text:
PRIME Education, Inc
20 - 49
5 - 10 Million
Services->Service Providers
SIC Code:
1721 - Painting and Paper Hanging
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Additional Info:
PRIME Education, Inc, a business led by CEO Kathleen Moreo, is part of the Service providers industry. PRIME Education, Inc email with the @primeinc.org format, you can check their Lead411 profile. They hold their main office in Tamarac, FL and more data like cfo contacts and linkedin data can be found within our profiles. If you sign up for our free trial you will see our firstname.lastname@example.com addresses.
Company Background:
Full company description is available with the free trial.
Ceo Reference:
Kathleen Moreo
Kathleen Moreo is PRIME Education, Inc's CEO. Their CEO/Co-Founder is Kathleen Moreo. Their Lead411 profile is categorized under the Service providers industry. If you're checking for PRIME Education, Inc email addresses, these are also available on Lead411 with the @primeinc.org email format and possibly Kathleen Moreo's email. PRIME Education, Inc is based in Tamarac, FL. You can also get Kathleen Moreo's linkedin info, twitter, phone numbers, wiki, and biography on their Lead411 profile. Their contact information is filed under the Service providers category. Some possible email formats for Kathleen Moreo are email@example.com, email@example.com, email@example.com, and email@example.com. If you sign up for our free trial you will see our email@example.com addresses.
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Company Directory > PRIME Education, Inc


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The Pet Company
Consumer Complaints and Reviews
In December 2010, my husband and I bought a Boston Terrier pup from the Milford, CT store and it was a terrible experience. Our poor pup was given a clean bill of health by the vet that the store recommended to us, and lo and behold, 3 days after his "clean" bill of health, he had pneumonia. $4,000, many vet visits, tears and 6 months later, we nursed him back to health, despite my vet (who is well-renowned in the area and treats our other, very healthy, dog as well) thinking that we were fighting a losing battle.
We filed a complaint with the company and tried to get reimbursed for some of the costs of saving our baby's life, but nothing. We were basically dismissed and told that we could give him back and get a new dog, but then what would happen to our poor sick baby that we had become attached to? Would they just let him die?
It was an overall deplorable experience and the only good thing that came out of this was that we were able to save our puppy's life and now he is a very happy and cherished member of our family. I highly recommend that you avoid the Pet Company at all costs, for the sake of the neglected animals it sells as well as your wallets.
Summer of 2011, I took my daughter to the pet company store in Newport Center Mall, Jersey City. We walk in and the lady worker comes up to us and said to my daughter, "Here, carry the dog. Maybe you can convince your mom in buying it." While she places the dog on my daughter's chest, the dog starts vomiting a whole lot on her jacket and OMG, on her five-day old new uggs! So the store manager Dan ** said, "No problem." Give me receipt and your uggs and we will refund your money back. Well, it's been seven months and I haven't received anything in the mail. I have his signature and writing stating he received receipt and uggs from me. Please I would like to resolve this matter as soon as possible. It's only fair to me. I've been patient but it came to a point that I'm upset that now the pet company is gone in JC Mall. Thanking you in advance!
I purchased a two and a half month old puppy at the pet company in the Staten Island mall. Upon his first vet visit, my puppy was diagnosed with two parasites. I immediately returned to the pet company and filed the necessary paperwork to receive compensation for my vet visit and the medications. It has been four months and I have not received a dime from them. I have tried calling the phone number on file and the message states the number has been disconnected.
They are horrible! I received my dog from the pet company over two years ago. Don't get me wrong, I love my dog. She is the sweetest thing ever! I just hate the company I had to deal with. When I got my dog, they said she was of great health, and had been spayed. My husband got it as a gift for me. We didn't have the money at the time, so we put her on as a charge, to pay her off monthly (big mistake). When we brought her home, we noticed she was coughing a lot, and didn't seem well. We had to do a vet check up anyway, so we took her in. She had an ear infection, and sinus infection, and had no shots. We got all her shots, which cost a fortune, and then her antibiotics.
Later on, when she got old enough, she got her period. She had not been spayed, like they had told us. So we had to pay for that as well! All in all, we had to pay about $2,000 in vet bills, due to shots, and having to get her fixed. The billing in Pet Company is ridiculous as well. If you send in the bill as well, better send it in the day you get the bill in the mail (if you get it in the mail), and if you send it in a few days after, they claim it's late, and you have to pay double for it. If you call it in, they will sit on your payment, and make it late, so you have to pay extra anyway. Do not buy from them! It's a horrible company, with horrible costumer service. We've even been told we could get a refund for one late fee, then they didn't give it to us. It was lie. This is the worst company ever.
Very disappointed and upset with the Pet Company. Their lack of concern regarding my puppy's health. Their promise to reimburse me for the kennel cough my pet came down with, within 5 days after my purchase. The manager Jaimie in the Staten Island Mall refused to come out of the back room to discuss my refund. I have tried to contact the telephone number that he supplied me with and it goes straight to voice mail with the mailbox being full. I was promised a refund within 4 weeks and it has been almost 12 weeks.
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I purchased a pet at the Pet Company at the Freehold Raceway Mall in Freehold NJ. After only seven months, the dog was diagnosed with encephalitis and almost died; $2400 in vet bills later. I filed a claim with the store in accordance with their state mandated warranty policy. I got the runaround for a month and a half and then the store went out of business. I was given the customer support number, only to discover that the mailbox is full and taking no more messages; more smoke and mirrors.
The Staten Island store which is still open, keeps referring people to that number which is no help. I'm ready to call the police and the state bureaus.
I was working in the pet company in Milford Mall, about 2 months ago now. I still didn't get my last 2 checks yet. I kept calling the store and a so-called manager named Jamie (when you get to see him, you would laugh on how he looks and talks). All he does is sit in the back and eat all day. But anyway, I kept saying he got his before I felt. And I kept calling that home office of Sheron ** and I went straight to the voice mail.
That store, the pet company in Milford Mall, is so nasty and got fleas from bringing in straight kittens off people who got kittens they don't want. Ask Jamie, the so-called district manager. He will tell you just like everybody else would tell you. And I strongly agree that the puppies are from puppy mills. I got every proof to know.
They are closing all their offices and have not answered me. I purchased an AKC French Bulldog and it has been sick since day one. I purchased the peace of mind pet policy and no one answered any of my calls. Please help!
I have a lot of background in animal care, having a pre-veterinary bachelors degree and having a job as an animal care provider at an animal hospital for 4 years now. I just started working at The Pet Company in Milford, CT as an animal care tech about a month ago as a second job, and what I've seen there has been atrocious.
Here is my laundry list: the whole place smells of feces and the cages have a distinct smell of ammonia. Many of the dogs have worms and kennel cough. I have a strong suspicion that they come from puppy mills. The back room looks like it have never been cleaned. I cleaned out one corner of it and found months- to years-old dog and rabbit feces. (I have no idea how rabbit feces got back there, since the rabbits never see the back room). Many techs don't wash out food bowls but simply spray them down with water. Proper disinfectant is rarely used, if at all.
I've been working there for a month and still haven't seen a paycheck. Ive heard from many other store associates that they have gone months without being paid. The manager, Jaime, is very weird and disappears into the bathroom for hours at a time or falls asleep at the food court or at his desk in the back room. He's also been hours late to work.
Overall, this business is shady in how it treats both its animals and employees. Please do not buy animals from this store. Let it go out of business.
I used to work at the pet company in the Danbury mall. Overall, the place was not kept up with and no matter what they tell you, the dogs are indeed from puppy mills. I had finally had enough after a year and gave my two weeks notice. Then the following day while I was working, people from home office came in and shut the store down. A month prior to that, we started not getting paid on time. Since then, I had not gotten my last paycheck. I called and called the home office in New Windsor and would always get a voicemail.
After a week of not getting a callback, I and my former co-workers decided to write a complaint to the Department of Labor. I just got my check Saturday, but it isn't even the correct amount. They basically did not pay me for my last day there. I know it's not much, but at this point, it's the principle. My co-workers still have not gotten their checks as well as those who worked at the store in Milford. I urge everyone reading this who works there to quit because this company lies, cheats and they will not pay you. I also urge those thinking of buying a puppy there to please go elsewhere. I know the puppies are cute and also deserve good homes, but you are just giving this company more money than they deserve and are helping keep puppy mills in business. This company needs to be shut down.
On May 30, 2011, I purchased an Anatolian Shepherd from the Staten Island Mall which cost me $1700. I was told this was a great house dog and good with children which was a very big concern of mine since I have a 6- and 9-yr-old. After having this dog for a month and giving her nothing but love, she became very vicious. My dog mainly stays in my yard and whenever anyone goes out there, she charges at them and bites. She has even come after me and tried biting me. I have elderly parents who live upstairs from me and my dog not only bruises them by jumping on them, she has bit them and broken the skin on numerous occasions. Not only is she biting everyone, she has destroyed my yard. She has eaten every plant that we planted. She ate two pool skimmers. She pulled off a window frame from my house and ate the screen. I can go on and on of all the damage she has done.
