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About Dee3
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on 19/05/2013
I have used this antibiotic in the past for cystic acne. It took a good 3-4 months before I even noticed any change but in the 5th month I was all clear. During this time I still had excessively oily skin, but I would try to cover that up with powder during the day. The clear skin lasted only for about 3 months and then after this slowly I started breaking out in little inflammatory spots, then eventually they became full blown cysts again. I regret not using a topical with this antibiotic because I think I could of maintained the clear skin for longer if it wasn't just relying on the antibiotics. I have to add the new resistant acne came back even worse than my previous cystic acne and I was truely dissapointed. These new cysts were deeper and more harder to treat. In the end I eventually got rid of them with isotretinoin.
Bottom line is this antibiotic will work for you if you have not used it before and provided you don't have any resistance. But eventually your spot causing bacteria grows an immunity and becomes resistant to this antibiotic, so it's best to use it in conjuction with another treatment. Antibiotics are only a temporary solution to a chronic condition.
on 19/05/2013
If you want a honest review from my point of view then read ahead. For quite a few years I suffered with cystic acne. It started off mild with just comedones and blackheads but with time it became more inflammatory, with pustules than eventually cysts that were the size of a marble deep in my cheeks. It carried on for a good few years between me being 17-21 years of age, and as my acne increased my self-esteem & confidence decreased.
During this time, I was put on antibiotics, which initially worked but after 6 months I became resistant to them. I was given differin which I used for a few weeks but after not being satisfied with results gave up on it. I then tried benzoyl peroxide which I found too irritative. Skinoren (azelaic acid) was given to me and was quite helpful but again, I was not satisfied with it. In hindsight I can see I did not give any topical a good chance. I was so convinced my acne was resistant and actually believed I would suffer with cysts forever.
When I was about 20 my family advised me to cut out junk foods (especially foods high in sugar and trans-fats) and dairy as these were rumored to encourage acne. I cut out bread, gluten, sugar and even tea and coffee and kept waiting for instant results. I even drank 8 glasses of water religiously and took up exercise. Of course, with my severe acne instant results were not possible and with my confidence being eroded with every new cyst I became quite depressed about it.
It was around this time I decided to go back to the doctors. I was very embarrased about my skin condition. I was excessively oily and flaky at the same time, with cysts all over my cheeks, nose and forehead. I was at the point where I was even embarrased to make eye contat with people because I thought they would think my skin was gross. Heck , even a stranger once told me to get medication for my skin.
Anyway, I told my GP everything and was in tears by the end, so he immediately reffered me to a dermatologist to be put on Isotretinoin. I was counselled that there would be side effects, but since my acne was severe and it was affecting me psychologically, that it would be a sensible and good option for me. In the UK women of childbaring age are recommended to take birth control whilst on this medication, as it toxic and can affect the development of foetuses. I was not sexually active at the time and decided not to take the Dianette contraceptive they were giving me. The dermatologist was not happy about this, but I signed a form which basically said I can take responsibility for my own vagina lol.
Fast forward some time and I had just completed my first 5 months. I was on a very low dose (about 10mg a day) and my weight was about 50kg, so it worked very slowly for me. I remember being quite down at this time because even though I had seen some improvements my face was still red and breaking out occasionally. I still wanted the clear skin instantly and craved for the results I'd read about on here. In hindsight, I can see it was actually working, but as I was constantly observing my skin daily I couldn't actually see a big difference. The thing with retinoids are they DO work, but any differences are very subtle. It took a good few months for me to be satisfied with results.
After a good 8-9 months on 10mg, I rememeber looking into the mirror and realising how far my skin had come. It was around this time the spots had stopped, redness from previous marks had finally faded and my skin actually glowed. It looked so fresh and I was delighted. I atually felt like a con at times as people started complimenting my skin and asking what creams and cosmetics I use. I found this so funny as I knew it's all down to the Isotretinoin.
After I completed the course the clear skin continued for a few months. After this I started getting quite oily again and breaking out with smaller spots. The comedones were back again, although a lot milder than what I had before. I was disappointed but went to the doctors and decided to use a topical retinoid and so far it has cleared my skin again. Bottom line is retinoids do work, inside or out, but you have to give them time. I have looked into the symptoms of acne and especially after treatment with Isotretinoin, I realised as long as I keep the skin cells from being blocked by an over production of keratin, keep my sebum controlled (which my isotrex topical retinoid does) and make sure the bacteria is not out of hand, then my skin can remain clear. If only I knew this before!
Overall, to get to my cumulative dose it took about a year and a half. I did experience side effects. Obviously the very dry and sensitive skin made my red marks and spots look a lot worse when beginning treatment, but as my skin improved and I adjusted to the sensitivity, it stopped being such a problem. To this day I still use a simple moisturiser without fragrance, don't over exfoliate with harsh scrubs and generally just leave my skin alone. This all helps with dealing with the extra sensitivity and you will soon find you and your skin can adapt to it. I also had bowel problems wit this. It seemed to upset my stomach, particularly in the last few months. I had excessive gas and diarreah. It happened even though I always took the capsules with food. It reduced significantly when I finished my course, but I still have an upset tummy at times. However, I don't regret taking this drug as it cleared my skin immensley. I got great results from it and most importantly, I have my confidence back. To those who are struggling with acne and it is affecting you psychologically, you really should not be afraid of the side effects. The damage to your confidence and self esteem can have long term effects in itself as it will inevitabley start affecting you everyday life, and acne is so not worth that damage. I will never regret taking Isotretinoin as it was the start of helping me get my confidence back. Having my confidence is helping me in my life to get a new job, have a career and even finding love. So if you have acne, don't feel it is something to hold you back as I did for many years. I am nearly 24 now and very happy :)


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Blues duo pleased with start
Michael Essien and Salomon Kalou are delighted Chelsea's Champions League campaign has started positively.
By Giscard Gourizro
Last Updated: 16/09/09 12:43pm
Michael Essien and Salomon Kalou are delighted Chelsea's UEFA Champions League campaign has started in a positive fashion.
The Blues edged past Porto on Tuesday evening at Stamford Bridge courtesy of Nicolas Anelka's winner shortly after half-time.
Essien believes it is crucial Chelsea pick up maximum points on home soil, while he attributes their below-par performance to Didier Drogba's absence.
"It's a good start for us in the Champions League," he told skysports.com. "The most important thing is to win your home games.
"People are talking about our performance, but we missed Didier Drogba like all teams would miss their main striker.
"We played well. We scored without conceding, so it bodes well for the rest of the competition."
Kalou has echoed Essien's sentiments by stating it was the perfect way to start their Champions League campaign by winning on home soil.
The Ivory Coast international knows he is behind the likes of Drogba and Anelka in Carlo Ancelotti's pecking order and hopes he impressed enough to give the Italian food for thought.
"It was fantastic to start the Champions League game," said Kalou. "It wasn't easy because Porto are a great team and used to playing in the Champions League.
"I set Anelka up for the goal. Didier will be back in the team very soon, but I want to make it difficult for the manager by showing him I want a place in his starting line up."

