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How to save a million bucks - MoneySense
How to save a million bucks
Becoming a millionaire is more painless than you think, even if you're starting with next to nothing.
by Dan Bortolotti Jul 29, 2010
Roger Hunter is 40 years old and owns a small construction company in St. John's. He earns about $80,000 a year. His wife Anna, 36, looks after the couple's three children and works for the family business during the busy season, earning an extra $35,000 or so. Roger enjoys playing soccer, and he and Anna love to eat in nice restaurants, though they indulge only a few times a year. In many ways, they're just like everyone else in their neighbourhood. Except for the fact that they're millionaires.
Roger is the first to admit he's no investing wizard. "I just figure if I throw enough stuff against the wall, some of it will stick." What the Hunters have mastered is the art of saving. As soon as he started working full-time, Roger arranged automatic payroll deductions that, over the months, eventually bought him $10,000 worth of Canada Savings Bonds. Whenever his job required him to relocate, he took the moving allowance and put it in the bank. If he had a little extra cash, he called his bank and asked them to increase his mortgage payments.
Thanks to that attitude, the Hunters (whose names we've changed to protect their privacy) have saved more than $700,000 in their investment accounts. They paid off the mortgage on their $300,000 house in nine years, and own two rental properties, a tract of land and a motor home, with a combined value of more than $400,000. All this despite never earning a $100,000 income, until they hit that milestone last year.
When the Barenaked Ladies wrote their classic song about being rich, they didn't call it "If I Had an Ample Nest Egg." There's no TV game show called "Who Wants Several Hundred Grand?" In the first Austin Powers movie, Dr. Evil didn't obtain a nuclear warhead and hold the world ransom for 70% of his pre-retirement income. No, in our culture, the number that symbolizes real wealth is still a cool million. "I think I'll need a million and a half to retire," says Hunter. The couple is already there in terms of net worth, and they should have a seven-figure investment portfolio well before Roger hits 50.
At MoneySense, we've received many letters and emails from middle-class readers like the Hunters who have saved a million, so we thought we'd help you figure out if you could do it, too. We're not going to pretend it's easy—it requires a steady income, a commitment to saving, short-term sacrifices, and a smart investment strategy—but if Roger can do it, so can you. Joining the ranks of the millionaires may be a more realistic goal than you think.
The first secret to saving a million dollars isn't a secret at all: spend less than you earn, then save and invest the difference. "That is so dirt simple," says David Christianson, a financial planner and portfolio manager with Wellington West Total Wealth Management in Winnipeg. "But I work with people who have accumulated significant net worth, and most of them have accumulated it by using that formula."
The percentage of your income you need to save depends on how much you earn, how many years you have before retirement, and what kind of return you expect on your investments. As a rule of thumb, Gail Vaz-Oxlade, financial author and host of 'Til Debt Do Us Part, says that people who start saving in their twenties can assure themselves a comfortable retirement by setting aside just 6% of their net (after-tax) income. For someone whose take-home pay is $50,000, that's an RRSP contribution of about $250 a month.
If your heart is set on saving a million, however, you'll likely have to sock away more: On the opposite page we've created a Model Millionaire and figured out how much he needs to save each year. We found that about 10% of his middle-class income should do it, if he wants to hit seven figures by age 65. That means in his thirties and forties, he'd have to save $300 to $500 a month. That's a challenge for someone earning $50,000 or $60,000, paying off a house and raising children. But remember the part where we said this wasn't going to be a breeze?
You can make it easier by setting up an automatic RRSP contribution on payday so you don't have a chance to spend your savings. "Pay yourself first" has been a mantra for decades—because it works. Most people never get behind on their income taxes, mortgages or car loans because they never see the money earmarked for those purposes. Make your savings a fixed expense, too, and you'll be well on your way to saving a million.
Living on less
When Thomas Stanley and William Danko wrote The Millionaire Next Door, they set out to examine the lifestyles of the wealthy. What they learned surprised them: the people who wore expensive suits, drove flashy cars and drank fine wine had high incomes, but they weren't necessarily wealthy. Most of the millionaires they studied, by contrast, dressed casually, drove Chevrolets and drank Budweiser. The authors summed up their observation simply: "Wealth is what you accumulate, not what you spend."
The lesson here is that if you want to become a millionaire without a huge income, you're not going to look like a millionaire. The Hunters are perfect examples: Roger is pretty sure his soccer teammates have little idea what he's worth. People who save 10% of their net income aren't typically paying $800 a month to lease an SUV, nor are they eating in restaurants three times a week. They buy what they need, and they recognize good value, but they don't indulge every desire. This frugality comes naturally to the Hunters, but there's hope for anyone who is truly committed to their financial goals, says Vaz-Oxlade. "There is no question that some people are born savers. However, I have gotten too many letters from too many people who were spend-crazy and who have subsequently seen the light. It's all about prioritizing."
One of the biggest barriers to saving a million-dollar portfolio is the priority we put on our homes. According to RBC Economics Research, owning a two-storey home costs the average Canadian household more than 46% of their pre-tax income. If you're pouring that much into your house for 25 years or more, your chance of saving a million is vanishingly small. The goal becomes realistic, however, if you buy a home you can afford to pay off in 15 years. Once the mortgage is gone, you can redirect the payments to your RRSP and see your portfolio suddenly jump to life. (We cost out this scenario in "The Late-Blooming Millionaire," below.)
Get time on your side
There's no question that starting early is a huge advantage. Any online savings calculator will show that you can save a million by tucking away just $500 a month if you have 40 years to do it (assuming a 6% return). Unfortunately, life isn't as simple as a savings calculator. "Those linear graphs that show how to achieve $1 million don't match the human life cycle," says Neil Murphy, a financial planner with Weigh House Investment Services in Toronto. "Your cash flow doesn't match that. The people who are aggressively saving are usually a bit older, their kids are gone, they're hitting their stride income-wise and their expenses are going down. But I doubt that many of them were doing massive savings in their twenties."
If you live below your means when you're young, concentrating on paying down debt rather than buying expensive toys, you'll likely have little trouble applying that same discipline to retirement savings as you get older. Once you're mortgage-free and your kids have moved out, you may well be able to save 30% or 40% of your net income during the last 15 years of your working career. But if you're spending more than you make and continually refinancing your home to bail you out, you're not going to suddenly morph into a super saver at age 50.
The slow-and-steady road to a million puts compounding on your side, but it does have one psychological pitfall: the finish line can seem so far away. Our Model Millionaire on page 68 starts saving 10% of his net income at 25, and two decades later his nest egg has grown to just $212,000. He's halfway through his 40-year savings plan, and yet and he's barely a fifth of the way to his goal. That can be awfully discouraging if you don't understand the nature of compounding: most of the benefit comes near the end. For instance, our investor's portfolio took 20 years to grow from zero to $212,000, but it will double in just eight more years. By the time it reaches half a million at age 55, a 6% return will be spinning off $30,000 of growth annually. That's more than our hard-working saver contributed during his first six years.
The tipping point comes when the dollar value of your portfolio's annual return exceeds the amount you're contributing. At 35 years old, three-fifths of our Model Millionaire's portfolio growth comes from contributions. Just five years later, however, the portfolio has grown to more than $115,000 and everything has changed. His portfolio's return is now adding more to his savings every year than his contributions. Once your portfolio is working harder than you are, your goal will feel a lot closer.
Keeping more for yourself
The final piece in your million-dollar puzzle is the right investment plan. It's possible for extreme savers and top-tier earners to amass a fortune in savings accounts and GICs. But if you're planning to hit seven digits by saving 10% of a modest income, you're going to need help from the markets.
Your first step is to check your expectations: if your map to a million includes 8% or 9% returns every year, you're likely to be disappointed. True, the markets have returned more than that historically: during the 25 years ending in 2007, even T-Bills averaged almost 7%, while bonds returned close to 11% and stocks almost 12%. But that included periods of double-digit inflation and steadily declining interest rates, two things we're not likely to see in the decade ahead. Neil Murphy says that high costs and bad decisions—things like chasing hot funds or panicking during market crashes—doom most investors to subpar returns. When he makes projections for his clients, he uses a 5% to 6% expected return for a portfolio of half equities and half bonds.
One of the best ways to conquer the one-two punch of high fees and self-destructive behaviour is to adopt the Couch Potato investment strategy. Low-cost index funds or exchange-traded funds (ETFs) are the best way to capture your fair share of the returns the markets deliver. A Couch Potato portfolio can easily cost less than 0.5% a year in fees if you manage it yourself in a discount brokerage account.
Have no illusions here: fees can destroy your returns and easily derail your million-dollar journey. Canadians pay some of the highest investing costs in the world: annual fees of 2% to 3% aren't unusual. If our Model Millionaire has his annualized return reduced from 6% to 4% because of mutual fund expenses or other fees, he'll fall well short of his million-dollar goal with just $672,000. Ask yourself whether it makes sense to put up all of the capital and assume all of the risk, while reaping only two-thirds of the return. If you don't end up being a millionaire, you can be sure your investment adviser will.
The million-dollar question
We hope we've shown you that saving a million bucks is a realistic goal for disciplined investors with a good (though not enormous) income, and several decades to make it happen. The question you need to ask yourself now is more introspective: is it worth it? Like any sacrifice, your long-term savings plan should be done with a higher purpose. Your ultimate goal, after all, is supposed to be happiness.
A funny thing can happen on the way to the Millionaire's Club. People who spend their whole lives scrimping and saving suddenly find themselves having to draw down their portfolio when they retire, and it doesn't come naturally. "I would bet that for 25% of our clients each year, our job is helping convince them that they can spend more money," says Christianson. "People who are good at saving often have trouble letting go."
Living frugally, paying off your debt and saving for retirement should be everyone's financial goal. But if you're turned off by the idea of scrimping for decades just so you can call yourself a millionaire, that's fine. "Don't start with the end result, start with the process," says Vaz-Oxlade. "It's less about a magic number and more about you deciding where you want to be, where you are now, and how you are going to close the gap."
Now there's advice that's worth a million bucks.
The model millionaire
Like a robot programmed to save, you contribute 10% of your net (after tax) income to your RRSP fromage 25 until age 65, and you turbocharge your savings by reinvesting your RRSP tax refund every year. You're comfortable with a balanced portfolio of stocks and bonds designed to achieve an annualized return of 6%.
Age Earned annual income Net annual after-tax income Monthly RRSP Contributions Annual RRSP tax refund (reinvested) RRSP value at year end
25 $40,000 $32,945 $275 $861 $4,156
35 $53,757 $42,125 $351 $1,324 $70,944
45 $72,244 $54,488 $454 $1,907 $211,701
65 $130,482 $89,380 $745 $3,968 $1,028,151
The super-safe saver
You can't get a return of 6% without risk. If you're the ultraconservative type of sticks to GICs and other safe investments, you may have to save a quarter of your net income to retire a millionaire. Here we assume you're maxing out your RRSP every year, so your annual contribution is 18% of earned income to a maximum of $22,000. (Since you're using up all your RRSP contribution room, you can't reinvest the tax refund.) We assume a low-risk annualized return of 3.5%
25 $40,000 $32,945 $600 $0 $7,200
35 $53,757 $42,125 $806 $0 $109,060
45 $72,244 $54,488 $1,084 $0 $286,757
65 $130,482 $89,380 $1,833 $0 $1,060,161