The minute we bring her in the house, it is non-stop barking along with biting whoever is near her. I have gotten her a trainer who had informed me this is a flock dog who should have never been sold in a pet store; it is not intended for a house pet. I have pictures and videos of all the bruises she has caused to my elderly parents. I would like to return this dog. I fear she will hurt one of my children. I would like the payments to be stopped on the card. If I don't hear back from someone in your company within 72 hrs, I will take legal action.
I used to work at The Pet Company in Arbor Place Mall, from February until May of this year. I was shocked to see the way the puppies were treated, and how the management neglected to inform consumers and concerned employees about the health and welfare of the puppies. I was a sales associate and my job was to sell puppies and lie to customers. It's a filthy place with a bunch of lazy employees and managers that leave puppies in the feces for hours.
I was one of 2 or 3 people who cared about these animals and cleaned up after them. I made sure they had water and clean crates. I also tried very hard to rotate puppies and bring a few out, each day I work, and hold them. It's the only time they get to come out. When customers want to see them, then I would bring them out, but usually the popular puppies got to come out of their horrible cages, and they play with customers. The rest never got to come out. I felt horrible for them being stuck in those cages all day, everyday, and watch other puppies playing or going home with a new family. It broke my heart. I cried and prayed everyday, for God to help me find good homes for the ones who had been at the store for several months, that got overlooked. When they find a home, I cry because I know they will be happy, they will be loved and they will be free from their prison.
I promised those puppies that I wouldn't close that place down, and I won't give up until I do. The puppies are all very sick, they never see vets. The time I was there, almost 2 months, the puppies one but he didn't bother looking at any of the puppies who were seriously sick. Those that had been in this tiny little room, called the "sick room", another thing customers don't know. Those puppies had been in that room for months, but all he did was look at the 2 brand new puppies that came in that day. The puppies are angels but they are yelled at, kicked around, and deprived of every comfort a puppy should have. There are no toys, no walks, and no companionship. Around the time when I quit, they were cutting back on the precious babies' food. They were starving them. I got pictures of an emaciated Great Dane puppy, nothing but ribs. All the puppies are starving and sick, you can see their ribs through their fur. I've been talking with PETA and WESTGA SPCA because I have to close them down. Please help me shut them down and expose the cruelty and neglect, for the puppies and for all the animals being neglected right now, in one of their stores. Thank you.
I purchased a purebred yorkie so I was told on 5/21 from The Pet Company. I purchased the dog for my 11-year-old. I was advised the puppy was hypoallergenic. Since bringing the puppy home, I have been sick with asthma attacks and never had one until bringing the puppy home. Also, the puppy has kennel cough and bites. I called the store 24 hours later to advise them of the difficulty I was having and requested a refund. I was advised I would only be given 60% of the $1262.51 I paid after deductions of the microchip registration and tax. They would refund me $653.
Are you kidding? I had the dog for 24 hours. I can't seem to get any assistance. They keep referring to the fact I have a contract with them. Nowhere in the paperwork does it say contract. It talks about warranties. I really wanted to keep the dog but I can't. My throat closes over and I can't breathe when I am around him. Very frustrated. The district manager advised me to get some Benadryl and go to the doctor. I almost cursed at the lady when she said that. I'm not sure what to do next.
Well I still work at the Pet Company, but that doesn't make me a bad person because I love animals; I needed a job. I've haven't even been there two months, and I'm in the process of doing everything in my power to have it shut down. I'm not going to abandon these puppies until I can free them from their prison because I made a promise to them; and that means more to me than anything in the world.
All sales people don't lie. It just so happens that we are lied to by management about the health and welfare of the puppies. But I know from experience, I'm the only person in my store who cleans their cages and cries when the ones who've been living in that hell for several months finally get homes. It isn't the puppies' fault they're neglected; they still need love, and they still need homes. I speak for those who do not have voices. And I will fight in their names until they are free, until they can be puppies, and until they can be loved and nourished. All the puppies at my store are starving because management has cut back on their food! They are heartless, and they must be stopped! I don't know how they sleep at night! We must put them out of business. Please help the puppies!
We purchased a puppy from The Pet Company at Menlo Mall in Edison, NJ because my kids fell in love with a puppy. The store clerks are cons. They tell you how the warranty is so great - you get reimbursed for any sickness and it comes with a free vet visit if you use their house vet. Turns out our puppy did get sick in 2 weeks and their house vet lied to us and said he was fine. Two days later I had to rush the puppy to an animal hospital where they diagnosed him with kennel cough and worms. We got an "unfit to purchase" notice from our vet. Now they won't reimburse us because the warranty is for 14 days and we took 17 days to go to their vet. The Pet Company knows that all puppies from their disgusting puppy mills get this sickness so they con their warranty contract to make sure no payments need to be made. This is not right and they need to pay for their ways!
My fiancé and I purchased a 3-month-old Puggle puppy from this store on February 11, 2011. The very next day, the puppy's eye appeared to be infected (swollen, red, oozing). On Monday, February 14, 2011, we took her to our own choice of vet only to find out that the dog has cherry eye, which is a hereditary condition which deems the dog unfit for sale. Since then, the puppy has become extremely aggressive, biting and attacking everyone in our household. When we called and reported these problems to the store manager, her response was, "The dog is teething and it's not a big deal about the cherry eye." The surgery to repair the dog's eye costs $1,000. We are not wealthy people and cannot afford such a steep amount for vet bills, especially after just having paid over $2,000 for the dog. When I researched the breeder the dog came from, I found that it is a well-known puppy mill. I plan on returning the dog to the store tonight.
First of all, the puppies at The Pet Company are from puppy mills. So you will be paying top dollar for badly bred animals. However, I love my little Chihuahua I bought just a few days ago even though he is sick and I have had to already start him on medicine. My complaint is more about the way I was tricked into purchasing their "Lifetime Guarantee" for $200.00. When I first showed interest in the pup, the store clerk, Connie, told me the price was $1300.00.
I said no way and somehow they magically dropped the price to $1099.00 I still said I wanted to think about it over night and left the store. She called my cell phone and offered me $800.00 if I bought the puppy that night. So I gave in and went back to the store with my kids in tow. Once there, after my kids are already excited about bringing a puppy home, Connie tells me the final price is $1049. She told me that included the Lifetime Guarantee that I had to purchase and it was not an option to decline it.
I told her I didn't want it and felt like I was being forced into purchasing it. In a very snotty tone she told me she would gladly void the whole contract out. At this point my kids were getting upset about me changing my mind. I went ahead and went with the purchase thinking it wouldn't hurt to have the guarantee. I got home and read over the guarantee and realized it is a total rip off. You have to go through major hoops, including an autopsy, if anything ever happens to your pet to even have the store honor the guarantee. I have tried and tried to no avail to have this warranty refunded.
The store clerks have been so ugly and unprofessional when speaking with me. I will never deal with this company and wouldn't recommend them to my worst enemy. I basically was lied to about it being required to purchase the warranty to take the dog home and now because I signed for it I am "bound by contract." It's all a bunch of bull. Its $200.00 wasted. Nowhere does the paperwork state that is a contract I signed. I just acknowledged receipt of the warranty, not a binding contract.
I purchased a puppy from this company and the sales were all deceitful. They claimed that the first puppy visit comes with a shot and check up. My puppy was sick and had the Kennel Cough. The puppy costs $1600 but the check up and medication was not expensive around $100. This amount was supposed to be covered under their policy. I never received my reimbursement and the office number they gave me to call was a cell phone number.
The company also states that they will reimburse me 100% if the puppy dies in 5 years due to any health conditions. I don't trust this company since they can't even reimburse me $100 for the check up and medication. I paid for the puppy at a higher price than market value because I thought that it comes with a great deal of benefits. However I didn't get the benefit that I was supposed to get. The market price for my puppy is $800; however, I paid $1600 for the additional benefits that were supposed to be but are not.
I purchased a puppy (and two additional "piece of mind" warranties) who turned out to have bilateral cherry eye which my vet described as "genetic defect" and told me to contact the pet store and question my warranty as this would be "expensive" to treat. I filed a claim with The Pet Company, sent in all the documentation they requested as well as an itemized estimate of the surgery bill (not done yet). A few weeks later, I received a denial in the mail from The Pet Company simply stating "items submitted for reimbursement not covered under the warranty". There was no explanation given and I am still not sure what is even covered under the two extra warranties I purchased. This company is a disgrace.
I in turn will be responsible for all of the charges, which are approximately $1000 when my puppy undergoes cherry eye repair tomorrow. This is not to mention the emotional toll this is taking on me. I now have to go through the process of pre-op care, putting my dog under anesthesia and post-op care.
