melanosomal antigen or the melanosome-associated glycoproteins tyrosinase, TRP-1, and TRP-2. J Invest Dermatol 106:28-35, 1996.
- Harley JB. The genetic etiology of systemic lupus erythematosus: a short dispatch from the combat zone. Genes Immun. 2002 Suppl 1:S1-4
- Gottlieb SL, Gilleaudeau P, Johnson R, Estes L, Woodworth TG, Gottlieb AB, Krueger JG. Response of psoriasis to a lymphocyte-selective toxin (DAB389IL-2) suggests a primary immune, but not keratinocyte, pathogenic basis. Nat Med. 1995 1:442-7.
- Casciola-Rosen L,Rosen A, Petri M, Schlissel M: Surface blebs on apoptotic cells are sites of enhanced procoagulant activity: implications for coagulation events and antigenic spread in systemic lupus erythematosus. Proceedings of the National Academy of Sciences of the United States of America. 1996 93:1624-9.


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After the success of the "How To Shop CVS" video I thought I would follow up with a "How To Shop Walgreens" video as well!
One of the biggest complaints I get from people trying to coupon is that the drug stores are just so confusing.
I think they are actually the most fun because it is where I see the biggest savings.
So this weekend I took the time to film the portion of my coupon class where I teach Walgreens in an effort to help all of you understand how it works.
Now the other part to understanding Walgreens is HOW to read the Walgreens deals on my website.
So let's take a look at a few sample deals and with your new found knowledge hopefully it will make more sense:
We will start with a simple one:
Morton Epsom Salt (4lbs) – $4.00
Get $4 RR
FREE after RR!
This means that when you get to the register you would pay $4 out of pocket. BUT you would get a piece of paper (Register Rewards) worth $4 off your next transaction at Walgreens!
Nexcare Blister Waterproof Bandages (6 pk) – $3.50
Get $3.50 RR
$0.55/1 Nexcare Bandages, exp. 5/31/13 (SS 04/07/13 R)
$1/2 Nexcare Bandages, exp. 5/31/13 (SS 04/07/13)
Better than FREE after RR!
In this case the bandages are $3.50. But you can use one of those two coupons to help you save. So let's say you have the $.55 of 1 coupon form the 04/07/13 Smart Source Insert. At the register you would pay $2.95 and then get a piece of paper good for $3.50 off your next transaction at Walgreens.
Ban Antiperspirant/Deodorant – $1.99
Get 1000 Balance Rewards Points wyb 3
$0.40/1 Ban Product, exp. 5/26/13 (SS 04/14/13 R)
$0.75/1 Ban Solid, exp. 5/26/13 (SS 04/14/13 R)
As low as $1.24 ea. + 1000 Balance Rewards Points wyb 3!
In this case you use the coupon to get a lower price but they will also load 1000 points onto your Balance Rewards Card. This is kind of like building up a Walgreens gift card. Check out the dollar value of the points:
I hope this clears up Walgreens for you!


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IMPORTANT: Compatible with iPad 2 and up, iPhone 4 and up and iPod touch 5th generation – WILL NOT RUN ON EARLIER DEVICES
The adventure continues with Runaway: A Twist Of Fate - Part 2.
The most famous couple in the history of adventure games is finally coming to iOS devices.
Plunge into the depths of a sinister adventure with an overriding element of humor and graphics worthy of the greatest 2D animated movies. For the first time ever in the Runaway series, the adventure has gone for a more balanced gameplay with gamers required to play some chapters as Gina and other chapters as Brian.
Runaway: A Twist of Fate offers an enhanced game experience with its all-new high-resolution graphics engine, with dozens of charismatic characters crossing your path in a variety of colorful settings.
Don't panic! If a challenge seems a bit too tough, an ingenious system of clues will guide you through the trickiest situations without actually giving you the solution to the game's 200 riddles and puzzles.
Get ready for an extraordinary adventure!
Runaway: A Twist of Fate - Part 2 is the direct sequel to the previous episode Runaway: A Twist of Fate – Part 1, available in the App Store.
• Thrilling puzzles and engrossing mysteries
• An enhanced graphics engine for superior visual and sound quality
• Graphics worthy of a major animated movie
• A remodeled and redesigned interface. A perfect game for your iPhone or iPad.
• An innovative, user-friendly help system
• Many charismatic characters
• Languages supported: English, French, German, Spanish and Italian
Runaway: A Twist of Fate - Part 2 size is 2Go but requires 4Go to be installed. To avoid this, you can download and install the game via iTunes.
About Pendulo Studios
About Numeric Pipeline
|Runaway 3 Vol 2
|Runaway 2 - Vol 2
|Runaway 2 - Vol 1
|Runaway: A Road Adventure
|Runaway: A Twist of Fate Part1
|Hollywood Monsters Lite
|Yesterday Lite
|Hollywood Monsters