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Registration for all students grades Pre-school through 8th grade will be held at Kirkland School on Wednesday, August 3rd from 8 am until noon. Please plan to attend!
School begins Monday, August 8th at 7:50 am for all students.
Class Supply Lists will be available soon!! Check Back!!


Welcome to Quote Meanings. This page lists the Frank Mankiewicz quotes we have in our database and soon will provide users a means to discuss the meanings of quotes listed here. You don't even need to sign up.
A politician will always tip off his true belief by stating the opposite at the beginning of the sentence. For maximum comprehension, do not start listening until the first clause is concluded. Begin instead at the word "but" which begins the second, or active, clause. This is the way to tell a liberal from a conservative -- before they tell you.
Thus: "I have always believed in a strong national defense, second to none, but ... " (a liberal, about to propose a $20 billion defense cut).


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Research Reveals 'Rich Get Richer' Scenario in Kindergarten Math
By Holly Kurtz — May 23, 2014 3 min read
Kindergarteners learn more math in classrooms with higher average levels of student engagement. That's the less-than-surprising conclusion of a study that appears in the current issue of the peer-refereed American Journal of Education.
More unexpected are findings about which students benefit most from classrooms with higher average levels of engagement.
You might think that less-than-motivated students would get more from classrooms with high average levels of engagement. In fact, that's what past research would suggest since students in such classrooms tend to help each other more and encourage one another's efforts.
But past research has not necessarily explored the interaction between the engagement levels of individual students and the overall environment of their classrooms.
That's where Keith Robinson, an assistant sociology professor at the University of Texas at Austin, and Anna S. Mueller, an assistant professor of sociology at the University of Memphis, stepped in.
What they discovered was that children who are, themselves, highly engaged make more math growth if their classmates are also highly engaged. So, too, do children who start the school year with better math scores.
"[H]ighly engaged students in highly engaged classrooms showed the largest achievement growth in math," Robinson and Mueller write. "This combination seemed to produce a 'rich get richer' scenario: More engaged students take an approach to schooling that is more conducive to learning, and this approach is then continually reinforced by similarly engaged classmates."
As for students with lower levels of engagement, they also do better in highly engaged classrooms. It's just that it makes less of a difference for them. And this can have long-term consequences.
"Lower individual engagement means that a given student will be slower to acquire essential math skills," Robinson and Mueller write. "Since these skills affect one's ability to learn more advanced math skills in subsequent grades, the combination of low individual engagement and low classroom engagement may lead to substantial achievement differences compared to highly engaged children in highly engaged classrooms by the end of kindergarten."
Robinson and Mueller base their findings on an analysis of 12,462 kindergarten students who took part in the U.S. Department of Education's Early Childhood Longitudinal Study of children who attended kindergarten in 1998 and 1999. These students took individually administered math tests in both spring and fall.
Given the shifts that have occurred in the kindergarten world since that time, it is certainly possible that they would get different results today, but Robinson doubts that it would have made much of a difference. He said he got similar results when he examined a different data set from 2003.
Another caveat is that the data set the researchers used only permitted them to examine one aspect of student engagement, namely, children's behavior as observed by classroom teachers. These teachers responded to six questions that asked them to assess the frequency of behaviors such as showing "eagerness to learn new things," working "independently," and keeping "belongings organized." The researchers then created average classroom-engagement ratings by averaging the individual scores.
Although behavior is a key indicator, it is not the only ingredient of student engagement. There are also emotional and cognitive aspects that are tougher to observe because they unfold inside a student's mind.
"Assessing the classroom environment is a difficult task given the complexities of classroom interactions, organization, and instruction," Robinson and Mueller conclude. "Learning environments are defined by physical, emotional, and behavioral characteristics. Our work emphasizes that the reasons why some students experience larger growth than others are complex and multifaceted, just as they are individual and contextual."
Holly Kurtz
Director, EdWeek Research Center
Holly Kurtz is the director of the EdWeek Research Center.
A version of this news article first appeared in the Inside School Research blog.
Student Well-Being Explainer How Should Schools Quarantine Students Exposed to Coronavirus? An Explainer
The Centers for Disease Control and Prevention is changing its quarantine guidelines for people who had close contact with COVID-19.
Sarah D. Sparks, December 3, 2020
Teaching & Learning Pandemic Learning Loss Heavier in Math Than Reading This Fall, But Questions Remain
Results from fall testing confirm that the pandemic has taken a toll on students' academic growth.
Students are reminded to wear a mask amidst other chalk drawings on the sidewalk as they arrive for the first day of school at Union High School in Tulsa, Okla., Monday, Aug. 24, 2020.
Mike Simons/Tulsa World via AP
Student Well-Being Children Account for More New COVID-19 Cases as the Pandemic Rolls On
A new study in the journal Pediatrics finds more than a half million children have been diagnosed with COVID-19 so far in the pandemic.
Mathematics Opinion Teach Math in Ways That Are 'Proactive' & Not 'Reactive'
Larry Ferlazzo, December 18, 2020

redpajama_set_name: RedPajamaCommonCrawl


Dr Carolyn O'Shea started at Greensborough Road Surgery in 2003 and obtained her Fellowship of the RACGP in 2004. She enjoys the variety of general practice and the surprises each day brings. She usually is available on Tuesdays all day and Thursday afternoons. As well as clinical work, she also has interests in medical education and in medical editing.