This review is on the management staff of PETCO in Independence, Missouri. I took my dog and cat to get their rabies shots at PETCO. I was bullied by the vet and his assistant to get more than just the rabies shot. I was made to feel like a bad pet owner if I did not get the $50.00 package, so I did to keep face. Then the vet shared his total disappointment that I had de-clawed my cat. The vet reached down and tried to muzzle my 50lb terrier mix, who is not aggressive. I asked him, "What are you doing?" He just looked at me and removed the leash around my dog's nose, then he bent down and I guess tried to squirt something up my dog's nose.
My first reaction was to grab my dog, as this sudden move from the vet upset my dog. I was thrown to the floor. I stood up and asked the vet what he was doing. He said he has to squirt the Bordetella medicine up my dog's nose. It would have been nice if he would have told me that. Also, as a certified vet, I believe that the vet's assistant should have been assisting and not just standing behind the table. Anyway, after I was thrown to the ground, I stood up with a bloody bruised up leg which was very painful. As I was trying to stop my leg from bleeding, I saw a puddle on the floor. That was the Bordetella medicine that was supposed to be shot up in my dog's nose, but ended up squirted on the floor.
I just had a hysterectomy 2 weeks prior and me being thrown to the ground put me in extreme pain. I was told I had to pay full price. No apologies were given. I left the store and on the way home, called PETCO. I spoke to the manager there. He took down all the info and said he would have his manager call me. I called him back the day after and advised I had not gotten a phone call regarding my accident on their property. He was not real concerned with me. Today is July 10th (7 days after my accident) and no follow-up from any managers. The bruising and scratches from my leg are still very apparent even today. I have taken photographs of all my injuries from this PETCO store. I am going to contact PETCO's home office and see what they say. I do not believe I should pay for any of the shots that my dog and cat received on that day (minimum).
I purchased a puppy from The Pet Company on 1/1/10. They claimed he came from a breeder and that he was "fit for sale". I came to find that he had a very severe case of Giardia, the parasite that is highly contagious to both other dogs and humans. They refuse to refund me the cost I incurred at the Veterinarian's office because I did not submit the receipts "on time".
When I first saw Rocky, he was in the crate with another dog, which obviously leads me to believe that the Giardia was spread to this animal, as well. What also concerns me is the fact that people come into this store with their children and pet these puppies, not realizing that it is a health hazard. This store should be shut down, along with the puppy mills they ship from. I incurred several hundred dollars of Veterinary bills, not to mention that this puppy has severe emotional issues.
We purchased a 12-week-old Yorkie puppy from the Towne Center Mall Pet Company store last week. I was adamant about questioning the health of the puppy because I have another dog at home that I did not want subjected to any form of illness. They assured us that this puppy was 100% healthy which was far from the truth! Within 3 days of having this puppy home, my 5-year-old Schnoodle, which has always been in perfect health, was hospitalized with a severe bacterial infection that nearly claimed his life. We took the new Yorkie puppy to the vet that the Pet Company deals with on the same day that my dog got sick and the puppy presented with bloody stools and was found to have a bacterial infection, severe skin irritation and scabbing from flea infestation (which we were told was scabbing from the identity chip), ear mites and a severe infection in both ears.
We brought the letter from the vet as well as the paperwork listing the expense and lab findings to the Pet Company and we were told they are not responsible for the illness of my dogs. This event has cost us $1183.06 in vet bills on top of the $1500.00 purchase price of what we were told was a healthy puppy. Not to mention the emotional distress to our family worrying about the welfare of our beloved 5-year-old dog that was hospitalized for 3 days. Bringing home a new puppy is supposed to be a positive experience for my children and this was nothing short of a nightmare!
I bought my English bulldog from The Pet Store in Sept. 2007. It is very expensive ($4,848.85). It included POM Warranty and Peace of Mind Warranty. I know it is expensive but as soon as I saw him, I fell in love with Fats Domino. The kicker is the insurance. They have no address or telephone number. The shop here closed down, with no forwarding address or telephone number. Fats needs surgery. Of course, it is very expensive. The policy is not worth the paper printed on. Can anyone help find the company? And of course, The Pet Company cannot be located.
I recently just brought a dog from the Milford, pet company store. She is the cutest thing, be warned that I took her home with kennel cough and it cost me 100.00 just to get meds and get her checked out. She cost a pretty penny too and I read her paperwork to find out that she was transported more than five times over and over again. I feel bad for these animals and only complain because I believe their prices are ridiculous. Although, the associates where very helpful and did provide with all her updated shot and where I can call if I had any questions for the doctor. I wouldn't recommend buying a dog from here, but if you ask them about the information they will fill you in. I read all the other stories on here and they should of been more upfront. To make this story end, she is healthy and my new best friend.
She ended up having kennel cough which cost 100.00 bucks meds and visit, I don't care about money, nor am I rich, it's just the case that these dogs should be more looked at from the vet that comes in to check them, or think about changing the vet to someone who cares. Thanks.
I applied for a Christmas job in 2006 at the Pet Company. I worked there for three weeks and to this day, 2010, I have not been paid a cent. I called and called and there is no reply.
I purchased an American Bulldog puppy at the Menlo Park Mall store #6. Bringing the dog home, I noticed that Mack was drinking a lot of water. I took him to the vet for a check up. The vet ran some tests and concluded that the puppy had Juvenile Renal disease. He had the kidneys of a 10 year old dog. The dog was purchased in late September. Numerous trips to the vet through the next months. The vet gave Mack until New Years Day of 2010. Mack, through the efforts of the vet, had lived past New Year's only to pass just recently, 3-26-10. The Pet Company has not been too responsive to the claims I have submitted. I have paid the vet through my Visa card but the Pet Company credits their store card. Meaning, I have credit to purchase items or a new pet.
I was in this store today when I saw a small puppy with an infected paw. His paw was raw and pink colored and looked very painful. The puppy was chewing at his paw and it was very obvious that these puppies are not taken care of at all. This poor puppy is in a lot of pain and I am honestly concerned for its well being. I am very upset and disturbed by this.
The policy of the store where I purchased the dog was that if a letter of "unfit" was provided, they would incur all expenses of making dog well. Dog's tail improperly "docked"; it fell off in my hand and the dog had worms. They refused to pay for office visits and medications. Janet is rude, inconsiderate, nasty and unprofessional. Now I realize they have many complaints filed against them.
On January 12th, 2010 I purchased a puppy from The Pet Company. On January 16th, she was diagnosed by a vet to have the parvo virus, which is a very serious and very contagious intestine virus. My puppy was in the hospital until January 19th, when she was released with antibiotics and other medications. On January 18th I brought to the store a certificate from the vet that had treated my puppy that stated she was unfit for sale. I also gave the store employees the vet bill and the diagnosis. The store employees had me fill out a form of election and told me they would give everything to the corporate office and that corporate would contact me. I have yet to hear anything from them and I have already sent two e-mails with no response. Because my puppy was so sick, I lost one day of work to take her to the vet. Also, because my puppy was in the hospital for four days, the bill now exceeds $1500.00. I would like The Pet Company to at least pay my vet bills because the puppy was sick when sold to me.
I purchased a Yorkshire terrier from this company on 12/19/09. This puppy was sold to me in a horrible condition as far a appearance. I paid $1669 for the dog and got it home and kept smelling this offensive smell. I took the pup to the vet and was told that he had a really bad ear infection for which he had for weeks if not months. The vet prescribed ear cleaner and antibiotic drops for which cost me $42. I went back to the store and explained to them that I felt like they completely ripped me off. After explaining my situation, I was told to make a claim for which I did to not receive any correspondence or feedback a month later. I never received the pups Pedigree for which I should have received the day of purchase but the manager didn't have it in the store because she said she may have misplaced it or she may have it home.
When I returned on 1-1-10 to complete the claim, I again asked about the Pedigree paper and was told that she mailed it out which was a lie because up until today I don't have the Pedigree paper and the person for which put through all of this headache name is Alex who is supposedly a manager but has no managerial skills.
So today 1-22-10, I called the pet company again and spoke to another one of their "managers" Amanda because I wanted to inquire about the claim and was told to e-mail the company that she knows nothing. I then asked about the Pedigree and was told she doesn't know anything about that either. She just got into the company a couple of days ago! This is an outrage! I want the $42 refunded back to me along with a refund of $1669.15 for the puppy.
When he was sold to me, he was out of date on all the shots they were supposed to give him. Why should I have to dish out so much money to do something that was their responsibility while in their care? They have already ripped me off. I want my money back I want someone to speak to me and resolve this ASAP! I am prepared to take this to court if need be, if it can not be settled! The price for him was absurd and to think I would have to spend a lot more money for shots they should have given him. I was told by the salesman Jon and the manager that he was so expensive because he would not need any shots or anything for at least another 2 if not 3 months! My son is clearly depressed because this has been such a nightmare! What should be making him happy is making him sad!
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Total number of Reitmans stores in Newfoundland and Labrador-Canada: 11
The biggest mall in Newfoundland and Labrador with Reitmans store: Avalon Mall (Kenmount Road at Thorburn)
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2271 Harvey Ave #180, Orchard Park, Kelowna, BC V1Y, Canada297 stores
100 City Centre Drive, Mississauga, ON, L5B 2C9


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The former X Factor winner took a moment on Twitter to reflect on the past few months ahead of ringing in the New Year.
