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Model is 5'5", wearing size Small with a 26" waist, and 38" hips.
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A new breed. Our Seamless Biker shorts are the first of their kind for Alphalete, not to mention the perfect workout bottom for the warmer months to come. With a three-tier, 8" inseam length and no front rise seam (to avoid any camel toe issues), the Seamless Biker will finally give you that stylish silhouette you've been wanting by way of top-notch craftsmanship. Subtle texture panels and rib detailing add visual interest to the garment. Five original colorways are available and meant to pair with the matching Seamless Crop. Our classic Forever Knit Alphalete logo is stitched into the back of the unique waistband. The launch of our Seamless Biker shorts signals a level-up for Alphalete womenswear, and it's only the beginning.
Size Guide:
Model is 5'4, wearing size S and has a 32" bust.
Material & Washing Directions:
Focusing on high functionality through simplicity of design, this all-new Surface Tri Bra is designed to move and perform with you. Made in our incredibly soft, weightless and high performance Surface material, this universal Tri Bra will be your new favorite staple.
Model is 5'4, wearing size S, with a 32" bust.
Brought back by popular demand, this Wrap Bra perfectly encompasses our mission to create pieces that you'll never forget. Made in our incredibly soft, weightless and high performance material, this Wrap Bra makes for the perfect everyday bra.


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From delicious food, to outdoor activities, to local Irish culture and heritage, you will be amazed at how much you will discover as you uncover all that makes this region so unique. You'll feel at one with nature during the day and the friendly Irish people will help you feel right at home as you embrace rural life. And by the time you leave, you'll have had a taste of Irish life that is guaranteed to leaving you wanting more.
Mayo is still a relatively untouched & undiscovered part of Ireland. It treasures many of our iconic landscapes & continues to be a photographer's haven for those promoting Ireland. It is here that you can still find so many of our more typical stone houses, untouched landscapes & traditional farming habits. It is best known for Ireland's most sacred pilgrim mountain – Croagh Patrick – that iconic "cone" that dominates so much of the landscape in this region and is still one of our most climbed & popular "pilgrim days" – especially on "Reek" Sunday!! Mayo's maritime history is long & fascinating, its ancient habitations date back to the time of the Egyptian Pyramids & everywhere you turn – there is more to discover, stories to hear & more beauty to be enthralled by.
Achill Island is Ireland's largest island & was first inhabited 5,000 years ago. Now accessible by a bridge from the mainland, it is simply oozing with great walks, amazing scenery & history in abundance. Famous for its soaring mountains and dramatic cliffs and seascapes you will relax into island life before you realise you are doing so as you explore the hidden treasures of this place.
Moving south, you reach the gaily painted Westport town & make your own pilgrimage to Croagh Patrick, Ireland's most famous pilgrim mountain. With breath-taking views over Clew Bay, dotted with a sparkling array of islands, on a clear day you can see north to Achill and south across Connemara. Visiting the largest of these islands, you will have one day on the magnificent Clare Island before undertaking your pilgrimage.
Your holiday then takes you south to another island - Inishbofin. Off the shore of Connemara, lies the beautiful island of Inishbofin (the island of the White Cow), a special area of conservation and protection. This island has been inhabited for over 6000 years and has a wonderful history. It is a fascinating place with an enthralling history, a peace & tranquillity that will infiltrate your soul, leaving you refreshed, relaxed & ready for life as you make your return journey home from here.
You arrive to the capital of Mayo – Castlebar town. Here, your Guide will meet you at 16.00 hours, introduce you to your other group members & whisk you away to the western reaches of this glorious region to reach Achill Island. This is your base for your next 2 nights and your Guide will brief you on the coming days of your holiday & ensure you are properly prepared for each day. You will then walk to a nearby restaurant to enjoy your first dinner together & experience island nightlife!
After a scrumptious breakfast and armed with your picnic lunch, you will depart from your accommodation to start your walk, discovering the delights of this wonderful region – the "deserted village", an old signal tower and some idyllic hidden lakes. Returning to your accommodation later that afternoon, you will be rewarded with a wonderful demonstration on how to make the perfect Irish Coffee. Your choice of walks today is:
From your accommodation, you walk up an old "bog" track to reach an old deserted village. With tales of the famine, and a traditional way of life long gone from Ireland, you then continue, passing an old Signal Tower and mining region, to reach the village of Dooagh. From here, those with energy enough can continue along the coast to see just what is was that so enthralled the famous painter Paul Henry to capture so many of the wonderful sights on this island.
Leaving your accommodation, you reach a magnificent lake hidden in the mountains in an idyllic setting which supplies most of the island with its water. From there, you continue across open mountain, moorland & bogland with no defined tracks as you continue to the northern coast of this island.
Here, you discover the delights of more hidden lakes, known only by the birds & keen walkers, as you follow across the hillsides to reach an old signal tower. Continuing on, you reach an old deserted village before re-joining your minivan & returning to your accommodation.
After your walk, you will have the opportunity to learn how to make the perfect Irish Coffee before enjoying your dinner & overnight.
Leaving this beautiful island, you then continue south east to reach the town of Mulranny. Just east of here, you will follow a wonderful track to the town of Newport. From here, you then continue south to reach your accommodation just outside the town of Westport. This is where you will be staying for your next 3 nights.
Before leaving Achill, your Guide will take you to see the beautiful Keem Beach – voted Ireland's best beach!! With glorious views across the island, the Wild Atlantic & south to Clare Island, you will be fascinated by the beauty of this region. From here, you start your walk just east of Mulranny and follow a beautifully prepared track to reach the town of Newport.
While you have time to enjoy some refreshments here, your Guide will collect your minivan & then return to bring you on to your accommodation for your next 3 nights. Dinner & overnight in Westport.
Also starting your walk just east of Mulranny, you follow a beautiful track into the foothills of the Nephin mountains – close to the amazing Ballycroy National Park. From here, you will then continue you circuit to enjoy the final part of your walk on a well prepared trail. Return to your minivan & continue to your accommodation in Westport for your next 3 nights. Dinner & overnight in Westport.
Your day starts today with a glorious drive around the shores of Clew Bay to then reach a small harbour on the western tip of these shores. From here, you take a small ferry across to the magnificent Clare Island. This is a legendary place – once home to our famous Pirate Queen – Grace O'Malley.
Discovering some of the delights of this island, you then return to Westport for an evening at your own leisure. If for any reason weather prevents this trip – then your Guide will take you on a lovely walk into the wilderness that few discover east of Croagh Patrick.
Following some of the little roads or "boreens" around the island, you will have the opportunity to reach the northern tip of this beautiful place with glorious views across Mayo & north back to Achill. History abounds here & you will learn much about the tales and heros that have made this place so famous.
Walking west from the pier, you will climb to the highest point of the island with wonderful 360 degree views all around. This is the largest island on Clew Bay and the western side of the island protects so much of the land from the ravages of the Wild Atlantic storms. With views south to Croagh Patrick & north to Slievemore on Achill, you will be spoilt with beauty.
Return to your accommodation in Westport for your overnight & a free evening at your leisure.
Today is your day for experiencing a pilgrimage as you hike the iconic mass of Croagh Patrick. No trip to Mayo is complete without a journey to the "Reek" and as it dominates the landscape, so it features in so much conversation around the locality. It is a glorious hike, and those that manage to complete it will have a huge sense of achievement. You have a choice of the following walks today:
Travelling south from Westport you reach the ancient woodlands of Brackloon. From here, you follow "Tochar Phadraig" part of the old pilgrim route from the monastic settlement at Aghagower. From here, you follow through woodlands and back country roads to reach the foothills of Croagh Patrick.
With a tough, short hike across moorland you then reach your highest point to then follow around the north eastern flanks of the mountain & finish at the Visitor Centre at the base of Croagh Patrick. There, you can enjoy some well-earned refreshments and read some of the history of the mountain if you wish.
Ascending across open mountain, you will be following the main Pilgrim Route that most people use from the northern shores of Croagh Patrick. Taken slowly, this is a wonderful route giving terrific views across Clew Bay.
Reaching the top of the mountain, you will find the famous Church there, have time to enjoy your triumph & then continue west to descend along a different route if weather allows. Returning by minivan to the base of the mountain, you may wish to enjoy some refreshments here before returning to your accommodation.
Driving back to your accommodation, you can enjoy the bustling town of Westport at your own leisure this evening.
Today, you travel south through a wild & untouched region of mountain and bogland to reach the village of Leenane at the eastern end of Ireland's only fjord – Killary Harbour. Discovering the delights of this wilderness region your choice of walks is as follows:
Under the shadows of the Sheffry Hills is a land that is untouched, untamed & unblemished by the test of time. Here, your Guide will take you on a beautiful walk, through forestry & beside a stream to emerge into open countryside with views that will literally take your breath away. Sometimes short & sweet walks are the best type you can encounter & we believe this is one of them. Returning to your minivan, you then continue west to the coast.
South west of Westport & on the southern foothills of Croagh Patrick, there is an expanse of blanket bog that is full of history. This in turn gives rise to the Sheefry Hills & it is in these foothills that your Guide will take you to discover some of the riches of this region. A super walk brings you closer to the village of Leenane and on re-joining your minivan, you then continue west to the coast.
At the end of your walk, you will have time for some light refreshments near Leenane, before continuing on through Connemara to reach Cleggan Pier. From there, you take a small ferry to the beautiful island of Inishbofin – awash with history, tradition & wonderful people. With time to discover some of the islands delights, you then have your dinner & overnight on the island. (PLEASE NOTE: early & late season holidays may not be able to achieve all of this due to ferry times. If your earlier walk is not possible – you will have all the more time to discover the delights of Inishbofin).
Your final day takes you around Inishbofin Island on a day of discovery as you enjoy a circular walk around this historical island. With fortresses dating back to the time of Cromwell and a rich mythological history, you will be enthralled by the beauty of this island. If time allows, it may be possible to reach the smaller Inishark Island as well, depending on weather & tide times. (This will be an optional extra trip).
Today is a day for one walk only and should you prefer to take some precious time to wander and enjoy nature away from the group – this is the day to do it as you soak up all that is wonderful around you in the most idyllic setting possible.
At the end of your walk, you return to your accommodation. Your final farewell dinner together is a great way to compare stories, reminisce and enjoy some great music before your onward journeys tomorrow.
After your final and substantial Irish Breakfast, you will take the ferry back to the mainland & transfer by minivan to reach the bus & train station in Galway. From Galway, you can then avail of the excellent bus/train service to all major airports, cities & ferry ports in Ireland. Your estimated arrival time to Galway is approx. 11.00am. (Please ensure any flights are booked for 17.00hrs earliest).
Please note : - It is extremely important that you read & understand the WALK DETAILS for each day & that you are able to achieve this. If you would like to discuss your Walking Ability with one of our experts – please arrange a telephone conversation & we will be delighted to assist you with your holiday choice.
Should you require extra night's accommodation before or after your holiday, please advise us at the time of booking.
Please visit www.irishrail.ie or www.buseireann.ie for public transport in Ireland
Please note that Ireland can be a bit 'damp' both underfoot and overhead, with some liquid sunshine! Irish weather is unpredictable and the nature of hikes can change quickly and dramatically because of the weather. This is one of the many pleasant aspects of hiking in Ireland. Benny's Ireland Vacations,Inc. reserves the right to alter this itinerary due to weather conditions or the walking ability of each group.
Not Included: Any boat trips, personal drinks, entrance fees to theatres, parks or museums etc., medical expenses or gratuities.
Comfortable: Terrain varied & occasionally wet underfoot. Best suited to people capable of walking up to 12kms (7.5 miles) daily. You encounter uphill & downhill sections with a max. height of 600 metres (1,950 feet) approx. Ideal first walking holiday or less experienced walkers.
Moderate: Takes you across open-mountain & bogland (wet conditions). Terrain is varied each day with uphill & downhill hiking, some of which may be steep. Max. height is 950 metres (3,100 feet) approx. Suitable for people with good level of fitness & capable of walking up to 20kms (12.5 miles) a day.
© Benny's Ireland Vacations Inc.
Florida Seller of Travel, Registration Number ST40279.
I've lived most of my life on the Dingle Peninsula, Ireland. My Itineraries demonstrate my knowledge of Ireland. which is why you will be in the best hands.You will be assured that your vacation will be most memorable. Benny's Ireland Vacations is proudly partnered with the most able, reliable & experienced ground handlers in the business in Ireland, The Abbey Group.
Only in Ireland!
Benny's Pint!
We provide..... Group Travel - Individual Travel - Self Drive Travel - Corporate Travel
Our mission is to provide you with as much information on Ireland as possible through our Itineraries, Tours & Vacation choices. so that you will experience this spectacular culture to the fullest.
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Alternative Energy Systems Category
No one is immune to the skyrocketing energy costs of today's world. Therefore, you, along with the many billions of other inhabitants of this planet, are increasingly finding yourself in the position to seek alternative energies, and hence here you are. A great many have come before you and others will follow you in the pursuit of information on alternative energy systems. Many respected authorities have written various helpful articles on different aspects of alternative energy systems, primarily solar panels and wind turbines, and here they are conveniently sorted for your reading to help you on how to take advantage of alternative energy systems:
Solar Panels / Solar Technologies Wind Turbines
Of those hit hard the most by the energy dilemma are the lower and middle classes of the economic bracket in our society.
In fact, according to the United States Census Bureau, over 35 million Americans are considered to be low-income earners, making it especially difficult for these Americans to make ends meet in today's escalating climate of housing energy costs. To try to appreciate this, understand these grim realities collectively identified in a publication by The National Fuel Funds Network, The National Low-Income Energy Consortium, and The National Energy Assistance Directors' Association merely based upon general periods of 1999-2000, a time when the high energy costs then were relatively lower than in 2008: The average low-income family spends approximately one out of every five dollars of their budget on housing energy costs every year. In other words, a middle-income family that makes an income of $50,000 a year facing the same inevitable energy-cost burden spends about $10,000 of that income solely on housing energy costs a year (such as to heat their home, prepare meals, etc.). Suffice it to say, it's a burden that all Americans endure, and it is, of course, more burdensome for the low- and moderate-income Americans who often live paycheck to paycheck.
With the price of a barrel of crude oil having already shown its ability to skyrocket to over $140 a barrel in 2008, in the words of the above energy watch organizations, the price of "energy stands as a massive roadblock between many Americans and self-sufficiency." It is, therefore, in everyone's best interests to seek and utilize alternative energy systems, such as solar energy (solar panels, etc.) and wind power (wind turbines, etc.).
It's no longer just noble to be "green," it is a personal necessity for us all to be "green."
Of course, "being green" has not only created a new working class of "green-collared" workers, it has brought upon a new fashion trend: Green clothes. It has also added to our entertainment media: Watch the Green Planet channel for yourself, a build-off of the renowned Discovery channel.
Being green is now not only noble, but also a necessity, a job-market creator, a fashion trend, and a major part of today's entertainment media. Join the green bandwagon because it is here to stay--since experts all agree the sustainability of our environment depends on it!
Ed the Handyman
Your Handyman Zone Team
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Ipreo is pleased to present the updated and enhanced 2013 Corporate Access Survey. The purpose of the survey is to offer detailed intelligence on the value of various corporate access services in the fast-evolving world of investor relations, in addition to providing benchmarks for corporate access activity.
Ipreo Global Corporate Access Report 2013
- Archives, Corporate Investor Relations
- Articles & Reports
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- Ipreo Staff