subset: commoncrawl


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Do you find Ryan Gosling good looking?
See pics: link
- YesVote A
- NoVote B
Most Helpful Girl
Yes, he is very attractive but not my type.
Do you find Ryan Gosling good looking?
See pics: link
Yes, he is very attractive but not my type.
Have an opinion?
he looks...fine? I don't know,i don't understand why he in particular is so fawned over.
I wouldn't say that he's ugly but I also don't find him attractive.
So very very very very very very much.
Yeah he's OK. He's not drop-dead gorgeous or anything. Just...okay looking.
What's that supposed to mean?
Attractive/good looking, but not my type
I do
Yup...he looks better as he ages.He is just one of those people.
Yes, I think he's pretty good looking.
MUCH better with facial hair though. That goes for Ryan Reynolds too.
I don't really think they're very cute without facial hair... but WITH it? Wow :-)
He's alright
Eh, he's alright
Yes but I don't see the hype over him
Yes, I think he is a nice looking man.
Yes he's gods creation (:
I think he needs some ink to make him more masculine. I forget the name of the movie but I saw one rather recently in which he was covered. It really suited him. Overall the guys not bad looking but then again... most aren't when you have a professional photographer on hand to highlight your best features. Definitely never shave off the stubble. He looks 16 otherwise.
I think he's a good-looking guy. No homo.
hes very feminine looking.
Yeah, I'd do him.
He's not that great looking
he looks goofy to me
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text:
Why? or why not?
Most Helpful Girl
I've wanted to for so long but gag wouldn't let me 😭😭😭😭😭😭😭😭😭😭11|00|0
i'm sorry about that girly!
Why? or why not?
I've wanted to for so long but gag wouldn't let me 😭😭😭😭😭😭😭😭😭😭
Have an opinion?
yeah i'm bored of it tbh, i have it for 2 years and a little bit more LOL
i'd rather call myself wid a name of some 80s album... it suits me better i believe
Ummm no cause i am single and pretty much the name suits me! LOL
But if i change it i would name it something similar to my field of interest! Like VFXcrazy or something like that LOL
I don't know I am neutral on the subject :p
Don't tell me what I am or what I am not :|
No I like mine. Pretty relieving...
I always had from the get-go, but most people are used to it by now.
I have been using this username since I weas a really young kid so its kinda nostalgic :P
llorando is too iconic to change, everyone block me if I changed my name from llorando.
I would because I don't find my soul as complicated as I used to anymore. :)
Heck no! My name will live in infamy forever! :)
I would, 'cause it seems too 'straight forward' haha
no i am content
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Photo: Don Jazzy recalls the time he used to wear artificial jewelry – Gistmaster (blog)
Gistmaster (blog)
Photo: Don Jazzy recalls the time he used to wear artificial jewelry
Gistmaster (blog)
Don Jazzy shared this throwback photo on social media, recalling the time he used to wear a lot of fake jewelry. The music label executive captioned the photo above: "Bae can you see my eyes? Somebody will just pack plenty fake jewelry and wear. Well …
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Welcome to watch UFC 207 Live Steam Nunes vs Rousey The Biggest Match is Stream Online Full Fight Watch Main Card, Prelims, Early You can easily watch Match UFC 207 Live streaming online on MAC, PC, your Electronic devise. Don't miss to watch the lovely match.Just connected our TV link …Read More »
Real Betis vs Real Madrid Live Stream 15 Oct 2016
If you, too, prefer my international break routine of hiding under a rock with a bottle of booze, here's what we've missed. Sergio Ramos is out for a bit with a knee injury. James Rodríguez is out with a calf injury, though his timetable to return is promising. Luka Modrić …Read More »
Arsenal vs Swansea City live Stream 15 Oct 2016
Bob Bradley has demonstrated his ability to talk the talk, as anybody present at his Swansea media unveiling will attest – now, he has to walk the walk, at a stadium where his side have fared well of late. Arsenal vs Swansea City Arsène Wenger said the American's appointment was …Read More »
Chelsea vs Leicester City Live Stream 15 Oct 2016
The Premier League champions from the last two campaigns meet at Stamford Bridge with Antonio Conte obliged to reiterate the strength of his relationship with the Chelsea hierarchy after various bookmakers closed the market on his premature departure on Thursday. "I'm trying to find out who put the money on," …Read More »
Blue Jays vs Indians Live Stream 14 oct 2016
Josh Donaldson, the 2015 American League MVP, was 7 for 13 (.538) in the ALDS and so far during the postseason is hitting a robust .500 (9 for 18) Blue Jays vs Indians with five doubles in four games. The third baseman was 8 for 21 (.381) with two home …Read More »
Chile vs Peru Live Stream 11 oct 2016
To watch this match online in the U.S. you can stream it on beIN Chile vs Peru Sports Connect. The match won't be shown online in Chile or Peru, but for streaming options in other countries you can check out Chile vs Peru LiveSoccerTV. It's been a rough road for the …Read More »
USA vs New Zealand Live Stream 11 oct 2016
The United States laboured in their friendly against Cuba, but the condition of the pitch did not encourage a high quality of technical USA vs New Zealand football. It is only the third occasion America has met the five-time Oceania Football Association champions, with the U.S. readying themselves for upcoming …Read More »
Bolivia vs Ecuador Live Stream 11 oct 2016
Ecuador, in contrast, have won five of their first nine, and have amassed sufficient points to sit third in the table behind Uruguay and Brazil. They certainly can't afford to take their foot off the pedal yet, however, with only tiebreakers keeping them above the fifth-place intercontinental playoff spot. They'll …Read More »
ALDS Game 3 Live Stream online
Indians vs Red Sox The 6:08 p.m. ET game will be televised by TBS, with Ernie Johnson calling the play-by-play alongside analysts Ron Darling and Cal Ripken Jr. and reporter Sam Ryan. The Boston Red Sox and Cleveland Indians were rained out on Sunday, so the two teams will resume …Read More »
Albania vs Spain World Cup Qualification UEFA 9 October 2016
Their goal though was fortuitous as it came from a baffling Gigi Buffon mistake and there may still remain the underlying feeling that for all their pleasing possession, Spain still lack a killer touch in front of goal. In qualifying for Euro 2016, Spain won their last three away games …Read More »


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Joy OBanionBuffalo, New York, US
We are what we repeatedly do; excellence, then is not an act but a habit.
I can bring an array of deliveries to meet your business needs. From the voice behind corporate videos and narrations to effective characterizations that will bring your story to life, I can get the work done. I will provide a believable and convincing sound that will cut through the noise and grab the customer's attention.
I am a professional storyteller with a background in theater who can think on her feet to provide the desired delivery. I understand how to tell the story of a client's project. I am a retired speech therapist and educator who has successfully used character voices in the creation of effective classroom lessons. My voice is compassionate, calming, warm, sincere, kind and fun-loving. I am interested in the following voice over opportunities: education, business, animation, video games and telephony.
English (North American), English
US African American, US South (Deep South, Dixie, Delta), African (General)
Child, Middle Aged, Senior, Teen, Young Adult
Special Skills
Audiobooks, Business, Cartoons, Documentaries, Educational, Internet, Movie Trailers, Podcasting, Radio, Telephone, Television, Videogames
I have mentored youth who aspire to improve their oral speaking skills. I have served as program emcee and narrator for many church activities and events. I continue to develop workshops through my local storytelling affiliate to assist new tellers in honing their techniques.
Such A Voice Training and Demo Production
Scarlett Studio CM25
Computer & Software
Envy Beats Audio & Audacity
Delivery Methods
Email, voices.com upload
Turnaround Time
24 - 48 hours; contact me for specifics
Service Description
I will first review and get an understanding of the story in the script and then produce a quality voice over product in the agreed upon format and time frame. My work style is professional and meticulous. My objective is to meet the needs of the client.
Payment Terms
Hire Joy as a voice actor. Payment is made through Voices.com SurePay, an escrow service that guarantees your work is done to your satisfaction. Send payment securely by Visa, Mastercard or PayPal through Voices.com then download your files from the website.
Watch a video to see how to make a payment
Next Steps
To contact Joy OBanion about your project, request a quote today. We'll walk you through the process step-by-step. It's fast and easy.
Hire Joy OBanion as a voice actor. Working with Joy OBanion is fast and easy. We'll walk you through the process step-by-step.
Request a quote for your project today.


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Spanish Teaching/Translating
25 simbi per unit - Virtual OK
I can translate documents and give lessons on a variety of topics in Spanish, including conversation.
Training & Qualifications
I am a senior Spanish student at the undergraduate level. I have spent time living in South America and have experience translating documents for a non-profit business.
Availability & Preferences
Trading Preference: I'm flexible, just hit me up!
Weekday evenings.
About Candace Ward
Foreign language major hoping to work with immigration services or go into the military. I have extensive experience in the Spanish language, beginning in childhood. I also have work experience in tra...nslating and speaking at a non-profit business. show moreOpen to other proposals
Candace Ward is looking for:
- Art & Design
- Fitness
- Experiences
- Learning
- Beauty
- Nailcare
- Skincare
- Makeup
- Hair styling
- Style & Fashion
- Beauty: Other
- Fun & Quirky


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About the Book
Features & Details
- Category Biographies & Memoirs
Standard Portrait, 7.75×9.75 in, 20×25 cm
48 Pages
- Publish Date Mar 11, 2010
See More
About the Creator
EPPING, Melbourne, Australia
I have had Simca's since I was a young boy (14yo) and have raced, restored, owned many types, I currently have a restored Vedette Bailieu and am restoring another for Historic Racing, I am the current President of the Simca Car Club of Australia and enjoy the involvement in the Club and it's members... I also like to find out about Simca Enthusiast's around the world and enjoy looking for those hard to find parts.....
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Christine Tripp became a professional photographer over a decade ago. At weddings and events, she observes and predicts what will happen next in order to capture the perfect moment. As a business owner, with employees, Christine is often called a leader and project manager. She has assisted many clients in ways above and beyond that of a typical photographer.
As an instructor, Christine has helped hundreds of eager new photographers learn how to use their camera properly and has shown them how to make money with their photographic art. She has spoken numerous times in front of business groups on topics such as business networking, collaborating with others, social media and unique marketing concepts and strategies.
Whether she is behind her camera or teaching how to take great pictures, Christine's proven skill, talent, patience and friendly demeanour is just a few of the many reasons she is a well-known and much-liked business person and photographer.


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Can Garuda's IPO Finally Take Off?
Indonesian carrier PT Garuda Indonesia has waited over a decade to go public, but has its window of opportunity passed?
The state-owned airline, which aims to raise US$500 million in an IPO, began pre-marketing on Tuesday. Sources close to the deal say the company will be in Singapore on Thursday and Friday this week, and Hong Kong next Monday and Tuesday for its roadshow.


text: [[{{SUBST:Popopp}}| ]] [[{{SUBST:Popopp}}| ]] Popopp Bestiary: Opo-opo Affiliation: Kazham [[{{SUBST:Popopp}}| ]] [[{{SUBST:Popopp}}| ]] Type: NPC Location: Kazham (H-9) Involved in Quests: The Opo-opo and I Notes Accepts the Wandering Bulb for The Opo-opo and I. Retrieved from "http://ffxiclopedia.wikia.com/wiki/Popopp?oldid=1579360" Ad blocker interference detected! Wikia is a free-to-use site that makes money from advertising. We have a modified experience for viewers using ad blockers Wikia is not accessible if you've made further modifications. Remove the custom ad blocker rule(s) and the page will load as expected. Categories: NPCsKazham NPCsOpo-opo NPCs Languages: Deutsch Español Français 日本語


