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Rush Limbaugh

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RUSH: Folks, the next caller wants to try to help me through my dictation problem here on my iPhone 4S. I realize this is kind of like talking about golf to some of you. “Stick to the issues!” But, believe me, it’s one of my passions here. So indulge me. This is Sean in Bloomington, Minnesota. What’s up? What, what, what, what what’s the story?

CALLER: Basically the way Siri works is there’s an activation ticket that gets sent to your phone every day. My guess is for some reason that’s expired, and it’s not getting renewed. The easiest thing you can do is go into Settings and then General and Siri and turn it off right there.

RUSH: Yeah?

CALLER: Then reboot your phone, go back into Settings, and turn it back on.

RUSH: You know, I thought about trying that, but when you try to turn Siri off it says, “We’re gonna take your kids and a bunch of other stuff, and it may be awhile before you get ’em back if you do this. Are you SURE you want to turn it off?” (chuckling)

CALLER: Yeah. It’ll come right back on.

RUSH: Okay, I’m gonna try that right now. You turn Siri off then shut down the phone?

CALLER: Yep. Turn the phone off then turn the phone back on.

RUSH: And then turn Siri back on?

CALLER: Turn Siri back on.

RUSH: What do you do for a living?

CALLER: I work with my father in a small business.

RUSH: Related to computers?

CALLER: No, it’s just a hobby of mine on the side.

RUSH: Yeah, that’s me, too. Me, too. Did this happen to you?

CALLER: Yes, I’ve had it happen a bunch of times. I’ve actually built servers to do what Siri does, but it doesn’t go through Apple.

RUSH: Well, now that’s fine for me. This is not that problem. Although Siri is working and it’s the dictation that’s not, it’s all the same thing.

RUSH: Okay that’s fascinating. So you just figured this out on your own because it’s a hobby of yours?

RUSH: Really, when you turn it off you get a message: “If you do this, you’re gonna lose everything Siri knows. It’s gonna be a while before it all comes back.” And I thought, “Well, I’ll try everything before I do that.” But, on your advice, I’ll do it even as we speak in the next commercial break.

CALLER: Sounds good.

RUSH: Now, how Applized are you? You have an iPhone obviously, right?

CALLER: Everything I own is Apple, practically.

RUSH: Yeah?

CALLER: If they make it, I’ve tinkered with it, Beta-ed it, anything you can imagine.

RUSH: Well, you have an iPad?

CALLER: I do have an iPad. My wife doesn’t.

RUSH: Well… Ho! Wait. Do you have a new Retina 15-inch MacBook Pro?

CALLER: I do not have one of the new MacBook Pros. I’ve wanted them and looked at them and drooled over them in the stores but haven’t had the cash to buy one.

RUSH: Well, I’ll tell you what. You stay on hold, and I will try your suggestion, and if it works I will send you a 15-inch MacBook Pro. I’ve got three of them sitting in there. I’ll send you one. You’ll have it tomorrow if it works, if your idea works. Are you game to try that?

CALLER: I am. I hope it works.

RUSH: I bet you do. (laughing)

CALLER: I have a couple other tricks that you could do, too, that aren’t the number one fix.

RUSH: Ohhhh, okay. All right. Well, I’ll play. I’ll play. So you hang on. This is Sean in Bloomington, Minnesota. You hang on. I’ll try this during the break, and if it works, you get the MacBook. By the way, your drooling is very justified. This is the fastest computer they’ve made. It’s the best computer they’ve made. The display will take you a while to grow into it, but there’s nothing like it out there. Okay, Sean, hang on. Thanks for the tip. That makes sense. My Siri ticket has expired. My certificate’s expired and I’ve got to restart it. I’ll try it. That sounds like it’ll work.

RUSH: All right, I have tried Sean’s method twice. I went in and disabled Siri. Shut the phone down, rebooted, enabled Siri, and it still isn’t working. There’s a real anomaly here, too. For those of you familiar with this, the alert tone you get when you either use Siri or hit the dictation button, my alert tone is half as loud, if that, as when it’s working normally. Now, what happens, your dictation’s sent to Apple servers. They transcribe it as text and send it back to your device.

It’s amazing. I mean literally what they’ve done is stunning. This happens in split seconds. But I got a server problem here ’cause I’m not getting anything back, and I don’t know if what I’m sending is getting to them. So now what do I do? Sean, I told him I’d send him a new Retina display MacBook Pro 50 if it worked. Snerdley’s being a hard guy. See, if I wanted to go the Obama route, I’d say, “Oh, well, I’ll give it to him anyway, even though that wasn’t the deal.” But he said he had other ideas if this didn’t work. So we’ll maybe see if we can get back in touch with him.

RUSH: Okay. So we’re gonna try again. We’re now back with Sean in Bloomington, Minnesota. Sean, I’ve tried it three times to no avail. I don’t know if you heard me say I’m running Beta on this.

RUSH: You heard that. Okay. I don’t want to be too loud about that if you get my drift here, but I’m running Beta. I’m running Beta 3. It worked for two days and then stopped. I’m running the same Beta on an iPad, no problems whatsoever. It’s just this one phone that is the problemo.

CALLER: I did look online a little bit while I was off when you were still on break and everything. There have been rumors from a couple people that I’ve seen that are big names in the iPhone world that have said Siri on iPhones iOS Beta 3 doesn’t work the first time when you install Beta 6. A lot of them have said if you restart and reinstall Beta 3, it should fix the problem.

RUSH: Yeah, that’s the last thing I was looking to do.

RUSH: That’s a pain in the rear.

CALLER: That was gonna be your last ditch. You wouldn’t want to do that.

RUSH: Well, it’s a three-hour project to do that.

CALLER: Yeah, exactly. But there’s one other thing I had that I’m praying will work ’cause I would love a MacBook Pro.

RUSH: (laughing) What is it?

CALLER: If you go into Settings and then General again, down at the bottom there’s Reset. If you Reset Network Settings, it could just be there’s something blocking the connection to Apple, and that resetting the network settings could free up that block.

RUSH: Well, yes, yes. I could do that. I’ll try it. I’ll lose all my network passwords, but that doesn’t matter, I’ll have to restore them.

CALLER: That’s the only thing you’ll lose is your Wi-Fi passwords that you entered.

RUSH: Okay, I’m doing that now. We’ll see what happens. So, Sean, hang on here. Don’t hang up. Can you hang on?

CALLER: I can certainly hang on as long as you’re willing to have me.

RUSH: Well, it’s not gonna be more than five or six minutes. I just have the rest of the show to do here.

CALLER: (chuckling)

RUSH: Just don’t go away. We’re gonna put you on hold, just hang on.

RUSH: Okay, Sean are you back? You there?

RUSH: I reset the network settings, I reestablished the password for the local Wi-Fi network here, and still it doesn’t work. However, since you eventually did tell me what will no doubt work, but that I had been putting off (and that is a clean reinstall of the damn thing), I’m gonna send up the Retina MacBook Pro since you did know what it ultimately would take to fix this.

CALLER: Well, thank you.

RUSH: I just wish your first idea had worked. I hadn’t thought of that. Well, I did think of it, but I thought it would be a hassle. It turned out not to be. Anyway, I appreciate your assistance. I’m glad you took the effort. Here’s a guy who recognized my passion and tried to help me. I like that. So, Sean, you’ll have your 15-inch MacBook Pro Retina display via FedEx tomorrow.

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S3 Barre

The only barre workout in the world designed and choreographed by a physiotherapist! It fuses elements of dance and pilates, cardio and endurance exercises to create an intense and effective full body workout. It’s the ultimate barre workout!

Clinical Pilates

S3 Clinical Pilates is instructed by a physiotherapist and provides an effective form of exercise rehabilitation. After a detailed physiotherapy assessment, we provide individualised programs that are based on your injury history, movement preference and specific health goals. Small group sizes allow us to closely monitor you when using the reformer and trapeze apparatus, ensuring correct technique is always maintained. This is the perfect class for individuals wanting to rehabilitate from injury, manage pain, improve posture and increase functional strength.

reformer pilates.JPG

Reformer Pilates

Our small group Reformer Pilates sessions are designed by a physiotherapist and all programs are specifically targeted to meet your individual needs. In contrast to Clinical Pilates, which is suited for individuals rehabilitating from injury or requiring closer guidance, our Reformer Pilates offers exercise to improve fitness and general well-being.

Mat Pilates

Designed by a physiotherapist, S3 Pilates builds upon traditional pilates principles and exercises to create the ultimate pilates based workout to Stretch, Strengthen and Stabilise! It is highly effective and efficient, but most importantly safe and fun!

A physiotherapist designed HIIT programs utilising suspension training, bodyweight exercises, kettlebells and weights. It’s intense, challenging, effective AND safe!

We offer a variety of yoga classes - Ashtanga, Yin and Hatha. Each is taught by expert instructors who live, breathe and dream yoga! Each class is tailored to suit all levels - from beginners to advance participants.

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Protecting DB pension schemes – A Stronger Pensions Regulator

On 26 June 2018, the DWP published the first of the consultations promised by this year’s White Paper (see our Alert), “Protecting [DB] pension schemes – a stronger Pensions Regulator”.

Click here for a PDF of this Alert.

In this Alert

Key points

The consultation seeks views on proposals in three key areas:

  • increasing TPR’s and trustees’ access to timely information to allow greater corporate oversight
  • extending the sanctions regime to deter wrongdoing and to punish it when necessary and
  • improving TPR’s existing anti-avoidance powers.