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- Home
- Departments
- Recreation
- Programs & Events
- Programs
- Youth Programs
Youth Programs
Check here often for updates and additional programs that will be added.
Below are our upcoming programs. Register online using the link on the left of this page or contact us for more information.
Click here for a printable registration form that can be mailed to us with payment to register for any of our classes or programs.
Unfortunately due to the current state of COVID-19 the Preschool Prom planned for Saturday, May 9 is cancelled. We hope to host this event in Spring of 2021.
Preschool Prom
Ages: 3 to 5 ONLY (Cannot be 6)
Cost: $15.00 per child
Saturday, May 9 (Date Subject to Change)
Location: Murrysville Community Center
11:00 a.m. to 12:30 p.m.
Calling all little ones! Come dressed in your best for Murrysville Recreation Department's first ever Preschool Prom. You'll get to show off your dance moves and learn some new ones with Luanne from Integral Enrichment Center in Murrysville. Carol Siefken with the Murrysville Community Library will also be with us to share a fun story. Enjoy snacks, entertainment, photo ops, and more! Dressing up is encouraged but not required. Parent participation required. Space is limited.
This program has been cancelled due to lack of registration.
Creative Madness
Kids will create beautiful initial room signs on canvas, make structures with marshmallows and toothpicks; make slime, and so much more! Children might get messy at times so please dress appropriately. There will be a few breaks with games so join us for some fun, creativity and new friends!
Ages: 8-11
Class Min: 10 Max: 20
Date: July 13-15 Time: 9:00 a.m. to noon
Location: Chambers Park
Instructor Ilona Ralston
Fee: $65.00
Late Fee: $10.00 (Effective July 6)
Ready, Set, Run 5K!
Have you ever wanted to run a whole 5K? Well, this is your chance!! Join Coaches Jim and Susie to learn how to safely train to run a 5K in this non-competitive training camp, we guarantee you'll have fun all summer long! The camp will conclude with all participants actually running a full 5K! This camp is sponsored by Pro Bike + Run and presented in conjunction with the National Alliance for Youth Sports.
Ages: 8-13
Class Min: 10 Max: 50
Date: Tuesdays & Thursdays: June 16-August 6
Time: 9:00 AM-10:00 AM
Instructors: Jim Passarelli & Susie Albert
Location: Murrysville Community Park
Fee: $65.00 (16 sessions at $4.00 per session) Register Online
Late Fee: $10.00 (Effective June 9)
Due to current COVID-19 precautions, please visit their Tinkergarten website for current information on class dates, locations, and availability.
Offered in our local parks, each class becomes a tight-knit group of children and adults who learn together through well-designed, outdoor play-based activities. Tinkergarten's approach helps kids develop a host of important capabilities, including empathy, collaboration, creativity, persistence and problem solving. Their expert-designed classes and activities help kids ages 6 months—8 years develop core life skills while enjoying healthy, fun, engaging experiences in the physical freedom of local green spaces.
Murrysville Community Park: Local Leader Amy Manuele
Bear Hollow Park: Local Leader Lauren Menzietti
Wildlife Events on the Westmoreland Heritage Trail at the Roberts Trailhead Murrysville Visitors Center
Join Murrysville volunteer Sue Miller on the last Sunday of each month (May through October) from 11:00 a.m. to 2:00 p.m. at the Roberts Trailhead Murrysville Visitors Center to interact with nature! Register for any of these events for FREE at https://www.eventbrite.com/e/95676128877.
- Sunday, May 31: Turtles, Frogs, and Salamanders of Murrysville
- Sunday, June 28: Birds of Murrysville
- Sunday, July 26: Mammals of Murrysville
- Sunday, August 30: Butterflies of Murrysville
- Sunday, September 27: Wildflowers of Murrysville
- Sunday, October 25: Trees of Murrysville
Wetlands Tour at Murrysville Community Park
Saturday, June 27 at 10:00 a.m.
Enjoy this free guided walk for all ages with Susan Miller, naturalist and local Murrysville resident, who will share MCP wetlands wildlife sightings. Get a peek at Purple Martin baby birds, check the Bluebird boxes and learn all about bears from Mike Papinchak with the PA Game Commission! Register for FREE at https://www.eventbrite.com/e/95631589659.