Looks like our bank accounts will be a little more empty than usual this month! Malaysians love to save money or get good bargains anytime so if you love shopping in pharmacies like Watsons, then you would be super happy to know that they are having a mega sale in their stores right now!
Based on a post on their Facebook page that has gone viral, they announced that the sale is available in all their outlets across Malaysia.
This mega sale, which has already started, will be going on for a month until September 3 for West Malaysia and starting from August 9 to September 12 for East Malaysia.
One of the most important things you should know about this sale is that they are having Buy One Free One promotions for a wide range of items. These include items ranging from personal hygiene, beauty, supplements, snacks, and many more.
Many popular brands are on sale too, such as Maybelline, Revlon, Silky Girl, Kiss Me, Dove, and lots of other brands as well. If you aren't able to visit their stores to buy these super cheap items, then don't worry because you can also shop online as Watsons Malaysia also has these promotions on their website.
Plus, it looks like if you shop during the weekends, there will be even more discounts with up to 50% off and five times more member points if you are a Watsons member.
Guess now is the best time to stock up on any essential personal care products you need! Can save money too!


Estate Sale Lot, owned by one family for many years. Close to the Elementary School, Mature trees, raspberries and rose bushes, great sunlight, zoned for multifamily, lot is stubbed for utilities. Priced below appraisal.
I was searching for a Property and found this listing (MLS® #18-18037). Please send me more information regarding 631 Mumford Street, Anchorage, Alaska, 99501. Thank you!
I'd like to request a showing of 631 Mumford Street, Anchorage, Alaska, 99501 (MLS® #18-18037). Thank you!


Intrepid investigative journalist Scout Davis has given herself a holiday, but when Hermione Longfellow accosts her in the supermarket, she stops to listen.
eccentric Anemone sisters. Always dressed in black, they rarely leave their home nestled in the hills – but Scout is sure that the drinking of chicken blood is just idle gossip. When Hermione asks Scout to track down her sister Nemony's AWOL husband, believed to have died at sea thirty years ago but recently popped up again on the Great Barrier Reef, Scout jumps at the opportunity.
Delightfully witty and addictively fast-paced, this is the second hilarious outing for unforgettable sleuth Scout Davis.
I wasn't sure whether this title by 2013 Davitt Award winner Maggie Groff (she scooped the Australian Sisters in Crime pool of Best Novel and Best First novel with MAD MEN, BAD GIRLS a few weeks ago) would actually be my cup of tea. It seemed that it would be "lighter" than my usual crime fiction fare. But then I chose it for my face to face reading group to read in the coming month, so in a sense I was committed.
I did have my doubts in the first 50 pages or so, but then things settled down a bit, and I must admit to enjoying both the plot and the plotting skill. The blurb on the front cover calls sleuth Scout Davis " a successor to Evanovich", and I thought I could detect a bit of Phryne Fisher there too.
I also enjoyed the quirky humour – who would call their cat Chairman Meow? – but underneath it all there is some serious, realistic characterisation and some careful plotting. There are a couple of other humour lines such as the guerilla knitting group that I thought were a bit superfluous but I guess they show another dimension of Scout's character.
International readers can find it here on Amazon US for Kindle or audio.
The second novel to feature Byron Bay based investigative journalist Scout Davis sees the heroine on the trail of a man thought to have died 30 years previously. She is first contacted by Hermione Longfellow who claims that a man whose photograph appeared in that week's newspaper was the same Mick O'Leary who had married her sister Nemony in 1983 and was thought to have drowned a few months later while sailing in Sydney Harbour during a freak storm. According to Hermione her sister has been in a deep depression since her husband's death and she wants Scout to prove that far from being a grieving widow Nemony should be angry about O'Leary's faked death and potential disappearance with the bulk of her inheritance.
The investigative thread of this book speeds along nicely and is full of suspense, especially the final quarter which sees Scout and her friend Daisy on the trail of their prey in Queensland's gorgeous Whitsunday Islands. In what is something of a rarity for crime fiction without a murder in sight Groff doese a nice job of making the reader care about the Longfellow sisters and the impact of Mick O'Leary's sudden appearance then disappearance in their lives and it's not hard to share the characters' desire to see the bad guy get his comeuppance. The fact that the entire book takes place against a backdrop of some fantastically depicted locations, especially Byron Bay is a bonus.
An equal amount of this novel's space is taken up with Scout's non-investigative activities which includes a secret life as a yarn bomber, a complicated love-life and a sister, four nephews and a brother-in-law who are in a bit of a pickle. Personally I found this all a bit too chick lit-y for my tastes, especially as every time she appeared we got a detailed description of Scout's outfits (fashion and I are complete strangers), but I am positive a lot of readers are looking for exactly this kind of combination. Scout's well-rounded home life offers most of the book's funnier moments and her family, including her faithful feline companion Chairman Meow, and friends are nicely drawn characters.
I do think the book is too long at 360+ pages for what is not a terribly complicated story but the publishing world seems to have universally agreed that bigger is better some time during the last decade and at some point I'm just going to have to accept that I'm the lone voice who still believes that less is more. Overall this is a very readable, very Australian, lighter style crime novel that I'm sure will have a broad appeal.


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A Description from 1872
Scottish Episcopal Church
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You are here: Home / Info / Accessibility
St Mary's is a Victorian building which was built with no regard for what we would now regard as basic accessibility requirements. However, a number of steps have been taken in order to make the building more accessible. The vocation of the congregation is to be a cathedral which is open, inclusive and welcoming.
The nave of the church has relatively easy wheelchair access. There are no steps into the church though the main door has a small lip of about an inch. Stewards are on duty at all Sunday services, Choral Masses and at diocesan services near the door to help open doors for those arriving and leaving the building. Help can be requested with managing these doors for midweek services by contacting the Cathedral Office in advance. Access is through the glass door on the left of the porch. The two wooden doors of the porch can also be opened for slightly wider access and are usually used for funerals and weddings.
Most of the seating is in pews which are on a raised, fixed base. Wheelchair users have several choices as to which part of the church to be in for services. There is a lot of space at the back of the church and there are two spaces at the front of the church which allow a non-wheelchair user and a wheelchair user to sit side by side.
Some midweek services and the 8.30 Sunday Services take place in the chancel. Most of the seating here is in the old choir stalls and the canon's stalls. Wheel chair access is by means of a removable ramp which stewards and clergy are happy to help with. The ramp is located behind the piano when not in use.
The ramp also can be used to give access to the platform at the crossing on which which the nave altar sits, thus ensuring that this altar is accessible to a celebrant in a wheel chair.
The Synod Hall and Church are on different levels. These are connected with an electrically operated wheelchair lift. The Synod Hall can also be accessed down a slope from the outside of the church through the door furthest from the main gate on Great Western Road.
There are four toilets available on the same level as the Synod Hall, down 4 four steps from the church level. Two of these are designated for men and two for women. There is one toilet on the same level as the church which is gender neutral and more accessible for wheelchair users. This is located in a corridor which can be found through the door of the oratory to the left at the front of the church on the same side as the pulpit. There is a ramp of a couple of inches at this door.
A sound amplification system is in use at the Sunday Services and weekday masses. A loop system is available in the pews in the nave of the church.
Most services use service sheets which are available in A5 and larger-print A4 versions. Liturgies can usually be emailed to members of the congregation in advance by the office manager by prior arrangement. This may be useful for people wishing to print the service out in giant print or in Braille.
The language used in the liturgy at the 11 am service on a Thursday and the 8.30 am and 6.30 pm services on a Sunday is the traditional form from the Scottish Prayer Book 1929. Modern language is used at all other services. A distinctive feature of the worship at St Mary's is an attempt to ensure that as much of the language of the hymnody as possible uses language which is inclusive of both men and women for human beings. The language used to refer to God is deliberately as rich and varied as that within the biblical tradition.
The service sheets at St Mary's carry more information than those in many churches and the congregation is invited to take them away each week both to use the prayers in their devotions and also to read the notices which are printed therein.
An audio relay of the services is carried in the Synod Hall and in the Meeting Room (close to the Synod Hall toilets).
BabySpace!
Members of the congregation with young children seeking sanctuary during quiet parts if the service are welcome to use the Meeting Room which is located on the Synod Hall level next to the Toilets. This room has an audio relay of the services from the church.
Members of the congregation who are breastfeeding infants are welcome to do so anywhere on the premises.
Baby changing facilities are available in the accessible toilet on Church Level in the corridor. (From the church go through the door on the side of the church near the front on the pulpit side.
This website uses WordPress and a recent version of the Genesis framework. This has been deliberately chosen to aid web accessibility. The Genesis Accessibility plugin is used on the site in order to try to make the site easier to navigate using screen-readers.
Audio and Loop System
There is an audio Loop System fitted in the church but there is no loop currently fitted in the Synod Hall.
Car Parking is difficult to regulate in the West End of Glasgow which makes it difficult to guarantee that parking right next to the Cathedral will ever be available for anyone. Car parking for Sunday services is restricted to members of staff and Blue Badge holders. Lots of street parking is available in the streets around the cathedral. Drivers should be careful to check the parking regulations which are different for different streets.
Making St Mary's More Inclusive
Comments about making St Mary's more inclusive are always welcome and can be made to the Provost or the Vestry Secretary via the Cathedral Office.
Next Sunday at St Mary's
Epiphany 2
0830 Holy Communion (1970)
1030 Sung Eucharist (1982)
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Upcoming midweek services
Episcopal Synod Eucharist
There will be a Eucharist for the Episcopal Synod on 18 January 2020 at 12 noon.
Regular Midweek Services
Morning Prayer is said at 9.30 am every day in the oratory. (On some feast days this is replaced by a communion service in the chancel).
11 am every Thursday
There is a Eucharist at 11 am every Thursday morning in the chancel followed by refreshments in the synod hall.
Hear a recent sermon
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The Cathedral Church of Saint Mary the Virgin, Glasgow (St Mary's Episcopal Cathedral)
is a charity registered with OSCR, number SC006225.


