Once again this year, pro hockey players will be using pink hockey sticks for three days beginning Friday. After game use, the sticks will be auctioned off on eBay to raise money for Breast Cancer research.
Last year, over $176,000 was raised.
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ATUL K THAKUR is a Views Columnist and Writer who specialises in the interface of politics and economics. His research and writing interests extend to macroeconomic policies and international affairs, with special focus on South Asia. He is an alumnus, inter alia, of Banaras Hindu University and has worked across sectors, spanning policy research, management consultancy, publishing and media.
India Now and in Transition is his second book as an editor. He has previously edited India since 1947: Looking Back at a Modern Nation (Niyogi Books, 2013), a significant work on modern India. He is currently working on the book project that deal with Nepal's complex political-economic transitions and ethnicity issues and another on India's journey with economic reforms.
What prompted you to do this sequel to your previous book - India's 70 years of democracy, or the surprising victory of the BJP in 2014? Was the latter, anyway, a critical moment for India?
Honestly, this was the first idea that confirmed my inner call to attempt to bring out a comprehensive collection of essays, written without any preoccupation or enter into the prognosis. As the centrality of thought rested with 'India', I naturally had to count on its brightest tribute, democracy – and inspire myself and fellow writers to delve with the complex subjects with which India was concerned then and will be in transition.
As an editor, I work on something to make it compatible with the readers' expectations. As a writer, first, I answer my own queries. Normally, I read a lot – not to write anything particular but to stay in the mental state where I can silently cope with the chaos of ideas.
The beauty of India is that there are many kinds of Indias. Understanding the fundamentals that have given birth to such multiplicity across various segments is especially imperative in the present day, when the 'Idea of India' is keenly contested.
India Now and in Transition is thus an enquiry into possible futures, based on current happenings.
In confession, I thought to work on a book after reading full-time for one-and-half decade – and writing extensively on opinion/edit pages of broadsheets. Being a compulsive reader, it was somehow natural to tempt and turn as a columnist and writer – to find a way of expressions.
How India Now and in Transition looks on India?
India Now and in Transition offers fresh insights into several crucial areas, elements that have shaped India into what it is today, whether that be the complex set of relations under the country's federal system, the challenges of territorial/cultural diversities, and the contradictory outcomes of economic reforms, among others. This book looks diligently at the successes and failures of India's tryst with democracy, which—despite having many flaws—is charting its course ahead.
India is the world's largest democracy with nearly 70 years of independent existence. Its unique and ever-changing nature has sparked a great degree of academic debate, both before and since Independence. The beauty of India is that there are many kinds of Indias. Understanding the fundamentals that have given birth to such multiplicity across various segments is especially imperative in the present day, when the 'Idea of India' is keenly contested. Our nation has the world's largest youth population and is undergoing tectonic social and political changes at present, therefore, understanding what directions India may take in the future is essential for every thinking individual.
India Now and in Transition is an enquiry into possible futures, based on current happenings. Featuring contributions from leading thinkers and scholars in diverse fields, each essay in this volume critically analyses a major theme of India's present, to propose the likely way ahead for our emergent nation. Covering the fields of politics and governance, economics and development, security and foreign policy, society and culture, and language and literature, the book shows that—while beset with both internal and external challenges on many fronts—India isn't waiting for its moment, it's making its moment happen.
When you're talking about India's future, how many years from now are you looking at?
On this, it would be hard to go through the figures. My first edited work, India Since 1947: Looking Back at a Modern Nation(2013) was a collection of essays on a nation that was still trying to come into its own. If we consider the state of our nation today, in certain aspects India has come a long way, while in many others it has a challenging journey and many tough transitions ahead.
This sequel, India Now and in Transition, is based on how 'India' is being shaped through contemporary political events and other key determinants. What this book intends is not a prognosis (which is often confused with prediction), but, rather, an inquiry into futures based on current happenings. This necessarily entails deconstructions of the past, as in the previous volume. A causal linearity is maintained, so that the futures proposed will be the likeliest. To that end, the exegesis is rigorously researched, referenced and argued. The book is not intended to be a mere warehouse of opinions. Together, the two volumes cover India's continuum from a nascent nation-state to a mature one.
How dominant the role of a governing party's ideology is in shaping India's future?