The Government aims to improve TPR’s oversight of corporate transactions by broadening the current notifiable events regime and introducing a new requirement for sponsors to produce a “declaration of intent” (to be addressed to the scheme’s trustees and shared with TPR) prior to certain business transactions.

The DWP proposes extending the existing penalty regime to include a new power to impose a civil penalty of up to £1 million for serious breaches and new criminal offences to punish wilful or grossly reckless behaviour in relation to a DB scheme.

The online consultation certainly raises the question of how strong TPR’s powers should be (“something stronger than tea?”)

The White Paper, “Protecting [DB] Pension Schemes” was published in March 2018. In it, the Government argued that the existing regulatory system is working well for the majority of DB pension schemes, members, trustees and sponsoring employers but that it could see ways in which it could improve the system further. It is now working to make these improvements and will be carrying out a number of consultations focused on different areas.

This first consultation sets out the Government’s proposals to improve TPR’s powers so that it:

  • can be more proactive and get involved earlier when employers make changes which could impact their pension scheme
  • can obtain the right information about a scheme and its sponsoring employer, and
  • is able to gain redress when things go wrong.

Corporate Transaction Oversight

Notifiable Events Framework

The purpose of the notifiable events regime is to assist TPR in reducing the risks of situations arising that may lead to calls on the PPF. When an event is notified to TPR, it is intended to serve as an early warning mechanism of potential financial difficulties, which in turn might result in the PPF having to assist a scheme.

The DWP considers that the notifiable events framework could be improved by broadening the range of employer-related events which need to be reported to include, for example:

  • the granting of security on a debt to give it priority over the scheme
  • the significant restructuring of the employer’s board of directors
  • the taking of independent pre-appointment insolvency / restructuring advice.

The DWP also proposes bringing the timing for notification forward and extending the reporting obligation to other parties, for example, the directors of a sponsor’s parent.

Declaration of intent

The Government proposes that, subject to certain risk criteria, particular transactions (such as the sale of a controlling interest in a scheme employer), should trigger the production of a “declaration of intent”. The aim being to oblige corporations to think about how their decisions will affect the pension scheme(s) “in more detail and at an appropriately early point in the transaction process”.

The declaration would be addressed to trustees from the transaction’s corporate planners (usually the board of directors), shared with TPR and should:

  • explain the nature of the planned transaction
  • confirm both that the corporate planner has consulted on its terms with the trustees and the trustees’ agreement (or otherwise) to the planned transaction
  • explain any detriment to the scheme and how this is to be mitigated.

Declarations of intent would work closely alongside the notifiable events framework but would be required at a later point in a corporate transaction, when there is greater certainty as to the nature of the transaction, whether it will go ahead and the implications for the scheme.

Voluntary clearance regime

Under the voluntary clearance regime, companies can seek confirmation from TPR that, in the circumstances set out in a clearance application, TPR does not consider that it would be reasonable to use its anti-avoidance powers to issue a financial support direction (“FSD”) or a contribution notice (“CN”).

TPR will be reviewing its current guidance on the clearance process with the aim of clarifying its expectations as to what employers and trustees should do.

Improved powers for TPR

TPR’s current powers are relatively limited in scope. For example, it is able to penalise individuals and corporate entities for non-compliance with a range of duties by imposing civil penalties of up to a maximum of £5,000 or £50,000 (respectively).

The Government proposes introducing additional options to enable TPR and/or the Courts to impose more severe penalties in certain circumstances. The new regime would include:

  • the continuation of the existing civil penalties for low-level non-compliance
  • a new TPR power to issue a civil penalty of up to £1 million for more serious breaches, such as those which have resulted in actual harm to the pension scheme or have the potential to do so if left unchecked
  • new criminal offences to punish “wilful or grossly reckless behaviour” in relation to a DB scheme, non-compliance with a CN and failure to comply with the notifiable events framework.

The DWP believes that the range of possible targets for these penalties should include all of those who have responsibility for the scheme, ie directors, sponsoring employers, any associated or connected persons and, in some circumstances, the trustees themselves.

In order to protect the benefits of pension scheme members and to ensure that pension liabilities are not avoided or unsupported, the Pensions Act 2004 gave TPR the power to issue:

  • CNs (requiring payment to be made into a scheme);
  • FSDs (requiring financial support to be put in place for a scheme).

Please see, “Anti-avoidance: TPR’s powers for further details”.

The DWP proposes technical changes to bolster both the CN and FSD regimes and, in particular, would like views on:

  • improvements to TPR’s current powers to make it easier to compel related companies to provide financial support to a scheme, and to require companies to compensate a scheme if they have caused loss or detriment to it
  • how this should be enforced.

Next steps

This consultation closes on 21 August 2018.   If the proposals are implemented in their current form, they will raise the stakes considerably for all employers and trustees involved in occupational pension schemes. The aim appears to be to change the nature of boardroom discussions on pensions so the situation is not reached where TPR needs to bring out the big guns.

Over the coming months, TPR will be talking to “interested stakeholders” on the design of clearer funding standards and this is intended to culminate in a formal consultation on a revised DB Funding Code of Practice in 2019. The DWP also plans to consult on the design of the legislative framework and authorisation regime for commercial consolidation of DB pension schemes later this year.

For more information

Janet Brown

+ 44 (0)20 7615 9554

Georgina Jones

+ 44 (0)20 7615 9596

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National Pet Month runs from April 1st to May the 7th and to celebrate, we’re giving away a Wi-Fi camera! As a nation of pet lovers, we know how much your furry friends mean to you, which is why we’re helping you keep an eye on yours. Whether you own a bird, a reptile, a rodent or a cat or a dog, there’s no doubting that a pet enriches your life.

45% of the UK’s population own a pet, with the most popular being a dog. However, with research showing that five dogs are being stolen every day across the UK, we thought we’d give you some tips on how to help you keep your dog safe.

It’s a legal requirement for a dog to be microchipped, but you should make sure that the details are up to date. Your dog should be microchipped from 8 weeks of age by law.

ID Tag
Another legal requirement, you should make sure that your dog wears an ID tag on its collar when it is in public. Put your name, address and mobile number on the tag, not the dog’s name, as this could encourage your dog to trust a stranger if it hears its name being called.

It is very tempting, but you should never tie your dog up outside a shop. Unfortunately, many dogs get stolen this way.

Similarly, don’t leave your dog alone in a car, as it can be an easy opportunity for thieves.

Try to vary the timings and routes of walks, as some dogs are specifically targeted and grabbed while out. You should also be wary of strangers asking you questions about your dog – particularly if you’ve never seen them before.

Pedigree vs Non-Pedigree
While pedigree dogs are more at risk of theft, it doesn’t mean that non-pedigree dogs are safe, as some thieves will rely on the owners offering a reward.

So, to help keep your pets safe in your home, we’re giving away a Yale Wi-Fi enabled Camera which means that you can check up on your furry friend whenever you want – with the added bonus of keeping your home safe too. The camera can detect motion, triggering HD 720p video recording which you can view on your smartphone, so you make sure your pets aren’t up to too much mischief while you’re away. You can also talk to your pets and hear what they say back to you!

All you have to do to enter is share a photo of you and your pet with the hashtag #SafeNPMComp on Facebook or Twitter, making sure to tag @TalkWithSafe too. The competition is open for just a week so make sure you enter now! Good luck!

Competition T&Cs

  1. The competition starts on Monday 30th of April and will run until midnight on Monday 7th
  2. The prize is one Yale Smart Living Wi-Fi Enabled IP Camera. If the prize is unavailable at the time of the competition ending, a prize of equal value will be provided.
  3. Entrants must be over the age of 18.
  4. To qualify, entrants must share a photo of themselves and their pet on Facebook or Twitter using the hashtag #SafeNPMcomp and tagging the relevant Safe social media profile.
  5. Entrants can enter once on each platform.
  6. UK residents only.
  7. This competition is not open to The Safe Shop Ltd employees, their families or any other person or company directly connected with this competition.
  8. Winner will be chosen within 7 days of the competition closing. Winner will be contacted on Twitter or Facebook and will be displayed on our Facebook and Twitter pages as way of notification.
  9. Once the winner has been notified it is the responsibility of the winner to confirm their full name and address. If no details are provided for any reason, The Safe Shop Ltd reserves the right to disqualify that entry and select an alternative winner.
  10. By entering this competition, you give The Safe Shop Ltd permission to re-use your photo on social media for marketing purposes.
  11. By entering this competition, you give permission for The Safe Shop Ltd to display your first name, surname and home town or county on our site and social media channels should you win the competition.
  12. Winner may be contacted by The Safe Shop Ltd for marketing purposes once the competition is closed.
  13. The Safe Shop Ltd accepts no liability for any loss of entries caused by a technical fault.
  14. Any personal data relating to participants will be used solely in accordance with the UK Data Protection Act 1998 and will not be disclosed to a third party without the participant’s prior consent.
  15. The Safe Shop Ltd’s decision is final and no correspondence will be entered into.
  16. The Safe Shop Ltd reserves the right to change these Terms & Conditions at any time.
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Case Study: Gopher Study

When a newly planted Thousand Oaks backyard sustained severe damage from gophers over a one year period, the homeowner was advised to use root cages when re-planting.