After a rocky time lately, James told fans: "Needless to say, 2014 is not a year I'm going to particularly miss aside from the interactions with my cool ass fans!
"2015 hurry up and come!"
James won the ninth series of X Factor and had enormous success with first single 'Impossible' and his self-titled debut album.
However, the past year hasn't been the easiest for the star who quit Twitter after finding it "too toxic" and found himself injured during a Polish bar brawl.
He also confirmed his departure from Simon Cowell's record label Syco, and later said he was leaving his management team to focus on a fresh start.
Reflecting on the past year, he told fans: "This Christmas has really made me fully appreciate the value of family and friends. I hope to strengthen those bonds in 2015. #2014TaughtMe
"2014 has also taught me that even when the chips are down I still have an unbelievable fan base worldwide! The support has been exceptional."
As well as working on new music and (hopefully) releasing a new album, the singer-songwriter has vowed to start a new healthy eating plan tomorrow.
So he made the most of his last day of comfort food, enjoying a McDonald's breakfast and a Gregg's roll.
"Crash diet starts tomorrow and for all of 2015 so I started my day at the Golden Arches with 2 mcmuffins n a sausage n bean melt ala greggs
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A new and updated version of this best-selling resource! Jones and Bartlett Publisher's 2011 Nurse's Drug Handbook is the most up-to-date, practical, and easy-to-use nursing drug reference! It provides: Accurate, timely facts on hundreds of drugs from abacavir sulfate to Zyvox; Concise, consistently formatted drug entries organized alphabetically; No-nonsense writing style that speaks your language in terms you use everyday; Index of all generic, trade, and alternate drug names for quick reference. It has all the vital information you need at your fingertips: Chemical and therapeutic classes, FDA pregnancy risk category and controlled substance schedule; Indications and dosages, as well as route, onset, peak, and duration information; Incompatibilities, contraindications; interactions with drugs, food, and activities, and adverse reactions; Nursing considerations, including key patient-teaching points; Vital features include mechanism-of-action illustrations showing how drugs at the cellular, tissue, or organ levels and dosage adjustments help individualize care for elderly patients, patients with renal impairment, and others with special needs; Warnings and precautions that keep you informed and alert.Professional Behaviors Nursing care during a shift is based on the content and the accuracy of shift reports for making clinical ... Electronic documentation systems can generate 8-hour or 12-hour shift reports, and if you have such a system ... The 2006 NPSG established by the Joint Commission helped many hospitals to adopt a standardized template for handoffs between shifts: a patient- centered, anbsp;...
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|Jones & Bartlett Publishers - 2010-11-15


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Peroxisome proliferator-activated receptor β/δ (PPARβ/δ) is a ubiquitously expressed gene with higher levels observed in skeletal muscle. Recently, our laboratory showed (Bonala S, Lokireddy S, Arigela H, Teng S, Wahli W, Sharma M, McFarlane C, Kambadur R. J Biol Chem 287: 12935–12951, 2012) that PPARβ/δ modulates myostatin activity to induce myogenesis in skeletal muscle. In the present study, we show that PPARβ/δ-null mice display reduced body weight, skeletal muscle weight, and myofiber atrophy during postnatal development. In addition, a significant reduction in satellite cell number was observed in PPARβ/δ-null mice, suggesting a role for PPARβ/δ in muscle regeneration. To investigate this, tibialis anterior muscles were injured with notexin, and muscle regeneration was monitored on days 3, 5, 7, and 28 postinjury. Immunohistochemical analysis revealed an increased inflammatory response and reduced myoblast proliferation in regenerating muscle from PPARβ/δ-null mice. Histological analysis confirmed that the regenerated muscle fibers of PPARβ/δ-null mice maintained an atrophy phenotype with reduced numbers of centrally placed nuclei. Even though satellite cell numbers were reduced before injury, satellite cell self-renewal was found to be unaffected in PPARβ/δ-null mice after regeneration. Previously, our laboratory had showed (Bonala S, Lokireddy S, Arigela H, Teng S, Wahli W, Sharma M, McFarlane C, Kambadur R. J Biol Chem 287: 12935–12951, 2012) that inactivation of PPARβ/δ increases myostatin signaling and inhibits myogenesis. Our results here indeed confirm that inactivation of myostatin signaling rescues the atrophy phenotype and improves muscle fiber cross-sectional area in both uninjured and regenerated tibialis anterior muscle from PPARβ/δ-null mice. Taken together, these data suggest that absence of PPARβ/δ leads to loss of satellite cells, impaired skeletal muscle regeneration, and postnatal myogenesis. Furthermore, our results also demonstrate that functional antagonism of myostatin has utility in rescuing these effects.
- PPARβ/δ
- myostatin
- skeletal muscle regeneration
the peroxisome proliferator-activated receptor (PPAR) ligand-inducible nuclear hormone receptor subfamily consists of three members, PPARα, PPARβ/δ, and PPARγ. The conformational change induced upon interaction of PPARs with their ligands activates the heterodimeric complexes that they form with retinoid-X receptors (8, 12, 16). These activated PPAR-retinoid-X receptor complexes are then able to bind to peroxisome proliferator response elements to activate gene transcription (6, 31). Classically, each of the three PPAR isotypes has been identified in species ranging from Xenopus to humans and are expressed in distinct tissue-specific patterns. PPARα (NR1C1) is involved in fatty acid catabolism and amino acid metabolism and is primarily responsible for body energy homeostasis. PPARα is highly expressed in liver, heart, skeletal muscle, intestinal mucosa, and brown adipose tissue and is metabolically very active (14). PPARγ (NR1C3), highly expressed in white and brown adipose tissue, colon, and spleen, is mainly involved in adipocyte differentiation and lipid storage in adipose tissue and also in enhancing body insulin sensitivity (36). In contrast to PPARα and PPARγ, which are highly expressed in a few tissues, PPARβ/δ (NR1C2) is expressed ubiquitously, but with varying levels in different tissues (3, 40). PPARβ/δ has been shown to be involved in lipid metabolism, energy homeostasis, and wound healing (41). PPARα, β/δ, and γ also play important roles in epidermal maturation and tissue repair processes (28). Whether PPARβ/δ is pro- or anticarcinogenic is still debated: both effects have been reported in various tumor types, which might reflect different genetic defects within the tumor (27, 33). In addition, PPARβ/δ has been implicated in increasing the β-oxidation of fatty acids in skeletal muscle and adipose tissue (9). Furthermore, PPARβ/δ plays a pivotal role in regulating hepatic gene expression, which modulates glucose homeostasis in liver (17).
Overexpression of PPARβ/δ has been shown to influence muscle metabolism. Previous studies have established that the mRNA expression of PPARδ is higher in oxidative soleus (Sol) muscle compared with the predominantly glycolytic extensor digitorum longus (EDL) muscle (19). It was further noted that oxidative muscles also display the highest levels of PPAR-β/δ protein. PPARβ/δ overexpression promotes hyperplasia of skeletal muscle, specifically resulting in an increase in oxidative muscle fibers and capillary density. In agreement with this, overexpression of a constitutively active PPARβ/δ in mouse skeletal muscle was found to induce differentiation of mitochondria-rich, oxidative type I muscle fibers (42). In addition, muscle-specific overexpression of PPARβ/δ has been shown to promote myonuclear density (13). PPARβ/δ also plays an important role in the adaptation of skeletal muscle to environmental changes, such as long-term fasting, by increasing the number of oxidative fibers (10). In line with these observations, muscle-specific ablation of PPARβ/δ causes a functional switch of the skeletal muscle fiber type toward lower oxidative capacity, which is followed by the appearance of age-dependent obesity and type 2 diabetes (38).
Furthermore, PPARβ/δ ligands may upregulate fatty acid transport and oxidation, thereby reducing fatty acid-induced inflammation and insulin resistance in skeletal muscle (5, 20). A recent report suggests that activation of PPARβ/δ, through addition of specific agonist, enhances myogenesis in C2C12 myoblasts by increasing both myoblast proliferation and differentiation (2). Consistent with this, loss of PPARβ/δ resulted in reduced proliferation of primary myoblasts and defective differentiation. In addition, a recent study reported that skeletal muscle-specific knock out of PPARδ in mice [PPARδ-conditional knockout (cKO)] leads to reduced satellite cell (SC) number and impaired skeletal muscle regeneration upon cardiotoxin-mediated injury (1). Recent results have revealed that PPARβ/δ positively regulates postnatal myogenesis through transcriptional activation of Gasp-1, leading to reduced activity of its downstream target myostatin (2).