A: Since 1947, India as a nation has made significant strides. However, those were not enough. The realisation is growing stronger, as democracy is deepening every day. Despite having followed a 'reluctant revivalist' tendency for close to seven decades, now, in an increasingly technocratic situation, the overall 'governance discourse' is gaining ground to charter something as desired by the people and emerging directly out of compelling necessities. In the early years of this decade it was perceived that 'policy paralysis' and lack of reform impetus in macroeconomic policies led to a downward spiral in business and mass sentiments, which eventually resulted in an alarming level of deceleration in economic growth. The UPA-II regime was blamed for that, which was justified to an extent too, but somewhere there is a need to see the real stumbling blocks. Those stumbling blocks are still existing and flourishing when a new government is helming at center that was voted to power with absolute majority in eventful Parliamentary elections of 2014.
It has to be admitted that India's administrative system has become largely non-functional and unresponsive to the interest of the masses. This book focuses on this crux of the problem through 37 essays from some of India's leading policy practitioners, scholars and young writers. Several of the essays seek to trace different aspects India's political trajectory, from the time of its birth to the modern day. At the heart of the book is the idea that India is struggling to establish a deeper, more definitive democracy. The book captures the centrist tendency in Indian politics, particularly at the national level. The book puts forward the case of political reforms, besides economic and administrative reforms—to bring in structural changes otherwise marred through surviving inconsistencies. Indeed, without a reformed culture of politics, it is naive dreaming of the fruits of economic reforms and that too with equity. Many of the essays from this book have a focus on the interface between politics and economics in India, which actually determines the path of progress for the country.
The essays also offer possible solutions to end the menace of corruption and for achieving inclusive growth—this comes while discussing among others, the pressing issues related to governance, the rise of new politics (through civic activism), growing inequality, alienation, the contradiction between identity politics and development. In the states, identities of various sorts still rule the course of political actions and outcomes. India is presently at a stage wherein the expectations of the electorate are quite diverse, apropos of how the system and its representatives respond to them. Without the freedom movement, India's nationhood would have been inconceivable, which means democracy too would've been inconceivable. This book and the previous volume, focus especially on the consolidation of national democracy after 1947, calling it the next remarkable event after India's independence—where the decisive leadership of Nehru played a major role.
While examining all these changes, the book also indicates the next course of development as far as democracy in India is concerned. In my own view, Indian democracy is the sort that becomes more progressive the more unsettling changes it comes across. After all, time and again, all kinds of political hiccups in India have been solemnized—although with varying degrees of success. Then again, the stakes are much higher at the moment, and forward-looking Indians can no longer trust a government that offers less than a two percent job growth rate, for example. Now is the time for political parties to be as prompt in terms of their actions as their electorates are with their expectations. Overlooking that would be detrimental for success in the political fray as other countries in South Asia have evidenced.
If we aren't able to predict how long the BJP is going to govern India at the federal level, then is it easy to do this prognosis?
Possibly yes, as it helps is knowing a predictable trend.
Often it's cited by the lots of escapists, believers and passive observers that the existing 'electoral process' is in middle of troubles that are defining India's democracy and million mutinies. As it is in reckoning, the electoral funding pattern has had diminished the political culture to the level where expecting politics to remain a saintly business, is too naïve a pre-thinking.
As the next Parliamentarian elections are round the corner, the ruling regime which has had failed to live on the expectations and hallucinations of the vast numbers of electorates, are offering enough sign to run on the turf that will have no qualifying criteria on policy issues. Shaken through the core, India's economy and polity are no longer in positions to carry the burden of non-performance and its ceremonial glorification like how followed in last four years.
India's much-celebrated growth story is on wane, it is badly affected with the protected scams, maligned judiciary – and targeted rapes, riots and encounters. What promises made turned-out to be nightmares in reality – and those who are on fringe are gravely threatened under the watch of a government which clearly has no vision to understand the finer elements of an idea that finally makes India.
Are you personally optimistic about India's future - if democracy, civil freedoms and inclusive development were the scale?
A: While policy intervention is subject to a totalitarian vision, it all appears stage-managed, when India's government in New Delhi, attempts to deal with states in its fold, wary neighbours – and the world beyond. At no point of time, a government can run the policies and meet the expectation without having the back-up of goodwill and auxiliary support of all stakeholders of the administrative processes.
The customized policy-making, death of institutions, gagging of voices and organised plundering of the banks by the protected elites are just among the few signals, which aptly make it clear that India's democracy has come a long way from the days of struggle when it kept 'idealism' in statecraft.