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India loves social networks. If you had any doubts about that, look to eMarketer's latest findings. The research firm says India will record the highest social networking growth in the world, with the number of new Indians logging on to Facebook, Twitter and the likes expected to increase by 37.4 percent this year. More interestingly, the report says India will have the world's largest Facebook population by 2016.
While India is expected to add the most new users, Indonesia's will be the second highest contributor to social networks with a 28.7 percent increase in usage, while Mexico is in third place with an expected growth rate of 21.1 per cent, reports The Economic Times. The research estimates Facebook will have a global monthly user base of 1.026 billion this year. And a massive 1.61 billion people will log on social networks overall, from all devices.
India loves Facebook
Based on this trend, India will beat the US in terms of the number of Facebook users by 2016. Currently 146.8 million, US citizens log on to Facebook and India is a distant second. India, with its large population and high expected growth rate in terms of new users and better connectivity, will outpace US in three years.
India would have had a harder chance of beating the US had Facebook been allowed in China, a country the research considers having zero users. Hypothetically speaking, if Facebook is legalised in China before 2016, it could very well beat India to the top spot.
Published Date: Nov 22, 2013 04:42 pm | Updated Date: Nov 22, 2013 04:42 pm


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Age-related loss of skeletal muscle mass and function is implicated in the development of disease and physical disability. However, little is known about how age affects skeletal muscle structure at the cellular and ultrastructural levels or how such alterations impact function. Thus we examined skeletal muscle structure at the tissue, cellular, and myofibrillar levels in young (21–35 yr) and older (65–75 yr) male and female volunteers, matched for habitual physical activity level. Older adults had smaller whole muscle tissue cross-sectional areas (CSAs) and mass. At the cellular level, older adults had reduced CSAs in myosin heavy chain II (MHC II) fibers, with no differences in MHC I fibers. In MHC II fibers, older men tended to have fewer fibers with large CSAs, while older women showed reduced fiber size across the CSA range. Older adults showed a decrease in intermyofibrillar mitochondrial size; however, the age effect was driven primarily by women (i.e., age by sex interaction effect). Mitochondrial size was inversely and directly related to isometric tension and myosin-actin cross-bridge kinetics, respectively. Notably, there were no intermyofibrillar or subsarcolemmal mitochondrial fractional content or myofilament ultrastructural differences in the activity-matched young and older adults. Collectively, our results indicate age-related reductions in whole muscle size do not vary by sex. However, age-related structural alterations at the cellular and subcellular levels are different between the sexes and may contribute to different functional phenotypes in ways that modulate sex-specific reductions in physical capacity with age.
- aging
- mitochondria
- muscle ultrastructure
- sarcopenia
age-related changes in skeletal muscle function underlie declines in functional capacity that lead to physical disability. While the loss of muscle mass plays a role in this functional decline [i.e., changes in muscle quantity (13, 21)], diminished whole muscle dynamic force production may persist after controlling for age-related muscle atrophy (21). Multiple studies report age-related reductions in whole muscle torque generation that exceed changes in muscle size (37), although this is not always the case (5, 37, 40, 42). When present, decrements in muscle quality (contractile performance per unit size) may be caused by changes in molecular and cellular level function. Indeed, multiple reports suggest single-fiber (28, 32, 71) and myosin-actin cross-bridge function (10, 19, 42, 48, 49) are diminished with age. Some of these adaptations may be explained, in part, by alterations in molecular and/or cellular muscle structure. Our understanding of how aging affects skeletal muscle structure at the molecular and cellular level in humans, and how these structural alterations relate to whole tissue and functional declines, however, is limited.
Aging alters human muscle structure at the tissue level, causing decreases in muscle performance. The most notable is the gross loss in muscle mass (31), but other structural alterations, such as a decrease in muscle pennation angle and fascicle length (46, 65), could contribute. These architectural changes, however, explain only a portion of the age-related decrease in whole muscle performance (65) and would not explain altered single-fiber contractile performance (28, 32, 71). Studies suggest that an age-related loss of myosin protein contributes to decreased single-fiber isometric tension (10), which may present structurally as a shorter thick-filament length and/or an altered thick-to-thin-filament stoichiometry. Moreover, our laboratory's previous data (43) from a model system (Drosophila melanogaster) shows age-related changes in myofilament ultrastructure that may have functional consequences. To our knowledge, however, no quantitative measurements of myofilament ultrastructure have been compared between muscles of young and older humans, nor have they been evaluated for their relationship to cellular- or tissue-level functional phenotypes.
Dysregulation of cellular metabolic processes has long been suggested as an impetus for aging (16). Recent studies have suggested that mitochondrial dysfunction may contribute to muscle atrophy [reviewed in Powers et al. (55)] and alterations in cellular-level muscle structure (7, 17, 74). For instance, age-related accumulation of mitochondrial deletions has been implicated in region-specific atrophy of skeletal muscle fibers in animal systems (7). With the linking of such changes to diminished muscle performance, studies suggest that altered mitochondrial function and morphology promote intracellular oxidative stress, which can interfere with myofilament function via oxidative modification of proteins or disruptions in myofilament protein metabolism (6). The relationship of alterations in mitochondrial biology to muscle fiber/myofilament structural and functional alterations with aging in humans, however, has not been systematically examined.
The present study was designed to investigate age-related changes in skeletal muscle structure at the tissue, cellular, and myofibrillar levels, including mitochondrial morphological adaptations, and to relate these parameters to skeletal muscle functional performance across the same anatomic levels. To accomplish this objective, we recruited healthy young and older men and women to have similar levels of habitual physical activity. Care was taken to account for age-related alterations in physical activity, as muscle use/disuse can impact whole muscle (14, 22) and single-fiber performance (10, 11), as well as mitochondrial function (3, 20, 25, 27, 29, 36). This consideration represents an advance on prior work in this area, as physical activity is not routinely objectively quantified in human aging studies. Thus some of the presumed age-related changes in skeletal muscle structure and function may be the result of reduced physical activity that frequently accompanies old age (38, 72).
Twelve young (5 men) and twelve older (5 men) participants were enrolled in the present study. Self-reported physical activity was minimally active (≤2 sessions of ≥30 min of exercise/wk) for the young volunteers and moderately active (3–5 sessions of ≥30 min of exercise/wk) for the older volunteers. None were engaged in a structured exercise program, and self-described exercise consisted primarily of walking. These recruitment criteria were used to correct for differences in self-efficacy and lifestyle differences across age groups (39, 72) and produced young and older groups that had similar habitual physical activity levels. To confirm achievement of this goal, daily physical activity was quantified using uniaxial accelerometers, as previously described (69), worn by each participant for 9.2 ± 0.3 days (Caltrac, Hemokinetics). All volunteers were healthy, with no symptoms or signs of heart disease, hypertension, or diabetes; normal resting electrocardiogram and response to an exercise stress test; and normal thyroid function and blood cell counts and blood biochemistry values. Volunteers were not eligible to participate in the study if they had participated in a weight loss or exercise training program in the past year; a history of smoking (within 1 yr); unintentional weight loss of >2.5 kg during the last 3 mo; a body mass index > 30; hospitalization longer than 3 days in the past 5 yr; active cancer, or history of cancer within the past 5 yr; or were taking/had taken hormone replacement therapy (combined estrogen/progestin for elderly women and testosterone for elderly men). None of the participants were taking 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors (statins) or oral corticosteroids. Young women taking oral contraceptives were included (n = 4), and all elderly women were postmenopausal (cessation of menses >1 yr). All participants signed an informed consent document before participation. The study's protocol was approved by the Committees on Human Research at the University of Vermont. Data on clinical characteristics (age, height, body and whole muscle mass, as well as physical activity level), whole muscle function, single-fiber tension, myosin-actin cross-bridge kinetics, and myosin heavy chain (MHC) isoform distribution from the volunteers in this study have been reported previously (42). The present study examines muscle structure at multiple anatomical levels with these clinical and functional characteristics.
Experimental protocol.
Eligibility was determined during screening visits, which also included whole muscle strength testing, a treadmill test, and resting and exercising electrocardiograms. At least 1 wk later, participants arrived fasted for body composition assessment, and muscle tissue was obtained via percutaneous biopsy of the right vastus lateralis, as described (68). The majority of tissue was immediately placed into cold (4°C) dissecting solution, dissected into bundles, tied to glass rods at 4°C, processed for single-fiber mechanical and morphological assessment, and stored at −20°C, as described (44). The remaining tissue was prepared for electron microscopy (EM) measurements, as described (45), or immunohistochemical assessment after fixation in paraformaldehyde. The remainder was frozen in liquid nitrogen and stored at −80°C until analysis.
Whole body and tissue morphology.
Body mass was measured on a digital scale (ScaleTronix, Wheaton, IL), and total and regional body composition was assessed by dual-energy X-ray absorptiometry (DEXA) using a GE Lunar Prodigy densitometer (GE Lunar, Madison, WI). Muscle mass was estimated using the leg fat-free mass (FFM) from DEXA, as described previously (18). Quadriceps femoris muscle cross-sectional area (CSA) of the right thigh was measured using computerized tomography. Participants lay supine on the exam table, and slice location was determined using a radiopaque bead placed at the midpoint of the thigh (halfway between the anterior superior iliac crest and the most proximal aspect of the patella). Data were analyzed using freely available software (Image J V1.44, National Institutes of Health, Bethesda, MD). A region of interest (ROI) was traced around the quadriceps muscle group, and all voxels outside this ROI were eliminated. Voxels within the ROI were then differentiated between muscle and fat based on radiodensity, measured in Hounsfield units (0 to 100 for muscle and −190 to −30 for fat). The sum of pixels corresponding to each tissue type was used to quantify their CSA. The average radiodensity of pixels within the specified region corresponding to lean muscle was used to indicate overall attenuation and used as a proxy for intramyocellular lipid content (26).
Single-muscle fiber morphology.
Muscle fiber CSA was assessed using immunohistochemistry (IHC), as previously described (66) using a polyclonal rabbit anti-laminin antibody (1:100, ab11575 Abcam) and a mouse anti-MHC I antibody (1:250, A4.951-c Developmental Studies Hybridoma Bank, University of Iowa) in 1% BSA in PBS. Visualization and imaging were performed using an Olympus BX50 microscope. CSA measurements were performed using image analysis software (Metamorph version 188.8.131.52, Molecular Devices, Sunnyvale, CA). This approach does not allow for the detection of MHC isoform coexpression in individual fibers and only distinguishes between fibers expressing MHC I and those that do not. However, in our hands (45) and others (10), fibers coexpressing both MHC I and various isoforms of MHC II are relatively rare (6% in present sample). Thus the average CSA of muscle fibers measured with this approach are referred to as MHC I and MHC II. Due to lack of tissue, IHC was not performed on two older men and one younger woman, meaning this analysis was performed on a total of 11 younger (5 men), and 9 older (3 men) adults.
Ultrastructural measurements.