UMC accepts all patients needing health care services. To assist you in paying for the health services provided by the team at UMC, the hospital accepts payment from Medicare, Medicaid, Medicaid commercial and many other health insurance plans. Typically, these insurers require the patient to pay part of the hospital bill, including co-pays and deductibles, or a deposit at time of service.
Residents of Louisiana may be eligible for Financial Assistance. Patients are encouraged to visit the Financial Counseling area in the first lobby of the Hospital for screening. You will be required to complete an application to be screened prior to your participation. Please contact Financial Counseling at 504.702.3500 and leave a detailed message. For those who are without coverage for all or a significant part of their bill, payment arrangements may be requested by calling 504.702.2081. Click here to learn more about Financial Assistance at UMC.
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Will The Killing Return For a Season 5 on AMC // Renewed or Canceled?
When Will The Killing Season 5 Release Date? Will The Killing return for a Season 5 on AMC? Whether The Killing is renewed for another season or canceled? Get acquainted with the latest reliable news regarding the upcoming season of The Killing on AMC. Track the The Killing renewal/cancelation status.
The Killing kicked off on April 3, 2011 on AMC. The Killing is a 60-minute scripted drama/crime/thriller television series, which is currently in its 4th season. The Killing airs by Fridays at 00:00 on AMC.
Unfortunately, AMC decided not to pick up The Killing for a 5th season. The Killing thereby is canceled and will not return for another round on AMC. If the show's status is changed somehow and AMC opted to revive The Killing for another round, we will update this page. So guys, we're regreat to report the bad news. Stay tuned for updates. We'll inform you if something has changed.
The Killing Season 4 Release Date: August 1, 2014
Previous Show: Will 'Halt and Catch Fire' Return For A Season 5 on AMC?
Next Show: Will 'Hell on Wheels' Return For A Season 6 on AMC?
Show Genres: Drama, Crime, Thriller


Once I realised that PMS is a real thing that happens to many women monthly, it helped me to feel less weirded out by it. I don't know the symptoms you experience, or what helps you with yours, but I wanted to share how I navigate mine.
My breasts started aching yesterday, and I immediately sped up on work ahead of the week. Once a month, my breasts get heavy and painful, so painful that even hugging someone hurts. I used to think it was weird that till I found out that many women actually experience this. And it's just one of the symptoms of PMS. I imagine that before calendars and period apps were a thing, this probably helped many women to 'tell time'.
Pre-Menstrual Syndrome (PMS) describes the symptoms one may have in the days leading to one's menstrual period. Another annoying PMS symptom I experience is moodiness that leads to crying. At some point in the next few days, I'll catch myself crying hard over something that's inconsequential but, at that moment, seems like a huge deal. Last month, it was because people were late for a meeting we'd set. Ladies, I tire!
So, my PMS starts with the breast ache, then graduates to the other symptoms, including fatigue that I cannot explain. One time, I slept for most of two days in a row. But PMS is different for everyone. I don't know how it is for you, or what helps you with yours, but I wanted to share how I navigate mine.
I try to do as much work ahead of time as possible, so that my schedule is as light as possible in the PMS week. It helps that I run my own business, so I can move things around as necessary. Some months though, I can't do that because clients have surprise needs. But, I've found that, the less I have to do in that window, the better for me. So, even if you can't do this, try to eliminate stress factors.
Even if you cannot sleep for most of two days in a row like I did, try to make the best of your nights. Get at least 7 hours of good sleep—this should be standard throughout the month, really—so that you can feel refreshed during the day and get an easier handle on whatever PMS symptoms you have.
I had to add 'right' because my body craves a lot of food in the PMS window, and when I don't watch what I eat, period bloat follows. Jeez, that's two weeks of my body not being mine, if I'm not careful (and I'm not even counting random ovulation pain). I've cut out sugar, caffeine, and alcohol from my overall diet, and I feel better for it. I'm still trying to get to the eating more veggies part.
Don't make that decision on your own, even when it's just supplements. I know some people have really terrible PMS symptoms—like migraines or throwing up often—so if you're one, see your doctor for medical advice, and use meds to help if need be.
I keep telling myself this, but it's a lie. Every month, I'm still caught unawares by something—it's usually the random tears in sometimes embarrassing places. Have you ever cried because the restaurant got your food order wrong? No? Ok. Maybe this should have said, "Don't feel alone" because you're not. Once I realised that PMS is a real thing that happens to many women monthly, it helped me to be less weirded out by it.
So, what's your PMS like, and how do you PMS in Peace, if there's such a thing?


This is cool. I wanted to contribute to GNOME documentation a few years ago and it was just really hard to find a way to jump in. Something like GitLab, with a workflow that's more familiar to some people, could really open doors.
My book has a chapter on Git and the host I chose to demonstrate it with is GitLab! GitLab is underrated.


Today a young married woman, excited about being pregnant, can present to her doctor for her first prenatal appointment and be asked about whether she 'wants' the pregnancy as a matter of routine.
Interesting article, I think it shows how abortion defines western civilisation.
Tour attitude can be summarised in the one sentence where you write "making every woman 'choose' ".
Your kind has been forcing women to do what you want for too many years. Now they are freely choosing to do what 'they' want and not what 'you' want, you are crying foul.
Get over it, you lost. Women can chose to have a baby, or not. You are simply "anti-choice". Now go away.
"When the nature of abortion coercion has become so insidious"? No evidence of any coercion in this article, just a couple of anecdotes and a whole lot of unsubstantiated allegations. Author might like to look up the definition of 'coercion' - providing information or even a recommendation isn't included. Asking someone if their pregnancy is wanted merely provides an opening for the woman to discuss her situation if she wishes and explore her options.
What a strange article. It is almost as if the author believes that doctors are forcing women to have abortions when they don't want to. Perhaps this is just the author projecting their own views of wanting to force women to maintain the pregnancy when they don't want to.
It is also odd that someone who wants to take choice away from women keeps banging on about choice.
And then there are the unsubstantiated assertions: "Doctors behave as though abortion is the default response to every pregnancy" Uh evidence needed Debbie.
Thanks Stezza and Candide for reading the article, however your comments typify the kind of ideology that fails to hear the real experiences of women.
Stezza, not all women experience 'choice' when it comes to freely choosing to have children, just as they don't all experience 'choice when it comes to abortion. When a woman is told she will not be supported if she continues a pregnancy, and sees abortion as her only option, that is not choice. If abortion advocates such as yourself are going to ever demonstrate concern for all women, you need to stop dismissing the stories of women whose experiences have resulted in grief and trauma. They have a right to be heard.
Candide, the fact that you see no coercion in the examples in the article is the very reason why we need to keep presenting them. When a woman is told she cannot continue her education unless she an abortion, what would you call that? When a parent withdraws support for their daughter unless they have an abortion, what do you call that? The 'anecdotes' are real women's stories.. only 3 of hundreds.
"When a woman is told she will not be supported if she continues a pregnancy, and sees abortion as her only option, that is not choice"
Yes it is. She clearly has a choice to continue the pregnancy without the support of whatever person demands otherwise, or, to not continue the pregnancy. There are consequences for either choice, but a choice none the less.
Seeing that you are actually responding to comments (I respect that). Could you please answer the following simple question.
Do you support the right for women to chose to have an abortion in any circumstance?