Instead of resorting to rodenticide, the homeowner acted on this advice and has found this approach to be effective, “Using the root cages couldn’t be simpler.  I simply inserted the root ball into the wire mesh pockets and planted as normal. One month on the plants are thriving and have not been attacked by gophers.”

Root cages are made of malleable wire mesh and manufactured in a range of gallon size pockets for all types of plants. They are available online and at hardware stores.

Pictured Root Cages Below:


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Airglow Disney

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About the collection

The exterior of the Airglow Disney tablet sleeves is neoprene which helps to protect your tablet against dust and scratches. In order to take the tablet safely to anywhere, we also added handles to the sleeves.


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Dobson's Bar & Restaurant

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Dobson's Bar & Restaurant

Dobsons Bar and Restaurant
956 Broadway Circle
San Diego, CA 92101
Lunch: Mon - Fri 11:30 a.m. - 3 p.m. Dinner: Mon - Sat 3 p.m. - 10 p.m.

Dobson's Bar & Restaurant Information

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Learn more about Dobson's Bar & Restaurant...

Quick Facts About Dobson's Bar and Restaurant:

  • San Diego Dobson's Bar and Restaurant is located in the Gaslamp District.
  • Dobson's Bar and Restaurant in San Diego is owned by and named after American professional bullfighter Paul Dobson.
  • San Diego's Dobson's Bar and Restaurant serves Californian cuisine with Italian, Spanish, French and Asian influences.

Ambiance: Wood-paneled walls, stained glass windows and plaques engraved with regulars' names are signature features at San Diego Dobson's Bar and Restaurant. However, the lunchtime clientele is what really creates the atmosphere as the San Diego politicos, lawyers, NBC staffers and the City Hall crowd gather in their power suites and ties to dine on Dobson's bar room burgers. The bar area is uniquely still set in the imported mahogany and tiger oak from England that was designed in 1913 as part of the Spreckels Theater buffet, which was the original establishment in 1913.

Why We Dine: The prix fixe menu at San Diego Dobson's Restaurant and Bar is convenient for guests who don't want to be overwhelmed with choices or prices. The prix fixe menu offers a little bit of everything with its limited menu of appetizers, entrees and desserts for you to choose from at a specific set price. Dobson's also presents a happy hour every weekday evening to help you de-stress from the work day, and for those that still look forward to dessert more than the meal, the restaurant offers an assorted dessert and after dinner drink menu.

  • Prix Fixe Menu: San Diego Dobson's Bar and Restaurant provides a predetermined menu, in which you can choose your choice of a starter, entree and dessert at a set price. The current prix fixe menu features your option of Dobson's mussel bisque in croute, salade mesclun or chicken liver pate for starters, seared sea scallops, grilled salmon or 6 oz. ribeye steak for dinner and either creme brulee, cappuccino brownier or banana strudel as a dessert all for a fixed fee of $35.
  • Happy Hour: Every Monday through Friday between 4pm and 6pm Dobson's bar hosts happy hour with $1.50 draft beers and $3 margaritas, which offer a sure way to kick back and unwind after a long day at work. Indulge in a strong cocktail at the historic 1913 wooden bar and let your stress melt away.
  • After Dinner Dessert and Drinks: San Diego Dobson's Bar and Restaurant understands that after dinner treats are the grand finale to your meal and therefore it offers a vast selection of desserts, spirits, cognacs and cordials to top off your decadent dinner. Berry cobbler, banana foster and sorbet are a few of the sweets that grace the dessert menu while Dobson's Huevo post-dinner cocktail is an inviting combination of Spanish liquor 43, steamed milk and espresso.

The Local Scoop: San Diego's Dobson's Bar and Restaurant is just a short walk away from the Convention Center, so it's no surprise as to why it's a business mecca perfect for a pick-me up between conference meetings at the center. The restaurant is also only one block from the Civic Theater making it the ideal spot to grab a pre-show dinner or cocktail.

What We Recommend:

  • Ravioli Trio: While Dobson's Restaurant and Bar serves an eclectic menu of internationally infused cuisine, this pasta dish is obviously Italian inspired with its wild mushrooms, roasted vegetables and four cheeses splashed with tomato sauce.
  • Fried Oyster Salad: A delicious combination of fried oysters, cherry tomatoes, avocado and smoked bacon drizzled with a cucumber avocado ranch, this dainty salad makes the ideal addition to the seared sea bass or linguine and clams.

  • Cuisine: American
  • Alcohol: Full Bar
  • Reservations: Reservations highly recommended
  • Price: $$$

Dobson's Bar & Restaurant Map


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The Sikh Project

March 8 @ 10:00 am - 5:00 pm

|Recurring Event (See all)

An event every day that begins at 10:00am, repeating until March 24, 2018

Sikhs have been a vital part of America for over 125 years.  The Sikh project is a collection of stunning portraits that capture the beauty and diversity of the community and recognize the challenges and triumphs of what it means to be a Sikh in America.

This exhibit, with images by London photographers Amit and Haroop, focuses on the turban, which is an integral part of the Sikh identity.  The turban, as an article of faith in Sikhism, is a public declaration of sovereignty and equality.  Not only beautiful, the turban represents distinction, tolerance and justice.

Many of those depicted are residents of the Washington, D.C. metro area including a U.S. Army captain, a former American Idol contestant, and the Sikh Captain America.

Sikh Project


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We’re Number One

No, not me. I don’t care much about my own market share, in case you haven’t noticed.

It’s Sony. They’ve once again launched a press release claiming being “first” at something, this time full frame interchangeable lens camera volume and dollar volume in the United States for the first six months of 2018.

Sorry for the very specific qualifiers, but this is how the statistics-into-press-release game is played.

Thing is, because the data is protected by NDA, I can’t really talk about or show the numbers, and it would really help to be able to be specific. It’s an ephemeral victory, if we can call it that, as Sony’s numbers are helped by being the only one to introduce a new full frame interchangeable lens camera in the period claimed, and you can’t generally get a meaningful long-term read off long-term sales in the first few months of a new camera introduction.

Meanwhile, Nikon’s D850 is still sales limited by how many NIkonUSA imports each month. Basically it’s a sold out camera whose upper end of sales volume is not known. And it’s more than holding it’s own against each of the Mark III A7 models.

What’s really confusing is that Sony likes to make these “wins” more dramatic by putting up the most confusing charts known to man. Like the following one:

bythom sony numberone

That chart looks really impressive, but if you read it correctly, it’s actually an indictment of where Sony was in 2016.

  • From 2016 to 2017, overall full frame dollars increased 3%
  • From 2017 to 2018, overall full frame dollars was flat (-0%)

So in two-and-a-half years the full frame camera market has remained about the same size. Meanwhile:

  • From 2016 to 2017, Sony’s dollars increased 67%
  • From 2017 to 2018, Sony’s dollars increased 78% (same six-month period)

What drove the 2017 and 2018 increases? The new A7Rm3, A9, and A7m3 models that were introduced. All higher priced cameras (the m2 models by that point were often highly discounted).

In that same period, Canon introduced the EOS 6Dm2, and Nikon the D850. In other words, Sony introduced three high priced models in the time period, Nikon one, and Canon introduced at the lower end of the spectrum (basically at the A7m3 price). Cameras such as the Nikon D610 and D750 were quite old during the measured period; I’d submit that most people that want one already have one.

So what does Sony’s claim really look like when graphed more appropriately? For dollars, it looks like the following (I don’t have the full set of NPD data for the entire time periods involved here, so I’ve had to guess a bit at some missing values, but these charts shouldn’t be off too far from the exact numbers):

bythom sony charted

Full frame sales in dollars*

*Yeah, Sony’s footnotes need footnotes. The above chart is based upon dollars. And that includes kit lenses, if included in the sale. Canon and Nikon already had a large number of full frame users prior to this period, so more of their sales were body only than Sony’s, which distorts the dollar numbers.

Don’t get me wrong: Sony managed to do something that nobody really thought was possible (reach Canon/Nikon level of full frame sales). They should be proud of that and promote the accomplishment, as they’ve done. But you’ll note that the pie charts above—which use the same numbers—don’t look quite as dramatic as Sony’s ;~).

Those of us who analyze the camera market generally look at longer-term patterns than the two year pattern Sony is pointing to. Why? Because new model introductions distort the overall picture, certainly for the six month period around the launch(es). Sony had a launch in the first half of 2018 while neither Canon nor Nikon did, and Nikon’s best selling full frame camera is still not being brought into the US market at the level of demand (e.g. it is still sold out nearly a year after being introduced).

Sony’s press release is carefully timed. Nikon is next to launch cameras in this category, and it should distort the numbers considerably in a different direction for the second half of the year. In fact, my prediction is that this will distort the numbers about as far as Nikon can manage to distort them in terms of shipping products (that’s a veiled way of saying that I believe we’re going to similar issues with their new full frame mirrorless system as they have with the D850: it will be out of stock due to demand exceeding supply).

Does it really matter?

Yes and no. No in the sense that all the cameras we’re talking about are fairly low in overall production numbers, typically near the 10k/month mark best case. But because of their high prices, they pull a lot of dollars. And because they’re high end cameras they pull a lot of Internet discussion about performance and features, and which one is “the winner."