EM measurements were conducted on intact (i.e., unskinned) skeletal muscle fiber bundles to assess myofibrillar ultrastructure. These measures were not obtained in one younger woman due to lack of tissue, meaning this analysis was performed on a total of 11 younger (5 men), and 12 older (5 men) adults. These measures included myofibrillar fractional area, thick-to-thin-filament ratio (measured in cross sections at the A-band with full overlap of thick and thin filaments), A-band and sarcomere lengths, as well as intermyofibrillar and subsarcolemmal mitochondrial fractional area, average area, and number. Our intermyofibrillar mitochondrial measurements were largely similar to those described previously (45, 68) with minor modifications, including that four images (each ∼152 μm2 with no evidence of structural damage) at ×3,000 magnification were measured for each subject, and mitochondria were highlighted using an Intuos Graphics Pad (Wacom, Vancouver, WA). These techniques have been shown to produce similar results to conventional stereological methods (24, 77) and afforded the opportunity to further interrogate additional mitochondrial morphological characteristics. A similar approach was used for assessment of mitochondria in the subsarcolemmal space. This space was defined as the region between the sarcolemma and the first layer of myofibrils. Images were taken in random locations along the sarcolemma, where mitochondrial density was greatest, typically with nuclei or blood vessels, where mitochondria tend to colocalize. This approach was used to ensure consistency with more recent, relevant publications (9, 47, 53). Subsarcolemmal mitochondrial abundance was quantified in two ways. First, the sum of CSAs for visible mitochondria was divided by the total area of the image, or field of view, similar to intermyofibrillar measures. This was referred to as mitochondrial fractional area and expressed as a percent. The sum of subsarcolemmal mitochondrial CSA was also expressed relative to the length of sarcolemma visible in the image (47), as well as the area of the total subsarcolemmal region, to account for differences due to orientation of the sarcomere, or irregularity in the shape of the sarcolemma. Finally, Z-band width was measured as a proxy of fiber type (64), as described (68).
Mitochondrial and nuclear DNA copy number.
DNA extraction was performed with 10–20 mg of muscle tissue per sample, and genomic DNA concentration was measured according to the manufacturer's instructions (QIAGEN QIAamp, Hilden, Germany). Plasmid DNA controls for human beta globin and cytochrome b were used, as described previously (73). These samples were kindly provided by Dr. Phillip Nagley (Monash University, Australia).
Whole muscle and single-fiber contractile function.
Whole muscle strength was assessed using an isokinetic dynamometer (Cybex, Computer Sports Medicine, Stoughton, MA), as described previously (69), with the change that peak torque was defined as the single repetition with the maximal value. Peak voluntary knee extensor torque was measured with the knee joint positioned in 70° of flexion (180° = full extension) and was corrected for differences in tissue size by covarying for leg FFM during statistical assessment. Measures of contractile function in single-muscle fibers were characterized by measuring maximally Ca2+-activated (pCa 4.5) tension and single-fiber mechanics, as described previously (44). Single-fiber mechanics was used to estimate specific steps of the myosin-action cross-bridge cycle, as previously described (44), including the rate of myosin force production, or the rate of transition between weakly and strongly bound states (78), and myosin attachment time (ton) (52).
Data are presented as means ± SE. All variables of interest were assessed for normality and statistical outliers (values 2 SDs from the inclusive mean). Using this approach, no data were excluded as outliers. Two-way analysis of variance (age × sex) was used to compare measured values for age and age × sex interaction effects. In cases where multiple observations were used to characterize a single participant (e.g., single-fiber CSA), a linear mixed model was used, including a random effect to account for clustering of observations within individuals. For all analyses, if a main or interaction effect was noted (age or age by sex), post hoc contrasts were performed to identify pairwise differences. Associations between measures were determined using linear regression analysis. Statistical analyses were considered significant at P ≤ 0.05 and were performed using IBM SPSS Statistics (version 20.0, IBM, Armonk, NY) and SAS (version 9.3, SAS Institute, Cary, NC).
Subject characteristics are listed in Table 1. There was a trend for young adults to be taller than older adults (P = 0.07), and young and older participants had similar body (P = 0.19) and FFM (P = 0.96). Physical activity as determined by accelerometry was similar between age groups (P = 0.71). For comparison, sedentary to minimally active older adults produce between 200 and 300 kcal/day using identical measurement techniques (44, 67), showing that, as expected, the walking activity in our moderately active older adults increased the physical activity values from sedentary levels. When statistically corrected for differences in muscle size, voluntary knee extension strength was not different between young and older participants (P = 0.12).
Whole body morphology.
Reduced quadriceps CSA (P < 0.01, Fig. 1A) and muscle attenuation (P < 0.01, Fig. 1B) was found in older vs. young cohorts using computerized tomography. When expressed as a percentage of body mass to adjust for the variation in body size [i.e., to account for any compensatory hypertrophy related to the reduced fractional contribution of fat-free tissue to body weight with age (Table 1)], leg FFM from DEXA was reduced in older vs. young groups (P < 0.05, Fig. 1D), similar to quadriceps CSA (Fig. 1A). However, expressed in absolute terms (kg), leg FFM was not different between young and older groups (Fig. 1C).
Single-muscle fiber morphology.
CSA results from single-muscle fibers measured using IHC are presented in Fig. 2. The CSAs from MHC I fibers were not different between groups (P = 0.56, Fig. 2A), while older adults had reduced CSAs in MHC II fibers (P = 0.04, Fig. 2B) compared with young adults. The CSA histograms for MHC II fibers in men (Fig. 2C) and women (Fig. 2D) illustrate the age-related differences between the sexes in their fiber-size distribution. Older men tend to have a loss of fibers with large CSAs (>2,500 μm2) compared with young men, while older women show a leftward shift to smaller fibers across the entire range of values compared with young women.
Ultrastructural measurements.
Subcellular measures of skeletal muscle structure revealed no differences in our cohort of young and older men and women (Fig. 3). Cross-sectional EM measures found no difference in myofibrillar fractional area (Fig. 3A) or thick-to-thin-filament ratio (Fig. 3C) between groups. Analysis of longitudinal EM showed A-band length (Fig. 3B), or thick-filament length, was similar between groups.
There was no age-related difference found in the average number of intermyofibrillar mitochondria observed in our samples (Fig. 4A). However, the average size of intermyofibrillar mitochondria decreased with age (P < 0.01, Fig. 4B), and there was a trend for an age × sex interaction (P = 0.08). Pairwise comparisons showed the smaller mitochondrial size with age was significant in women (P < 0.01), but not in men (P = 0.43). Fractional area of intermyofibrillar mitochondria (Fig. 4C) was not different with age. These findings were recapitulated by the assessment of mitochondrial and nuclear DNA copy number (Fig. 4D). Analyses of the images used to measure intermyofibrillar mitochondrial morphology showed a uniform distribution and no differences between groups for Z-band width, indicating no fiber-type differences between groups. Furthermore, no associations were found between Z-band width and other measures of myofibrillar or mitochondrial morphology.
Mitochondria in the subsarcolemmal region were not morphologically different (number or size) between groups. Mitochondrial density in this region was also not different between groups, regardless of whether the sum of mitochondrial area was normalized to the total field of view (Fig. 5C) or the length of visible sarcolemma (Fig. 5D).
As changes in mitochondrial structure and/or function may be linked to alterations in single-fiber structure (58, 74), we examined the relationship between the intermyofibrillar mitochondria CSA and indexes of fiber structure and function (Fig. 6). The average CSA of mitochondria in the intermyofibrillar space was not correlated to single-fiber CSA in MHC I (P = 0.16) or IIA fibers (P = 0.11). However, average intermyofibrillar mitochondria CSA was inversely related to isometric tension in MHC I (R2 = 0.21, P = 0.03) and IIA fibers (R2 = 0.33, P < 0.01; Fig. 6A), as well as myosin attachment time in MHC IIA fibers (R2 = 0.28, P = 0.02), and directly related to rate of myosin force production (R2 = 0.32, P < 0.01; Fig. 6B) in MHC IIA fibers. Although these coefficient of determination (R2) values are moderate to low, these results show that the average intermyofibrillar mitochondrial CSA explains 28–33% of the variation in isometric tension and cross-bridge kinetics in MHC IIA fibers, a potentially relevant finding considering the variety of ways tension and cross-bridge kinetics can be modified. The coefficient of determination values were lower in MHC I fibers, explaining only 21% of the variation in tension. Exploring these relationships in the sexes independently, most remained significant in women, but not in men, suggesting these correlations were primarily driven by the women. Specifically, average mitochondrial CSA was inversely associated with MHC I (R2 = 0.32, P = 0.05) and MHC IIA tension (R2 = 0.43, P = 0.02) in women, but not in men (P = 0.57 and 0.21, respectively). Average intermyofibrillar mitochondria CSA was directly related to MHC IIA rate of myosin force production in men (R2 = 0.53, P = 0.04), while a trend for this relationship was observed in women (R2 = 0.31, P = 0.06). Myosin attachment time in MHC IIA fibers was negatively associated with average mitochondrial CSA in women (R2 = 0.36, P = 0.04) but not men (P = 0.39). No significant associations were found between these measures and the morphology of subsarcolemmal mitochondria. To explore the potential that enhanced mitochondrial volume leads to reduced tension via reduced myofibrillar density, we examined the relationship between mitochondrial fractional area and measures of myofibrillar density and single-fiber tension. Mitochondrial fractional area was inversely correlated to myofibrillar fractional areas (R2 = 0.21, P = 0.03), but no such relationship existed between mitochondrial fractional area and tension in MHC I or MHC IIA fibers (P = 0.69–0.88).
Aging human skeletal muscle is typically characterized by reductions in size and alterations in contractile performance from the tissue to the single-fiber level. While reports in the literature describe these measures in older humans (61), we are not aware of any studies that have comprehensively evaluated the role of age-related changes in cellular or subcellular (i.e., myofilament) structure. Furthermore, although studies have long considered a link between mitochondrial biology and sarcopenia, only a few studies have investigated the effects of age on mitochondrial morphology in humans (9, 47, 51, 54), and none has sought to relate mitochondrial adaptations to age-related changes in single-fiber function. Although our sample size was relatively modest, it is fairly comparable with the range in previous investigations, which studied between 10 (47) and 56 adults (51). In contrast, none of the aforementioned studies have controlled for habitual physical activity, health status, and medication use, as we have in the present study, to attempt to define primary aging effects and minimize the significant variability in physical activity observed across the human lifespan (38, 72). Our results show no effects of age on myofilament ultrastructure. However, we did observe that older adults had smaller CSAs in MHC II fibers, and, in women, aging reduced the size of intermyofibrillar mitochondria. Smaller mitochondrial size was related to increased isometric tension and reduced myosin-actin cross-bridge kinetics, contractile measures that were also altered primarily in older women (42). Collectively, these results highlight unique age-related structural adaptations in skeletal muscle that may partially contribute to sex-specific adaptations in muscle performance with age.
The effects of gross changes in skeletal muscle tissue mass or CSA with age to reduce functional capacity is well-accepted (33), but we know little about how other alterations in muscle structure at the subcellular and molecular level may contribute because few studies have performed such assessments, and we know of no study that has assessed muscle size/structure at all of these anatomic levels in the same cohort. To our knowledge, this is the first study to unambiguously assess the effects of age on myofilament ultrastructure in human skeletal muscle. Unlike variability noted at the cellular level, however, we found no effect of age on myofilament quantity or structure. Specifically, thick-filament length (A-band length), thick-to-thin-filament ratio, and myofibrillar fractional area were not different between young and older men and women, in contrast to our laboratory's previous findings in a model system (43). Parenthetically, this discrepancy between an animal model of aging and human aging should be a cautionary note for extrapolation of results about muscle morphometry across species. Our findings suggest maintenance of structural proteins within the myofilament lattice and are supported by our finding of no age effect on MHC protein content (42). Our data in healthy, older adults suggest alterations in skeletal muscle myofilament content/architecture do not play a role in the atrophy process beyond an assumed overall loss of parallel sarcomeres due to reduced CSA, nor do they appear to mediate age-related differences in contractile function. This is in contrast with some reports (10), but apparent conflict in these results may be explained by physical activity between groups (11), a caveat that we attempted to control in the present study.