Even with basic understanding, the generations who are living in the present time and their successors, will be kinder to the forefathers of the Indian democracy than those who are helming the authority in unprecedented fashion.
Notwithstanding the challenges, I don't keep a pessimistic view about the future of India. Its fundamentals are strong. Lack of greater socio-economic inclusion and growing violations of democratic and civil freedoms remain the matters of big concern. India's role at global stage will be decided by the home work of its policy-makers' at home which presently is not up to mark.
You have been known for your writing on South Asian affairs, please do share your views on Modi government's foreign policies in nieghbourhood?
A: Apparently, Modi government's pet foreign policy, 'Neighbourhood 1st', is not serving India's causes on the expected lines in Nepal and letting China pursue its nasty expansionist policies.
With other SAARC Countries too, things are not moving up in the directions to broaden the base of regional economic and strategic cooperation.
If you think India is currently fast moving towards crony capitalism?
A: For long, India has been gripped through the spectre of 'crony capitalism'. For sure, it is an old phenomenon and there is no sign that it is on wane. The present regime is Delhi is devoid from the existing scenario and is rather letting the policies support this endemic malady that hurts terribly to India's otherwise a tall standing as the 'world's largest democracy'.


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Aja Waalwijk
Menno Grootveld
Radio Rukstad
Aja Waalwijk is artist and the founder of the futurologic symposia
http://www.wittereus.net/aja/
As a university-dropout, Menno Grootveld started doing pirate television in Amsterdam with PKP TV and Rabotnik TV in the early eighties. Rabotnik TV was the media-branch of an extensive underground-culture that existed in Amsterdam during the eighties, which also included a concert hall (NL-Centrum) and a political party (De Reagering). In the mid-80s Menno started organizing major media-conferences, the first of which was the European Media Festival in 1985 (mainly focused on radio), followed by the Wetware Convention (1991) and four Next 5 Minutes-conferences that introduced the concept of 'tactical media' (1993, 1996, 1999 and 2003). In the mid-90s Menno had a short stint as a programme editor of "W.E.B.", a bi-weekly series of programmes on national television about the so-called 'digital revolution.' Menno currently works as a translator and a journalist, runs his own publishing house in Amsterdam, and is a member of DiEM25 in the Netherlands
Radio Rukstand will do the Q&A on the friday with Cody Hochstenbach, Brian Doucet and Andrej Holm
A patafysic radioshow at Radio Patapoe
with AK Bouwman, Mc Alfredex and Naaktslak
https://www.facebook.com/radio.ruk.patapoe

redpajama_set_name: RedPajamaCommonCrawl


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Director of the Army Staff sworn in as vice chief of staff
By Army Public AffairsJuly 26, 2019
1 / 3 Show Caption + Hide Caption – U.S. Army Chief of Staff Gen. Mark A. Milley hosts a promotion ceremony in honor of Lt. Gen. Joseph M. Martin, at the Pentagon, Arlington Va., July 26, 2019. (U.S. Army photo by Spc. Keisha Brown) From left to right, Gen. Joseph M. Martin, his wife Mrs. Leann Martin and Gen. Mark A. Milley. (Photo Credit: Spc. Keisha Brown) VIEW ORIGINAL
2 / 3 Show Caption + Hide Caption – U.S. Army Chief of Staff Gen. Mark A. Milley hosts a promotion ceremony in honor of Lt. Gen. Joseph M. Martin, at the Pentagon, Arlington Va., July 26, 2019. (U.S. Army photo by Spc. Keisha Brown) Gen. Joseph M. Martin at the lectern. (Photo Credit: Spc. Keisha Brown) VIEW ORIGINAL
WASHINGTON -- Gen. Mark Milley, the 39th Chief of Staff of the Army, promoted Lt. Gen. Joseph M. Martin to general and swore him in as the Army's 37th Vice Chief of Staff on Friday.
Martin, who was serving as the Director of the Army Staff, replaced Gen. James McConville, who will become the 40th Chief of Staff of the Army in the coming weeks.
"As I said before, I am humbled and grateful for this tremendous honor," Martin said. "I have had no greater privilege than leading and serving with the great men and women of our United States Army, and am truly blessed to be able to continue being by their side as Vice Chief of Staff."
Martin, from Dearborn, Michigan, is a former commander of the 1st Infantry Division and a class-of-1986 West Point alumnus.