Be thankful we live in a time when we’ve got plenty of choices, and very good ones, at that. We haven’t had such a hotly contested three way competitive race in ILC since Minolta introduced autofocus back in the film SLR era. If you don’t remember that period, that was also a time when Canon and Nikon ratcheted up their development to match an upstart. Competition is good for all users. Let’s just welcome it and not get too hung up on who’s number one, two, and three, as it’s almost certainly going to bounce around as new cameras are introduced.

text and images © 2018 Thom Hogan
portions Copyright 1999-2017 Thom Hogan-- All Rights Reserved
Follow us on Twitter: @bythom, hashtags #bythom, #sansmirror


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Worldwide Delivery
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When I found your website, I fell in love with the look of that key and debated a couple days before ordering.  I am sure glad I did.  The keys are beautiful!   One for me and one for each of my two girls who will have this tradition with their families for years to come.  This year, I’ll start it and my Grandson will be thrilled!  Next year, I think I’ll get us Santa’s Wish Angel  :)  Thanks again!   Denise P. Dear Santa’s Official North Pole Mail, My lil guy finally received his letter and Santa's magic key, I've never seen him more excited!!! He wanted to hang the key already, to make sure he doesn't forget lol I'm so happy I did this, well worth it!! Thank you Official North Pole Mail. - Robbie V. Dear Santa’s Official North Pole Mail, THANK YOU for bringing an almost unbelievable level of excitement, joy and happiness to an 8 yr-old boy and to his 6 yr-old sister with your Letters from Santa, Certificate, snow and Santa’s Key ! 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202 Jaffe Building

PDF icon Curriculum Vitae

David Brownlee is a historian of modern architecture whose interests embrace a wide range of subjects in Europe and America, from the late eighteenth century to the present.

Professor Brownlee has won numerous fellowships, and his work has earned three major publication prizes from the Society of Architectural Historians. He is a recipient of the University of Pennsylvania's Lindback Award for Distinguished Teaching.

After chairing the committees that proposed the reshaping of the University's undergraduate residences in 1997, he directed the implementation of a comprehensive system of College Houses and served as Director of the Office of College Houses and Academic Services for four years.

See Professor Brownlee’s lecture “The Fall and Rise of the World Trade Center,” given at the University Museum on the tenth anniversary of 9/11, at http://www.youtube.com/watch?v=qnLqLDFquUo

His film "Philadelphia: Our Nation's First World Heritage City," produced and directed by Sam Katz, was made in 2016 to explain Philadelphia's new designation, for which he had worked.  It is viewable at https://youtu.be/Jktrd4I681Q

Selected Publications

His books include Louis I. Kahn: In the Realm of Architecture (with David G. De Long,1991, translated into four other languages), Making a Modern Classic: The Architecture of the Philadelphia Museum of Art (1997), Building America's First University: An Historical and Architectural Guide to the University of Pennsylvania (with George Thomas, 2000), Out of the Ordinary: Robert Venturi, Denise Scott Brown and Associates: Architecture, Urbanism, Design (with David De Long and Kathryn Hiesinger, 2001), and The Barnes Foundation: Two Buildings, One Mission (2012).

Courses Taught

History of Art 100 Freshman Seminar: Building Philadelphia (Spring 2015)
History of Art 101 Introduction to Western Art, from 1400 to the Present (Spring 2013)
History of Art 270 The Modern City (Fall 2014)
History of Art 271 Modern Architecture I, 1700-1900 (Fall 2016)
History of Art 277 The Rise of Modernity: Arts of the Nineteenth Century, with Andre Dombrowski (Fall 2013)
History of Art 281 Modern Architecture II, 1900-present (Spring 2017)
History of Art 300 History of Art Methods: Architectural History and Theory (Fall 2010)
History of Art 301 Undergraduate Seminar: Frank Lloyd Wright (Spring 2013)
History of Art 303 Undergraduate Seminar: Introduction to Museums, with Ann Blair Brownlee (Spring 2017)
History of Art 571 Modern Architectural Theory (Fall 2016)
History of Art 581 Architects, Historians, and the Invention of Modern Architecture, with Daniel Barber (Spring 2014)
History of Art 771 Seminar in Nineteenth-century Architecture (2010 topic: Gothic Revival)
History of Art 781 Seminar in Twentieth-century Architecture (2013 topic: Paul Philippe Cret)

Field of Study


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Markets eye Bank of Canada rate cut for first time as oil rout damage deepens

(January 15, 2015 , posted in Economy)

Collapsing oil prices and a weakening economy are pushing markets to start pricing in a potential interest rate cut by the Bank of Canada this year.Those expectations grew Tuesday after Bank of Canada deputy governor Timothy Lane gave a speech in Madison, Wisc., that economists saw as tilting more dovish than usual. Mr. Lane’s speech focused on the economic effects of dropping oil prices, which has become a central concern for policymakers in Canada.“Lane’s final phrase that ‘however things play out, we have the tools to respond’ highlights that lower rates are an option if conditions weaken sufficiently,” said Benjamin Reitzes, senior economist at BMO Capital Markets.  -


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3358 164th St

"Morgan Creek - Exceptional, 7,100sf home on a spectacular 20,000sf lot adjacent to Morgan Creek Golf Course w/ Mtn views. This grand home greets you at its entrance w/ soaring ceilings and an abundance of natural light. Quality construction and attention to detail is evident throughout with gorgeous hardwood floors, arched doorways and extensive millwork. Gourmet kitchen is a delight for entertaining w/ quality appliances & adjacent prep kitchen. Also on the main is the lrg, inviting Mstr bdrm w/ elegant ensuite and his/hers closets. Upstairs is 2nd Mstr bd with 2 other spacious bdrms. Walkout bsmt is very bright w/ wine rm, games rm & gym. Backyard is entertainer's dream w/ huge covered deck & large pool. Call today!

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House/Single Family
2 Storey w/Bsmt.
October 2014
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V3S 0G5

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Sasso Home Marketing Group HomeLife Benchmark Realty (White Rock) Corp. Phone: 604-531-1111 Fax: 604-648-8048 Toll Free: 1-800-521-9666


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C. Savio Chan, PhD

Email | Twitter | Pubmed | GoogleScholarNU | NUIN

Dr. Chan started his research group in 2012 at Northwestern University, Department of Physiology.

The overarching research objective of his laboratory is to study cellular communications in the brain and how disruption of these processes contributes to neurological dysfunctions. The primary focus has been on reconstructing the electrical properties, signal transduction mechanisms, and anatomical connectivity of identified neuron classes in the external globus pallidus (GPe). The yielded knowledge should inform the roles of the GPe in controlling motor function in both health and disease. The impact of Dr. Chan's work is demonstrated by the clinical trials driven by his research.

Alexandria Granados

Alexandria received her undergraduate degree in Biology from North Park University, Chicago, IL.  After working in an emergency veterinarian clinic, she joined the Chan laboratory in October 2016.  She enjoys volunteering and making a commitment to programs that assist inner city youth.  Alexandria is interested in the Master of Public Health Program at Northwestern.

Nicole Curtis

Nicole received her undergraduate degree in Molecular and Cellular Biology from the University of Illinois at Urbana-Champaign, along with a minor in Chemistry in 2017. She joined the Chan Lab in August 2018 after moving back home to Chicago. She enjoys spending time with family and exploring what the city has to offer. She plans to continue on to graduate school once she has been able to explore more fields and job opportunities.

Brianna Berceau

Brianna earned her Bachelor of Science in Neuroscience and Behavioral Biology in 2015 from Emory University. She joined the Chan lab in January 2017 and is particularly interested in understanding the neural mechanisms that underlie neurodegenerative disease. Brianna is a sports enthusiast with a passion for the outdoors, working out and spending time with family. She plans to pursue a Doctor of Physical Therapy with a specialization in neurology.

Qiaoling Cui, PhD

Qiaoling received her PhD from the Chinese University of Hong Kong. She exchanged in Chan lab during the last two years of her PhD study. After graduation in 2012, she joined Chan lab as a postdoctoral fellow. Utilizing mostly ex vivo approaches, she has been studying synaptic transmission in the basal ganglia and how it is altered in mouse models of Parkinson's disease. She is interested in continuing research with the basal ganglia and integrating more studies with intact animals. After work, she enjoys hiking, classical concert and appreciates the nature beauty of the US.

Harry Xenias, PhD

Harry received his PhD from Rutgers University. He is a post-doctoral fellow studying alterations of pallidostriatal input in both healthy rodents and rodent models of Parkinson’s Disease with the goal of understanding normal basal ganglia circuit function and how it goes awry in disease.  He uses both ex vivo and in vivo techniques that include whole-cell recording and optogenetics.  On his off-hours, he enjoys working out and running.

Suraj Cherian, PhD

Suraj received his PhD from the University of Vermont. He is currently trying to understand how intrinsic and synaptic properties of striatal projection neurons are altered in dysregulated neural circuits related to Parkinson's disease and dystonia. Apart from work, he enjoys spending time with his family.

Arin Pamukcu

Arin is a graduate student in the Northwestern University Interdepartmental Neuroscience Program. She received her Bachelor of Science in Neuroscience with a minor in Chemistry from Duke University. During her undergraduate studies, she worked with Dr. Cagla Eroglu on astrocytic regulation of synapse formation for her graduation with distinction project and received HHMI undergraduate fellowships for two years. For her graduate work, she is interested in understanding how alterations in the basal ganglia circuits lead to movement disorders. Outside of lab, Arin enjoys running, traveling, and being outdoors.