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Muscle hypertrophy in the mdx mouse model of Duchenne muscular dystrophy (DMD) can partially compensate for the loss of dystrophin by maintaining peak force production. Histopathology examination of the hypertrophic muscles suggests the hypertrophy primarily results from the addition of myofibers, and is accompanied by motor axon branching. However, it is unclear whether an increased number of innervated myofibers (myofiber hyperplasia) contribute to muscle hypertrophy in the mdx mice.
To better understand the cellular mechanisms of muscle hypertrophy in mdx mice, we directly compared the temporal progression of the dystrophic pathology in the extensor digitorum longus (EDL) muscle to myofiber number, myofiber branching, and innervation, from 3 to 20 weeks of age.
We found that a 28% increase in the number of fibers in transverse sections of muscle correlated with a 31% increase in myofiber branching. Notably, the largest increases in myofiber number and myofiber branching occurred after 12 weeks of age when the proportion of myofibers with central nuclei had stabilized and the mdx mouse had reached maturity. The dystrophic pathology coincided with profound changes to innervation of the muscles that included temporary denervation of necrotic fibers, fragmentation of synapses, and ultra-terminal axon sprouting. However, there was little evidence of synapse formation in the mdx mice from 3 to 20 weeks of age. Only 4.4% of neuromuscular junctions extended ultra-terminal synapses, which failed to mature, and the total number of neuromuscular junctions remained constant.
Muscle hypertrophy in mdx mice results from myofiber branching rather than myofiber hyperplasia.
Duchenne muscular dystrophy (DMD) is the most common dystrophy affecting approximately 1:4,000 boys, and is caused by mutations in the dystrophin gene [1, 2]. A characteristic feature of DMD patients is the transitory hypertrophy of certain muscle groups, such as the gastrocnemius muscle. Direct correlations between computer tomography and histology of muscle biopsies demonstrate that an increase in myofiber number contributes to a transitory period of true hypertrophy in some DMD patients [3–5]. Ultimately, the failure of the muscle stem cells to continually regenerate the necrotic fibers leads, in part, to the replacement of muscle with adipose and connective tissue [6–9]. Muscle hypertrophy is found in most muscles in the mdx mouse model of DMD between 10 and 40 weeks of age and functionally compensates, in part, for the lack of dystrophin [5, 10–13]. While the area of individual myofibers in mdx mice is highly variable, the average area is unchanged when compared to wild-type myofibers . Similar to the DMD patients, estimations of myofiber number in transverse sections of mdx muscles are increased when compared to wild-type myofibers . The endogenous mechanisms for increasing the number of myofibers is of considerable interest for muscle replacement strategies to treat muscular dystrophy and sarcopenia. However, it is unclear whether the additional muscle results from myofiber branching and/or from the formation of new, innervated myofibers (myofiber hyperplasia).
Several considerations suggest that the increase in myofiber number in mdx mice could result from myofiber hyperplasia. Satellite cells associated with myofibers can begin proliferating and differentiate into new myotubes in culture . Furthermore, proliferative expansion of an activated satellite cell in vivo can contribute to the regeneration of clusters of adjacent fibers [16–18]. Muscle necrosis in mdx mice can initiate the expression of growth-associated protein 43 (GAP43), a marker of axonal branching, in motor neurons . While satellite cells are evenly distributed along a myofiber, a satellite cell resides in close proximity to the neuromuscular junction . Innervation of regenerating fibers may be beneficial as direct stimulation of muscle can improve the engraftment of satellite cells . Finally, myofibers can generate force through myomuscular junctions without having to extend from tendon to tendon . Here, we directly compared the temporal progression of dystrophic pathology in mdx 4cv mice to innervation, myofiber number, and myofiber branching. Our results demonstrate that the increase in myofiber number in transverse sections of mdx EDL muscles results from myofiber branching rather than myofiber hyperplasia.
We generated the mdx 4cv : Thy1-CFP mice by breeding mdx 4cv C57Bl/6 females with C57Bl/6 mice homozygous for the Thy1-CFP transgene . We utilized the male offspring, which were all mdx 4cv and expressed the CFP transgene under the control of the Thy1 promoter. For myofiber branching experiments we utilized mdx 4cv mice expressing the DsRed transgene in every cell. Mice were genotyped as previously described . All experiments were performed in accordance with the guidelines approved by the Institutional Animal Care and Use Committee of the University of Washington.
Wholemount immunostaining was performed as previously described . Briefly, the mdx 4cv : Thy1-CFP mice were examined at 3 weeks (n = 4), 4 weeks (n = 4), 12 weeks (n = 6), and 20 weeks of age (n = 4). The mice were anesthetized with 2,2,2-tribromoethanol and perfused with 2% paraformaldehyde (PFA) in 1× phosphate buffered saline (PBS) by cardiac infusion. Cervical dislocation of the mouse was immediately followed by dissection of the lower limb such that the extensor digitorum longus (EDL) was the only muscle still attached to the bone and was incubated for 2 hours in 2% PFA at 4°C. The EDL muscles were excised from the bone and the distal tendons were isolated. The fascicular outlines of four muscle groups can be followed from tendon to tendon . We stripped each of the four muscle groups that comprise the EDL using the distal tendons and retained the third group that normally inserts on the distal phalanx of the third digit of the foot. The third compartment of the EDL was incubated in 0.1 M glycine (in 1× PBS) for 1 hour and in blocking solution (1% BSA, 0.05% triton X-100, 1× PBS) overnight at 4°C. The muscles were then incubated in α-bungaratoxin conjugated to tetramethylrhodamine (TRITC; 1:800; Life Technologies) and GAP43 conjugated to DyLight 650 (1:800; Novus Biologicals) at room temperature on a rotating platform for 1 hour. For analyses of immune cells the muscles were incubated in Alexa-647 conjugated CD4, FITC-conjugated interferon-γ, Alexa488-conjugated CD8a, or FITC conjugated Mac-1 (1:50; BD Pharmingen). The muscles were then washed 3 × 10 min in 1× PBS and loaded onto superfrost+ slides with ProLong Gold antifade mounting medium containing 4′,6-diamidino-2-phenylindole (DAPI; Life Technologies). A composite image of the entire third muscle compartment was visualized and imaged using a Leica SP5 confocal microscope.
We quantitated the total number of synapses in the wholemount images using the count tool in Adobe Photoshop. Ultra-terminal branches were defined as motor axons that extended from the synapse. Those that terminated on an AChR cluster were labeled synaptic and those that did not terminate on an AChR cluster were labeled non-synaptic. The proportion of ultra-terminal synapses was calculated by dividing the total number of ultra-terminal synapses by the total number of neuromuscular junctions.
Once the innervation of the third compartment of the EDL had been imaged the slide was incubated overnight in 2% paraformaldehyde in 1× PBS on a rotating table at room temperature to allow the coverslip to release from the slide without affecting the integrity of the muscle. The muscle was then placed in 20% sucrose for 2 hours at 4°C and frozen in OCT in 2-methylbutane in liquid N2. Adjacent 10 μm sections were stained with hematoxilyn and eosin or wheat germ agglutinin (WGA) conjugated to fluorescein isothyocyanate (FITC; 1:100; Vector Laboratories). The sections stained with WGA were washed 3× 10 minutes in 1× PBS, mounted with ProLong Gold antifade mounting medium (Life Technologies). The sections were imaged using a Nikon Eclipse E1000 fluorescent microscope. The total number of myofibers in the third compartment of the EDL was quantitated using the slides stained with WGA using the count tool in Adobe photoshop. The myofiber areas were measured using the FIJI computer software (NIH). We measured the areas of 167 myofibers from n = 4 wild-type mice and 265 myofibers from n = 4 mdx mice.
The entire EDL muscles from mdx 4cv : DsRed mice aged 3 weeks, 4 weeks, 12 weeks, and 20 weeks were immediately digested in 6,000 Units of collagenase II (Worthington; NJ) for 60 minutes at 37°C with gentle agitation every 15 minutes. The collagenase II solution was exchanged with 1× PBS containing Alexa488-conjugated αBTX (1:800; Life Technologies) and incubated on a rotating table for 1 hour at room temperature. The muscles were washed three times in 1× PBS. The DsRed was expressed in every fiber, but quickly disappeared upon necrosis. The healthy DsRed fluorescing fibers were then carefully teased on a superfrost+ slide in ProLong Gold mounting medium containing DAPI. The fibers were quantitated and imaged using a Leica SP5 confocal microscope to gain sufficient resolution in the Z-direction as well as the X/Y planes. We quantitated 289 fibers at 3 weeks of age (n = 5), 256 fibers at 4 weeks (n = 3), 365 fibers at 12 weeks (n = 6), and 327 fibers at 20 weeks (n = 4). A myofiber with multiple branches was quantitated as a single branched myofiber. We also compared the myofiber diameters of unbranched (61 myofibers) and the combined diameters of branched myofibers (42 myofibers) in teased muscle preparations from n = 4, 5-month-old mdx 4cv : DsRed EDL using FIJI.
Comparisons of muscle mass and myofiber areas were compared using a Students t-test. Myofiber number, ultra-terminal axon branches, and myofiber branching were analyzed using a one-way ANOVA with a Tukey post-test. Direct comparisons of synapse number with myofiber number were made using a two-way ANOVA with a Tukey post-test. All data analyses were performed using the PRISM software.
To better understand the cellular mechanisms of muscle hypertrophy in mdx mice we directly compared the number of myofibers to the number of neuromuscular junctions. To visualize innervation of skeletal muscles we generated mdx 4cv : Thy1-CFP mice that express CFP in the motoneurons. We chose to examine the extensor digitorum longus (EDL) muscle as the anatomy of the EDL is well described . The EDL has a single proximal tendon that attaches the lateral epicondyle of the distal femur to the distal phalanx of the foot through four distal tendons. The four muscle fascicles extend from tendon to tendon and can be easily and consistently separated. We chose the third muscle group because it is flat, small, and amenable to future muscle stem cell treatments.