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Of course Google isn't spinning it that way. According to Eric Schmidt, Google's executive chairperson, the €60-million is for a "Digital Publishing Innovation Fund to help support transformative digital publishing initiatives for French readers".
In many ways Google has gotten off lightly. The company allegedly offered French media firms a €50-million settlement in January, only to have them demand double that amount. And while €60-million is an enormous amount of money, it is relatively small by comparison to the open-ended "link tax" that the French government was mooting.
This tax would have been levied every time Google linked to the websites of any French publishers. By indexing these sites and displaying snippets of their news on its search results pages, Google is essentially profiting from their copyright without paying for the right to do so. Or so the Gallic logic goes.
Nevermind the fact that news websites (and indeed all websites) rely on Google and other search engines for a large chunk of their traffic (typically between 25-50%), from which they make their own revenue. Or that this content is often repeated by several different news providers without much material difference in substance.
But Google has been doing this for years, so why has this come to a head now? Simple, the French government has found its coffers bare and is casting about for ways to extract more revenues. And who better to target than the big, "crass" American corporation swallowing up the profits of the beloved French press?
Google is also an easy target because of its tax policies. By channelling all its foreign revenue through its Irish office, which enjoys one of Europe's lowest corporate tax rates, Google avoids paying large amounts of tax on its operations in France.
Earlier in the decade, when times were good, European governments looked the other way. But with tax revenues shrinking and public anger growing, they are being pressured into acting. It doesn't help that Google's profits are growing healthily while Europe struggles to stay afloat.
The thing is, Google isn't doing anything illegal, and it isn't doing anything that other multinational corporations don't do.
Late last year protesters picketed Starbucks' UK operations when it was discovered that the company had avoided paying corporation tax using a scheme similar to Google's. Starbucks has since agreed to pay £20-million over two years in restitution.
Squeezing corporations is a great lark. Governments get to look tough, tax revenues rise and voters are thrilled. But is this really the message that Europe wants to send out: "Invest in France! Our brand of extortion is so much more stylish than China's."
By capitulating to the French, Google has given clear directive to meddling governments around the world. Already the European Publishers Council has demanded that Google pay the rest of the continent's publishers the way it has France's. What's next after Europe? Japan? South America? This Pandora's box is not easily closed.
Regardless of how we feel about Google, the company has done an incalculable amount to advance the internet around the world. Its search engine is still the first port of call for billions of people around the world.
Taxing Google will not fix what is fundamentally broken in the publishing industry nor will it help solve the world's sovereign debt crisis.
By bashing Google, publishers and governments send a clear message to investors around the world: "We do not want your innovations or your disruptive business models. We want your money – as much of it as we can get. And we're prepared to play as dirty as we need to to get our way."