The mitochondrial morphological data reported here are generally in agreement with previous studies that describe reductions in the average size of skeletal muscle mitochondria with age (51, 54). However, this observation is not universal (9, 47) and appears to be at least somewhat dependent on cellular localization (intermyofibrillar vs. subsarcolemmal) (9, 47) and sex, as we found alterations only in older women. Our findings are most appropriately compared with those of Crane et al. (9), who report maintenance of intermyofibrillar mitochondrial size, but decreased fractional area, in healthy older adults compared with young. However, the participants described in Crane et al. (9) were significantly more active than our relatively sedentary population, with their participants engaged in alternate modes of physical activity; young performed primarily aerobic exercise, while older adults had just completed a twice weekly strength training intervention. Although we recently reported that resistance training does not alter mitochondrial content/morphology (68), aerobic exercise is a well-known modulator of mitochondrial biology (4), suggesting differences in the type of activity of the populations may explain the discrepancy with our findings. Of further interest is the apparent greater durability of subsarcolemmal mitochondria across age groups in our study. Building on previous work describing greater responsiveness of subsarcolemmal mitochondria to acute disuse in young and older men (47), these results collectively suggest intermyofibrillar mitochondrial morphology are more sensitive to the overall effects of age, whereas subsarcolemmal mitochondria may respond more dramatically to changes in physical activity. However, it should be noted that recent evidence suggests greater interaction between these mitochondrial subfractions than previously thought (53). Indeed, the mitochondria are increasingly appreciated as a dynamic reticulum, and it is possible that morphological changes in the subsarcolemmal fraction may be obscured by the relatively fewer physical constraints placed on those mitochondria compared with the effects of the ultrastructure of the contractile machinery on intermyofibrillar mitochondria.
Although controversial, mitochondria are frequently identified as causal agents in the process of cellular aging (16, 63). Multiple investigations have suggested or implied causal relationships between mitochondrial dynamics and atrophic processes in skeletal muscle (58, 59, 76). A recent animal study suggests mitochondrial fractionation occurs as a primary consequence of healthy aging in rats (23), and others have suggested this may be the case in humans (2). Potential relationships between mitochondrial dynamics and atrophic processes are supported by studies that demonstrate a reduction in muscle atrophy (58) or protection of ischemia-reperfusion injury (50) by blocking mitochondrial fractionation. In the present study, older women had reduced individual intermyofibrillar mitochondrial size, which correlated with increased tension and slower myosin-actin cross-bridge kinetics, measures that were also primarily altered in older women (42). We observed age-related alterations in mitochondrial morphology that are linked, either directly or as an epiphenomenon, with age-related changes in skeletal muscle function, perhaps via signaling pathways involving peroxisome proliferator-activated receptor-α/β coactivator-1 (60). Here again, we are cautious not to imply cause-effect from our cross-sectional associations, but they are nonetheless compelling in supporting a long-held link between mitochondrial biology and age-related alterations in skeletal muscle. It is tempting to speculate that mitochondrial fractionation, as evidenced by reduced mitochondrial size, contributes to an intracellular environment characterized by enhanced reactive oxygen species (76) that may alter contractile function via posttranslational modification of myofilament proteins (56).
We have also identified morphological distinctions at the whole tissue level of young and older adults. We found age-related muscle atrophy, evidenced by reduced quadriceps CSA (cm2) and leg FFM (%body weight). However, absolute leg FFM (kg) was not different between young and older groups, despite similar height, weight, and %FFM in young and older individuals. Clearly, our cohort did not fit a clinical definition of sarcopenia, consistent with our efforts to ensure the older cohort in this study was well-matched to the young in health and physical activity. Despite this, we still found tissue and cellular level evidence for age-related morphological adaptations consistent with sarcopenia. The implication of this finding being that the phenotypes we have identified were robust enough to be detectable in an aged cohort that does not show manifestation of clinically apparent muscle wasting. However, we acknowledge that whole tissue imaging techniques may suffer from imprecision related to the measurement itself and confounding factors inherent to a between-subject design in human subjects (8). In contrast, muscle atrophy was apparent at the single-fiber level. Specifically, age-related atrophy was found in MHC II fibers, consistent with other reports in the literature showing age-related muscle atrophy is typically more prominent in MHC II fibers (34, 35). On closer examination, the age-related atrophy appears different between the sexes, as the distribution of fiber sizes was largely similar in young and older men, with younger men simply having slightly more very large (CSA > 2,850 μm2) fibers. In contrast, older women had a noticeable shift in fiber size distribution with a skew toward smaller fiber sizes. Together, these findings highlight the overall loss of muscle in cross section with age and suggest a greater contribution of MHC II fibers to that loss, with the most dramatic differences observed in older women. We also observed sex specificity in associations between intermyofibrillar mitochondrial size and indexes of single-fiber function (Fig. 6), wherein significant associations observed in the entire cohort persisted when assessed in women alone, but trended or were not significant in men. These sex-specific associations are consistent with observations in this cohort of age-related differences in skeletal muscle morphology being more pronounced in women then men. A few important caveats to our interpretation of the data presented here are warranted. Worth noting is the potential effect of oral contraceptives on physiological outcomes in the younger women in this study (taken by 4 of the 7 volunteers). While some studies performed in animals (41) and humans (1) demonstrate a net anabolic effect of estrogen, evidence that hormone replacement/supplementation increases muscle size and strength in younger adult women is limited (12). At least one study has shown decreased myofibrillar synthesis rates in young women taking oral contraceptives (15), while studies in postmenopausal women by our laboratory and others suggest no effect of hormone replacement therapy on skeletal muscle size and function (70, 75). Regarding physical activity assessment, our measures relied on a single summary value that was relatively insensitive to variations in the intensity of physical activity performed by our participants. However, our participants were not engaged in strenuous exercise by self-report and referred to walking as their primary form of physical activity, minimizing the potential effects of variations in intensity between age groups. Finally, we acknowledge the inherent limitations associated with performing correlation analyses with small sample sizes in a cross-sectional study. These types of analyses are prone to type I statistical error and, despite our careful matching for health status and habitual physical activity levels in study volunteers, it is possible, as with any correlation analysis, that we have uncovered false-positive associations. Nonetheless, the variables used in the present correlation analyses were chosen based on prior evidence and classical physiological relationships between muscle protein structure and function. While these data are perhaps not definitive, they provide compelling support for future research involving larger cohorts.
Our findings illustrate the complexity of physiological properties inherent in the age-related phenotype of skeletal muscle and the potential sex-specific nature of these adaptations at the cellular and subcellular levels. Despite the atrophic effects of age and sex at the cellular level, subcellular myofilament ultrastructure (thick-filament length, thick-to-thin-filament ratio, and myofibrillar fractional area) remained unchanged. In addition, mitochondrial fractional area and number were maintained, regardless of cellular location, suggesting maintenance of oxidative capacity across age groups (62) with similar physical activity levels (27). However, here again, sex specificity in the aging response was noted in average intermyofibrillar mitochondrial size, with greater reductions in older women. In these healthy adults, matched for physical activity level, it is unlikely that overall oxidative capacity was different between groups (3, 25, 27, 29, 30, 57), but associations between mitochondrial morphology and muscle function at the fiber level suggest coordination between cellular metabolism and single-fiber function. Future studies should be directed at characterizing the functional metabolic consequences of altered mitochondrial morphology with age and sex, and specific perturbations to contractile proteins that might be responsible for the structural and functional phenotypes observed.
This work was supported by the National Institutes of Health [grants T32-HL-007647 (D. M. Callahan), K01-AG-031303 (M. S. Miller), R01-AG-033547 (M. J. Toth), M01 RR-000109].
No conflicts of interest, financial or otherwise, are declared by the author(s).
Author contributions: D.M.C., N.G.B., M.S., J.B., M.J.T., and M.S.M. analyzed data; D.M.C., P.A.A., M.J.T., and M.S.M. interpreted results of experiments; D.M.C. and M.S.M. prepared figures; D.M.C., M.J.T., and M.S.M. drafted manuscript; D.M.C., M.J.T., and M.S.M. edited and revised manuscript; D.M.C., N.G.B., M.S., J.B., P.A.A., M.J.T., and M.S.M. approved final version of manuscript; N.G.B., M.S., J.B., and M.S.M. performed experiments; P.A.A., M.J.T., and M.S.M. conception and design of research.
We gratefully acknowledge the time and efforts of volunteers who participated in this research. We also appreciate the gift of plasmids for quantification of mitochondrial and nuclear DNA from Dr. Philip Nagley, Professor Emeritus at Monash University.
- Copyright © 2014 the American Physiological Society
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PeaceHealth is seeking a Physician - Internal Medicine based in the Eugene, OR community.
PeaceHealth is a well-established financially stable multi-specialty provider group looking for physicians interested in outpatient Internal Medicine opportunities to BE A PART OF THE EXCITING FUTURE OF PEACEHEALTH.
Diagnosis and non-surgical treatment of diseases and injuries of internal organ systems. Provide care mainly for adults who have a wide range of problems associated with internal organs. Examine patients using up-to-date medical instruments and equipment. Order and/or execute various tests, analyses, and diagnostic images to provide information on the patient's condition. Analyze reports and findings of tests and examinations, and diagnose conditions. Administer or prescribe treatments and drugs. Advise patients concerning diet, hygiene, and methods for prevention of disease; and document care. Prepare and complete records, work with team members for the efficient and orderly flow of patients.
If you are interested in this career opportunity, please contact Dorothy Reed.
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About PeaceHealth
PeaceHealth, based in Vancouver, WA, is a not-for-profit Catholic health system offering care to communities in Washington, Oregon, and Alaska. PeaceHealth has approximately 16,000 caregivers, a multi-specialty medical group practice with more than 800 physicians and providers, a comprehensive laboratory system, and ten medical centers serving both urban and rural communities throughout the Northwest. In 1890, Sisters of St. Joseph of Peace founded what has become PeaceHealth. Today, PeaceHealth is the legacy of its founding Sisters and continues to serve communities when invited to do so with a spirit of collaboration and stewardship – the spirit of health.
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Posting Notes: Eugene, OR || Physician; Physician - Primary Care || Full Time || INTERNAL MED SVCS