Transverse sections of the third compartment of the wild-type: Thy1-CFP EDL revealed that less than 1% of the myofibers had centrally located nuclei, a marker of skeletal muscle regeneration (Figure 1A). Centrally located nuclei in the mdx 4cv : Thy1-CFP EDL were evident by 4 weeks of age (6% of muscles), while their numbers had peaked by 12 weeks (68%; P <0.001), and had stabilized until at least 20 weeks of age (68%; Figure 1). Thus, we chose 3 weeks (onset of necrosis), 4 weeks (evidence of regeneration), 12 weeks (peak of central nucleation), and 20 weeks (stabilization of dystrophic pathology) for the time points for this study. The third compartment of the EDL mass was increased by 82% in mdx compared to wild-type at 20 weeks of age (Figure 1C). While the myofiber areas were highly variable in the mdx mice at 20 weeks of age, the average areas remained unchanged (P = 0.71). Thus, the dystrophic pathology in the third compartment of the EDL led to significant hypertrophy in mdx mice, which did not result from changes in the average myofiber area.
Progression of dystrophic histopathology in the third compartment of the extensor digitorum longus (EDL) muscle. (A) Hematoxylin and eosin stained frozen sections from 3-month-old wild-type and mdx 4cv muscle. Note the central nuclei in the mdx 4cv myofibers. Scale bar = 50 μm. (B) Proportion of central nuclei (+/- S.D.) in the third EDL compartment from 3 weeks to 20 weeks of age (n = 4-6). Note the apparent stabilization of dystrophic histopathology from 12 to 20 weeks of age. ***P <0.001 at 12 weeks compared to 4 weeks of age. At some time points, the standard deviation is too small to see. (C) The mass of the third compartment of the EDL at 20 weeks of age. P <0.001 compared to wild-type. (D) Box-whiskers plot of median +/- 75% of myofiber areas in wild-type and mdx mice at 20 weeks of age.
High-resolution confocal images of wholemount preparations of the third compartment of the EDL revealed that the motor nerve trunk traverses the skeletal myofibers to innervate the postsynaptic acetylcholine receptor (AChR) clusters (Figure 2A). The transgenic expression of CFP does not influence the innervation patterns in mice . The innervation patterns were qualitatively normal when comparing wild-type and mdx 4cv : Thy1-CFP muscles at 4 weeks of age (Figure 2A). At 3 to 4 weeks of age we noticed a large number of small extrasynaptic AChR clusters within the mdx 4cv : Thy1-CFP muscles (Figure 2A). Detailed analyses of the wholemount preparations revealed that mononuclear inflammatory cells including activated CD4 positive T-helper cells expressing interferon-γ (Additional file 1: Figure S1A), CD8 positive cytotoxic T-lymphocytes (Additional file 1: Figure S1B), or macrophages (Additional file 1: Figure S1C) could express AChR, as previously described . We found no direct association between the immune cells and the neuromuscular junctions.
Innervation in the third EDL compartment. (A) The transgenic cyan fluorescence protein expression in neurons is pseudo-colored in green to demonstrate the innervation patterns in wild-type and mdx 4cv muscles at 4 weeks of age. Note the profound infiltration of small acetylcholine receptor (AChR) patches in synaptic and non-synaptic regions within the mdx 4cv muscles. Scale bar = 100 μm. (B) Shown are examples of ultra-terminal synapses (arrows) in 4-week-old muscle. Note that the ultra-terminal synapses are immature plaques. (C) Graph shows the mean +/- S.D. total number of ultra-terminal synapses demonstrating a modest reduction with age (P = 0.056; n = 4-6). (D) Shown is an example of denervation (arrow head) and non-synaptic ultra-terminal branching (arrow) in 20-week-old muscle. (E) The mean +/- S.D. total number of non-synaptic ultra-terminal branches increased with age (n = 4-6). **P <0.01 compared to 4 weeks of age. Scale bar for B and D = 30 μm.
The generation of new, innervated fibers requires synapse formation in the postnatal mice. Therefore, we performed a detailed examination of the wholemount preparations for evidence of synapse formation in mdx 4cv : Thy1-CFP EDL muscles. Neuromuscular junctions form as a plaque, and mature into a donut shape, and ultimately to a pretzel-like profile . The presynaptic motor nerve terminal directly apposed the postsynaptic AChRs in wild-type muscles (Figure 2A) . While the formation and maturation of the primary postsynaptic apparatus of the neuromuscular junction was normal in mdx mice (Figure 2A) , we found that motor axons could extend beyond the synapse (ultra-terminal axon sprouting) (Figure 2B-E). On average, only 4.4% of the ultra-terminal axon sprouts innervated immature secondary synaptic plaques (Figure 2B). The number of ultra-terminal synapses reduced from approximately 16 per muscle (5.1%) at 3 weeks of age to approximately 12 per muscle (3.9%) at 20 weeks of age in mdx mice (P = 0.056; one-way ANOVA; Figure 2C). Furthermore, we found no evidence for the maturation of the ultra-terminal synaptic plaques to a donut or pretzel profile in any of the muscles examined. Most ultra-terminal axon sprouts in mdx 4cv : Thy1-CFP muscles did not terminate on to AChR clusters (Figure 2D, E). Non-synaptic ultra-terminal axon sprouts significantly increased with age, with approximately one per muscle at 3 weeks of age up to approximately 47 per muscle at 20 weeks of age (Figure 2D, E; P <0.01; one-way ANOVA). Thus, ultra-terminal synapse formation was evident in the mdx EDL muscles, but they were few in number, decreased with age, and failed to mature.
GAP43 is expressed in newly growing motor axons, terminal Schwann cells, immune cells, and parasympathetic nerves in blood vessels . To determine if skeletal muscle necrosis in mdx 4cv : Thy1-CFP EDL muscles could initiate motor axon branching and synaptogenesis we examined the synapses at 3 and 4 weeks of age in wholemount preparations. It is well established that synapses transition from the normal pretzel profile to the fragmented grape appearance upon muscle necrosis in mdx mice [30, 31], but what happens in between to both the pre- and postsynaptic apparatus is unclear. Here, we found that the onset of skeletal muscle necrosis, as determined by Alexa488-IgG positive fibers, led normal pretzel profiled synapses (for example, Figure 3, synapse 1) to express GAP43 in the presynaptic nerve terminals (for example, Figure 3, synapse 2, 3, and 4). The early stage of necrosis, as determined by the localization of IgG on the surface of the muscle without overt cellular infiltrates, was accompanied by the retraction of the presynaptic nerve terminal from the postsynaptic apparatus (for example, Figure 3, synapse 3). The GAP43 in synapse 3 is expressed in the terminal Schwann cell, as previously described . Infiltration of mononuclear cells into the necrotic myofibers led to the loss of the postsynaptic AChR clusters and the presynaptic nerve terminal (for example, Figure 3, synapse 4). Another example of the loss of innervation can be found in Figure 2D (arrow head). The regenerating fibers, as determined by the central nucleation without surface localized IgG, were reinnervated with a fragmented grape-profiled pre- and postsynaptic apparatus (for example, Figure 3, synapse 5). Thus, skeletal muscle necrosis in mdx 4cv : Thy1-CFP EDL muscles initiated a temporary denervation of the myofibers rather than directly evoking motor axon branching from the nerve terminals.
Skeletal muscle necrosis initiates temporary denervation. The CFP is pseudo-colored in yellow to allow the visualization of multiple fluorophores. Necrotic IgG positive fibers are shown in green. Note we numbered the synapses in the second panel. Synapse 1: Normal synapse in a non-necrotic fiber (no IgG). Synapse 2: Expression of GAP43 in a pre-necrotic fiber (IgG is next to the fiber). Synapse 3: Onset of necrosis (green fiber without overt cellular infiltrate) leads to the activation of the Schwann cell expressing GAP43 that retracts the presynaptic nerve terminal from the postsynaptic acetylcholine receptors. Synapse 4: Infiltration of cells into the necrotic fibers led to complete retraction of the nerve and loss of the AChR clusters. Synapse 5: Re-innervation of a fragmented postsynaptic synapse in a post-necrotic fiber (note the central nuclei and absence of IgG (green)). Scale bar = 30 μm.
The number of myofibers and the number of neuromuscular junctions in the wild-type EDL remains constant in maturing wild-type mice  (Additional file 2: Figure S2). Despite the profound changes in motor axon plasticity in the mdx 4cv : Thy1-CFP EDL muscles, we found no significant change in the total number of neuromuscular synapses from 3 weeks to 20 weeks of age (Figure 4; P = 0.65 one-way ANOVA). To directly compare the number of synapses to the number of myofibers we reprocessed the same EDL muscle compartment for histological sections and stained the sections with wheat germ agglutinin conjugated to fluorescein isothyocyanate (FITC). We examined sections through the mid-belly of the EDL to coincide with the placement of the synapses. Quantitation of the total number of mdx 4cv : Thy1-CFP myofibers revealed a 28% increase from 3 weeks to 20 weeks of age (Figure 4; P <0.001; one-way ANOVA). Interestingly, the total number of fibers increased by 19% from 12 weeks to 20 weeks of age when the dystrophic histopathology had seemingly stabilized (Figure 1). Thus, an increase in myofiber number in hypertrophic mdx muscles was not accompanied by a change in the total number of neuromuscular junctions.
Direct comparison of myofiber number with synapse number in the third EDL compartment. Note that myofiber number in transverse sections increases with age while the synapse number remains unchanged (n = 4-6). *P <0.05 and ***P <0.001 fiber number compared to synapse number.