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Thanks, Amanda, for inviting me to the Siren/BookStrand blog. I can't believe I made it again! Hey, I'm getting good at this!
Just to let everyone know who I am, my name is Audrey Godwin and for the most part I write Gothic stories richly bathed in erotica and paranormal activity. You will find the tortured hero, and a beautiful heroine going through a challenging situation filled with dark characters of all kinds. Witches, ghosts, spell-beings and shapeshifters may show up at any time—or they may be the main character! My novels are full, rich and engaging. I come from Dallas, Texas but when I went to work for the federal government, I moved to the east. My first release for Siren was Dancing with the Devil. I also write for BookStrand where my book, Sin City will be coming out soon. These are two really great books, so I hope you will look them up and see what they're all about. You'll be seeing promos now and again with blurbs and excerpts, some of them pretty steamy. I've got more coming out soon, in fact I've probably worn Amanda ragged with all my submissions. I really love Siren, and BookStrand as well. There's some really great people connected to these publishing houses, and the authors are top of the line. I am honored to be among them.
Thanks for letting me ramble on. It's been great!
Audrey Godwin
Saturday, May 3, 2008
Audrey Godwin's Intro
Thanks, Amanda, for inviting me to the Siren/BookStrand blog. I can't believe I made it again! Hey, I'm getting good at this!


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Chocolate Sponge cake or soft amaretto cookie
Chocolate mousse cream and fresh raspberries
Chocolate Sponge cake
Chocolate mousse cream and fresh raspberries
Chocolate icing
Fruit on the surface
Sponge cake
g 250 ALMOND PASTE T.P.T.
g 200 EGG YOLK (TO WHIP)
g 5 EGG WHITE POWDER
g 300 EGG WHITE
g 80 SUGAR (WHIP UNTIL STIFF PEAKS FORM)
g 200 DARK CHOCOLATE GROUND THICKLY
g 180 SIFT FLOUR
Soft chocolate amaretto cookie
g 150 SUGAR
g 250 EGG WHITE (TO WHIP)
g 100 SUGAR
g 100 ALMONDS ( TO GRIND)
g 20 COCAO
g 50 FLOUR (TO SIFT)
g 50 MELTED CHOCOLATE
Chocolate and raspberry mousse
g 180 YOLK
g 150 RASPBERRY JUICE
n 1 GRATED ORANGES
g 150 SUGAR
g 500 MELTED CHOCOLATE SAMBIRANO 75%
g 1100 SHINEY WHIPPED CREAM
Neutral gelatin
g 600 WATER
g 80 SUGAR
g 16 PECTIN (MIX WITH SUGAR)
g 300 GLUCOSE
g 760 SUGAR
g 35 LEMON JUICE
Royal icing
g 150 WHIPPED CREAM (BOILED)
g 75 MILK CHOCOLATE
g 600 WARM NEUTRAL GELATIN
g 135 DARK CHOCOLATE 75% COCOA MASS
Sponge cake
Whip the egg yolks with the almond paste up to obtain a stabile and consistent lather. Whip the egg whites with sugar: the mass needs to be shiny and consistent. Grate the chocolate into thick grains and sift the flour. Put one third of the egg whites in the egg yolks, delicately stir, add chocolate and flour. Fold everything and complete the mixture incorporating the rest of the egg whites. Form discs thick 7-8mm. Cook at 220°C for 4-5 minutes with open throttle.
Soft chocolate amaretto cookie
Whip the egg whites until stiff peaks form, thinly grind the almonds with sugar, sift the flour, cocoa, almonds and sugar; incorporate delicately with a spatula. Form some discs, as big as the cake, using a piping bag with a 6mm smooth tin, or using Teflon stencils. Cook at 220°C for 12 minutes; lightly dust caster sugar before cooking.
Raspberry and chocolate mousse
Gently fold the mixture with egg, raspberry, one third of whipped cream, and then melted chocolate at 40-45°C, and finally the rest of the whipped cream. The cream must be shiny and homogeneous. After putting a layer of chocolate mousse for the filling, incorporate fresh raspberries, around 60 g for each layer.
Neutral gelatin
Put everything in a pan and cook at medium flame. Cook up to 67°Brix, measure at refractometer.
Royal icing
Boil the cream, incorporate the milk chocolate, melt, add the warm neutral gelatin and complete stirring and adding the dark chocolate. To obtain a good icing: melt the icing at 36-38°C, let it rest a room-temperature for 20 minutes: you will obtain a shiny covering mixture without air bubbles.


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Nathan Mark Ditum[1] (born May 25, 1981)[2] was a member of the Yogscast, working at YogTowers, and a part of PlayStation Access. On November 4, 2013, it was announced that PlayStation Access had joined the Yogscast.
Turps announced the arrival of Nathan, Rob, and Dave by saying, "We are really excited to welcome Nathan, Rob and Dave to the Yogscast team. Their skills, personalities and the videos they make are the perfect fit for the Yogscast family."
- Nathan has run marathons for the charities GamesAid and SpecialEffect.
- Nathan is married to Sarah Ditum.
- Nathan has a daughter named Maddy.
- Nathan has a son named Jay whom was born when Nathan was 20 years old.
- Nathan's favorite video games are the Doom series and Uncharted 2: Among Thieves.
- Nathan has been a barman, a tour guide, and has worked at a video library, and has taught at a university.
- Nathan used to work on Official Playstation Magazine and Official Playstation 2 Magazine.
- Nathan's favorite films are Taxi Driver, Rushmore, Alien, 2001: A Space Odyssey,The Conversation, and The Conformist.
Notable QuotesEdit
- "Yeah, exactly."
- "In your stupid face!"
- YouTube
- Website
- PlayStation UK Website
- Twitter (1)
- Twitter (2)
- Vine
- The Mispronounced Item Website
- The Mispronounced Item iTunes
- Google+
- ↑ https://www.youtube.com/watch?v=DqCEZdMFXP8 lists the Playstation Access guys' full names
- ↑ https://twitter.com/NathanDitum/status/735158244235055106
Community content is available under CC-BY-SA unless otherwise noted.


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Veggies & Herbs
What we're Growing
We dug our very first bed in the fall of 2018 to plant garlic. In the spring, we dug 9 more beds. This year, we chose an assortment of specialty crops to kick off the farm: funky round stuffing peppers, basil, lemongrass, sweet heirloom melons, bright orange winter squash and more.
Our veggies and herbs are available for purchase. We sell and deliver direct to restaurants, or you can also place an order to pick up on the farm. Email: email@example.com for more information.
With the first heavy frost on November 1st, our 2019 season came to a close. Our beds are spending the winter under cover crops and mulch, and we'll get to work planting again in the spring.


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I decided to try out my new Christmas present and take some pics of Noah tonight and get is 10 month session in. The lights are great and so powerful I only needed one! Woohoo!
I had to have DH on hand to wrangle the little guy because he was ALL OVER!
I do have a Christmas wrap up post for you all but I haven't had time to finish it. Maybe during our low key New Years I'll manage to get it done:) I didn't get as many pictures as I'd hoped unfortunately.


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9,458 Followers
Meet David Bogard, a 23-year-old from Fullerton, California.
"I made my playlist for myself. It was a way to have easy access to my favorite artists."
Name one of your favorite albums of all time?
One of my favorite albums at the moment is Tame Impala's Innerspeaker. A good combination of rock and psychedelia.
Name your top 3 favorite artists and why?
HOMESHAKE, Tame Impala, and King Gizzard & The Lizard Wizard. All three are really innovative and continue to put out music I love.
What music did you grow up listening to as a young kid?
As a kid, I grew up around a family that loved to listen to country music, but I personally can't stand it. Nothing wrong with it, I just can't get into it.
What artist, dead or alive, who would you interview and why?
I'd like to talk with Mac DeMarco. He's such a character and I feel like he'd have some pretty deep insight on everything from music to just life in general.
What is the best concert you've ever been to?
It's a tie. The best performance/show that I have seen was Arcade Fire closing out Coachella a couple of years ago. The most fun I've had at a concert though was seeing King Gizzard & The Lizard Wizard at the Hollywood Palladium. More of a massive mosh!


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Our History
Company History
In 1946, when Mr A.H. Butcher started the firm with his RAF gratuity, centuries of London's architectural heritage had been badly bomb damaged in the Blitz. Beautiful moulded ceilings, columns, arches, fountains, and other features belonging to some of London's treasured buildings, houses, hotels, restaurants and public buildings, stood in sore need of restoration.
To meet the demand for this highly skilled work, A.H. Butcher gathered together into the firm a team of the finest craftsmen available. In doing so, he laid the foundations for Butchers' present reputation as the finest source of traditional decorative plasterwork in London.
Now, over fifty years later, the present Butcher Plasterworks staff are as skilled as their forebears. It's a rare skill these days. And not surprisingly, examples of Butchers' mastercraft can be found not only in this country, but all over the world.
History of Plaster
Fibrous plaster is a tough, versatile material, widely used in 18th and 19th century houses for decorative effect, as cornices, ceiling roses, mirror frames, fireplace surrounds and a wealth of other elements. Made from a mixture of plaster and hessian, it is formed in moulds, allowing craftsmen to achieve a finesse of detail that only carved wood can match. Fibrous plaster is, of course, quick to make and far less expensive than carved wood; prefabricated in the workshops, it is rapidly installed on site, and then needs only final decorative finishing.
Butchers' premises house a matchless collection of moulds; a treasure house of architectural detail and a vital resource for restoring period houses. Where they cannot match from existing moulds, new ones can be made by a complex process of clay modelling. So important is the collection that it is currently in the process of being photographed for an extensive historical archive. In time, all these items will be featured on this site.