Here, using a germ line deleted PPARβ/δ knockout mouse model (PPARβ/δ-null), we have further characterized the role of PPARβ/δ in postnatal skeletal muscle growth and regeneration. Given the increased myostatin activity in PPARβ/δ-null muscle (2), we hypothesize that postnatal myogenesis is impaired in PPARβ/δ-null mice. Consistent with this, PPARβ/δ-null mice showed impaired muscle regeneration, evidenced by reduced muscle weight and decline in regenerated myofiber size and reduced centrally located myonuclei number, 28 days post-notexin administration. We also observed increased inflammatory response with reduced myoblast proliferation during later phase of regeneration in PPARβ/δ-null regenerating tibialis anterior (TA) muscle. On the other hand, antagonism of myostatin in PPARβ/δ-null mice resulted in increased body and muscle weight and significant hypertrophy of muscle fibers. Subsequent blockade of myostatin using the myostatin inhibitor soluble activin receptor IIB (sActRIIB) improved skeletal muscle regeneration by increasing the number of centrally formed nuclei and promoting hypertrophy of regenerated muscle fibers. Therefore, we conclude that PPARβ/δ positively regulates postnatal skeletal muscle myogenesis through reducing myostatin activity in mice.
PPARβ/δ-null mice were gifted from Professor Walter Wahli (University of Lausanne, Lausanne, Switzerland). Animals were housed and maintained at a constant temperature (20°C) with a 12:12-h light-dark cycle with ad libitum access to water at the Nanyang Technological University animal facility. Wild-type (WT) mice (C57BL/6) were purchased from the Center for Animal Resources, National University of Singapore, Singapore. All animal procedures were reviewed and approved by the Institute Animal Ethics Committee, Singapore.
Muscle injury model.
Six-week-old male WT and PPARβ/δ-null mice were anesthetized by intraperitoneal injection of a mixture of 10 mg/ml ketamine and 1 mg/ml xylazine at 0.1 ml/10 g body wt. Fifteen microliters of notexin (10 μg/ml in 0.9% saline; Latoxan, Rosans, France) were injected into the TA muscle of the left leg using a 28-gauge syringe (Hamilton, Whittier, CA). The TA muscle from the contralateral limb was used as the uninjured control. TA muscles were harvested on days 3, 5, 7, and 28 after notexin-induced injury. For the sActRIIB myostatin antagonist trial, mice were anesthetized with ketamine and xylazine, as stated above. Fifteen microliters of notexin (10 μg/ml) were injected into the TA muscle of the left leg with a 28-gauge syringe, and the contralateral limb was used as an uninjured control. The mice were injected intraperitoneally with sActRIIB (43) (4 μg/g body wt) three times per week for a period of 4 wk. TA muscles were harvested on day 28 after notexin-induced injury for further histological and molecular analysis.
Histological assessment of muscle regeneration.
Muscle tissues were embedded in optimal cutting temperature (Tissue-Tek, Sakura Fine TEK, Torrance, CA) compound and then frozen in liquid nitrogen cooled isopentane. Serial cross sections (10 μm) were cut from the midbelly of the muscle and mounted on cryoslides for histological, immunochemical, and metabolic staining. Hematoxylin and eosin (H&E) and Van Gieson's staining were performed according to the manufacturer's instructions [catalog no. 115973-1 (solution A), 115973-2 (solution B) Merck Millipore, Singapore]. For H&E staining, the cryosections were stained with hematoxylin for 1 min and rinsed with tap water. Following 2 × 1 min washes in Scott's tap water, the sections were stained with eosin for 2 min and rinsed three times in 50% ethanol and then in 70% ethanol. Sections were further rinsed for 2 min in 95% ethanol, washed 2 × 2 min each in 100% ethanol, followed by 2 × 5 min in xylene. The stained sections were mounted with DPX mounting reagent and allowed to dry overnight. Images were captured using the Leica CTR 6500 microscope equipped with the Leica DFC 310 FX camera (Leica, Singapore). ImagePro Plus software (Media Cybernetics, Bethesda, MD) and ImageJ software (National Institutes of Health) were used for image analysis. H&E stained images were used for cross-sectional area (CSA) measurement, and fibrotic tissue was assessed through Van Gieson's stain. The area of interstitial fibrosis was quantitatively assessed using Van Gieson's stained images and was measured according to Luz et al. (21). Five images (magnification, ×10) around the lesion area from each sample were used for quantification, according to Ge et al. (11), and calculated as the ratio of fibrotic area to CSA (%) of the images. For the contralateral uninjured control, the CSA from 1,000 myofibers from randomly selected fields were counted. For regenerated myofibers, the CSA of centrally nucleated myofibers within the field were measured.
Immunohistochemical staining for Mac-1.
Frozen muscle sections (10 μm) were stained for macrophages according to the previously established protocol (11). Briefly, sections were fixed in 2% paraformaldehyde for 5 min and then permeabilized with 0.3% Triton X-100 in PBS for 5–10 min. The sections were then blocked with 10% normal goat serum (NGS) in Tris-buffered saline (TBS) for 1 h at room temperature and then incubated with primary rat anti-mouse Mac-1 antibody (1:100; BD Pharmingen, San Diego, CA) in TBS overnight at 4°C. Following incubation with goat anti-rat IgG biotinylated (1:400) secondary antibody, in 5% NGS in TBS for 1 h at room temperature, the sections were then incubated with streptavidin conjugated Alexa Fluor 488 (1:400; Invitrogen) tertiary antibody in 5% NGS in TBS for 30 min. Nuclei were counterstained with 4′6-diamidino-2-phenylindole (DAPI) (1:1,000; Invitrogen Molecular Probes, Singapore) and mounted with ProLong Gold Antifade mounting reagent (Invitrogen). Mac-1-positive cells were counted and expressed as a percentage of DAPI-positive nuclei.
Immunohistochemical staining for Pax7 and MyoD.
TA muscle sections (10 μm) were fixed in 4% paraformaldehyde for 5 min and then permeabilized with 0.2% PBS-Tween 20. The sections were then blocked with a solution containing 6% mouse IgG blocking reagent (MOM Immunodetection kit; Vector Laboratories) and 3% bovine serum albumin (BSA) in PBS for 1 h, followed by blocking again with MOM protein diluent with 1.5% BSA in PBS, as per the manufacturer's instruction. Muscle sections were then incubated with either mouse monoclonal anti-Pax7 (1:1,000; Developmental Studies Hybridoma Bank; DSHB, Iowa City, IA) or anti-MyoD (1:25; BD Pharmingen, San Diego, CA) primary antibody in 1.5% BSA in PBS overnight at 4°C. Following incubation with biotinylated horse anti-mouse IgG (1:500; Vector Laboratories), rabbit polyclonal anti-laminin (1:1,000; Sigma-Aldrich, Singapore), and rabbit polyclonal anti-MyoD (1:40; Santa Cruz) antibodies for 3 h, the sections were then washed and incubated with streptavidin conjugated Alexa Fluor 488 (1:1,000; Invitrogen) and goat anti-rabbit Alexa Fluor 594 (1:1,000; Invitrogen) for 30 min. Nuclei were counterstained with DAPI (1:5,000; Invitrogen Molecular Probes) and mounted with ProLong Gold Antifade mounting medium (Invitrogen). Pax7+/MyoD− cells were quantified in the stained sections and expressed as number of Pax7+/MyoD− cells per 100 myofiber.
Succinate dehydrogenase staining.
Succinate dehydrogenase (SDH) activity used to determine the overall oxidative capacity of skeletal muscles was measured using a colorimetric assay, as described by Masuda et al. (22). Muscle sections were air-dried for 30 min and incubated in prewarmed PBS buffer containing 50 mM sodium succinate and 0.6 mM nitro blue tetrazolium (Sigma-Aldrich, Singapore) for 25 min at 37°C. The reaction was terminated by rinsing the sections thoroughly with distilled water. After dehydration and clearance by xylene, the sections were mounted using DPX (Sigma-Aldrich, Singapore). Images were captured using the Leica CTR 6500 microscope, equipped with the Leica DFC 310 FX camera and ImagePro Plus software (Media Cybernetics, Bethesda, MD). SDH activity was quantified using ImageJ software (National Institutes of Health) by converting the image to gray scale and measuring the gray intensity of the muscle section. The mean of the three sections was used to determine SDH activity.
Statistical analysis.
Statistical differences between groups was determined using unpaired two-tailed Student's t-test, and the results were considered significant at P < 0.05 (*), P < 0.01 (**), or P < 0.001 (***). Data are expressed as means ± SE.
PPARβ/δ-null mice exhibit pronounced skeletal muscle atrophy.
We observed reduced body weight and a significant decrease in TA, m. gastrocnemius, EDL, and Sol muscle weights in PPARβ/δ-null mice, compared with WT (Fig. 1, A–C). Although no significant difference in m. quadriceps muscle weights was noted, there was a trend toward reduced muscle weight in PPARβ/δ-null mice (Fig. 1B). Consistent with the reduced muscle weights, a significant reduction in TA muscle fiber CSA was observed in PPARβ/δ-null mice, compared with WT mice (Fig. 1D), although no significant difference was noted in myofiber number (data not shown). SCs play crucial roles in postnatal muscle growth and maintenance (32). As such, we next quantified the number of Pax7+/MyoD− SCs in muscle fiber sections through immunohistochemical analysis. Results revealed a significant reduction in the number of Pax7+/MyoD− SCs in resting muscle fibers of PPARβ/δ-null mice, compared with WT controls (Fig. 1E).