We next examined whether the increase in myofiber number in transverse sections of the third compartment of the mdx 4cv : Thy1-CFP EDL muscles correlated with an increase in myofiber branching. Here, we digested the entire mdx 4cv : Thy1-CFP EDL muscles with collagenase II and quantitated the proportion of branched fibers (Figure 5). To easily count the muscles we utilized the mdx 4cv : Thy1-CFP expressing DsRed. We found three types of myofiber branching including branching from the middle of the myofiber (53% of myofibers with branches; Figure 5A), branches that re-entered the original myofiber (13% of myofibers with branches; Figure 5B), and myofiber branching at the ends of the myofiber (13% of myofibers with branches; Figure 5C). Of the myofibers with branches, 21% had multiple branch points (Figure 5D), with various combinations of the above. We found that the proportion of branched red myofibers increased from 2% at 3 weeks of age to 33% at 20 weeks of age (31% increase; P <0.001; one-way ANOVA), which was consistent with the 28% increase in the number of fibers in transverse sections. Interestingly, the proportion of branched fibers increased by 21% between 12 weeks and 20 weeks of age (Figure 5E), when the dystrophic histopathology had stabilized (Figure 1). The combined average diameter of a branched myofiber was increased by 76% when compared to the unbranched mdx myofibers at 5 months of age demonstrating that myofiber branching led to myofiber hypertrophy (Figure 5F; P <0.001). While we found that 1.4% of the unbranched fibers had multiple synapses (Additional file 3: Figure S3), all of the branched fibers were singularly innervated at all ages examined (Figure 5), as previously described . Thus, the temporal increase in myofiber number in transverse sections of mdx 4cv : Thy1-CFP muscles directly correlated with the increased number of branched myofibers.
Myofiber branching in the EDL. (A) A singularly innervated branched myofiber expressing DsRed, DAPI in blue and AChR cluster in green. Scale bar = 50 μm. (B) Branches can also rejoin the initial fiber and/or (C) branch at the ends of myofibers. Percentages in the images in A-C show the proportion of myofibers with the respective branching phenotype. (D) Shown is an example of a myofiber with multiple branch points. Approximately 21% of myofibers with branches had multiple branch points. (E) Mean +/- S.D. of fiber branching increases with age. **P <0.01 compared to 4 weeks and ***P <0.001 compared to 12 weeks (n = 4-6). (F) Median +/- 75% diameter of unbranched mdx EDL myofibers compared to the combined diameter of branched myofibers at 5 months of age. ***P <0.001.
The transitory muscle hypertrophy in mdx mice can lead to a partial functional compensation for the lack of dystrophin [5, 10–13]. For example, larger muscles in mdx mice generate greater force than in wild-type mice, but they do not develop greater levels of specific force and they continue to display cycles of necrosis and regeneration . Muscle necrosis leads to a potent regenerative response in mdx mice that leads to the functional hypertrophy [6–9]. To better understand the cellular mechanisms for muscle hypertrophy in mdx mice we directly compared the temporal progression of dystrophic pathology in the third compartment of the EDL in mdx 4cv : Thy1-CFP mice to myofiber number, innervation, and myofiber branching. Similar to previous studies we found an increase in the number of myofibers in transverse sections . Despite profound changes to the innervation of mdx muscles, there was no change in the total number of neuromuscular junctions. Rather, the increase in myofiber number quantitated in transverse sections correlated with an increase in myofiber branching. Thus, our data suggest that myofiber branching rather than the formation of new, innervated myofibers (myofiber hyperplasia) contributes to the muscle hypertrophy in mdx mice.
Fiber branches can form through the generation of a new myofiber segment physically connected to a pre-existing myofiber or by splitting a fiber into two. Consistent with the former possibility, we found that all branched fibers in the mdx mice had central nuclei in at least one of the branches (Figure 5). Furthermore, fiber branches in mdx mice express developmental myosin . Activated satellite cells could potentially generate the fiber branches by fusing into nascent or pre-existing myofibers in a non-linear pattern . Satellite cells are also required for the increase in number of fibers that is associated with experimental induction of muscle hypertrophy by mechanical overload . Our results confirm previous reports that the most severe dystrophic histopathology occurs during maturation of the mouse from 3 to 12 weeks of age [12, 36–38]. Interestingly, the greatest changes in myofiber number and myofiber branching occurred between 12 and 20 weeks of age when cycles of necrosis and regeneration had reached a steady state level. The stabilization of dystrophic histopathology during this later period requires the activation of satellite cells to support myofiber regeneration . Therefore, it is likely that the potent regenerative response in mdx muscles leads to hypertrophy through the generation of myofiber branches rather than forming entirely new innervated myofibers.
While skeletal muscle necrosis can lead to overt changes in GAP43 expression in mdx muscles , it was unclear whether this represented overt changes to innervation of the skeletal muscles because GAP43 can label multiple cell types. Our detailed examination of wholemount preparations demonstrated profound changes to the innervation of mdx 4cv : Thy1-CFP muscles. We found that GAP43 was expressed in the motor nerves and terminal Schwann cells during the temporary denervation of the necrotic fibers. The terminal Schwann cell normally envelops the motor nerve terminal when synapses are eliminated during early postnatal development . A similar process in mdx mice could potentially function to protect the nerve terminal from the profound inflammatory response within the muscle . Skeletal muscle necrosis did not directly elicit ultra-terminal axon sprouting, which was prevalent at all ages examined. Only a small portion of these axonal extensions formed ultra-terminal synaptic plaques, which never developed into the donut or pretzel profiles of maturing synapses. The non-synaptic ultra-terminal axon sprouting was most prevalent between 12 and 20 weeks of age similar to the time course of myofiber branching. The excitation-contraction coupling is disturbed in branched myofibers , and this could potentially impair synaptic transmission leading to the presynaptic axonal extensions. We found that branched myofibers were singularly innervated, as previously described , demonstrating that multiple innervation did not influence the stability of the presynaptic terminals. We found no evidence of fiber branching between multiple fibers in the EDL like previously shown for the soleus muscle . It would be interesting to examine whether a multi-syncytial reticulum could influence innervation of the mdx myofibers, as myofibers are normally singularly innervated. It is also unlikely that the ultra-terminal sprouting results from the absence of dystrophin within the central nervous system (CNS). Full-length dystrophin stabilizes GABAergic receptor clusters in the CNS . However, impaired inhibitory innervation in adult mice would predictably increase motor nerve excitation and restriction of the motor axon branches . Furthermore, the mdx 4cv mouse strain retains the truncated Dp116 dystrophin isoform in Schwann cells such that axon conductance is unlikely to be changed , and no myofiber abnormalities have been observed in transgenic mdx mice expressing full-length dystrophin only in striated muscle . While the profound changes to innervation are an integral part of the dystrophic pathophysiology in mdx mice, we found no change in the total number of synapses that would be consistent with the formation of new, innervated myofibers.
Myofiber branching ensures that the developing myotubes are innervated irrespective of the site of injury. Considering the increased muscle in our study resulted almost entirely from myofiber branching, it is likely that myofiber branching helps to maintain the peak force capacity of mdx muscles . While there are clear benefits of myofiber branching, the branch points in mdx mice are primary sites of calcium mishandling and contraction-induced injury [33, 45–47]. Thus, it would be preferable to reverse muscle loss with the formation of entirely new, innervated myofibers. Multiple studies have suggested that prospective cellular therapies for DMD can form new fibers in mdx muscles. For instance, direct administration of fibroblasts genetically modified to form myofibers can form multiple dystrophin positive myotubes in mdx 4cv muscles, although it was not determined whether these were either innervated or attached to pre-existing myofibers . Delivery of isolated satellite cells contributed to the regeneration of a myofiber that only expressed the donor GFP and not the recipient DsRed . Transplantation of myogenic progenitors derived from induced pluripotent stem cells can also contribute to innervated fibers within the recipient . We also found that myofiber transplantation increased the number of myofibers in transverse sections of aged (28-32 months) tibialis anterior muscles . However, none of these studies demonstrated that the donor cells formed a whole innervated myofiber without the contribution from the endogenous host cells. Our current study demonstrates that the formation of new, innervated myofibers is not a natural process of muscle regeneration in the mdx 4cv mice. However, it remains important to examine whether various experimental manipulations utilizing diverse prospective cellular therapies and delivery techniques can form new, innervated muscle fibers, which could be important for reversing the loss of muscle mass in older DMD patients.
Muscle hypertrophy is a transitory feature of some muscles in DMD and is a prevalent phenotype of the mdx mouse model of DMD. Analysis of muscle histopathology suggests the formation of new myofibers contributes to the hypertrophy. New myofibers require innervation to survive. However, it is not clear whether the regenerative response to muscle necrosis in mdx mice leads to the formation of new, innervated myofibers. Here, we demonstrate that the new muscle receives innervation by branching from the existing myofibers, rather than directly from the motoneuron. Furthermore, the propensity of myofibers to branch increased once the mdx mouse had reached maturity. These results have important implications for muscle replacement strategies for muscular dystrophy and sarcopenia.
This work was supported by grants from the MDA and AHA (to GBB) and NIH grant AR40864 (JSC).
RMF contributed to experimental design, performed experiments, and helped draft the manuscript. JKH imaged the 5-month mdx innervation and edited the manuscript. JSC contributed resources and edited the manuscript. GBB conceived the project, contributed to all experimental designs, performed experiments, and helped draft and edit the manuscript. All authors read and approved the final manuscript.