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Irrigation Services Fall City
Although rain water is one of the best ways for a lawn or garden to receive water, it's not the most reliable. Among several efficient irrigation systems, sprinkler systems are preferred by many people in the Fall City, WA area.
Sprinklers installation ensures:
- Regular and adequate irrigation
- Prevention of water waste
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Considering the increasing demand, many companies are offering their irrigation services for the installation of sprinkler systems including designing, repair or replacement. We at Cedar Country Landscaping, Inc. offer our professional guidance and irrigation services to Fall City residents.
Due to our practical suggestions and cost-effective services for our clients, we are a trusted name among companies offering irrigation services in the area.
Lawn Irrigation Fall City
The amount of water required for lawns depends upon the type of soil and the size of your property. For stronger and deeper roots, lawn irrigation should be deep and intermittent. An efficient lawn sprinkler system should be installed for proper lawn irrigation from reliable irrigation services providers.
We are specialists in lawn irrigation systems and can help you with the installation of sprinkler systems for your lawn. In addition, our skillful and creative technicians can also provide their expert lawn irrigation services to create and maintain an attractive landscape for your house as well.
We offer our professional lawn irrigation services for the installation of automatic sprinkler systems to Fall City residents with:
- Thought-out designs
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The fact remains that cost of installation of a sprinkler system depends upon the area of the lawn. However, we assure our best lawn irrigation services to our clients at the most reasonable prices.
Garden Irrigation Fall City
Garden irrigation, unlike lawn irrigation, is based upon water distribution at low pressure through a network of pipes meant for each plant. Drip irrigation and soaker hoses systems are most preferred modes of garden irrigation and are best suited for vegetable garden irrigation.
We specialize in the installation of drip irrigation and soak hoses systems for vegetable garden irrigation systems. If you plan to install or repair any sprinkle, drip or soaker hoses systems for garden irrigation in Fall City, you want professionally qualified technicians.
You can rely on us as, we are:
- Highly experienced
- Committed to quality
- Guaranteed to please
If you need lawn and garden irrigation in Fall City, contact Cedar Country Landscaping, Inc. at (425) 358-2779.


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With more than 24% of websites on the Internet running WordPress, WordPress security is becoming an increasingly important factor in an organization's security posture. Unfortunately, thousands of WordPress plugins contain high-severity vulnerabilities which could allow attackers to gain access to the WordPress administrative interface.
Scan for Vulnerable WordPress Plugins
Acunetix identifies WordPress installations, and will launch security tests for WordPress plugins and WordPress core vulnerabilities. The WP plugins detected, are listed in the WordPress plugins Knowledge Base including a description, version number and latest version of plugin to update to.
WP Configuration File Disclosure and Username Enumeration
An administrator might sometimes need to alter certain settings from wp-config.php directly as opposed to the WordPress interface. To do this, a backup of the known working configuration is created, before proceeding with manually altering the file. However, the backed up file then becomes available to whoever is able to guess the name of the backup file.
Not just WordPress


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When editing or creating new articles, a set of rules must be followed:
General Rules
FIRST OF ALL: This is NOT your place to come in and create/write about a Freak from thin air. What this wikia aims for is to have concise but informative articles about TF2 characters who appear in various videos (Garry's Mod or SFM) that people have already made and posted on YouTube.
Failure to adhere to the rules, especially when deliberate/repeating, may result in a block. Read the Blocking Policy to learn more.
- To earn an article on this wiki, a TF2 Monster has to have at least one notable YouTube video appearance which provides a good depiction of the Monster's nature, habits and traits. Even a few extremely short videos and cameos are not enough to validate an article on their own. Videos which are considered as notable must have a minimum of 2000 views (or 7500 for Classic Monsters) and a positively good reception (substantially more likes than dislikes).
- Take the information only from reliable sources. Videos of the Monster's creator are obviously the best, but videos by other authors that are popular and have been accepted by the community are also a valuable source of data.
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Article Layout
The heading must include a properly filled character infobox template of colour corresponding to the particular TF2 Freak. Each infobox template page contains an appropriate guideline.
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Following the character infobox, an easily identifiable quote should follow. Afterward, include a brief introduction to the article. Standard intro template:
"Generic is a COLOUR Class TF2 Freak created by YouTube user YTUser (creator's name linked to their YouTube profile)."
May include short information about the Monster's theme(s).
Main Body
An optional section which details the Freak's appearance. May contain links to specific items equipped, custom models/skins etc.
For characters that appear in video series with defined storylines one can write a concise summary of their adventures. If a character has a known origin, but otherwise has no defined story, the section should be called Origin and be written accordingly.
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An important section that describes the above traits of the Monster. Habits, quirks, individual preferences, hobbies and character traits should be included here.
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Contains information on the known and/or theorised weaknesses and exploitable faults of the character in question, like vulnerability to specific things or personality traits that may be taken advantage of by potential opponents.
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Notable Videos
A vital section that includes a list of links to videos where the Freak appears. Videos listed in this section must feature the Freak prominently, and behaving in a manner consistent with the way the Freak is depicted by the creator. In addition, the videos should have good reception. There is no definite upper limit regarding the number of videos listed, but 15-20 should be plenty enough.
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If a recognised TF2 Freak appears in an episode of a video series where one is a recurring character, such episodes might be listed regardless of the view count. In case where the recognised TF2 Freak does not have many appearances in general, all videos featuring the character might be listed as long as they have good reception.
Remember to list the videos chronologically.
Remember to properly categorise the article. Creator, class, morality alignment and team colour categories are applicable to all TF2 Freaks. Others concern their fighting styles, nature and habits. Check the existing categories and add the relevant ones.
Arrange the categories in an alphabetic order.


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UnMakerBot was a Lightweight built by Caustic Creations that competed in RoboGames 2015.It was a Silver, two-wheeled, invertible robot armed with a very powerful drum spinner. UnMakerBot did well at RoboGames 2015, winning the Gold Medal on its only appearance so far. The team that built UnMakerBot also built BattleBots competitor Poison Arrow that competed in season 2 of the ABC Reboot, and were likely unable to attend RoboGames 2016 due to the close timing of the two events.
Robot History Edit
UnMakerBot's first ever match was against the powerful Brazilian bar spinner RIP. This fight started with UnMakerBot getting up to speed, while RIP avoided it to get its weapon spun up. Once RIP was spun up the two bots collided, with UnMakerBot's drum sending RIP several feet into the air.
RIP tried to get away and get its bar spun up but UnMakerBot then caught up to it by the rails, and delivered three huge hits. Each one sending RIP flying, and it landed immobilized with a chain hanging out. RIP then tapped out giving UnMakerBot a win by knockout in its first RoboGames match. UnMakerBot's next fight was against another Brazilian robot, the vertical spinner K-Torze. This fight started with both bots spinning up, and colliding weapon to weapon, however both robots stayed on the ground. UnMakerBot then hit K-Torze on the side, sending sparks flying, it followed this up with another hit that popped K-Torze into the air.
K-Torze then attempted to attack with its vertical spinner, but UnMakerBot met it weapon to weapon, and sent it flying again. Once K-Torze landed it was clear that it was immobilized, and UnMakerBot did a victory dance as it was counted out. This meant that UnMakerBot had won its second fight in a row by knockout.
This win put UnMakerBot into the Lightweight Quarter-Finals against yet another Brazilian machine, and defending RoboGames Gold medalist, the drum spinner of Federal M.T. In what would be the first of three matches between the two in the event.
This match started with both robots spinning up, UnMakerBot was the first to strike, landing a hit on Federal M.T.'s wedge. UnMakerBot, and Federal M.T. then collided weapon to weapon several times before UnMakerBot landed a hit that managed to flip the Brazilian drum spinner. This allowed UnMakerBot to come in and hit Federal M.T. again, sending it flying.
UnMakerBot followed this up with another hit, this one righted Federal M.T. and tore a piece off of it. UnMakerBot, and Federal M.T. then drove to the middle of the arena, where UnMakerBot launched another attack, popping Federal M.T. into the air. It repeated this attack near the rails, and followed this up with another attack that bent Federal M.T.'s wedge upwards.
Now in the middle of the arena again UnMakerBot flipped Federal M.T. yet again, it followed this up with a second attack that righted it, and a third attack which peeled up more of Federal M.T.s wedge. UnMakerBot then delivered a severe hit to Federal M.T., this attack tore both of its wheels off. The mangled hulk of Federal M.T. was then counted out giving UnMakerBot its third win by knockout.
Results Edit
Wins/Losses Edit
- Wins: 5
- Losses: 1