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James Hamblin
James Hamblin, M.D., is a staff writer at The Atlantic. He is also a lecturer at Yale School of Public Health and author of the forthcoming book Clean.
That seems like a lot of green, right?
But then you zoom in, and the colors are people. There are around 1,278,838,000 Facebook accounts right now, each allotted an equally-sized plot of pixels on the new website "The Faces of Facebook." Natalia Rojas of Barcelona launched it last week. The site has since been intermittently debilitated by heavy traffic.
Mark Zuckerberg, a California man, has pole position in the upper left. The newest person to join is on the lower right. Can you see them? If you zoom, you can see everyone.
You can also sign in through Facebook and find yourself. Or just spend years combing the dots to find yourself. The site updates in real time, so each position is constantly shifting. You can improve your position and get closer to Mark by eliminating the people between you ... if you get what I'm saying.
Or you can click on any square and find a random person. Then maybe add them as a friend and send a message: "Hey, I found you on that site with all of the people on Facebook. How is your day going? Mine is fine."
Rojas told CNN, "I was playing around with Facebook API, and I discovered that there is a way to access everyone's public information with a very simple (but not obvious) algorithm." She said she was inspired by the idea that Facebook profile pictures are an example of a person's best self.
"There is a mix of people from all over the world," she said, "And somehow we are all telling our friends: 'Look, this is me, when I like myself.'"
This post originally appeared on The Atlantic.
Now more than ever, public transportation is not just about ridership. Buses, trains, and subways make urban civilization possible.
The coronavirus crisis stands to dramatically reshape cities around the world. But the biggest revolutions in urban space may have begun before the pandemic.
What do we know so far about the types of places that are more susceptible to the spread of Covid-19? In the U.S., density is just the beginning of the story.
As reports of harassment and assault against Asian Americans increase, community advocates are finding new ways to tackle the spread of xenophobia.
To help get essential workers around, cities are revising traffic patterns, suspending public transit fares, and making more room for bikes and pedestrians.


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(CNN) -- Arsenal striker Eduardo could face a two-match Champions League ban if European football's governing body UEFA decide to charge him with diving.
Eduardo celebrates after scoring his controversial opening goal in Arsenal's win over Celtic on Wednesday.
UEFA disciplinary officials are reviewing the incident when the Croatia striker won a penalty against Celtic on Wednesday before deciding whether he will be charged.
A UEFA spokesman told Press Association Sport: "We are reviewing the match to see whether a disciplinary investigation should be launched."
Under UEFA rules, if charged and found guilty Eduardo could face sanctions up to a two-match ban in European competition.
Scottish Football Association chief executive Gordon Smith has called for Eduardo to face action and UEFA president Michel Platini confirmed he could be suspended.
Platini, speaking in Monaco, said: "There are disciplinary procedures at UEFA and the procedure could be taken to suspend the player. Scotland often start such procedures, last time it was a Lithuania player who was sanctioned."
Platini said his plan of having two additional assistant referees, one behind each goal-line, would cut down on diving. The scheme is being trialled in this season's Europa League.
He added: "One day players will give up simulating because referees will see them. For years players have cheated because the referees were not of a good enough quality.
"I am convinced if you have referees close by that will prevent players from simulating and players will take the right decision. I have always said better to have more referees than a multiplication of disciplinary procedures," Platini continued.
SFA chief Smith wants UEFA to act retrospectively to punish Eduardo in the same way they dealt with Lithuania striker Saulius Mikoliunas, who cheated to earn a spot-kick against Scotland at Hampden Park in September 2007.
Video evidence was used to sanction Mikoliunas, who was banned for two matches. Smith said: "Eduardo is a terrific player who has battled back from a serious injury to resume playing at the highest level.
"However, last night he showed disrespect to the game by his actions in winning a penalty against Celtic.
"Since I came into this post, I have raised the issue of simulation time and time again -- both here in Scotland and with FIFA and UEFA.
"I don't think that I have received enough support in my efforts to eradicate what I believe to be one of the most serious threats to the integrity of football. Last night showed exactly why we must take this issue seriously.
"We have shown the courage to use retrospective punishment when it comes to simulation and I would urge UEFA to do so in this instance. Everything that can be done to stamp it out must be done -- starting right now.
"Last night's incident also brings the whole issue of video evidence to the fore. I see absolutely no reason at all why we cannot use technology to assist referees -- particularly in live games.
"I know that some people say that TV evidence would damage the flow of a game, but I believe the proposal that I put forward to both FIFA and UEFA whereby football would adopt a similar approach to tennis in offering a set number of challenges can work."