2 (quote) No such issues here!
Announcement from Vipul Jha: First build of LineageOS 13.0 for Android One first gen devices.
LineageOS is a free, community built, aftermarket firmware distribution of Android 6.0(Marshmallow), which is designed to increase performance and reliability over stock Android for your device.
@jackeagle Can you please move the thread to Here? I mistakenly selected this forum to create my DevDB.
Ty will be testing it. Can u add feb security patch!? Or in lineage OS it's not merged till now!?
It's not merged in LineageOS 13.0 and I guess they are not going to update LOS 13.0 anymore.
Btw. Is this anyway linked to the nougat lineage os for sprout?


text:
Massachusetts School Suspends Eight Year Old for Drawing Jesus on the Cross
TAUNTON, Massachusetts, December 15, 2009 (LifeSiteNews.com) - An 8-year-old boy was sent home from Maxham Elementary School and required to undergo a psychological evaluation after he drew a stick-figure picture of Jesus Christ on the cross.
The boy's father, Chester Johnson, said he got a call earlier this month from the school informing him that his son, a second-grade student with special education needs, had created a violent drawing and was being sent home. The image depicted a crucified Jesus with Xs covering his eyes to signify that he had died on the cross.
"As far as I'm concerned, they're violating his religion," Johnson said. "They told me he would have to leave the school and get a psychological evaluation, which I didn't see necessary for the picture that was drawn. Especially after I told them he went to the La Salette on Thanksgiving with his mom. I didn't see anything wrong with the picture that was drawn."
The boy and his family had recently gone to see a Christmas display at the National Shrine of Our Lady of La Salette, a Catholic retreat center in Attleboro.
Toni Saunders, an educational consultant with the Associated Advocacy Center who is working with the boy and his parents, told the Taunton Gazette, "I think what happened is that because he put Xs in the eyes of Jesus, the teacher was alarmed and they told the parents they thought it was violent. They weren't looking at the fact that this is an 8-year-old child with special needs."
"They made him leave school, and they recommended that a psychiatrist do an evaluation," Saunders said. "When I got that call, I was so appalled that I had to do something," she added.
Maxham School principal Rebecca Couet refused to comment to the media about the event and referred all questions to the superintendent's office.
Superintendent Julie Hackett told the Taunton Gazette that district policy prevents her from discussing a "confidential matter regarding a student."
School committee member Christine Fagan told WBZ radio, "I find the decision very disappointing. But I think there's so much pressure now on people to look for all kinds of things. I think that's what generates these types of responses. I think we really need to be careful about how far we want to take this idea of political correctness."
The boy's father said the school overreacted and his son was traumatized by the incident. The school district subsequently approved the family's request to have the child transferred to another school.
"This is a highly intelligent kid. He gets 100's on his tests," Johnson told WBZ.
"I want him transferred to another school and I want something done about this. They owe my family an apology and they owe me an apology and what they can do is keep giving my son the education that he needs and work with him."
Kerri Augusto, a professor of psychology and family studies at Becker College told WBZ that the school did more harm than good for the boy.
"More disturbing than the knee-jerk interpretation of this child's drawing, is the response of the school," Augusto said.
"The extreme lengths to which the administration went to 'protect' the child, resulted in punishment for the child and his/her family and shows blatant disregard for the child's social and emotional needs."
To contact Maxham Elementary School with your opinion/comment:
Rebecca Couet - Principal
Lowell M. Maxham School
Email: RCouet@tauntonschools.org
To contact Superintendent Julie Hackett with your opinion/comment:
Taunton Public Schools District Office
Dr. Julie Hackett - Superintendent of Schools
110 County Street
Email: jhackett@tauntonschools.org
URL: http://www.lifesitenews.com/ldn/2009/dec/09121509.html
Posted by Robert Ritchie at 10:51 AM
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