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Spinocerebellar ataxia (SCA) type 7 is an inherited neurodegenerative disorder caused by expansion of a polyglutamine tract within the ataxin-7 protein. To determine the molecular basis of polyglutamine neurotoxicity in this and other related disorders, we produced SCA7 transgenic mice that express ataxin-7 with 24 or 92 glutamines in all neurons of the CNS, except for Purkinje cells. Transgenic mice expressing ataxin-7 with 92 glutamines (92Q) developed a dramatic neurological phenotype presenting as a gait ataxia and culminating in premature death. Despite the absence of expression of polyglutamine-expanded ataxin-7 in Purkinje cells, we documented severe Purkinje cell degeneration in 92Q SCA7 transgenic mice. We also detected an N-terminal truncation fragment of ataxin-7 in transgenic mice and in SCA7 patient material with both anti-ataxin-7 and anti-polyglutamine specific antibodies. The appearance of truncated ataxin-7 in nuclear aggregates correlates with the onset of a disease phenotype in the SCA7 mice, suggesting that nuclear localization and proteolytic cleavage may be important features of SCA7 pathogenesis. The non-cell-autonomous nature of the Purkinje cell degeneration in our SCA7 mouse model indicates that polyglutamine-induced dysfunction in adjacent or connecting cell types contributes to the neurodegeneration.
- polyglutamine
- ataxin-7
- neurodegeneration
- Purkinje cell
- non-cell autonomous
- truncation
- proteolytic cleavage
The spinocerebellar ataxias (SCAs) are a group of inherited neurological disorders that share the common feature of cerebellar degeneration. Spinocerebellar ataxia type 7 (SCA7) is classified as an autosomal dominant cerebellar ataxia type II (ADCA II), because affected patients display retinal and brainstem degeneration (Enevoldson et al., 1994). Neuropathological examination corroborates the clinical picture, revealing marked atrophy of the cerebellar vermis, the inferior olivary nucleus, and the dentate nucleus (Weiner et al., 1967). Neuronal loss and degenerative changes are consequently greatest in the Purkinje cell layer of the cerebellum and in the inferior olivary complex.
A compelling feature of SCA7 is genetic anticipation (Enevoldson et al., 1994). On the basis of this observation, a repeat expansion was sought as the cause of SCA7, and an expanded CAG tract, ranging from 38 to >250 triplets, was identified (David et al., 1997). The CAG repeat encodes a run of glutamines in the ataxin-7 protein, placing SCA7 in a category of diseases caused by polyglutamine tract expansions. The CAG/polyglutamine repeat disease group consists of at least nine inherited neurodegenerative disorders, including spinal and bulbar muscular atrophy (SBMA), dentatorubral-pallidoluysian atrophy (DRPLA), Huntington's disease (HD), and six types of spinocerebellar ataxia (SCA1, -2, -3, -6, -7, and -17) (Zoghbi and Orr, 2000; Nakamura et al., 2001).
With the exception of SCA6, all of the polyglutamine repeat diseases involve expansion beyond a threshold of ∼35 glutamines, resulting in a change in the conformation of the protein. The transition to a novel conformation may be detected by antibodies directed against extended glutamine runs (Trottier et al., 1995), and the adoption of an altered conformation is hypothesized to underlie a toxic gain-of-function effect. Studies done on animals and in cell culture suggest that the mutant polyglutamine-containing protein (or a peptide fragment thereof) must localize to the nucleus to initiate pathogenesis (Klement et al., 1998; Saudou et al., 1998). Indeed, our recent work on the molecular basis of SCA7 retinal degeneration supports such a model (La Spada et al., 2001). Once in the nucleus, the polyglutamine-expanded protein or peptide fragment can interfere with the function of transcription factors or coactivators (McCampbell et al., 2000; Orr, 2001). Expanded polyglutamine tracts are also relatively resistant to proteasomal degradation via the ubiquitin pathway (Paulson, 1999), and this leads to the accumulation of polyglutamine-containing peptide fragments within the cell. In SBMA, HD, DRPLA, SCA1, SCA3, and SCA7, aggregates of polyglutamine-containing fragments form nuclear inclusions (NIs) within neurons (Paulson et al., 2000).
To advance our understanding of polyglutamine neurodegeneration, we have generated a mouse model for SCA7. Lines of transgenic mice expressing ataxin-7 with 92 glutamines developed a neurological phenotype presenting as a gait ataxia. Despite the absence of expression of polyglutamine-expanded ataxin-7 in Purkinje cells, we documented severe degeneration of cerebellar Purkinje cells in these mice. We observed NIs consisting of N-terminal truncations of polyglutamine-expanded ataxin-7 and were able to detect an N-terminal truncation fragment of ∼55 kDa in protein lysates from affected tissues. The appearance of NIs in cerebellar neurons coincides with the onset of a coordination defect in the SCA7 transgenic mice, suggesting that nuclear localization of the truncated mutant ataxin-7 correlates with the ability to initiate pathogenesis. The non-cell-autonomous nature of the Purkinje cell degeneration in this model implies that dysfunction in adjacent cell types may play a prominent role in SCA7.
Transgenic mice. The generation of the SCA7 transgenic constructs and the production of the PrP-SCA7-c92Q and PrP-SCA7-c24Q transgenic mice have been described previously (La Spada et al., 2001).
Immunohistochemistry. Deeply anesthetized mice were perfused transcardially with 4% paraformaldehyde in 0.1 mphosphate buffer (PB), pH 7.4. The brain was removed, placed in paraformaldehyde for 4 hr, and cryoprotected in 10% sucrose and then 30% sucrose in PB. Parasagittal frozen sections were cut at 30 μm thickness on a sliding microtome. Immunohistochemistry (IHC) was performed on free-floating sections after blocking in 10% goat serum, 1% BSA, and 0.3% Triton X-100 in PBS, and the primary antibody was diluted in 0.3% Triton X-100 in PBS. The antibodies used and their respective dilutions are as follows: anti-ataxin-7 antibody A, 1:300 (La Spada et al., 2001); anti-ataxin-7 antibody K, 1:2000 (La Spada et al., 2001); expanded polyglutamine tract antibody 1C2, 1:1000 (Chemicon); HDJ-2, 1:500 (NeoMarkers); and Hsc-70, 1:200 (StressGen). Primary antibody staining was visualized with the ABC Vector elite kit (Vector Laboratories) using diaminobenzidine as a chromagen.
Western blot analysis. Protein lysates were obtained by homogenizing tissues in sample buffer (62.5 mmTris-HCl, pH 6.8, 4% SDS, 200 mm dithiothreitol, 10% glycerol, 0.001% Bromophenol blue) at a ratio of 1:10 (w/v) and then boiling. Nuclear extracts were prepared using the NE-PER Nuclear and Cytoplasmic Extraction Reagents Kit (Pierce). Protein samples were resolved by SDS-PAGE (8% acrylamide), transferred to nitrocellulose, and probed with antibody K (La Spada et al., 2001) or 1C2 antibody (Dako) or p44/42 MAP kinase antibody (Cell Signaling Technologies) at 1:1000 dilution in TBS containing 0.1% Tween 20 and 5% BSA, after membrane blocking in TBS with 0.1% Tween 20 and 5% non-fat dry milk. Antibody 1598, produced by Yvert et al. (2000), was kindly provided by J.-L. Mandel (Institut de Génétique et de Biologie Moléculaire et Cellulaire, Institute National de la Santéet de la Recherche Médicale, Strasbourg, France) and was also used at a dilution of 1:1000. The primary antibody was visualized with horseradish peroxidase-coupled anti-rabbit antibodies (Amersham) at 1:2000 dilution and Enhanced Chemiluminescence (Amersham).
Behavioral analysis. Mice of varying ages and genotype were assessed with four different behavioral tests in a blinded manner by investigators over the course of four successive days. The "clasping test" assessed whether mice would clasp their forelimbs and hindlimbs into their bodies or would splay their limbs when suspended by their tails (Lin et al., 2001). The "activity test" measured the activity of mice after removal of their cage lid. Normal "active" mice typically explore their cages when the lid is removed, whereas neurologically affected mice remain inactive or show enhanced exploration of their surroundings (Lin et al., 2001). The "ledge test" (which we developed) involved placing a mouse on the ledge of a cage and observing the response of the mouse to this predicament. Although normal mice either scurry along the bar of the cage and jump down without a problem, mice with neurological dysfunction typically freeze in place or fall into their cages. Finally, we determined the coordination and motor functions of the mice by performing rotarod testing with an Economex Accelerating Rotarod apparatus (Columbus Instruments). The speed of the rod was set to 4 rpm and increased to a final speed of 40 rpm at a rate of 0.1 rpm/sec, and latency to fall was measured in the best four of five daily trails over the course of 4 d. Performance on the rotarod was statistically compared by two-factor ANOVA (Microsoft EXCEL, Office 98).
Light microscopy. Mice were killed, and the brain was removed and immersed in a fixative consisting of 1.6% paraformaldehyde, 2.5% glutaraldehyde, 0.05% MgCl2 · 6H20, and 0.04m sucrose in 0.08 m PIPES buffer at pH 7. After washing, brains were secondarily fixed with 1% osmium tetroxide for 1 hr. A graded alcohol series (methanol or ethanol) was then used to dehydrate the brains: 35, 70, 95, and 100%, each 15 min per change. After three propylene oxide transition washings, brains were embedded in epoxy, and the propylene oxide was allowed to evaporate from the mixture overnight on a rotating shaker. The embedded brains were transferred to molds, and after hardening, the resulting blocks were sectioned on an ultramicrotome. One-micrometer-thick sections were cut and mounted on glass slides after immersion in 50% (v/v) Richardson's stain (sodium borate, Methylene blue, and Azure II, each at 1% w/v) in 0.1m dibasic sodium phosphate solution, pH 8.8.
Confocal microscopy. Free-floating 40 μm brain sections were blocked with 10% goat serum, 1% BSA, and 0.3% Triton X-100 in PBS for 1 hr and then incubated with antibody K (1:2000) and anti-calbindin (1:1000) in PBS containing 0.3% Triton X-100 for 48 hr at 4°C. After three washes with PBS, Alexa Fluor 488 anti-mouse IgG (Molecular Probes) at 1:100 dilution, Cy3 anti-rabbit IgG (Jackson ImmunoResearch) at 1:200 dilution, and 4′,6′-diamidino-2-phenylindole dihydrochloride (DAPI; Molecular Probes) at 1:10,000 dilution were applied to the sections and incubated together overnight at 4°C. After washing, the sections were mounted on glass slides and coverslipped in a medium of 90% glycerol and 10% phosphate buffer with n-propyl gallate added at a final concentration of 0.5% to reduce fluorescent label bleaching. The sections were viewed, and digital scans were recorded using a Zeiss 510 multiphoton nonlinear optics confocal microscope system. Digital imagez-stacks were created, and projections were made from them using the Zeiss AIM LSM software and the NIH Image J program (http://rsb.info.nih.gov/ij/).
Characterization of the SCA7 transgenic mice: expression pattern and aggregates
To produce a mouse model of SCA7, we inserted the ataxin-7 coding region with either 24 or 92 CAGs into the MoPrP expression vector to yield two transgenic constructs: PrP-SCA7-c24Q and PrP-SCA7-c92Q. PCR screening identified five founders (one PrP-SCA7-c24Q mouse and four PrP-SCA7-c92Q mice). As described previously, we determined the expression level of the ataxin-7 transgene in brain RNA samples from representative individuals for each available line and confirmed expression of full-length ataxin-7 protein (La Spada et al., 2001).
To study the expression pattern of ataxin-7 in the CNS, we immunostained frozen sections from our transgenic mice. We found that ataxin-7 is widely expressed in neurons throughout the CNS in the 92Q transgenic mice, but we observed no appreciable increase in ataxin-7 immunostaining in 92Q cerebellar Purkinje cells in comparison with 24Q and non-transgenic control mice (Fig. 1) (data not shown). Lack of transgene expression in Purkinje cells is a feature of the MoPrP construct and has been observed repeatedly (Borchelt et al., 1996; Schilling et al., 1999a,b). In the 92Q transgenic mice, there was intense nuclear staining of neurons, with especially dense staining noted in the granule cell layer of the cerebellum (Fig. 1A,B), pyramidal neurons, and dentate gyrus granule neurons of the hippocampus (Fig.1C,D), the pontine nucleus (Fig.1E), and the inferior olivary nucleus (Fig.1F). At higher magnification, this nuclear staining is clearly punctate with usually one or two dense regions of immunoreactivity (Fig. 1G,H). These densely stained structures resemble the NIs reported in other polyglutamine repeat diseases and mouse models (Ross, 1997) and could be detected with antibodies directed against polyglutamine expansion tracts or heat shock chaperones (1C2, HDJ2, Hsc-70; data not shown). We observed variation in the intensity of ataxin-7 immunoreactivity in NIs between transgenic individuals of the same line and of different lines (data not shown). The intensity of anti-ataxin-7 antibody staining increases with transgene expression level and with age, suggesting that ataxin-7 protein is accumulating in NIs over time.
PrP-SCA7-c92Q mice develop ataxia
The first sign of a neurological dysfunction in the PrP-SCA7-c92Q mice is an unsteady gait beginning at 8–15 weeks of age (Table1). The gait ataxia gradually progresses until the mice display a wide-based stride with occasional falling. The movement disorder then becomes more complicated, and the mice start to shudder and startle easily. The mice become less explorative and a chronic whole-body tremor eventually ensues. By this time, the PrP-SCA7-c92Q mice are significantly smaller in size than their non-transgenic littermates. Such phenotypically affected transgenic mice show decreased survival, with the most severely ill individuals of the highest expressing line (i.e., 6080) dying or requiring euthanasia at 13 weeks of age (Table 1). Despite high level expression of the ataxin-7 transgene in heart and kidney, necropsies performed on these affected mice found no non-neural pathology or obvious cause of death (data not shown). In contrast, the eldest PrP-SCA7-c24Q transgenic mice (1 year of age) show no visible signs of neurological disease and display no increased mortality.
To determine the nature of the behavioral abnormality and the timing of its onset in the SCA7 transgenic mice, we performed a series of four tests to gauge neurological function: clasping test, activity test, ledge test, and rotarod test (see Materials and Methods). Because of the difficulty in maintaining lines 6080 and 6561, we focused our behavioral testing on one high-expressing PrP-SCA7-c92Q line (i.e., 6076), one low-expressing PrP-SCA7-c92Q line (i.e., 6529), and the high-expressing PrP-SCA7-c24Q line (i.e., 6129). Although all tested mice performed all four paradigms at 4 weeks of age without significant differences, 92Q transgene-positive mice from line 6076 exhibited a significant impairment in rotarod function by 8 weeks of age (Fig.2). At 12 weeks of age, performance on the rotarod considerably worsened for line 6076 mice, and the performance difference became even more apparent. This was accompanied by abnormalities in the other testing paradigms, with 50% of the 12-week-old line 6076 92Q mice being classified as "claspers," "inactive," or failing the ledge test (data not shown). No functional deficits were noted in these three testing paradigms for comparably aged non-transgenic littermates or for younger (i.e., 4 and 8 week old) line 6076 92Q mice. Once line 6076 mice become visibly ataxic at 13–15 weeks of age, virtually all such mice display abnormal behaviors in all three of these paradigms. Line 6529 mice that express the ataxin-7 92Q transgene at levels less than endogenous, however, continued to perform comparably on the rotarod to aged-matched littermate controls when tested at ages beyond 1 year, as did the line 6129 PrP-SCA7-c24Q mice (data not shown).
Neurodegenerative changes in the cerebellum occur in the absence of apoptosis or significant neuronal loss
Because the neurological dysfunction in the SCA7 mice resembles the presentation of patients with cerebellar ataxia, we evaluated the CNS of our transgenic mice for neurodegenerative changes with particular emphasis on neuroanatomical analysis of the cerebellum. Using a basic dye stain (Richardson's), we examined the cerebella of PrP-SCA7-c92Q mice from line 6076 at 20 weeks of age and found marked histopathology and degenerative changes (Fig.3). Although the cerebella of non-transgenic littermate controls displayed Purkinje cells of typical morphology, the PrP-SCA7-c92Q cerebella consisted of Purkinje cells that were much smaller and shrunken by comparison. Instead of a normal cuboid appearance, the Purkinje cells of the line 6076 PrP-SCA7-c92Q mice were flattened and exhibited less dendritic arborization. The nuclei of the 92Q Purkinje cells revealed occasional invaginations and appeared granular. Despite the observation of degenerative changes in cerebella of PrP-SCA7-c92Q animals killed at end-stage disease, granule cells and Purkinje cells were not labeled by the terminal deoxynucleotidyl transferase-mediated biotinylated UTP nick end labeling method of apoptosis detection (data not shown). Furthermore, there was no obvious difference in the number of neurons within PrP-SCA7-c92Q cerebella immunoreactive for NeuN or microtubule-associated protein 2 (data not shown). These findings suggest that functional deficits develop in PrP-SCA7-c92Q mice without significant neuronal loss.