Histological analysis of skeletal muscle during early regeneration.
To further study the effect of loss of PPARβ/δ on postnatal myogenesis, skeletal muscle regeneration was assessed in WT and PPARβ/δ-null mice injected with notexin. The uninjured TA muscles from both PPARβ/δ-null and WT mice are shown in Fig. 2A, and, upon injury, both of the genotypes showed complete and extensive muscle degeneration 3 days post-notexin-induced injury (Fig. 2A). However, more extensive necrosis was seen on day 3 post-notexin injection in PPARβ/δ-null mice, compared with WT mice (Fig. 2A). At day 5 postinjury, a mixed population of hyperstained necrotic myofibers and newly developing myofibers were observed in TA muscle from both PPARβ/δ-null mice and WT controls (Fig. 2A). At 7 days postinjury, nascent myofibers, characterized by centrally located nuclei and small fiber size, were abundant in TA muscle from both PPARβ/δ-null mice and WT controls; however, visibly smaller myofibers were observed in PPARβ/δ-null mice compared with WT controls (Fig. 2A). Immunohistochemical analysis with Mac-1 antibodies revealed increased infiltration of macrophages in PPARβ/δ-null mice at day 3 post-notexin injection (Fig. 2B). However, no significant difference in the percentage of Mac-1-positive cells was noted between PPARβ/δ-null mice and WT controls 28 days following notexin injection (Fig. 2C). Collectively, these data suggest that loss of PPARβ/δ affects the early stages of muscle regeneration.
Reduced numbers of proliferating myoblasts in PPARβ/δ-null regenerating muscle.
We next performed MyoD immunohistochemical analysis on notexin-injured TA muscle sections to assess whether or not loss of PPARβ/δ affects SC activation. Results revealed a significant reduction in MyoD-positive myoblasts from 3 days post-notexin injection, with greater than 50% reduction in MyoD-positive cells noted at day 3, ∼38% reduction at day 7, and ∼50% reduction at day 28 postinjury in PPARβ/δ-null TA muscle, compared with respective WT controls (Fig. 2D). These data suggest that loss of PPARβ/δ significantly reduces the pool of proliferating myoblasts present in injured and regenerating skeletal muscle.
We further assessed SC self-renewal in PPARβ/δ-null muscle through MyoD and Pax7 immunohistochemical analysis on regenerated (day 28 post-notexin injection) TA muscle sections. After injury and regeneration, we still observe a significant reduction in SC number in PPARβ/δ-null mice compared with WT mice (Fig. 2E). Upon further analysis, we did not find any significant difference in SC number between uninjured and regenerated TA muscle in both the genotypes (comparison not shown). These data suggest that the self-renewal capacity of SCs remains unaffected in PPARβ/δ-null mice.
Loss of PPARβ/δ results in reduced centrally placed myonuclei in regenerated muscle.
Histological analysis was performed to quantitatively examine muscle regeneration 28 days post-notexin-induced injury (Fig. 3A). Morphologically, we noted an observable reduction in myofiber size in regenerated TA muscle from PPARβ/δ-null compared with WT controls (Fig. 3A). Subsequent analysis of myofiber CSA confirmed the reduced myofiber size in regenerated TA muscle from PPARβ/δ-null mice (Fig. 3B), which was consistent with the atrophy phenotype noted in PPARβ/δ-null mice before injury (Fig. 1D). Consistent with this, the weight of regenerated TA muscle was significantly lower in PPARβ/δ-null mice compared with WT controls (Fig. 3C). As regenerated myofibers are characterized by the presence of centrally located myonuclei (34), we next assessed the number of central myonuclei per myofiber in regenerated TA muscle from WT and PPARβ/δ-null mice. As can be seen in Fig. 3D, loss of PPARβ/δ led to a significant increase in myofibers with one centrally placed nuclei, concomitant with a significant reduction in the percentage of myofibers with two and three or more centrally placed nuclei, compared with WT controls (Fig. 3D). Specifically, the number of myofibers with one centrally placed nuclei was found to be 52.99 ± 2.01% in WT and 66.76 ± 1.78% in PPARβ/δ-null mice, whereas the number of myofibers with two centrally placed nuclei were found to be 33.07 ± 0.7% in WT and 26.03 ± 1% in PPARβ/δ-null, and greater than three centrally placed nuclei were found to be 13.9 ± 1.53% in WT and 7.2 ± 0.87% in PPARβ/δ-null mice (P < 0.01, P < 0.001) (Fig. 3D).
Loss of PPARβ/δ does not significantly alter scar tissue formation or metabolic properties of regenerated muscle.
The final phase of muscle regeneration is usually characterized by fibrotic tissue formation, which contributes to incomplete functional recovery (15). To examine the extent of fibrotic tissue formation in regenerated TA muscle of WT and PPARβ/δ-null mice, muscle sections were stained with Van Gieson's stain, and the extent of fibrotic tissue was quantified. Subsequent quantification of fibrotic tissue formation revealed that there was no significant difference in the area of fibrotic tissue in regenerated TA muscle sections between WT and PPARβ/δ-null mice (Fig. 4A).
Skeletal muscle regeneration has been shown to increase the number of oxidative muscle fibers (4). Hence, we further assessed the proportion of oxidative muscle fibers in regenerated (day 28 post-notexin injection) TA muscles through assessing SDH activity (22). As expected, there was an increase in SDH activity, as measured through increased SDH staining, in regenerated TA muscles from both WT and PPARβ/δ-null mice, compared with respective uninjured controls. However, it is noteworthy to mention that SDH staining, and thus activity, was comparable between uninjured TA muscle from WT and PPARβ/δ-null mice and between regenerated TA muscle from WT and PPARβ/δ-null mice (Fig. 4, B and C). These results indicate that loss of PPARβ/δ does not lead to a change in oxidative capacity in injured skeletal muscle tissue.
Blockade of myostatin leads to skeletal muscle hypertrophy in PPARβ/δ-null mice pre- and postinjury.
Myostatin has been established to bind with high affinity to sActRIIB (18), inhibiting myostatin signaling and contributing to increased musculature. Hence, we tested the effect of myostatin inhibition in PPARβ/δ-null mice using sActRIIB. Increased body weight was observed in PPARβ/δ-null mice administered sActRIIB (4 μg/g body wt), compared with dialysis buffer (DB) injected control mice (Fig. 5A). However, no significant difference in muscle weights was observed in PPARβ/δ-null mice treated with sActRIIB, compared with control-treated mice (Fig. 5, B and C). We further noted an increase in muscle fiber CSA in sActRIIB injected PPARβ/δ-null mice (Fig. 5D) compared with control-treated mice, which is consistent with skeletal muscle hypertrophy and loss of myostatin activity. These data suggest that the reduction in body weight, muscle weights, and muscle CSA observed in PPARβ/δ-null mice may be due to enhanced activity of myostatin.
We further tested the effect of sActRIIB injection on skeletal muscle regeneration in PPARβ/δ-null mice. We observed no significant change in regenerated (day 28 post-notexin-induced injury) muscle weights of PPARβ/δ-null mice treated with sActRIIB, compared with respective DB treated control (data not shown). Despite this, we did find a significant increase in muscle fiber CSA, consistent with hypertrophy, in regenerated TA muscle sections of sActRIIB treated PPARβ/δ-null mice, compared with respective DB-treated control (Fig. 5E). A significant increase in the number of centrally formed nuclei was also observed in regenerated TA muscle sections from PPARβ/δ-null mice treated with sActRIIB, compared with respective DB treated control (Fig. 5F).
Taken together, these data suggest that sActRIIB-mediated blockade of myostatin is able to improve skeletal muscle regeneration in PPARβ/δ-null mice in response to injury.
Overexpression of constitutively active PPARβ/δ in mouse skeletal muscle promotes muscle development and enhances myogenesis by increasing both myoblast proliferation and differentiation in C2C12 myoblasts (2, 13, 42). In this study, we used notexin-induced muscle injury to analyze the regeneration capacity of PPARβ/δ-null muscle and, therefore, understand the role of PPARβ/δ in postnatal myogenesis.