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Here is the second video comparing the 120Hz Samsung 2233RZ LCD display with a 60Hz Benq G2220HD LCD display and in this video you can see bigger difference compared to the one comparing the LCD with CRT at 120 Hz. The freeze frames below are from the original video, before being compressed and uploaded to youtube, so that you can compare the detail level of frames displayed on both monitors. On the freeze frames you can clearly see the advantages of the 120Hz LCD panel – less ghosting on fast moving objects, less tearing of the image with vsync set to disabled and more fluid movement of the surrounding area when you are panning faster in the game.
Take a note of the lights in the back of the last freeze frame, they do seem tripled on the 120Hz Samsung and just doubled on the 60Hz Benq monitor. Now this is clearly visible only on stop frames, but when looking at the video it is more like an advantage than a disadvantage. The thing is that this "tripling" of the objects makes the movement more fluid and natural that the doubled version, where you are like skipping the central part and the image seems much more jumpy.


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It may seem early to start thinking about fall — as the days grow longer, temperatures increase and the workload may, too. But once the summer sun has reached its zenith, the crops you plant thereafter will be growing and maturing in gradually shortening days and cooling weather. It's time to start planning your plantings so crops are ready to harvest when you need them, right into the end of the season.
Putting the principles of succession planting into practice helps take some of the guesswork out of planning, and brings a steady supply of produce — ready for harvest over the longest possible period — within reach. Succession planting gives you the ability to:
- Maximize space
- Extend the harvest window
- Maintain a continuous supply
- Optimize quality and yield
Several proven strategies can help to ensure a continuous supply of fresh produce into the fall and winter:
- Start planting varieties that are adapted to mature in cooler temperatures.
- Plant several varieties of the same crop that have different days to maturity.
- Incrementally time successive plantings more closely together, as they will be maturing more slowly into the fall.
- Adopt season extension technology for crops that mature into the fall, to cover and hold them in the field without damage from early winter weather.
Read on to learn more about each of these strategies.
Crops are bred for various traits, including heat and cold tolerance. Within a crop, some varieties perform better in cool weather and some in warm weather. If you grow only one variety, you may find that it falls short of its potential at some point or another during the season. By growing several varieties, you can span a longer season and still offer consistently high quality. Depending on the crop, our planting plans recommend different varieties depending on the time of year, and/or planting multiple varieties with different maturity dates to spread the harvest from a single planting.
Succession planting systems can become increasingly more refined, complex, and productive with experience. The intervals can be tweaked by factoring in regional or individual farm-record data, and by adopting more innovative and advanced techniques, such as season extension methods.
Johnny's Research team has created a set of charts showing recommended planting intervals for crops especially well-suited for repeated plantings of the same crop.
Download our calculator
Visit PlantMaps to obtain average frost date in your area
Planting tips and notes are provided, and the charts can also help you decide which crops to grow concurrently.
To forecast the dates of your successive plantings, try our Succession Planting Calculator. The chart denotes crops that are customarily started indoors for transplanting versus direct-sown.
You also can use a combination of transplants and direct seeding to effectively succession plant. For example, grow transplants of crops you normally direct-seed, such as arugula, cilantro, cucumbers, parsley, spinach, squash, and sunflowers. When you plant them outside, direct-seed some of the crop at the same time. The transplanted crop will be ready for harvest first, and the direct-seeded crop will mature a few weeks later.
Planting programs differ from interval succession planting in that they generally involve planting crop varieties that have varying days to maturity, as well as planting different varieties depending upon the season, to produce a continuous supply. As with interval succession planting, many growers apply season extension methods as an integral part of their planting programs.
Visit the Planting Programs section of our website to learn more about the details of implementing a successful program.
Finally, protected cropping bears mention, as it can help you expand the limits of your growing season significantly, allowing for production earlier in spring, later into fall and winter and, for some growers, year-round production.
Use several types of season-extension structures to tailor the protection to the crop. The possibilities are numerous. Here are just a few examples:
- Plant low-growing crops such as greens in Quick Hoops™ low tunnels, or cover them with floating row cover or Quick Hoops to hold them in the field when cold weather arrives.
- Cover peppers and eggplants with row cover to help them survive the first frost or two. There is frequently a return of mild weather following the first frost, that can help some tender crops survive into that period.
- Plant a late crop of determinate tomatoes in a hoophouse, or keep a main season planting of indeterminate hoophouse tomatoes productive after field crops have slowed down.
- Plant cold-loving crops in early autumn in a hoophouse or caterpillar tunnel to harvest all winter.
- Overwinter some crops under Quick Hoops to give them an early start the following spring.
Succession planting may seem complicated at first, but with practice you'll get the swing of it. Start with a few main crops and project your harvest dates, then use these four strategies to find opportunities to extend the harvest. Do the same thing with additional crops next season. Try a few new varieties from the Planting Programs to see how they produce for you. Experiment with high tunnels and low tunnels.
Keep track of the details, then analyze the results. You'll soon be on your way to creating a succession planting plan that provides for abundance and quality — and strong sales — over the longest possible season.
Planting Intervals for VEGETABLES • Chart
Planting Intervals for HERBS • Chart
Planting Intervals for FLOWERS • Chart
Succession Planting CALCULATOR • XLS
Scheduling Vegetable Plantings for Continuous Harvest • ATTRA Sustainable Agriculture • PDF