text:
A FAMOUS Adelaide mansion with a colourful past has sold for $5 million.
The Myrtles, at 7 Myrtles Court, was once the home of former bankrupt property identities Cathy and Myles Pearce.
The home settled on Friday and Harcourts Brock Williams agent John Williams, who sold the property with his wife Stephanie, said it was a landmark sale.
"You don't see too many $5 million private residential sales in South Australia, and I think this is the first one for a couple of years," Mr Williams said.
"It's a standout home and it has everything in a good location."
Mr Williams said a Chinese man with local connections bought the home.
"They know the area and they know South Australia," Mr Williams said.
'The Myrtles sold for $5.2 million in April 2006, and then sold again in July 2007 for $3.9 million.
The renovated 1890-built home has six bedrooms in the main home and a separate self-contained apartment with a lounge, bedroom and bathroom.
The home boasts 850sq m of indoor space, a formal entrance gallery, a study, a formal dining room, a drawing/billiards room, a casual lounge/home theatre room and a formal lounge room.
It has a chef's kitchen with four ovens, two dishwashers and a cold room.
Under the home are three connecting wine cellars and the home also features a floodlit synthetic tennis court, a heated pool and spa and an outdoor kitchen.
The home has featured in the movies Shine, Kiss or Kill and Sample People, and the television show McLeod's Daughters.
Mr Williams said the top end of the market was performing strongly and that 4 Victoria Ave, Unley Park, selling through agent Michael Brock, was under contract for more than $5 million.
"So that's two $5 million sales our office has had in the past couple of months," Mr Williams said.
"The top end of the market has been very robust for the past two or three years and there's consistently those sorts of properties coming on.
"Stephanie and I are selling five or six properties over $2 million every month."
Last year's top residential sale in South Australia was 11 Robe Tce, Medindie which sold for $4.917 million.
The most expensive residential sale in SA history is Glenelg's historic Stormont mansion, which sold for $6.5 million in 2010.