During postnatal myogenesis PPARβ/δ-null mice show reduced body weight, reduced TA, gastrocnemius, EDL, and Sol muscle weight (Fig. 1, A–C). However, in contrast to the results presented here, Angione et al. (1) have shown no significant change in body weight and muscle weights in skeletal muscle-specific PPARβ/δ knockout mice (PPARδ-cKO). It is quite possible that the differences noted in body and muscle weights between Angione et al. and the present study could be due to the different transgenic mouse models used. In particular, the Angione et al. study made use of muscle-specific PPARβ/δ knockout mice, whereas we have used germ line-deleted PPARβ/δ-null mouse model. However, it is important to highlight that Angione et al. assessed for differences in body weight between female WT and PPARδ-cKO mice, whereas we have assessed differences in body and muscle weights between male WT and PPARβ/δ-null mice. Thus the variation in body weights and muscle weights observed between the study by Angione et al. and our present study could be due to sexual dimorphism, as previous reports indicate that hormones such as estrogen influence muscle growth (7, 24). However, further research will need to be performed to ascertain whether PPARβ/δ influences estrogen levels and thereby affects muscle mass. We further noted decreased muscle fiber size (atrophy) in PPARβ/δ-null mice compared with WT mice (Fig. 1D), with no appreciable change in fiber number (data not shown). Such atrophy could be due to reduced SC number and impaired SC function. Previous work from our laboratory has also demonstrated that myostatin is a potent negative regulator of SC activation and function (25), and excess myostatin levels have been shown to promote muscle wasting (26). Since PPARβ/δ-null mice have been previously shown to have increased myostatin activity (2), it is quite possible that the observed atrophy may be due to increased myostatin activity. In agreement with this, Pax7 immunostaining on muscle sections confirmed there was a significant reduction in SC number in TA muscles of 10-wk-old PPARβ/δ-null mice. These data are consistent with the Angione et al. study that reported a reduction of 40% in the number of Pax7-positive SCs in PPARδ-cKO mice. Given that the number of Pax7+/MyoD− quiescent SCs between resting muscle and regenerated muscle (day 28 post-notexin injection) in PPARβ/δ-null mice are comparable, we suggest that SCs from PPARβ/δ-null mice are able to self-renew their population normally during postnatal growth (Fig. 2E). Given that SC self-renewal may not be impaired in PPARβ/δ-null mice, we predict that the reduction in SCs is due to alterations in the specification of SCs during embryonic/fetal development (30) in PPARβ/δ-null mice. It was previously shown that a subset of Pax3/Pax7 expressing myoblasts in dermomyotome of embryonic days 16.5 to 18.5 mature into SCs (35). Perhaps lack of PPARβ/δ is responsible for either specification of these myoblasts in the dermomyotome or for their replication. Much more extensive investigations are required to investigate the precise mechanism of PPARβ/δ in regulating SC specification during fetal growth. Interestingly, in Xenopus development, PPARβ/δ is essential for muscle and neural differentiation as early as in gastrulation when PPARβ/δ governs a massive wave of transcriptional modifications affecting the later differentiation of muscle and brain (37).
SCs are proven muscle stem cells that give rise to new muscle fibers during skeletal muscle regeneration (32). Therefore, we next assessed the myogenic function of PPARβ/δ-null SCs by studying muscle regeneration. During the early phase of muscle regeneration, we found significantly increased macrophage infiltration in PPARβ/δ-null injured muscle after 3 days of notexin-induced injury (Fig. 2, A and B). In agreement with the data presented here, reduced macrophage infiltration has been reported in diabetic nephropathy mice treated with PPARβ/δ agonist and activation of PPARβ/δ has been further shown to inhibit macrophage recruitment and vascular inflammatory gene expression (23, 39). We also observed reduced numbers of MyoD-positive activated SCs at day 3 in regenerating PPARβ/δ-null TA skeletal muscle (Fig. 2D). Since PPARβ/δ-null mice have reduced SCs to begin with, which have previously been shown to proliferate slower (2), we speculate that both of these factors contribute to the reduced number of MyoD-positive myoblasts observed at day 3 of regeneration. In addition, previously published results from our laboratory have revealed increased myostatin activity in PPARβ/δ-null mice, which leads to reduced proliferation and differentiation of primary myoblasts (2). Thus it is quite possible that the reduced numbers of MyoD-positive myoblasts in PPARβ/δ-null mice during regeneration is due to increased expression/activity of myostatin observed in these mice. It is noteworthy to mention that, despite increased macrophage infiltration and impaired SC activation in PPARβ/δ-null mice, we observed no difference in fibrotic tissue formation in regenerated muscle (day 28 post-notexin injection) between WT and PPARβ/δ-null mice (Fig. 4A).
In agreement with Angione et al. (1), we also observed a reduced differentiation potential of myoblasts as the histology on PPARβ/δ-null regenerated skeletal muscle at day 28 confirmed a severely atrophied regenerated muscle fiber with lower number of centrally formed nuclei (Fig. 3, B and D). Several factors have been shown to affect SC activation, proliferation, and differentiation (1, 29). Previously, our laboratory has shown that myostatin is a potent negative regulator of SC activation and myoblast proliferation (25). Therefore, lack of myostatin improved muscle healing by increasing both myoblast proliferation and differentiation. Since the PPARβ/δ-null mice used in this study have increased myostatin activity (2), it is quite possible that the impaired SCs function and reduced myogenesis observed in these mice could be due to increased myostatin. To confirm the role of myostatin in PPARβ/δ-null mice during regeneration, we induced muscle injury via notexin injection and blocked excess myostatin signaling via treatment with a dominant-negative soluble receptor decoy (sActRIIB) (44). The results confirmed that blockade of excess myostatin signaling in PPARβ/δ-null mice resulted in increased muscle hypertrophy of not only resting muscle, but also regenerated (day 28 post-notexin injection) muscle. Therefore, we propose that increased myostatin activity is at least in part responsible for the atrophy phenotype observed in PPARβ/δ-null mice.
In summary, PPARβ/δ plays a critical role in muscle regeneration from early inflammatory response, primary myogenesis, and formation of completely regenerated myofibers. Based on the results from this study, we propose that PPARβ/δ regulates SC number, function, and myoblast differentiation via regulation of myostatin.
We are indebted to National Research Foundation (CRP) Singapore for financial support.
No conflicts of interest, financial or otherwise, are declared by the author(s).
Author contributions: P.C., R.M., X.G., and S.B. performed experiments; P.C., R.M., C.M., M.S., W.W., and R.K. analyzed data; P.C., R.M., C.M., M.S., W.W., and R.K. interpreted results of experiments; P.C. prepared figures; P.C. drafted manuscript; P.C., C.M., M.S., W.W., and R.K. edited and revised manuscript; P.C., R.M., X.G., S.B., C.M., M.S., W.W., and R.K. approved final version of manuscript; C.M., M.S., W.W., and R.K. conception and design of research.
We thank Developmental Studies Hybridoma Bank (Iowa City, IA) for some of the antibodies used in this study.
- Copyright © 2015 the American Physiological Society


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Luton Murders - One Victim, Mum, Is Named
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Fifth Varshavyanka submarine joins Russia's NavyMilitary & Defense October 26, 12:11
Russian Baltic Fleet frigate arrives in Cuba on visitMilitary & Defense October 26, 11:57
Air Defense drills involving various aircraft kick off in four CIS statesMilitary & Defense October 26, 11:34
MP Savchenko arrives in Moscow to attend hearing on Ukrainian nationalistsWorld October 26, 11:03
Bulgaria and Russia sign agreement to settle debt on Belene NPP project — ministerBusiness & Economy October 26, 10:38
Russia honored all commitments on S-300 supplies to Tehran — ambassadorWorld October 26, 9:04
Kyrgyz president signs decree on government's resignationWorld October 26, 8:47
Display of rare impressionist masterpieces from Russian collector wows Parisian art loversSociety & Culture October 26, 8:46
Russia ready to resume humanitarian pauses in AleppoWorld October 26, 7:42
{{element.title}}{{element.heading}} {{element.date}}
ST. PETERSBURG, October 16 (Itar-Tass) —— Young hooligans and the pirate flag were taken down from the mast of the Aurora cruiser, a source in the local law enforcement agencies told Itar-Tass on Sunday.
Two young men and a young woman spent five hours on the mast of the Aurora cruiser, the deputy chief of the information and public relations department of the police force in St. Petersburg and the Leningrad Region Elmar Shakhirzayev said. Young hooligans went aboard the cruiser at about 4 p.m. Moscow time and separating into several groups were seeking to climb the Aurora masts, he said. The Aurora crew thwarted an attempt at climbing the mast. Six people were detained and brought to the police station. The pirate flag and the pieces of metal tubes were confiscated from them. However, three hooligans managed to climb the mast and hoist the Jolly Roger.
The rescuers and police took the young hooligans off the mast. The offenders put up resistance. Neither drizzle nor cold winds (the air temperature is 7-9 degrees Centigrade in St. Petersburg) frightened them. The young hooligans were taken at about 9.40 p.m. Moscow time off the mast. The detainees were brought to the police station.
"The offenders do not confess in their crime, but just keep silence. So, they cannot be identified as members of the art group Voina (War) or any other groups," Shakhirzayev said.
All detainees were charged under Article 20 Part 1 of the Criminal Code for petty hooliganism.