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yeah that's right, but you're helpful tho, I mean, 2 weeks of holiday and what should I do??
that's okay, I didn't mind my RHG getting locked....
I may be bad at grammar, and I'm sorry for not taking ur advice...
Btw, that's just a troll after all.....xD
Nah, it was all Flunk, Loops and Kanga. You're fine lol
Yeah...I'm not ready too!, I like rhg battles but I didn't even start to practice animations, I just know how to draw, and besides I didn't even finish my RHG , but now I know how it's gonna looks like!
So we should take our time to practice , don't ya' think that?
Well, I was thinking so many ideas for my RHG but...there so many characters with the same powers and abilities that I was thinking, so I'm searching some original ideas.like a gay gosth robot of the future with neko ears- wait thats a terrible idea ._. ,lol, do you have any idea 4 me? :3 (fuk I'm so bad at english)
Ok, I joined.
'They' dislike weaklings so they tend to go toward stronger opponent for their own satisfaction. 'A one hit battles boring' - Bacchus.
(basically if your better than me at animating I'm gonna challenge myself and fight you lol)
Yeah that would be nice. I am probably getting rid of my old RHG though.
Return of Asshat Supreme
Infinate Inferno
Arzone The Animator
Gears in motion
wenas :v
The Universe In My Eyes
The Iron BEAST