To determine the timing of aggregate formation relative to the onset of neurological dysfunction, cerebellar sections from SCA7 transgenic mice at 4, 8, and 13 weeks of age were double labeled with antibodies recognizing ataxin-7 and the Purkinje cell-specific calcium binding protein calbindin. Although 4-week-old PrP-SCA7-c92Q mice from line 6076 do not display ataxin-7-positive aggregates in cerebellar neurons, NIs are clearly visible in cerebellar granule cell neurons at 13 weeks of age in c92Q mice from line 6076 (Fig.4). Although NIs can be detected in non-Purkinje cell neurons of the molecular layer (such as stellate, basket, and Golgi cells), NIs are not visible in the Purkinje cells themselves, confirming that the MoPrP promoter does not drive expression in this cell type. Interestingly, detection of NIs in the granule cell layer and the molecular cell layer of the cerebella of the line 6076 mice first becomes apparent at 8 weeks of age (Fig. 4). The NIs are few in number at this age and accompanied by diffuse nuclear staining in a subset of cerebellar granule neurons, suggesting that accumulation of the polyglutamine-expanded ataxin-7 first becomes appreciable around this time. Despite the absence of expression of polyglutamine-expanded ataxin-7 in Purkinje cells, calbindin immunoreactivity in Purkinje cell dendrites was markedly decreased in both 8- and 13-week-old line 6076 transgenic mice (Fig. 4). These findings demonstrate that ataxin-7-containing NIs and non-cell-autonomous Purkinje cell abnormalities develop coincident with the onset of neurological dysfunction in the line 6076 SCA7 mice (Fig.1). IHC analysis of line 6129 ataxin-7 24Q mice and of low-expressing line 6529 ataxin-7 92Q mice revealed no loss of calbindin immunoreactivity or NI formation in individuals at 1 year of age (data not shown).
Ataxin-7 undergoes proteolytic cleavage
As we reported previously, affected PrP-SCA7-c92Q mice produce full-length ataxin-7 protein with 92 glutamines, but the soluble, monomeric form of polyglutamine-expanded ataxin-7 is only readily detectable before the onset of a phenotype (La Spada et al., 2001). With advancing age and neurological dysfunction, little of the full-length monomeric form of ataxin-7 is seen on Western blot analysis, but instead, insoluble immunostaining material tends to be seen in the stacking portion of polyacrylamide gels (La Spada et al., 2001). Inspection of Western blots, which we probed with antibody K raised against the N-terminal portion of ataxin-7, also reveals intense bands migrating at 50–60 kDa (Fig.5A). These bands appear specific to SCA7 transgenic mice that express the ataxin-7 transgene with either 24 or 92 glutamines, because they are not observed in non-transgenic littermate controls.
To confirm the existence of this truncation fragment in the PrP-SCA7-c92Q mice, protein lysates were generated from various tissues from a line 6076 individual and a non-transgenic control and probed with the 1C2 antibody after immunoblotting. The 1C2 antibody, which is directed against expanded polyglutamine tracts and has already been shown to successfully detect polyglutamine-expanded ataxin-7 (Trottier et al., 1995; Lindenberg et al., 2000), also identifies an ∼55 kDa fragment in the PrP-SCA7-c92Q mice (Fig. 5B). Using the 1C2 antibody, no such fragments are detected in non-transgenic littermate controls (as shown) or in PrP-SCA7-c24Q mice (data not shown). Furthermore, protein lysates from the fibroblasts of an affected SCA7 patient reveal a fragment of similar size when probed with the 1C2 antibody, whereas fibroblast lysates from two human controls yield no such fragment. An N-terminal ataxin-7 truncation fragment of comparable mobility is also apparent in protein lysates obtained from the occipital lobe of an unrelated SCA7 patient (data not shown). Interestingly, the amount of detectable fragment in the line 6076 SCA7 transgenic mice varies according to tissue, with heart showing the largest quantity. To verify that ataxin-7 does undergo proteolytic cleavage, we performed IHC analysis on brain sections from PrP-SCA7-c92Q mice with antibody 1598 (Yvert et al., 2000) directed against a C-terminal epitope of the ataxin-7 protein. Although brain sections immunostained with antibody K reveal obvious NIs (Figs. 1, 4), antibody 1598 did not detect NIs or show appreciable staining in transgene-positive mice beyond 4 weeks of age (data not shown). When used to probe Western blots, antibody 1598 could detect full-length ataxin-7 protein but did not identify a fragment specific to SCA7 transgenic mice (data not shown). Because a Northern blot survey of ataxin-7 expression revealed only a single 7.5 kb mRNA species in humans (David et al., 1997), independent detection of a 50–60 kDa protein with polyglutamine-directed and ataxin-7 N-terminal-directed antibodies suggests that this protein product is the result of proteolytic degradation. However, until the proteolytic enzyme is identified or the truncation fragment is peptide sequenced, other possible explanations, including alternative splicing, cannot be excluded.
We have generated a representative mouse model of SCA7 by expressing a human ataxin-7 transgene with 92 glutamines in the CNS. The behavioral phenotype observed in the PrP-SCA7-c92Q mice includes features common to SCA7 patients, including prominent gait ataxia. The neurological phenotype progresses to include tremors and hypokinesis. Despite the complexity of the phenotype, the SCA7 transgenic mice display expression of mutant ataxin-7 in the cerebellum, basis pontis, and inferior olivary nucleus, tissues of primary pathological importance in SCA7. The PrP-SCA7-c92Q mice show intense nuclear staining in neurons expressing the ataxin-7 transgene. In humans, ataxin-7 is normally expressed in both the nucleus and cytoplasm of neurons in the pons, inferior olive, cerebellum, thalamus, and striatum (Lindenberg et al., 2000). Studies of SCA7 patient material, however, suggest that this cytoplasmic staining gives way to intense nuclear staining and nuclear aggregate formation, perhaps reflecting relocalization of the polyglutamine-expanded ataxin-7 to the nucleus (Holmberg et al., 1998; Einum et al., 2001). The anti-ataxin-7 antibody used primarily in this study, antibody K, appears specific for human ataxin-7 because it fails to recognize murine ataxin-7. Antibody K immunostaining of transgenic brain sections primarily yields a nuclear pattern, suggesting that the PrP-SCA7-c92Q mice recapitulate the nuclear relocalization of polyglutamine-expanded ataxin-7 observed in SCA7 patients.
In SCA1 transgenic mice and in a striatal neuron model of HD, localization of polyglutamine-expanded protein to the nucleus is required for pathogenesis (Klement et al., 1998; Saudou et al., 1998). In SCA7 patients, however, NIs occur at high frequency in both affected and unaffected brain regions (Holmberg et al., 1998), suggesting that although nuclear localization is necessary to initiate pathogenesis, it is by no means sufficient. Lack of correlation between NI distribution and neurodegeneration has been established similarly for other polyglutamine repeat diseases (Ross et al., 1997; Becher et al., 1998). Additional studies report onset of neuronal dysfunction in the absence of NIs (Klement et al., 1998; Saudou et al., 1998; Hodgson et al., 1999), leading some workers to suggest that nuclear aggregate formation is a protective response by the cell (Sisodia, 1998). Indeed, impaired ubiquitin-proteasome function yielded fewer NIs but accelerated disease pathology in a mouse model of SCA1 (Cummings et al., 1999). Other investigators nonetheless argue that the process of aggregate formation is pathogenic, because development of NIs typically precedes onset of neuronal dysfunction (Perutz and Windle, 2001). In the PrP-SCA7-c92Q transgenic mice, nuclear aggregate formation in granule cell neurons and in neurons in the molecular layer is prominent, with virtually all of these neurons showing NIs when a visibly ataxic phenotype is detectable (Fig. 4). Furthermore, although presymptomatic line 6076 mice lack detectable aggregates, the development of NIs in these mice occurs at 8 weeks of age and coincides with the onset of impaired performance on the rotarod. Thus, it is the accumulation of polyglutamine-expanded ataxin-7 within neuronal nuclei that best correlates with the onset of neurological dysfunction in our model, indicating that once a sufficient quantity of the altered ataxin-7 conformer is present in the nucleus, the disease process is under way. Formation of nuclear aggregates corresponds to the achievement of this threshold and may serve as a useful marker for disease progression. Whether NIs themselves cause or contribute to the disease process or are solely a protective cellular response in our SCA7 transgenic mice and in polyglutamine disease pathogenesis, however, remains to be determined.
A feature of the PrP-SCA7-c92Q mouse model that appears relevant to the human disease is the production of an N-terminal ataxin-7 truncation fragment. Previous studies of HD, DRPLA, and SBMA have yielded evidence that N-terminal truncation fragments accumulate in the nuclei of neurons from brain and spinal cord tissues in affected patients (Li et al., 1998; Schilling et al., 1999a,b). For HD, DRPLA, and SCA7, analysis of transgenic mouse models by immunoblotting and immunostaining suggests that N-terminal truncation fragments are produced from the full-length proteins (Schilling et al., 1999a,b;Yvert et al., 2000). In the present study, we detected N-terminal truncation fragments of ataxin-7 in PrP-SCA7-c92Q and PrP-SCA7-c24Q mice with an ataxin-7-specific antibody. We and others (Yvert et al., 2000) have found that ataxin-7-positive NIs in transgenic mice lack C-terminal epitopes, indicating that N-terminal truncated forms are accumulating in the nucleus. We, however, additionally used the polyglutamine-specific 1C2 antibody to probe protein lysates and were able to detect an N-terminal truncation product in the ataxin-7 92Q mice. Interestingly, with this antibody, we also detected an N-terminal truncation fragment of ataxin-7 in SCA7 patient material, migrating at the same molecular weight position as the truncation fragment present in the SCA7 transgenic mice. The presence of an N-terminal truncation fragment of ataxin-7 in transgenic mice and in SCA7 patients is consistent with the detection of an N-terminal truncation fragment in DRPLA transgenic mice and patients by Schilling et al. (1999b).
Of the polyglutamine-expanded proteins responsible for human disease, huntingtin, the androgen receptor, atrophin-1, ataxin-1, and ataxin-3 can each be cleaved by caspases to generate proteolytic truncation fragments (Wellington et al., 1998). Caspases are cysteine-dependent aspartyl-directed proteases involved in both signal transduction and the execution of the apoptotic cascade (Stennicke and Salvesen, 1998). In some cases, the cytotoxicity of the polyglutamine-expanded protein appears to be dependent on caspase cleavage (Wellington et al., 1998; Ellerby et al., 1999). Interestingly, tissue culture cells expressing polyglutamine-expanded ataxin-7 recruit the active form of caspase-3 into NIs, and CNS tissue from SCA7 patients appears immunoreactive for the activated form of caspase-3 (Zander et al., 2001). This observation suggests that proteolytic processing of ataxin-7 may also be mediated by caspases. However, although the ataxin-7 protein contains several caspase consensus cleavage sites (DXXD), none of these optimal sites is located in a region of the protein that corresponds to the molecular weight of the N-terminal truncation fragment observed in SCA7 transgenic mice and patient material. Indeed, whether proteolysis of ataxin-7 is required for toxicity is not yet known. The goal of future studies will be to determine how the ataxin-7 truncation product is generated and what its role in cerebellar injury and dysfunction is.
In a recent study, Dyer and McMurray (2001) sought to determine whether the huntingtin N-terminal truncation product is generated from polyglutamine-expanded huntingtin or from the normal huntingtin protein product in human HD brains. Using the 1C2 antibody, these workers reported that polyglutamine-expanded huntingtin remains full length, whereas the normal huntingtin protein product is subject to proteolytic cleavage. Although the N-terminal truncation fragment of huntingtin appears to be generated from the normal huntingtin protein, our data and that of others respectively suggest that N-terminal truncation fragments of ataxin-7 and atrophin-1 do derive from the polyglutamine-expanded versions of these proteins (Schilling et al., 1999b; Yvert et al., 2000). Thus, although loss of normal huntingtin function caused by enhanced proteolytic degradation may contribute to the pathogenesis of HD, differences in protein metabolism in the non-HD polyglutamine repeat diseases may indicate that a corollary process of loss of normal function does not occur in all polyglutamine repeat diseases.
A significant feature of the PrP-SCA7-c92Q mouse model is the degeneration of cerebellar Purkinje cells despite the absence of expression of polyglutamine-expanded ataxin-7 in this cell type. To assist in the interpretation of this result, it is useful to consider previous studies of SCA7. Although Purkinje cell degeneration and loss are hallmarks of SCA7, immunostaining of human SCA7 cerebella from both juvenile and late onset patients reveals that few, if any, surviving Purkinje cells contain ubiquitinated NIs (Holmberg et al., 1998; Einum et al., 2001). Furthermore, when Yvert et al. (2000) generated SCA7 transgenic mice expressing ataxin-7 90Q protein at high levels exclusively in Purkinje cells, these mice remained normal beyond 1 year of age, ultimately showing a phenotype and neurodegeneration at 16 months of age. When this group directed high-level expression of polyglutamine-expanded ataxin-7 throughout the cerebellum and brainstem with the platelet-derived growth factor B promoter, however, a motor incoordination phenotype appeared at 3 months of age (Yvert et al., 2000). Our results, taken together with these studies, indicate that expression of polyglutamine-expanded ataxin-7 in neurons that synapse with or receive input from Purkinje cells may underlie the Purkinje cell degeneration in SCA7. Ubiquitinated NIs are most frequent in brainstem neurons in the basis pontis and inferior olive of SCA7 patients (Holmberg et al., 1998). As shown in Figure 1, these brainstem regions contain numerous NIs in our PrP-SCA7-c92Q mice.
What then is the mechanism of Purkinje cell degeneration in the PrP-SCA7-c92Q mice? A well recognized function of synaptic connections between communicating neurons is to provide neurotrophic support (Sofroniew et al., 2001). Members of the neurotrophin family, including brain-derived neurotrophic factor (BDNF), are believed to perform this function in both a retrograde and an anterograde manner (Nawa and Takei, 2001). In HD, a reduction in BDNF levels in corticostriatal projection neurons was found in transgenic mice and patients, suggesting that loss of striatal neurons in HD may involve withdrawal of trophic support (Zuccato et al., 2001). The non-cell-autonomous nature of Purkinje cell degeneration in our SCA7 mouse model could similarly stem from a loss of trophic support involving cerebellar synaptic interconnections. Inferior olivary neurons as well as deep cerebellar and brainstem nuclei are among the principal populations of neurons with which Purkinje cells synapse. Granule cell neurons and Bergmann glia (in the Purkinje cell layer) also show expression of polyglutamine-expanded ataxin-7 in the PrP-SCA7-c92Q mice and could similarly be involved in Purkinje cell degeneration. Whatever the molecular basis of this phenomenon, our SCA7 mouse model clearly demonstrates that Purkinje cell abnormalities develop without intrinsic expression of a polyglutamine-expanded protein, supporting the hypothesis that "murder" by adjacent, dysfunctional neurons or glia does occur in the polyglutamine repeat expansion diseases.
This work was supported by research funds from the University of Washington, by a generous gift from a Utah SCA7 family (Y.-H.F.), and in part by National Institutes of Health Grant NS31775 to R.S.M. We thank G. Nicholson, J. Christodoulou, and T. Bird for patient samples and D. Borchelt for the MoPrP vector.
Correspondence should be addressed to Dr. Albert R. La Spada, Department of Laboratory Medicine, University of Washington Medical Center, Box 357110, Room NW 120, Seattle, WA 98195-7110. E-mail:laspada{at}u.washington.edu.