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Note 4 for CHM 218 with Professor Berger at IPFW
Note 4 for CHM 218 with Professor Berger at IPFW
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Date Created: 02/06/15
CHI218 1 RVCKLO Chapter 4 a The elemmrse madel is a madel afbanding that assumes that a crystal Bf a metal cansists afpasidve ians at the lattice paints within a delacalized sea afvalence elecsmns b The unit cell is the smallest buxrlike pmiun nf a crystal lattice Emm which the entire lattice can be neated by stansladng in three dimensians c An allay is a cumbinadan aftwa ur mare metals in the salid state a A crystal latriceis the three dimensianal repeating pattern afatums ar ians in a aystalline salid b The caurdinatian number is the number afnearest neighbars ta an atam ar inn in a crystal c An amalgam is ahamageneaus mixture ufmercurywith same cther metal Amang the charaderisdcs ufmeuls are i Highthree dimensiunal cmductivity at SAT ii Decreasing mndtctiyity with increasing temperature i Highthennalcmdtcdyity iy Highretlediyity y Highbu ing palm 3p 35 crystal of Mg Iran aluminum supper and zinc are the mast widely used metals The everlapinenergyaftheap and3s quot M9 3mm band means that each ufthesewill be partially lled and will therefure allcw fur cunducdun Depmding an the degreem which the 3s andap bands ave ap the band diagram will lack samething like 31 H crystal of Al 3F 35 ans AI atom 10 ll 12 13 14 15 In the BCC unit cell there is one atom at each comer as well as one atom Metallic behavior depends on the interaction of a large number of atoms giving rise to bands of crystal orbitals In the gas phase the metal exists as isolated atoms or discrete clusters of at most a few atoms so these typical band structure of a metal cannot be obtained Like hydrogen three periods above it K is likely to form a diatomic molecule K2 in the gas phase The MO diagram 43 is shown to the right T XI T 45 n i 45 Cubic and hexagonal are the two types of layer H P arrangements in metals and hexagonal is the more efficient N of the two CF43 In the hcp arrangement every other layer repeats in an ABABAB arrangement In the ccp arrangement every third layer repeats in an ABCABC arrangement In the SC unit cell there is one atom at each corner Since each comer is shared by eight unit cells only 18 of each atom belongs to one of the unit cells 8 x 18 1 atom per unit cell in the center of the unit cell The comer atoms are counted as above and the atom in the center of the unit cell belongs exclusively to that unit cell for a total of 2 atoms per unit cell The atoms must be similar in size and in chemical properties and they must adopt the same type of crystal structure Potassium is significantly larger than zinc radius 227 pm as opposed to 133 pm for zinc The metals adopt different crystal structures K is BCC while Zn is hcp K is significantly more reactive than Zn Body centered cubic In a simple cubic unit cell the atoms touch along an edge as shown above The length of the unit cell edge e is equal to 2 times the radius of the atom and since the volume of the unit cell is e3 the volume of the unit cell is 813 The volume of the atom is 43 1113 and since there is only one atom per unit cell the fraction of the unit cell which is occupied is 119 3 052 E 8r3 6 The fraction of empty space is 1 7052 048 or 48 16 Body Centered Cubic atoms touch along the cube diagonals b cube diagonal 4r f2ezez2e2 b e b2ezf23e2 f e e b 3 Body centered cubic c 4r 36 4 e r Volume of unit cell c3 6 r3 There are two atoms per unit cell so the 3 3 fraction of the unit cell Which is occupied is The fraction of empty space is l 7068 032 or 32 17 Face Centered Cubic atoms touch along a face diagonal f face diagonal 4r 62 62 f2 e b f2 262 f V56 f9 8 i f 41 Face centered Cubic 4r e 18 Body Centered Cubicatoms touch along the cube diagonals b cube diagonal 4r f28262262 e b b262f2362 f e e b e Bodyecenlered cubic 4r e 4 e 1 J 19 From the previous problem 139 W 125 pm 288 pm x 1 m 288 x 1o X cm 1010 pm V e3 288 X 10398 em3 239 X 103923 cm3 m 2 atoms X X L 1727 X 103922 g 1 atom 6022 X 1023 amu 22 density i 239 X 1023 cm3 cm3 13733 amu 1 g x 20 mass of unit cell 2 atoms X 1 atom 6022 X 1023 amu 4561 x 1022 g 22 volume of unit cell mass 1393 X 10 22 cm3 density 3 50 g cm3 3 edge length of unit cell 1393 X 103922 em3 507 X 10398 cm x 1010 pm 507 x 102 pm 1 cm 507 x 10398 cm 10787 mu 1 g x 71651 X 103922 g 1 atom 6022 x 1023 amu 4 a N 21 mass of unit cell 722 mashs 71651 x 10 g 6824 x 1023 cmg densuy 1050 i cm3 3 edge length of unit cell 6824 x 10 23 em3 4086 x 10 8 cm volume of unit cell 10 4086 x 10 8 cm x lo Pm 4086 x 102 pm 1 cm 22 If the surfaces were smooth and clean at the molecular level they would lse together in the vacuum of outer space
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A retired Detroit police officer whose wife was forced into a government employee union because the couple opposes paying "union dues" to care for their two developmentally disabled adult children at home is "an idiot" according to a leading proponent of Proposal 4, the Detroit Free Press reports.
Patrick Wright, director of the Mackinac Center Legal Foundation, explains in the Free Press story the relationship between the Service Employees International Union and a shell corporation designed to help the union skim $6 million a year in "dues" from people who care for disabled loved ones.
The MCLF is representing Patricia Haynes, whose husband Rob Haynes was insulted by Dohn Hoyle in the article.
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Jack In The Box - Review about Tacos from Irving, Texas
- Irving, Texas
- May 27, 2015
- 141 views
- 2 comments
Update added by user May 27, 2015
The employees there a this location Montrose /Westheimer Are Very Unprofessional
Original review posted by user May 27, 2015
I go to the Jack in the Box on Montrose just about every morning but the service and food are just a day to day you might get great tacos morning.The staff absolutely is a *** poor excuse workers .
No hospitality whatsoever. I have other choices that are very much nearby ,but I still try and give them a chance bit I'm quickly losing faith that this paticular Jack n the Box has no hope. The misrepresentation is appalling. I'm sick n tired of playing we hat kinda serve will I encounter this morning days.
I really think this business should be shut down.
JIB#3619.You can never read the receipt to do the survey and receive 2 free tacos!
More Review Details
|Delivery Service
|Discounts and Special Offers
|Diversity of Products or Services
|Product or Service Quality
|Nutrition Description
- Reason of review:
- Poor customer service
- Product or service
- Tacos
- Review category
- Fast Food
Author wants to be contacted by the company. Learn more ›
May 29, 2015
If the receipt prints like that every day it is because their printer is messed up. I have no comment about the food and am not going to be a *** like the guy making that first comment, but it is possible the employees don't realize the code is not printing properly and don't think it is a big deal. It looks as though they may have tried correcting it because that is new ink. But they don't realize the problem is the receipt printer. Local management are unlikely to be responsive to you because that printer may cost them money or be a pain to fix.
If you have complained locally with no resolution, here is what uou need to do. Contact JIB Guest Relations at (85 522-4716 Monday-Wednesday 5am-9pm, Thursday & Friday 5am-Midnight, Saturday 7am-Midnight, and Sunday 7am-5pm (PST). Tell them there is a problem at the Irving unit with the receipt printer and that 1. You don't know if perhaps they are overcharging you and you have no way to reconcile your credit card, 2. you have told local management and they won't correct issue 3. it is a shame because you can never do the survey and you want to say how much you LOVE JIB food, but at this point you are so frustrated over the receipt printer you are starting to have doubts about how great JIB is.
Keep the call positive and friendly (FAKE IT) and do not vary a bit from this general script and you will find the receipt printer to be corrected within 72 hours... (legal requirements and merchant rules - they can't ignore it) and more than likely a nice gift card coming in the mail to you. Show more
May 27, 2015
Well, this isn't the web site for Jack In The Box. I have a question why do you keep going back being you are unsatisfied with the service? It sounds like you are a glutton for punishment. Furthermore, why would anybody want to eat out every morning, or for that matter every day? How are the employees professional and what is your idea of professional? It might be completely different from what other people expect.3 2 Reply
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text: Locations Fairborn Home Event Back to Calendar Thursday 05/19 Thursday 05/19 Colorful Rain 7:00 - 9:00PM Purple Rain - Prince Tribute Night!! 7:00 - 9:00PM This painting is as romantic as it is a lot of fun to create. It allows lots of creativity by using different colors to make your own work of art! Join us for a night of PRINCE! Paint your purple rain as we channel our inner rock star and jam to some classic Prince songs. Adult class ages 16+ Share This Event Not Available $35.00per painter View Photos Share Collect Corks with this purchase You are joining the waiting list for: Pinot's Palette - Fairborn Address: 2610 Colonel Glenn Highway, Fairborn, OH 45324 Painting: Colorful Rain Time: Thu May 19, 2016 7:00-9:00PM Seats First Name Last Name Phone Email Enter your contact info and request details below, and we will contact you with details about your private party! Back to Top