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10, du Terroir street, Lévis, QC, Canada, G6V 9J3
Phone: (418) 835-5605 Fax: (418) 835-9054
Supports Green Practices
"Supports Green Initiatives" designates a hotel's participation in an optional environmental program that includes the use of energy-efficient lighting, guestroom towel/linen re-use, and on-premise recycling. "Supports Green Initiatives" does not represent an official certification of any kind.
Join free while you book
There is no catch. Join for free, and get access to exclusive perks!
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Exclusive flexible rate for Choice Privileges members when you book direct at ChoiceHotels.ca or through the Choice Hotels Mobile App. Valid at most International and U.S. Choice Hotels locations. Must be or become a Choice Privileges member prior to making the booking. Discount rate is non-transferable or redeemable for cash, cannot be used for future stays or existing reservations and may not be combined with other promotions, offers or discounts. Unless otherwise stated, quoted rates are per room, per night, based on single/double occupancy and do not include taxes, gratuities or incidental charges. Early departure fees, deposit and cancellation restrictions may apply and will vary by hotel. Not valid at vacation rental properties.
The Comfort Inn Lévis (Quebec, Canada) is located on the south shore of Quebec City, near Highway 20 (Exit 325). The ferry, which will take you to the very heart of Old Quebec, is located only a few minutes away from the hotel. (Please ask about our 'Sail to the heart of Old Quebec' that can be add to your account upon your arrival, which includes a shuttle service to the ferry as well as the fare tickets.) We are situated halfway between Ontario and the Maritimes.
Travellers staying at the Comfort Inn Levis will find the main attractions of the region nearby:
Travellers staying at the Comfort Inn Levis (Quebec, Canada) will never run out of activities to do during their stay. You can enjoy a beautiful day biking along the St. Lawrence River, and appreciate the breathtaking scenery. It is also possible to play golf and, in winter, to do some cross country or alpine skiing, dog sleigh riding, and snowmobile excursions. Tourists wishing for a less eventful vacation can go shopping or make their choice among the multitude of restaurants and lounge bars in proximity of the hotel.
Guests staying at the Comfort Inn Levis can enjoy the following free commodities:
Completely renovated in 2015, our commodities and services are adapted to the present needs of our clientele. All the rooms are decorated with style and are equipped with a 32-inch flat screen television (with cable), a Keurig coffee maker, a hair dryer, as well as an ironing board. Several rooms are equipped with a refrigerator and a microwave oven.
Our self-service parking allows for most guests on the ground floor to park in the front of their room; Ideal for motorcycles, snowmobiles and persons with reduced mobility. We accept pets for a small $35 fee (per day, per pet). Currency exchange and dry cleaning services are also available.
The Comfort Inn in Levis is the perfect hotel for your business or leisure trips, be it your final destination or if you're simply passing through. Our choice location, our exceptional commodities, and the courteous and professional customer service make the Comfort Inn the perfect choice in the region. Reserve your room on our website today and let us create for you a haven far from home.
Check-In Time: 16:00 Check-Out Time: 12:00 Guest Rooms: 96


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Collins hoping for better fortunes at home
NEW YORK -- Manager Terry Collins is hopeful that his club can turn around its fortunes at Citi Field as it begins a 10-game homestand.
"We've got to play better at home, which the last two years really kept us from being a team that was in the hunt," Collins said.
In 2012 the Mets were 36-45 at Citi Field and 38-43 anywhere else; last season the splits diverged further, as New York was 33-48 at home and 41-40 on the road.
The 2014 season has barely begun, but the first homestand and road trip have followed the same trend. New York went 2-4 to start the season at home but went 6-3 while visiting the Braves, Angels and D-backs.
Collins reiterated that the issue was addressed in Spring Training and that the home pregame routine was altered to match what's done when the Mets are the away team.
"We're trying to get a little bit more similar to what we do on the road," Collins said. "They're aware that's an issue with everybody, including them, that we've got to play better."
Some of the discrepancy is just circumstance and the opponent, especially in the small sample of the season's first three weeks. The Mets batted .178 with a .597 OPS in those six home games while averaging 3.5 runs per game; on the road the offense had a .257 average and .669 OPS while scoring 5.2 runs per game.
"[During] our first homestand," Collins said, "as we reviewed a lot of the tape, [we saw that] we fouled a lot of pitches off that we should have hit hard -- real hard."


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Choose Your Event in Homewood !
Step 1 - Use Calendar's Scroll bar to view entire Month's Events.
Step 2 - Click image, view full event details and scroll to the bottom to register.
Step 3 - Click Register Now and join the fun!
Don't see an event that works for you? Contact us for a private party!