Zack Abecassis

Zack is a third year medical student at the Feinberg School of Medicine at Northwestern University. He also received undergraduate degrees in Industrial Engineering and Economics from Northwestern University. He was recently awarded a Howard Hughes Research Fellowship and will be spending the year in the lab working to classify a distinct class of neuron within the external globus pallidus. Outside of the lab, Zack enjoys spending time with his family, watching Chicago sports (with the exception of the White Sox) and spending time outdoors.

Daniela Garcia, MD

Daniela received her medical doctor degree in 2014 from the Central University of Venezuela. She is passionate about neuroscience and came to United States pursuing an academic career within a residency in Neurosurgery. Outside the lab, Daniela enjoys eating in restaurants, traveling, and playing ukulele.

Xixun (Flora) Du, PhD

Xixun received her PhD from the Medical College of Qingdao University in China. Her scientific work has focused on the effects of ATP-sensitive potassium channel activations on iron transport in dopaminergic cells during the development of Parkinson’s disease. She joined the Chan Lab in July 2018 and is interested in the important role of external globus pallidus in the modulation of movement in Parkinson’s disease. Outside of the lab, she likes to listen to music and enjoys life with her family.

Isabel Fan

Isabel is a part of Northwestern University’s class of 2019 where she is studying Neuroscience and Global Health. She began working in Chan Lab her freshman year of college and is currently researching the role of lactate shuttle systems in supporting mouse motor behavior. Isabel has many random interests such as knitting and fishkeeping, but most often spends her free time exercising at the university gym, cooking food, or spending time with friends. Her future plans include attending medical school and becoming a physician.

Jeff Win

Jeff is an undergraduate student at Northwestern University. He is currently majoring in Biological Sciences with a concentration in physiology and minoring in Economics. He joined the Chan Lab in January 2017 and is interested in studying the cellular makeup of the GPe and the neuronal pathways that could contribute to Parkinsonian symptoms. In his free time, he plays piano or goes to the gym.

Ahana Narayanan

Ahana is a sophomore at the Illinois Mathematics and Science Academy. She joined the Chan Lab in June of 2018, and is interested in how disruption of cellular communications in the brain can contribute to neurodegenerative diseases such as Parkinson's, and what we can do to develop novel treatments. Apart from working at the lab, Ahana enjoys singing, the arts, and spending time with her family and friends

Shubha Verma

Shubha is a junior at the Illinois Mathematics and Science Academy. She joined Chan Lab in September 2017, and she's interested in understanding the neural pathways and interactions behind Parkinson's disease. She hopes to study biology in the future, and in her free time she writes, plays volleyball, and plays music.

Alyssa Bebenek

Alyssa is a junior at St. Charles East High School. She joined Chan lab in June of 2018, with an interest in understanding the neuroanatomical and neurophysiological basis for Parkinsonian symptoms. Apart from the lab, Alyssa enjoys playing on her school's volleyball team, reading, and being outside with her dogs, family and friends.

Together. Everyone. Achieves. More.

Alumni & current positions

Jason Pitt, PhD

Assistant professor, University of Evansville

Kelly Glajch, PhD

Scientist I, Neurology Research, Biogen

Vivian Hernandez, PhD

Scientific writer, Takeda

Alan Goldberg, MD

Cardiology fellow, Rush University Medical Center

Katherine Young, MD

Pulmonary critical care fellow, Loyola University Medical Center

Tina Huang, MSc

Research Tech II, Department of Neurological Surgery, Lurie Children's Hospital

Ellie Hong

M.D. student, Northwestern University

Mike Fiske

Ph.D. student, Northwestern University

Elizabeth Augustine

Medical student, Chicago Medical School, Rosalind Franklin University


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1 bedroom Flat for rent: Brunswick Place, Hove

  • reception rooms 1
  • bedrooms 1
  • bathrooms 1
Reference: 36064_10015638

Key Features

  • One Bedroom Patio Flat
  • Contemporary Style
  • Lounge
  • Spacious Fitted Kitchen
  • Appliances Included
  • Utility Area
  • Available 23rd January
  • Patio Garden

A stunning and recently refurbished (2013) one bedroom lower ground floor flat with patio area. Modern contemporary design to include good size lounge with doors to patio, open plan and spacious fitted kitchen with breakfast bar to include integrated appliances, utility area to include washing machine, beautifully fitted bathroom suite with shower, sliding door leading to double size bedroom, large walk-in wardrobe. East facing patio area. Sought after Hove location having easy access to city centre & Hove seafront. Available from 23rd of Jan , Unfurnished. No pets. EPC E(43)

13' x 12'4 (3.96m x 3.76m)

13' x 6'8 (3.96m x 2.03m)

Tenant info

Rent in advance: 1 month
Deposit: 1 and a half months
Admin fee per tenant £200.00
Guarantor fee (if required) £30.00
TDS registration fee £50.00 If Sawyer and Co registers the deposit, £0.00 If the landlord registers it.

Holding fee/bond £250.00 If property is under £1000.00, £500.00 If over taken in advance. This forms part of the above costs and is subject to contract and conditions.

We wish to inform prospective purchasers that we have prepared these sales particulars as a general guide. We have not carried out a detailed survey, nor tested the services, appliances and specific fittings.

Room sizes are approximate.

Back to top ^

Reference: 36064_10015638

Contact Agent

Tel: 01273 778844


text:
Smug Parents of Good Eaters, Please STFU

Smug Parents Of Good Eaters, Please STFU

After several years of parenting, several thousand parenting articles written, and several million parenting articles read — I’ve learned one thing about being a parent: you should only speak for yourself. Assuming all parents should be able to duplicate your parenting “successes” is just dumb.

Celebrity chef Curtis Stone thinks it’s super easy to get children to eat well, because he happens to have two good eaters of his own. He and his actress wife have a garden where they grow fresh veggies – and Stone uses those freshly grown, beautiful celebrity veggies to make his son a green juice every morning. His son loves freshly squeezed green juice. And yours would too if you would just start parenting.

“Your kid is going to embrace whatever you expose them to, right, that’s just a fact of life,” Stone recently said while promoting his cookbook Good Food, Good Life. “People tell you, ‘no, no my kid likes this or my kid likes that’. My opinion is, that’s just not accurate.”

No! Your kids don’t have tastes of their own. They will literally eat whatever you put in front of them. You’re just not trying hard enough. (Please read the sarcasm here.)

Curtis may have lucked-up with some children who eat everything he feeds them, but just because he’s not currently experiencing the struggle, doesn’t mean it isn’t real. Picky eaters come from all different types of households. If you don’t happen to have one you should thank your lucky stars, not assume parents who do aren’t trying. I’ll also mention here that his kids are three and one — so he should seriously consider shutting up before his smug-parenting karma comes back to bite him in the ass.

When my first child started eating, he shoved anything I put in front of him into his mouth. I still remember his first bite – smooth, pureed avocado.  I was totally delighted when as a toddler he started popping capers, olives, and feta cheese into his mouth gleefully. Then he turned three and decided spaghetti and PB&J were the staples he’d like to have in his diet, thankyouverymuch. My two-year-old still loves everything I put in front of her, but I’m sure that will be changing soon. Another thing I’ve learned about parenting — never speak too soon.

Don’t expect Stone to offer his kid a hot dog either, because those are fucking poison: “Someone said to me on a TV show in America ‘But how do you stop your kid from eating hotdogs?’ I’m like that’s pretty easy, my kid has never eaten a hotdog because it’s full of shit. I don’t want him to have all the nitrates and crap that’s in a hotdog. Of course one day he will be invited to a party at a fast food restaurant and I’m not going to say no, you can live a life of course, but you are in charge of his day to day.”

He has admitted in the past that his kids love foie gras and Vegemite. Foie gras is made by force-feeding male ducks so they become so obese they can’t move, their livers basically turn into pure fat, and rich people around the world rejoice and gobble them up. Vegemite is full of preservatives, but who cares? Doesn’t matter. All I’m saying is, STFU, Curtis. Nobody’s perfect.

Apparently no one has told Stone the cardinal rule of parenting: anything you act smug and superior about will come back to haunt you. Just wait.

Related post: 25 Reasons My Kid Won’t Eat That


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Arizona E-Z Fletch Fletching Tool

Item No. 1790-7190

Add to cart options

Product Actions

Additional Information

Product Description

This carbon straight fletching tool is perfect for arrows 5/16" (.3125) diameter or smaller with a very slight offset. The straight works well with both right wing feathers and vanes of any style up to 5" in length. While the E-Z Fletch "Mini" lets you fletch short BLAZER style vanes up to 2 ¼" with maximum helical for more accurate arrow flight specifically designed for shooting tighter more consistent groups when shooting with broad heads.
  • Faster broadhead stabilization
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  • Fastest easiest most accurate fletching tool
  • Fletches 3 vanes at one time
  • Customize your arrows the way you want
  • Compact so you can fletch anywhere
  • Have fun - save money the e-z fletch way

Product Reviews


text:
Scholle Law Hero Banner

Stone Mountain, Georgia Auto Accident

Practice Area photoUnfortunately almost everyone who drives a car regularly will at some point in their life, be involved in a car accident. That accident can happen anywhere, even on the scenic roads in Stone Mountain, Georgia. When this happens, you should call Stone Mountain car accident lawyer Charles Scholle so that you have an experienced attorney fighting for your legal rights.  Luckily, most small collisions do not result in severe injuries, but a serious car accident can present a whole range of problems for the people involved.