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Recently renovated to a good standard. Pleasant welcome, but having pre registered, I was surprised that they wanted my Passport details again. Requested a no-smoking, dog friendly room and got a pleasant room at the end of the corridor where we would not be destereb...More
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Le agradecemos enormemente sus comentarios en relación a su estancia en ibis Oviedo. Es siempre un placer recibir...More
Very comfortable bed and pillow, quiet room overlooking front of hotel. Clean linen and towels, generous size bathroom with good shower. Thirty minute drive from airport after a 24 hour flight meant it was the perfect stopover on the trip to Portugal. Breakfast was excellent...More
"2nd floor overlooking carpark in front of hotel."


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NAHC Board Announces Strategic Planning
Help Build the New NAHC – Send Us Your Nominations for the Board of Directors
Hospice Quality Updates – Deadline Tomorrow!
CMS Launches Hospice COMPARE Quality Website
Home Health Value-Based Purchasing Program Payment Adjustment Process and Enforcement of Service Codes on Home Health Claims
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How to Fix the Face-to-Face Requirement
In the various roles he has undertaken through the years, Val J. Halamandaris has been a singular driving force behind the policy and program initiatives resulting in the recognition of home health care as a viable alternative to institutionalization. His dedication to consumer advocacy, which enhances the quality of life and dignity of those receiving home health care, merits VNA HealthCare Group's highest recognition and deepest respect.
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Home health care agencies do such a wonderful job in this country helping people to be able to remain at home and allowing them to receive services
- U.S. Senator Debbie Stabenow (D-MI) Chair, Democratic Steering and Outreach Committee
Home care is a combination of compassion and efficiency. It is less expensive than institutional care...but at the same time it is a more caring, human, intimate experience, and therefore it has a greater human element...it's a big mistake not to try to maximize it and find ways to give people the home care option over either nursing homes, hospitals or other institutions
- Former Speaker of the U.S. House of Representatives Newt Gingrich (R-GA)
Medicaid covers long-term care, but only for low-income families. And Medicare only pays for care that is connected to a hospital discharge....our health care system must cover these vital services...[and] we should promote home-based care, which most people prefer, instead of the institutional care that we emphasize now.
- Former U.S. Senator Majority Leader Tom Daschle (D-CD)
We need incentives to...keep people in home health care settings...It's dramatically less expensive than long term care.
- U.S. Senator John McCain (R-AZ)
Home care is clearly the wave of the future. It's clearly where patients want to be cared for. I come from an ethnic family and when a member of our family is severely ill, we would never consider taking them to get institutional care. That's true of many families for both cultural and financial reasons. If patients have a choice of where they want to be cared for, where it's done the right way, they choose home.
- Donna Shalala, former Secretary of Health and Human Services
A couple of years ago, I spent a little bit of time with the National Association for Home Care & Hospice and its president, Val J. Halamandaris, and I was just blown away. What impressed me so much was that they talked about what they do as opposed to just the strategies of how to deal with Washington or Sacramento or Albany or whatever the case may be. Val is a fanatic about care, and it comes through in every way known to mankind. It comes through in the speakers he invites to their events; it comes through in all the stuff he shares.
- Tom Peters, author of In Search of Excellence
Val's home care organization brings thousands of caregivers together into a dynamic organization that provides them with valuable resources and tools to be even better in their important work. He helps them build self-esteem, which leads to self-motivation.
- Mike Vance, former Dean of Disney and author of Think Out of the Box
Val is one of the greatest advocates for seniors in America. He goes beyond the call of duty every time.
- Arthur S. Flemming, former Secretary of Health, Education, and Welfare
Val has brought the problems, the challenges, and the opportunities out in the open for everyone to look at. He is a visionary pointing the direction for us.
- Margaret (Peg) Cushman, Professor of Nursing and former President of the Visiting Nurses Association
Although Val has chosen to stay in the background, he deserves much of the credit for what was accomplished both at the U.S. Senate Special Committee on Aging, where he was closely associated with me and at the House Select Committee on Aging, where he was Congressman Claude Pepper's senior counsel and closest advisor. He put together more hearings on the subject of aging, wrote more reports, drafted more bills, and had more influence on the direction of events than anyone before him or since.
- Frank E. Moss, former U.S. Senator
Val's most important contribution is pulling together all elements of home health care and being able to organize and energize the people involved in the industry.
Anyone working on health care issues in Congress knows the name Val J. Halamandaris.
- Kathleen Gardner Cravedi, former Staff Director of the House Select Committee on Aging
Without your untiring support and active participation, the voices of people advocating meaningful and compassionate health care reform may not have been heard by national leaders.
- Michael Sullivan, Former Executive Director, Indiana Association for Home Care
All of us have been members of many organizations and NAHC is simply the best there is. NAHC aspires to excellence in every respect; its staff has been repeatedly honored as the best in Washington; the organization lives by the highest values and has demonstrated a passionate interest in the well-being of patients and providers.
- Elaine Stephens, Director of Home Care of Steward Home Care/Steward Health Systems and former NAHC C
Home care increasingly is one of the basic building blocks in the developing system of long-term care. On both economic and recuperative bases, home health care will continue to grow as an essential service for individuals, for families and for the community as a whole.
- Former U.S. Senator Olympia Snowe (R-ME)
NCOA is excited to be part of this great event and honored to have such influential award winners in the field of aging.
- National Council of Aging
Health care at home…is something we need more of, not less of. Let us make a commitment to preventive and long-term care. Let us encourage home care as an alternative to nursing homes and give folks a little help to have their parents there.
- Former President Bill Clinton
I've said before that wireless technology is reprogramming human behavior. I've worried that we are becoming dependent on instruments that were intended to free us but are actually captivating us with their incessant demands. We are becoming addicted to the ping of an arriving call or text that triggers a burst of endorphins which stimulate the reward centers in the brain and urge us to want more. Eighty-five percent of Americans are never more than an arm's length from their phones and can't imagine what life is like without the pings. I worry that it is so hard for us to get away from our cell phones that there is no longer a life between the pings. I also want to tell you that the cell phone will change the practice of medicine in wonderful ways.
We are in the midst of a culture shift in health care delivery, moving from an interventional model to one that focuses on prediction and prevention. The new technology will help patients manage their health problems with recommendations from their doctor. Mobile apps for smartphones and tablets will let patients gather diagnostic data or help coordinate care, giving them an easy way to keep track of their conditions and treatments. Consumers are increasingly armed with "wellness" apps — simple devices to monitor diets, exercise, and weight to help them stay out of the doctor's office — that make up most of the 97,000 health-related mobile-apps on the market.
Devices that were once only in doctors' hands are now in the hands of consumers. They'll be able to purchase phone apps to monitor their heart problems by taking an ECG and performing an ultrasound or echocardiogram. An ECG app costing $199 records and transmits your cardiac status to your doctor's phone. A microscopic chip the size of a grain of sand is being developed that will circulate in your bloodstream and can pick up the warning signs of an impending heart attack. In the event of a cardiac arrest, there's also a CPR app that can guide someone through the steps of performing CPR and using an automated electronic defibrillator.
In addition, there are a number of mobile tools to help people with diabetes lower their blood glucose levels. Type in diabetes on your phone, and you can download apps at costs ranging from free to $12. You have many different diabetes apps to choose from to quickly record your blood sugar, blood pressure, pulse, weight, medications, food (usually carbohydrates), and exercise. You can even print or email your blood glucose record to your health provider.
The new technology actually allows doctors and patients to transmit data while talking to each other. Even if it's only for five minutes, they'll focus on each other. It's a relationship, and it's changing the way doctors and patients approach health care. Take it from Eric Topol, a cardiologist and genomics professor at the Scripps Research Institute in La Jolla, California. Topol had just taken a seat on a cross-country flight when he received an urgent e-mail from a 63-year-old patient. The man's heart was racing and he wanted to know what to do about it. After receiving data from the patient's phone app that analyzes heart rhythms, Topol recommended a higher dose of medicine and calmed his patient, who suffers from atrial fibrillation. "It's good I got on the Internet on the plane, otherwise he would not have had an answer for a long time," said Topol, who prescribed an ECG app for his patient. "Many times this helps keep a person from having to go to the emergency room."
Like Topol, many doctors think the apps are useful time savers and have the potential to make health care more efficient by speeding diagnosis, improving patient monitoring, and reducing unnecessary visits to the hospital or physician. The health care of the future is not about intervention but prediction and prevention. People will be monitoring their own bodies, listening to what it's telling them, and making some intelligent choices about how to come to what they are facing. This means we can heal ourselves at home and in supportive communities that care about our wellbeing. This is one form of human behavior that we shouldn't try to reprogram or change.
Carl A. Hammerschlag, M.D., is a psychiatrist, author, and professional keynote speaker. He is an authority in the science of psychoneuroimmunology — mind, body, and spirit medicine — and speaks about health and wellness, healing, leadership, and authenticity. He has delivered motivational keynote speeches to corporate and business clients around the world. For more information, visit www.healingdoc.com.
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text:
Hello there!
It's been a while since the previous chapter, isn't it?
well… see you later ^_^
Broccoli + Kirin (giraffe) + Banana = Brokkina
Several days later.
I and Firia who are undertaking the gathering medicinal herbs request as usual, feel that the atmosphere inside the forest is a bit strange, different from usual.
"…Firia, do you feel that there's something strange here?"
"Perhaps something happened here. I can feel a remains of magical energy with greatly different density from the other."
Firia makes a stern expression.
Considering about it by combining her statement with the presence I feel, it seems like it's quite a formidable fellow.
"You sure are amazing, to be able to feel the remains of magical energy."
"Even if I look like this, I'm an elf, after all. Or rather, how could you notice this abnormality, Yuri-san?"
"Intuition. Also, if I should say it, perhaps because the smell of the forest is slightly different from usual."
"I think you're the one amazing, though…."
Anyhow, I think without a doubt there's something here.
Unable to conceal my elated feeling, a smile floats at my face. I want to travel this vast world more. And then, I want to fight against many strong opponents.
But unfortunately there's no subjugation request at E rank requests.
But, be that as it may, if I don't undertake the request then my rank won't raised.
The only way to solve those problems in one go is none other than my "great plan of defeating a magical beast when we were gathering medicinal herbs".
"You sure have an amazing naming sense, aren't you, Yuri-san?"
"Don't peek at my mind! Good grief…."
Seems like Firia used her "Mind read" and peeked at my mind.
Nevertheless, this presence.
It isn't a presence of a magical beast that usually lives at such a forest mean for beginner.
That means, we must defeat it by any means, don't we?
Or rather, such a thing is unrelated, I don't see other option but fight it.
"Walking to search for it seems like a pain, isn't it? So let's flying for a bit"
"Flying? Yuri-san, what are you— kyaa!"
I'm flying.
My body is gradually floating, and finally surpassing the height of trees. And then I search for the figure of this magical beast— find it.
The first one comes into my sight is its surprisingly long neck.
Looking at its body that almost equal to the trees around it, perhaps its height is not less than then meters.
Perhaps it's trying to mimicking the trees around it, with a green colored body, its neck has a similar green color of tree leafs.
Its face is covered by a green colored shaggy fur, and there's a yellow fruit-like thing similar like a banana atop its head.
After confirming its appearance I return to the ground.
"I found it, Firia."
"Before that, could you please explain to me what you just did?"
"What I just did… I was flying. If you keep kicking the air before your body fallen, you could keep flying, right? Something like that."
"I see. I understand that it won't be any use as reference at all."
When I tell Firia about this magical beast's traits, Firia's face is slightly stiffened.
"That… perhaps it's brokkina. I'm not fully remember about it, but I think at least it is supposed to be a B rank magical beast."
According to Firia, seems like Brokkina tend to attack by swinging its long neck.
And then, above all, it seems like it's a strong magical beast that may endanger the balance of this forest.
"Any adventurers who come here perhaps would got instantly killed by it, right? We have no choice but to defeat it, isn't it? Haa, such job is…."
"It seems strong, isn't it? I'm looking forward to fight against it."
I can feel my body and my emotion in excitement. My blood is gushing strongly, and flowing through my whole body.
Fresh, without a doubt this is a fresh feeling. Without a doubt I'm alive right now.
"Why did you say such battle junkies words?"
"Having an opponent where you can crash your power till your heart content sure makes you thrilled, isn't it?"
"I don't feel it at all, though…."
Seems like Firia doesn't get the point here.
"Good grief, this is why Firia is…."
"Eh, am I the one strange here?"
Firia opens her eyes wide as if surprised.
Thinking about it logically with common sense, without a doubt the one strange here is Firia.
If she thinks about it, she should be able to understand that soon, though.
"Then, What should we do, Yuri-san? Should we make a strategy or something?"
"Hmm, let's see…. This time I'll show you the amazingness of my muscle magic."
I fold over my arms.
Simultaneously, seems like can't endure it for any longer, she opens her mouth.
"Then, it seems like this time there's no need for me to take any action, isn't it~? Is there anything I can help you?"
"No, no problem."
"Then, I'll watching you from distance. I have a considerably good eyesight, after all. Which direction is it?"
"Perhaps, around forty degree to the left."
"I got it. I'll wait from atop this tree."
Saying so, Firia floats her body and then sits at a branch atop the tree.
So wind magic could also be used that way, huh. I can't imitate it with my muscle magic, but it seems very convenient.
"Ah, I can see it. Uwah, it sure is big, isn't it?"
"I see, then I'm going."
"Ah, Yuri-san."
When I'm intending to run, Firia addresses me.
"…do your best. Please don't die on me."
"Ou, just look at how I go rampaging there."
I return a thumb up to Firia along with a wild animal-like smile.
◇ ◇ ◇
I run at my full speed toward where brokkina is.
I can feel its presence immediately, after I run toward that direction for a while more I finally make a contact with it.
"It sure is big, isn't it?"
I put my impression into words.
Seems like the brokkina sense me as a threat and it start gathering magical energy at its mouth.
"Good, come at me!"
I slightly pull my right hand.
Only that. With only that the brokkina makes a behavior as if it's flustered.
As I thought this one is strong. It has a great ability to sense danger.
I calmly looking at the magical beast before me.
To be able to understand the dreadful of my muscle magic, this fellow has quite a good eyes.
Brokkina lifts its long neck to its limit, and swings it as if a hammer.
To gauge its strength, I receive that attack upfront.
Unexpectedly it has a considerable strength. With that much strength, it seems like I need to take it seriously.
While shivering in excitement, I remove my body limiter inside my head.
Power is overflowing from the depth of my body.
Simultaneously with the transformation of my body, power is overflowing through my whole body after such a long time.
"Sorry, you damn giraffe. Seems like I can't holding back against you."
Brokkina is standing facing me, and firing magic from its mouth.
Since I can't see it with my eyes, perhaps it's a wind magic.
If I feel the air movement I might be able to evade it, but I don't need to evade it.
I receive brokkina's wind magic with my body.
"That was quite a good magic. If it's not against me, it should be an useful weapon, isn't it?"
Not getting injured at all, I grin at brokkina.
"Firia, look closely. The amazingness of muscle magic."
Speaking by myself to Firia who should be watching from atop the tree, I put a considerable strength at my right arm.
Sensing danger from it, brokkina swing its long neck as if a pendulum and then bends it over at me, but— that's too late already.
"Eat this."
I swing my arm while saying so.
My punch which is swung upward doesn't hit brokkina.
But, the punch from the me who have released my limiter has a speed exceeding the speed of sound.
And then, my punch which is swung with speed exceeding the speed of sound creates a terrific shock wave.
The shock wave is flying directly toward brokkina.
"Pan!" together with such snapped-like sound, brokkina's body explodes.
The only remained part is its head which is rolling on the ground.
The splinters of brokkina's body are fluttering midair as if a falling petals.
"…hmm? Did I overdo it?"
To think that even this brokkina left without almost of its figure.
To the point the only remained part is its head.
Well, it was sufficient to get a passing mark, wasn't it?
My punch is surpassing the speed of sound. –its name is 'Pistol punch'.
For me who don't have any talent at any elemental magic, this magic is the only ranged magic I have.
I look at brokkina's head near my feet.
It was an opponent that has some backbone. So that was a B rank, huh.
If that the case, perhaps an S rank is would be utterly stronger than me, isn't it?
If that's the case, seems like I need a more intense training, don't I?
Finding a new objective, I return to Firia's place with a refreshed expression.
"I'm back, Firia."
"Welcome back~… wait doesn't your left arm got injured! Please show it to me!"
I show my left arm as per Firia says.
My left arm is slightly swollen. Perhaps it was because that first hammer attack, wasn't it?
As expected at my normal shape, receiving that attack heads on perhaps was a bit too rash. Deep inside my heart, perhaps I had a negligence.
I must reflect on it.
Firia lays her small hands at my swollen arm.
Before long my arm is covered by a soft white light, when the light disappears my arm return to the way it was.
"Okay. With this it has been healed."
"Oh, thanks. You sure are amazing…. By the way, should I pay for it?"
"As expected I'm not greedy enough the even taking money from my own comrade. Since the request's rewards are divided evenly by two, after all."
"Firia, unexpectedly you're quite a good fellow, aren't you?"
"Shut up. Please shut your mouth."
Since I expressly praise her so it would be good if she just honestly delighted, though. What a not so cute fellow.
"By the way, Yuri-san, your last attack, what was that? I felt like seeing brokkina exploded, though."
"That technique, huh? That was pistol punch. It was amazing, right? My punch force was flying with a boom."
When she hears it, somehow Firia makes a doubtful expression.
When I say 'boom' again, her expression becomes more doubtful.
"…I deeply understand that Yuri-san are an existence outside the corridor of common sense."
"That fellow was also considerably strong, you know? Because of that my motivation was blazing."
"Why did your motivation got elated…?"
Firia says so and sighs once.
I see, Firia didn't fight that brokkina, after all.
"Sorry, you must be wanted to fight it too, don't you? I'll teach you a good way to train your muscle so please forgive me."
"I can't believe it that you actually say that with such serious look. As I thought you're a muscle-brain, aren't you?"
"Please don't praise me like that, it embarrasses me, you know."
We decide to return and reporting the case about brokkina to the guild. Aah~, today sure was a good day.