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Early College of Muskegon County (ECMC) recognized its 2019 cohort of 43 students, who successfully completed the rigorous three-year program, with a special celebration in Muskegon Community College's Overbrook Theater on May 1.
The event included student speakers, a certificate presentation, and a reception. A highlight came when the students simultaneously unveiled placards on the Overbook stage revealing the next step in their respective educational careers.
The 2019 cohort hailed from several county high schools: Mona Shores, Montague, Muskegon, North Muskegon, Oakridge, Orchard View, Ravenna, Reeths-Puffer and Whitehall. The students, who took courses at MCC while extending their high school graduation by one year, started the program as high school juniors and all 43 students are now eligible for an associate's degree.
"This group of students worked hard," said Early College Dean Val Shelby. "Completing this journey is not easy. With an average of 62.4 credits, most will enter their four-year university with junior or close to junior status. Many faced financial barriers that would have made it difficult, if not impossible, to attend college. Many are the first in their families to attend and complete college. They made sacrifices to reach this milestone and dedicated themselves to their education. I am very proud of their accomplishments."
Collectively, the students achieved a GPA of 3.1, completed 95 percent of the credits they attempted, will receive more than $800,000 in financial aid/scholarship funds for their future education, and saved $580,000 on college tuition, books and fees.
Shelby and Early College Mentor Denise Brown coached and supported the students during their three years in the program.
"The students are pursuing a variety of interests including technical degrees and careers in education, health sciences, business, technology, engineering technology and many others," added Shelby. "All of the students have been accepted to a four-year university, will continue their degree at MCC, will pursue vocational training, or are beginning their work career."
The list of transfer colleges includes Michigan State University, Grand Valley State University, Ferris State University, Michigan Technological University, University of Michigan, Western Michigan University, and out-of-state schools Colorado State University, University of Alaska Anchorage, and Wayne State University.
"Completing Early College gives our students an advantage in the talent development domain," noted MCC President Dale K. Nesbary. "With this important credential in hand, success at a transfer institution or in the workplace is that much more certain. Thank you to our brilliant students, along with their families and supporters for making Early College Muskegon County an ongoing success."
Muskegon Area Intermediate School District Superintendent Dr. John Severson added, "We are incredibly proud of our Early College students and their accomplishments during the last three years. Their ability to successfully complete this special program demonstrates that they are well positioned to meet the next opportunity before them. We wish them the very best."
In 2018, the program expanded by adding the Accelerated Technical Institute, which now covers many areas of applied technology. High school students have the option of taking classes at their home high school, the Muskegon Area Career Tech Center, and MCC's Sturrus Technology Center while working toward obtaining a degree in Manufacturing Engineering Technology or another STEM related field. The Institute also has an articulated agreement with Ferris State and Western Michigan University, allowing students to easily transfer their credits to these institutions.
ECMC recently announced the selection of its eighth cohort of 80 students that will begin the program in August 2019 with Early College Orientation Camp on the MCC campus. This fall, 200 students representing all public schools in Muskegon County will participate in the program. To learn more visit www.muskegoncc.edu/ecmc.
The list of the 2019 Early College of Muskegon County completers follows:
- Laney Baldwin, Reeths-Puffer
- Joseph Barringer, Reeths-Puffer
- Shaina Benedict, Oakridge
- Trinity Bentley, Mona Shores
- Emma Berends, North Muskegon
- Katelyn Broughman, Muskegon
- Dareae Brown, Muskegon
- Samuel Brunink, Whitehall
- Alexis Carroll, Oakridge
- Zaria Coleman, Mona Shores
- McKenna Davis, Oakridge
- Megan Delgado, Reeths-Puffer
- Corinn Dykes, Reeths-Puffer
- Rylee Eklund, Orchard View
- Ethan Epplett, Oakridge
- Jenel Erickson, Reeths-Puffer
- Lauren Erndteman, North Muskegon
- Teresa Hall, Oakridge
- Tia Harris, Whitehall
- Ruth Hernandez, Muskegon
- Renee Hirsch, Reeths-Puffer
- Joseph Like, Orchard View
- Alexx Lohman, Montague
- Katherine Mitcheltree, Reeths-Puffer
- Kaylynn Moschke, Reeths-Puffer
- Mickayla Munroe, Reeths-Puffer
- Vanessa Padilla, Muskegon
- Delaney Parmley, Whitehall
- Hunter Pilkington, Reeths-Puffer
- Kacey Pittmann, Orchard View
- Madison Rigby, Whitehall
- Sunny Ross, Oakridge
- John Rybik, Whitehall
- Ethan Schaeffer, Whitehall
- Calvin Smith, Reeths-Puffer
- Tamera Smith, Mona Shores
- Maya Straley, Reeths-Puffer
- Kayla Thompson, Orchard View
- Zachary Tindall, Oakridge
- Marie Townsend, Ravenna
- Samantha Vallier, Reeths-Puffer
- Makayla Villanueva, Mona Shores
- Christopher Wyatt, Mona Shores