Drivers must be responsible when on the road, both to themselves and those around them, each time they get behind the wheel. Impatience and distraction while driving lead to more preventable deaths than any other type of accident. Up to 80 percent of serious car accidents are caused by distracted driving and speeding just five seconds before the accident, according to the National Highway Traffic Safety Administration. Once these accidents happen, they contribute to the leading cause of brain injuries and spinal injuries in the United States, both of which may lead to permanent disability like paraplegia.

Additionally, many severe medical injuries that result from auto accidents are also accompanied by long-term financial and emotional burdens that require a period of recovery for both the victim of the accident and his family. Long-term physical injuries sustained in a car accident might not be immediately apparent. In many cases what seems like a minor personal injury can evolve into to permanent back or neck pain, herniated disks, ruptured spinal disks or traumatic brain injuries.

At Scholle Law, you can get the experience and expertise you need to build a strong case. Call now for a free consultation so that Charles Scholle can get you the maximum compensation you deserve. He is here to help you through this difficult time.
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"We're building a rocket.  We're building it bigger" -  Copenhagen Suborbital.
"We've got the biggest balls of them all" - AC/DC

I'll steal UniverseToday's summary, then tell you to skip reading everyone else's coverage of it (even mine):
Copenhagen Suborbitals, headed by Kristian von Bengtson and Peter Madsen, hope to launch the world’s first amateur-built rocket for human space travel. As of this writing, the launch countdown clock on the Copenhagen Suborbitals’ website reads 7 days and 12 hours, which would put the launch on August 30 at about 1300 GMT.
Let's skip the boring blah blah journalism stuff.  This is adventure, folks!  These folks have been working since 2004 to build the sucker, and there's a ton of construction pictures and 'rocket porn'.  Theirs is the ultimate DIY.

So drop everything and read the actual team's story on this SA thread.  You get dozens of pics and the entire week-by-week epic, from February 2004 to now, straight from the people doing it.

Why are you still here?  Okay, if you want 'context' or 'framing', rather than tons of pics and insight from the people actually doing it, fine.  There's a quote from the fictional Protagonist in Snow Crash, by Neal Stephenson:
Until a man is twenty-five, he still thinks, every so often, that under the right circumstances he could be the baddest motherfucker in the world. If I moved to a martial-arts monastery in China and studied real hard for ten years. If my family was wiped out by Colombian drug dealers and I swore myself to revenge. If I got a fatal disease, had one year to live, and devoted it to wiping out street crime. If I just dropped out and devoted my life to being bad. Hiro used to feel this way, too, but then he ran into Raven. In a way, this was liberating. He no longer has to worry about being the baddest motherfucker in the world. The position is taken.
Copenhagen Suborbitals says the same, in even fewer words.  In response to "You're sending a dude into space from a floating sea launch pad", they note:
I really don't know how to mention that we'll be towing the sea launch platform to location using our submarine without somehow coming across smug. Sorry.
The new space race just got even cooler.  We live in excellent times.

Satellite details on ProjectCalliope ('Music from Space', Launching Spring 2011)
Every Tuesday at The Satellite Diaries, every Friday at the Daytime Astronomer


text:
Development of an Efficient Haptic System for Tooth Processing

Article Preview

This paper focuses upon the research and development of a method for modeling human teeth. By the use of virtual reality and haptics technology an application was created, that allows dentists to prepare their next procedures or students to learn dental skills by visualizing a three-dimensional virtual human tooth and feeling real tactile sensations while touching or deforming the surface of the tooth.

Advanced Materials Research (Volumes 463-464)

Edited by:

Wu Fan

R. E. Sofronia et al., "Development of an Efficient Haptic System for Tooth Processing", Advanced Materials Research, Vols. 463-464, pp. 651-654, 2012

Online since:

February 2012

[1] Information on http: /dictionary. die. net/virtual%5C%20reality.

[2] Information on http: /en. wikipedia. org/wiki/Haptic_technology.

[3] R. Webster, R.S. Haluck, G. Zoppetti, A. Benson, J. Boyd, N. Charles, J. Reeser, A Haptic Surgical Simulator for Laparoscopic Cholecystectomy using Real-time Deformable Organs, in: Proceedings of the IASTED International Conference Biomedical Engineering, pp.219-222, (2003).

[4] M. Downes, M. Cavusoglu, W. Gantert, L. Way, F. Tendick, Virtual Environments for Training Critical Skills in Laparoscopic Surgery, in: Proceedings Medicine Meets Virtual Reality Conference, pp.316-322, (1998).

[5] L. Thurfjell, A. Lundin, J. McLaughlin, A Medical Platform for the Simulation of Surgical Procedures, in: Proceedings of Medicine Meets Virtual Reality Conference, pp.509-514, (2001).

[6] D.X. Wang, Y.R. Zhang, Y. Wang, P.J. Lü, R.G. Zhou, W.L. Zhou, Haptic rendering for dental training system, in: Science in China Series F: Information Sciences, Vol. 52(3), pp.529-546, (2009).

[7] C. Luciano, P. Banerjee, T. DeFanti, Haptics-based virtual reality periodontal training simulator, in: Virtual Reality, Vol. 13, pp.69-85, (2009).

[8] Information on http: /support. denx. com/dentsim_system_desc. html.

[9] Information on http: /www. kavousa. com/Default. aspx?navid=5210&oid=009&lid=Us.

[10] Information on http: /www. nissin-dental. net/index. html.

[11] J.F. Ranta, W.A. Aviles, The Virtual Reality Dental Training System- Simulating dental procedures for the purpose of training dental students using haptics, in: Proceedings of the Fourth PHANTOM Users Group Workshop, Vol. 4, pp.67-71, (1999).

[12] L. Johnson, G. Thomas, S. Dow, C. Stanford, An Initial Evaluation of the Iowa Dental Surgical Simulator, in: Journal of Dental Education, Vol. 64(12), pp.847-853, (2000).

[13] K. Montgomery, E. Herbranson, P. Brown, A haptically enabled dental simulator, in: Medicine Meets Virtual Reality (MMVR 13), (2005).

[14] L. Kim, Y. Hwang, S.H. Park, S. Ha, Dental Training System using Multi-modal Interface, in: Computer-Aided Design & Applications, Vol. 2(5), pp.591-598, (2005).

[15] C.J. Luciano, Haptics-based virtual reality periodontal training simulator, Phd. Thesis, Chicago, (2006).

[16] Information on http: /www. chai3d. org.

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The goal of the scientists, Stanford University cryptographer Dan Boneh and geneticist Gill Bejerano, along with their students, is to protect the privacy of patients who have shared their genetic data. Rapid and affordable genome sequencing has launched a revolution in personalized medicine, allowing doctors to zero in on the causes of a disease and propose tailor-made solutions. The challenge is that such comparisons typically rely on inspecting the genes of many different patients—including patients from unrelated institutions and studies. The simplest means to do this is for the caregiver or scientist to obtain patient consent, then post every letter of every gene in an anonymized database. The data is usually protected by licensing agreements and restricted registration, but ultimately the only thing keeping it from being shared, de-anonymized or misused is the good behavior of users. Ideally, it should be not just illegal but impossible for a researcher—say, one who is hacked or who joins an insurance company—to leak the data.

When patients share their genomes, researchers managing the databases face a tough choice. If the whole genome is made available to the community, the patient risks future discrimination. For example, Stephen Kingsmore, CEO of Rady Children's Institute for Genomic Medicine, encounters many parents in the military who refuse to compare their genomes with those of their sick children, fearing they will be discharged if the military learns of harmful mutations. On the other hand, if the scientists share only summaries or limited segments of the genome, other researchers may struggle to discover critical patterns in a disease’s genetics or to pinpoint the genetic causes of individual patients’ health problems.

Boneh and Bejerano promise the best of both worlds using a cryptographic concept called secure multiparty computation (SMC). This is, in effect, an approach to the “millionaires’ problem”—a hypothetical situation in which two individuals want to determine who is richest without revealing their net worth. SMC techniques work beautifully for such conjectural examples, but with the exception of one Danish sugar beet auction, they have almost never been put into practice. The Stanford group’s work, published last week in Science, is among the first to apply this mind-bending technology to genomics. The new algorithm lets patients or hospitals keep genomic data private while still joining forces with faraway researchers and clinicians to find disease-linked mutations—or at least that is the hope. For widespread adoption, the new method will need to overcome the same pragmatic barriers that often leave cryptographic innovations gathering dust.

Answers Hidden and Sought

Intuitively, Boneh and Bejerano’s plan seems preposterous. If someone can see they can leak it. And how could they infer anything from a genome they can’t see? But cryptographers have been grappling with just such problems for years. “Cryptography lets you do a lot of things like [SMC]—keep data hidden and still operate on that data,” Boneh says. When Bejerano attended Boneh’s talk on recent developments in cryptography, he realized SMC was a perfect fit for genomic privacy.

The particular SMC technique that the Stanford team wedded to genomics is known as Yao’s protocol. Say, for instance, that Alice and Bob—the ever-present denizens of cryptographers’ imaginations—want to check whether they share a mutation in gene X. Under Yao’s protocol Alice (who knows only her own genome) writes down the answer for every possible combination of her and Bob’s genes. She then encrypts each one twice—analogous to locking it behind two layers of doors—and works with Bob to find the correct answer by strategically arranging a cryptographic garden of forking paths for him to navigate.