text:
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text:
New Delhi, June 27: The Employees Provident Fund Organisation today cracked the whip on Industrial Finance Corporation of India, the funds biggest defaulter, reports our special correspondent.
The funds central board of trustees asked the corporation to cough up Rs 5,000 crore in arrears. We have asked IFCI to start paying up immediately, labour minister Sahib Singh Verma said today at a press conference, after a board meeting. The board met the corporation representatives on May 22 to strike a deal on the repayment of the Rs 420-crore borrowed from the fund.
At the meeting today, the board laid down the conditions for repayment. IFCI should pay us at the earlier coupon rate, ranging between 12 and 14 per cent, for the period between March 2002 and March 2003, Verma said. From March 2003 onwards, the corporation can repay at 10 per cent over the next 10 years.
These conditions, approved by the trustees, will be communicated to the IFCI. It is in their interest to agree to them, said Hansubhai Dave, a trustee and general secretary of the Bharatiya Mazdoor Sangh.
The fund rejected the corporations offer to repay at 9 per cent rate of interest. We insist on a 10 per cent repayment rate, Verma said. Both the finance and the labour ministries, he said, had stepped up pressure on the corporation.
Next on the list of defaulters is the Bangalore-based Hindusthan Machine Tool with a Rs 240-crore arrear.
According to Verma, the fund was making good progress in recovering arrears from defaulters. As much as Rs 1,200 crore was yet to be recovered. Of this amount, 70 per cent was locked in litigation.
To speed up the recovery process, the board of trustees today sanctioned the setting up of a directorate of recovery and a directorate of audit. This will strengthen the process of recovery. The directorate of recovery will maintain dossiers on major defaulters, the minister said.
The fund has recovered Rs 750-800 crore since 1998. The organisation has filed 7,000 criminal cases against defaulters. There has been a recovery of 800 per cent since last year, Verma said.
The board today also decided to give social security numbers to 25 lakh construction workers and set up a sub-committee to work out the modalities of the process. The workers will then be able to move and operate their accounts wherever they move, Verma said.
XLRI project
The director of the Xavier Labour Relations Institute, Father P.D. Thomas, has confirmed that the institute has submitted a project proposal for PF restructuring to the Centre.
A team comprising top PF department officials from the central and state governments visited the college campus in November last year and had an elaborate discussion on the project, he said.
A four-member team headed by E.M. Rao, dean of academics, had prepared the project, Thomas added.


text:
What are your thoughts when you see someone of opposite gender with good well maintained bod? (Be completely honest or don't answer)
For guys,
Good squat butt, Well maintained legs and toned belly.
For girls,
Buffed chest, muscled arms, toned abdominals, wide shoulders and built legs.
Most Helpful Girl
I just think "well, he works out" or "he's sexy and he knows it" and then that stupid song pops up in my head.00|00|0
Lol does that really happen
- Show AllShow Less
oh i don't notice that really on the opposite gender... guys usually wear baggy clothing anyways. well, baggier than women's clothes
I meant what's attractive on em
Most Helpful Guy
"She looks nice."00|00|0
Bexause she keeps fit?


text:
Thanks to hackers and YouTube, pop fans are now able to listen to a slew of unfinished demo material that was probably never meant for public consumption. It's great (for us…not the artists). Sometimes, a demo ends up being way more awesome than the finished product. Sometimes, a demo never sees the light of day and it's a massive injustice! Check out a list of some of my favorite demos and unreleased jams after the jump. Continue reading
News booty call, britney spears, demi lovato, demos, dj is my lover, ester dean, femme fatale, girl gone wild, heart attack, hook up, i do not hook up, i need a change, katy perry, ke$ha, kelly clarkson, lana del rey, let me love you (until you learn to love yourself), livvi franc, madonna, national anthem, ne-yo, nikki williams, rosette, ryan tedder, save the day, selena gomez, shellback, sia, stargate, tear the club up, the outsyders Leave a comment


text:
Why is Middleton known as the "Good Neighbor City"? Green businesses like Capital Brewery are one good reason.
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