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To prevent another round of million dollar scandals due to fraudulent manipulations on spreadsheets, regulatory bodies have launched major offensives against these well-loved User Developed Applications (UDAs). Naturally, internal auditors are front and center in carrying out these offensives.
While regulations like the Sarbanes-Oxley Act, Dodd-Frank Act, and Solvency II can only be effective if end users are able to carry out the activities and practices required of them, auditors need to ascertain that they have. Sad to say, when it comes to spreadsheets, that is easier said than done.
Because spreadsheets are loosely distributed by nature, internal auditors always find it hard to: locate them, identify ownership, and trace their relationships with other spreadsheets. Now, we're still talking about naturally occurring spreadsheets. How much more with files that have been deliberately tampered?
Spreadsheets can be altered in a variety of ways, especially if the purpose is to conceal fraudulent activities. Fraudsters can, for instance:
- hide columns or rows,
- perform conditional formatting, which changes the appearance of cells depending on certain values
- replace cell entries with false values either through direct input or by linking to other spreadsheet sources
- apply small, incremental changes in multiple cells or even spreadsheets to avoid detection
- design macros and user defined functions to carry out fraudulent manipulations automatically
Recognising the seemingly insurmountable task ahead, the Institute of Internal Auditors released a guide designed specifically for the task of auditing user-developed applications, which of course includes spreadsheets.
But is this really the weapon internal auditors should be wielding in their quest to bring down spreadsheet fraud? Our answer is no. In fact, we believe no such weapon has to be wielded at all because the only way to get rid of spreadsheet fraud is to eliminate spreadsheets once and for all.
Imagine how easy it would be for internal auditors to conduct their audits if data were kept in a centralised server instead of being scattered throughout the organisation in end-user hard drives.
And that's not all. Because a server-based solution can be configured to have its own built-in controls, all your data will be under lock and key; unlike spreadsheet-based systems wherein storing a spreadsheet file inside a password-protected workstation does not guarantee equal security for all the other spreadsheets scattered throughout your company.
Learn more about Denizon's server application solutions and discover a more efficient way for your internal auditors to carry out their jobs.
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Squish Coco 4.2 introduces Code Complexity Metrics And Unifies Cross-platform Code AnalysisRead more
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