She sets up outer “doors” to correspond to the possibilities for her gene. Call them “Alice doors”: If Bob enters door 3, any answers he finds inside will assume that Alice has genetic variant 3. Behind each Alice door, Alice adds a second layer of doors—the “Bob doors”—corresponding to the options for Bob’s gene. Each combination of doors leads to the answer for the corresponding pair of Alice and Bob’s genes. Bob then simply has to get the right pair of “keys” (essentially passwords) to unlock the doors. By scrambling the order of the doors and carefully choosing who gets to see which keys and labels, Alice can ensure that the only answer Bob will be able to unlock is the correct one, although still preventing herself from learning Bob’s gene or vice versa.

Using a digital equivalent of this process, the Stanford team demonstrated three different kinds of privacy-preserving genomic analyses. They searched for the most common mutations in patients with four rare diseases, in all cases finding the known causal gene. They also diagnosed a baby’s illness by comparing his genome with those of his parents. Perhaps the researchers’ biggest triumph was discovering a previously unknown disease gene by having two hospitals search their genome databases for patients with identical mutations. In all cases the patients’ full genomes never left the hands of their care providers.

Proof of Possibility

In addition to patient benefits keeping genomes under wraps would do much to soothe the minds of the custodians of those genome databases, who fear the trust implications of a breach, says Giske Ursin, director of the Cancer Registry of Norway. “We [must] always be slightly more neurotic,” she says. Genomic privacy likewise offers help for “second- and third-degree relatives, [who] share a significant fraction of the genome,” notes Bejerano’s student Karthik Jagadeesh, one of the paper’s first authors. Bejerano further points to the conundrums genomicists face when they spot harmful mutations unrelated to their work. The ethical question of what mutations a genomicist must scan for or discuss with the patient does not arise if most genes stayed concealed.

Bejerano argues the SMC technique makes genomic privacy a practical option. “It’s a policy statement, in some sense. It says, ‘If you want to both keep your genome private and use it for your own good and the good of others, you can. You should just demand that this opportunity is given to you.’”

Other researchers and clinicians, although agreeing the technique is technically sound, worry that it faces an uphill battle on the practical side. Yaniv Erlich, a Columbia University assistant professor of computer science and computational biology, predicts the technology could end up like PGP (“pretty good privacy”) encryption. Despite its technical strengths as a tool for encrypting e-mails, PGP is used by almost no one—largely because cryptography is typically so hard to use. And usability is of particular concern to medical practitioners: Several echo Erlich’s sentiment that their priority is diagnosing and treating a condition as quickly as possible, making any friction in the process intolerable. “It’s great to have it as a tool in the toolbox,” Erlich says, “but my sense…is that the field is not going in this direction.”

Kingsmore, Erlich and others are also skeptical that the paper’s approach would solve some of the real-world problems that concern the research and clinical communities. For example, they feel it would be hard to apply it directly to oncology, where genomes are useful primarily in conjunction with detailed medical and symptomatic records.

Still, Kingsmore and Erlich do see some potential for replacing today’s clunky data-management mechanisms with more widespread genome sharing. In any case, the takeaway for Bejerano is not that genome hiding is destined to happen, but that it is a technological possibility. “You would think we have no choice: If we want to use the data, it must be revealed.” Now that we know that is not true, it is up to society to decide what to do next.


text:
Jan van Deursen was baffled by the decrepit-looking transgenic mice he created in 2000. Instead of developing tumours as expected, the mice experienced a stranger malady. By the time they were three months old, their fur had grown thin and their eyes were glazed with cataracts. It took him years to work out why: the mice were ageing rapidly, their bodies clogged with a strange type of cell that did not divide, but that wouldn't die.

That gave van Deursen and his colleagues at Mayo Clinic in Rochester, Minnesota, an idea: could killing off these 'zombie' cells in the mice delay their premature descent into old age? The answer was yes. In a 2011 study, the team found that eliminating these 'senescent' cells forestalled many of the ravages of age. The discovery set off a spate of similar findings. In the seven years since, dozens of experiments have confirmed that senescent cells accumulate in ageing organs, and that eliminating them can alleviate, or even prevent, certain illnesses (see 'Becoming undead'). This year alone, clearing the cells in mice has been shown to restore fitness, fur density and kidney function. It has also improved lung disease and even mended damaged cartilage. And in a 2016 study, it seemed to extend the lifespan of normally ageing mice.

“Just by removing senescent cells, you could stimulate new tissue production,” says Jennifer Elisseeff, senior author of the cartilage paper and a biomedical engineer at Johns Hopkins University in Baltimore, Maryland. It jump-starts some of the tissue's natural repair mechanisms, she says.

This anti-ageing phenomenon has been an unexpected twist in the study of senescent cells, a common, non-dividing cell type first described more than five decades ago. When a cell enters senescence—and almost all cells have the potential to do so—it stops producing copies of itself, begins to belch out hundreds of proteins, and cranks up anti-death pathways full blast. A senescent cell is in its twilight: not quite dead, but not dividing as it did at its peak.

Now biotechnology and pharmaceutical companies are keen to test drugs—known as senolytics—that kill senescent cells in the hope of rolling back, or at least forestalling, the ravages of age. Unity Biotechnology in San Francisco, California, co-founded by van Deursen, plans to conduct multiple clinical trials over the next two-and-a-half years, treating people with osteoarthritis, eye diseases and pulmonary diseases. At Mayo, gerontologist James Kirkland, who took part in the 2011 study, is cautiously beginning a handful of small, proof-of-concept trials that pit senolytic drugs against a range of age-related ailments. “I lose sleep at night because these things always look good in mice or rats, but when you get to people you hit a brick wall,” says Kirkland.

No other anti-ageing elixir has yet cleared that wall, and for a few good reasons. It's next to impossible to get funding for clinical trials that measure an increase in healthy lifespan. And even as a concept, ageing is slippery. The US Food and Drug Administration has not labelled it a condition in need of treatment.

Still, if any of the trials offer “a whiff of human efficacy”, says Unity's president, Ned David, there will be a massive push to develop treatments and to better understand the fundamental process of ageing. Other researchers who study the process are watching closely. Senolytics are “absolutely ready” for clinical trials, says Nir Barzilai, director of the Institute for Aging Research at the Albert Einstein College of Medicine in New York City. “I think senolytics are drugs that could come soon and be effective in the elderly now, even in the next few years.”

Credit: Nature, October 24, 2017, doi:10.1038/550448a

The dark side

When microbiologists Leonard Hayflick and Paul Moorhead coined the term senescence in 1961, they suggested that it represented ageing on a cellular level. But very little research was done on ageing at the time, and Hayflick recalls people calling him an idiot for making the observation. The idea was ignored for decades.

Although many cells do die on their own, all somatic cells (those other than reproductive ones) that divide have the ability to undergo senescence. But, for a long time, these twilight cells were simply a curiosity, says Manuel Serrano of the Institute for Research in Biomedicine in Barcelona, Spain, who has studied senescence for more than 25 years. “We were not sure if they were doing something important.” Despite self-disabling the ability to replicate, senescent cells stay metabolically active, often continuing to perform basic cellular functions.

By the mid-2000s, senescence was chiefly understood as a way of arresting the growth of damaged cells to suppress tumours. Today, researchers continue to study how senescence arises in development and disease. They know that when a cell becomes mutated or injured, it often stops dividing—to avoid passing that damage to daughter cells. Senescent cells have also been identified in the placenta and embryo, where they seem to guide the formation of temporary structures before being cleared out by other cells.

But it wasn't long before researchers discovered what molecular biologist Judith Campisi calls the “dark side” of senescence. In 2008, three research groups, including Campisi's at the Buck Institute for Research on Aging in Novato, California, revealed that senescent cells excrete a glut of molecules—including cytokines, growth factors and proteases—that affect the function of nearby cells and incite local inflammation. Campisi's group described this activity as the cell's senescence-associated secretory phenotype, or SASP. In recent unpublished work, her team identified hundreds of proteins involved in SASPs.

In young, healthy tissue, says Serrano, these secretions are probably part of a restorative process, by which damaged cells stimulate repair in nearby tissues and emit a distress signal prompting the immune system to eliminate them. Yet at some point, senescent cells begin to accumulate—a process linked to problems such as osteoarthritis, a chronic inflammation of the joints, and atherosclerosis, a hardening of the arteries. No one is quite sure when or why that happens. It has been suggested that, over time, the immune system stops responding to the cells.

Surprisingly, senescent cells turn out to be slightly different in each tissue. They secrete different cytokines, express different extracellular proteins and use different tactics to avoid death. That incredible variety has made it a challenge for labs to detect and visualize senescent cells. “There is nothing definitive about a senescent cell. Nothing. Period,” says Campisi.

In fact, even the defining feature of a senescent cell—that it does not divide—is not written in stone. After chemotherapy, for example, cells take up to two weeks to become senescent, before reverting at some later point to a proliferating, cancerous state, says Hayley McDaid, a pharmacologist at Albert Einstein College of Medicine. In support of that idea, a large collaboration of researchers found this year that removing senescent cells right after chemotherapy, in mouse models for skin and breast cancer, makes the cancer less likely to spread.

The lack of universal features makes it hard to take inventory of senescent cells. Researchers have to use a large panel of markers to search for them in tissue, making the work laborious and expensive, says van Deursen. A universal marker for senescence would make the job much easier—but researchers know of no specific protein to label, or process to identify. “My money would be on us never finding a senescent-specific marker,” Campisi adds. “I would bet a good bottle of wine on that.”

Earlier this year, however, one group did develop a way to count these cells in tissue. Valery Krizhanovsky and his colleagues at the Weizmann Institute of Science in Rehovot, Israel, stained tissues for molecular markers of senescence and imaged them to analyse the number of senescent cells in tumours and aged tissues from mice. “There were quite a few more cells than I actually thought that we would find,” says Krizhanovsky. In young mice, no more than 1% of cells in any given organ were senescent. In two-year-old mice, however, up to 20% of cells were senescent in some organs.

But there's a silver lining to these elusive twilight cells: they might be hard to find, but they're easy to kill.

Out with the old

In November 2011, while on a three-hour flight, David read van Deursen and Kirkland's just-published paper about eliminating zombie cells. Then he read it again, and then a third time. The idea “was so simple and beautiful”, recalls David. “It was almost poetic.” When the flight landed, David, a serial biotech entrepreneur, immediately rang van Deursen, and within 72 hours had convinced him to meet to discuss forming an anti-ageing company.

Kirkland, together with collaborators at the Sanford Burnham Medical Research Institute in La Jolla, California, initially attempted a high-throughput screen to quickly identify a compound that would kill senescent cells. But they found it to be “a monumental task” to tell whether a drug was affecting dividing or non-dividing cells, Kirkland recalls. After several failed attempts, he took another tack.

Senescent cells depend on protective mechanisms to survive in their 'undead' state, so Kirkland, in collaboration with Laura Niedernhofer and others from the Scripps Research Institute in Jupiter, Florida, began seeking out those mechanisms. They identified six signalling pathways that prevent cell death, which senescent cells activate to survive.

Then it was just a matter of finding compounds that would disrupt those pathways. In early 2015, the team identified the first senolytics: an FDA-approved chemotherapy drug, dasatinib, which eliminates human fat-cell progenitors that have turned senescent; and a plant-derived health-food supplement, quercetin, which targets senescent human endothelial cells, among other cell types. The combination of the two—which work better together than apart—alleviates a range of age-related disorders in mice.

Ten months later, Daohong Zhou at the University of Arkansas for Medical Sciences in Little Rock and his colleagues identified a senolytic compound now known as navitoclax, which inhibits two proteins in the BCL-2 family that usually help the cells to survive. Similar findings were reported within weeks by Kirkland's lab and Krizhanovsky's lab.

By now, 14 senolytics have been described in the literature, including small molecules, antibodies and, in March this year, a peptide that activates a cell-death pathway and can restore lustrous hair and physical fitness to ageing mice.

So far, each senolytic kills a particular flavour of senescent cell. Targeting the different diseases of ageing, therefore, will require multiple types of senolytics. “That's what's going to make this difficult: each senescent cell might have a different way to protect itself, so we'll have to find combinations of drugs to wipe them all out,” says Niedernhofer. Unity maintains a large atlas documenting which senescent cells are associated with which disease; any weaknesses unique to given kinds of cell, and how to exploit those flaws; and the chemistry required to build the right drug for a particular tissue. There is no doubt that for different indications, different types of drug will need to be developed, says David. “In a perfect world, you wouldn't have to. But sadly, biology did not get that memo.”

For all the challenges, senolytic drugs have several attractive qualities. Senescent cells will probably need to be cleared only periodically—say, once a year—to prevent or delay disease. So the drug is around for only a short time. This type of 'hit and run' delivery could reduce the chance of side effects, and people could take the drugs during periods of good health. Unity plans to inject the compounds directly into diseased tissue, such as a knee joint in the case of osteoarthritis, or the back of the eye for someone with age-related macular degeneration.

And unlike cancer, in which a single remaining cell can spark a new tumour, there's no need to kill every senescent cell in a tissue: mouse studies suggest that dispatching most of them is enough to make a difference. Finally, senolytic drugs will clear only senescent cells that are already present—they won't prevent the formation of such cells in the future, which means that senescence can continue to perform its original tumour-suppressing role in the body.

Those perks haven't convinced everybody of the power of senolytics. Almost 60 years after his initial discovery, Hayflick now believes that ageing is an inexorable biophysical process that cannot be altered by eliminating senescent cells. “Efforts to interfere with the ageing process have been going on since recorded human history,” says Hayflick. “And we know of nothing—nothing—that has demonstrated to interfere with the ageing process.”

Fans of senolytics are much more optimistic, emboldened by recent results. Last year, van Deursen's lab went beyond its tests on super-aged mice and showed that killing off senescent cells in normally ageing mice delayed the deterioration of organs associated with ageing, including the kidney and heart. And—to the joy of anti-ageing enthusiasts everywhere—it extended the animals' median lifespan by about 25%.

Successful results from mouse studies have already lured seven or eight companies into the field, Kirkland estimates. At Mayo, one clinical trial has opened, pitting dasatinib and quercetin in combination against chronic kidney disease. Kirkland plans to try other senolytics against different age-related diseases. “We want to use more than one set of agents across the trials and look at more than one condition,” he says.

If eliminating senescent cells in humans does improve age-related illnesses, researchers will aim to create broader anti-ageing therapies, says David. In the meantime, researchers in the field insist that no one should take these drugs until proper safety tests in humans are complete. In rodents, senolytic compounds have been shown to delay wound healing, and there could be additional side effects. “It's just too dangerous,” says Kirkland.

Van Deursen says that continuing to answer basic biological questions is the field's best shot at success. “Only then will we be able to understand what ageing really is, and how we can, in an intelligent way, interfere with it.”

This article is reproduced with permission and wasfirst publishedon October 24, 2017.


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ILCPA > Volume 70 > Preparation and Characterization of Superabsorbent...
< Back to Volume

Preparation and Characterization of Superabsorbent Polymer (SAP) by Graft Polymerization of Carboxymethyl Cellulose

Full Text PDF

The synthesis of superabsorbent polymer with Carboxymethyl cellulose using ceric ammonium nitrate (CAN) initiated acrylamide (AA) monomer through a solution based graft copolymerization has been conducted. The characterizing studies were performed using Fourier transform infrared (FTIR) spectroscopy, Atomic force microscopy (AFM) and swelling studies. FTIR spectra established crosslinked polymeric network structure of hydrogels through graft copolymerization reaction between CMC and acrylamide indicating incorporation of acrylamide monomer resulting the formation of carboxamide group (>C=O). AFM showed the surface morphology or properties of superabsorbent. The hydrophilic properties of the superabsorbent were identified by the swelling percentage or degree of swelling.

International Letters of Chemistry, Physics and Astronomy (Volume 70)
A.B.M. Nazmul Islam and M. Anisul Islam, "Preparation and Characterization of Superabsorbent Polymer (SAP) by Graft Polymerization of Carboxymethyl Cellulose", International Letters of Chemistry, Physics and Astronomy, Vol. 70, pp. 27-32, 2016
Online since:
September 2016

[1] K. Horie et al., Definitions of terms relating to reactions of polymers and to functional polymeric materials, Journal of Pure and Applied Chemistry. 76 (2004) 889–906.

[2] K. Kabiri, Synthesis of fast-swelling superabsorbent hydrogels: effect of crosslinker type and concentration on porosity and absorption rate, European Polymer Journal. 39 (2003) 1341–1348.

[3] F.L. Buchholz, A.T. Graham, Modern Superabsorbent Polymer Technology, Elsevier, Amsterdam, (1997).

[4] L.B. Peppas, R.S. Harland, Absorbent Polymer Technology, Elsevier, Amsterdam, (1990).

[5] A. S. Hoffman, J.C. Salamone, Polymeric Materials Encyclopedia; CRC Press, Boca Raton, FL, (1996).

[6] R. Bodvik et al., Aggregation and network formation of aqueous methylcellulose and hydroxypropylmethylcellulose solutions, Colloids and Surfaces A: Physicochemical and Engineering Aspects, (2008).

[7] M.H. Rafie et al., Grafting of methacrylic acid to loomstate viscose fabric using KMnO4/NaHSO3 system, Journal of Polymers and polymer composites. 2(2) (1994) 99-104.

[8] A. Hebeish, A. Katouch, M.H.I. EL-Rafie, Graft copolymerization of vinyl monomer with modified cotton. II. Grafting of acrylonitrile and methyl methacrylate on acetylated cotton, Journal of Applied polymer science. 15(1) (1971) 11-24.

[9] G.F. Fanta, Synthesis of graft and block copolymers of starch, Block and graft copolymerization. 1 (1973) 11.

[10] P. Liu et al., Radiation preparation and swelling behavior of sodium carboxymethyl cellulose hydrogels, Journal of Radiation Physics and Chemistry. 63 (2002) 525- 528.

[11] N. Nagasawa et al., Radiation crosslinking of carboxymethyl starch, Journal Of Carbohydrate Polymers. 58 (2004) 109-113.

[12] E. Valles et al., Equilibrium swelling and mechanical properties of hydrogels of acrylamide and itaconic acid or its esters, Polymer Bulletin. 44 (2000) 109-114.

[13] M. Sadeghi, M.N. Esmat, F. Shafie, Preparation, characterization, and optimization of grafting parameters, Academic Journals Scientific Research and Essays. 7 (2012) 511-521.

[14] K. Pal, A.K. Banthia, D.K. Majumdar, Polymeric Hydrogels: Characterization and Biomedical Applications – A mini review, Designed Monomers and Polymers. 12 (2009) 197-220.

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