Among his awards and honors are the Distinguished Service Medal, the Defense Superior Service Medal, the Legion of Merit, the Bronze Star Medal with "V" device, the Meritorious Service Medal, the Army Commendation Medal with "V" device, as well as the Combat Action and Parachutist badges.
Martin has a master's degree in education from the University of Louisville, and is a graduate of the U.S. Army Command and General Staff College and the U.S. Army War College.
December 30, 2019Maj. Gen. LeMaster, Command Sgt. Maj. Charpentier relinquish command and responsibility of RHC-P
December 30, 2019Army selects MICC civilian for professional development opportunity
December 23, 2019Soldier wins 2019 U.S. Boxing Olympic Trials; on the road to Tokyo
December 20, 2019Army Pacific Commander concludes visit to Japan
December 20, 2019The big ask: upgrade graduate education for acquisition professionals
December 19, 2019'Army allowed me to go pro': MoH recipient delivers remarks at Infantry officer graduation
December 17, 2019Staff sergeant feels fortunate to be home for the holidays
December 17, 2019Army selects AMCOM solution as single technical manual viewer
December 17, 2019Fort Bragg's Soldier Support Center dedicated to 'Father of the Airborne'
December 13, 201925th Infantry Division
December 13, 2019Maj. Gen. George to CCDC DAC: 'You are the secret to our success'
December 12, 2019Troxell reflects on four years in military's top enlisted post
December 12, 2019Milley details DOD operations throughout the Middle East
December 10, 2019MHS GENESIS insights: Brig. Gen. Jeffrey Johnson tours Madigan
December 9, 20193rd Special Forces Group (Airborne) Hero Commemorated at Rogers High School


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← Polar bear population now officially 13,071-24,238 says IUCN Polar Bear Specialist Group
Chukchi-Beaufort sea ice atlas: check out polar bear habitat 1850-2013 →
Figure 1. Upper graph uses totals reported in PBSG status tables, with min/max; Lower graph uses the same figures, but adds back in the so-called "inaccurate" estimates dropped 2005-2013. The 1960 figure * is a ballpark estimate
What is apparent is that the global population of polar bears has not declined over the last 30 years, as the PBSG status tables indicate.
Although it's true that the official estimates for 2005 and 2009 publicized by the PBSG ("20,000-25,000") also indicated no recent change, the numbers listed on their status tables don't tell the same story. What's the point of insisting on supposedly more accurate "scientific" estimates if you don't use them to generate your official total?
Note that the most recent status table released last week, for 2013, did not include a new total — if you wanted to know if the global total had changed (and if so, by how much), you had to add the figures up yourself. Nowhere on the PBSG website does it now list an official population estimate. What's that about?
Finally, note that I've included a ballpark estimate for 1960 that reflects international concern that many years of unregulated hunting had seriously depleted populations, as occurred for numerous other species (indicated as a broad range rather than a single figure). And while it is true that no one truly knows how many polar bears there were in 1960, it is also true that by that time, over-hunting had occurred on a large scale for decades, and that there were fewer bears then than there are now (see another discussion of that topic here).
UPDATE 5 December 2014: Links to more recent posts relevant to this issue added below:
Status of Canadian polar bear populations has been changed – more good news October 28, 2014
W Hudson Bay polar bear population no longer "declining" – where are the headlines? October 29, 2014
The Politics of Polar Bears documentary [excerpt links] September 3, 2014
NOTES ON METHODS
Where the PBSG status table for any given year (list below) gives a total range of estimates (maximum and minimum), as in 2001, I've used the PBSG totals. Where the status tables do not give a total for the maximum, minimum and average numbers (i.e., 2005, 2009, 2013), I've used those listed in the first column of each table (Fig. 2 below, and upper panel of Fig. 1). For example, the min/max and average estimates (rounded to nearest 10) from the status tables for 2005-2013 are:
2005 15,130-27,760 (average 21,420)
Fig. 2 Graph using the figures listed in PBSG status tables only.
While I acknowledge that earlier estimates (from the 80s and 90s) used different methods than later ones, which may have made them less accurate, they were the "best available science" at the time. The purpose of this exercise is to compare the PBSG published numbers from these documents:
1981 8th Meeting – Oslo, Norway (Anonymous 1985: Table 1)
1993 11th Meeting – Copenhagen, Denmark (Wiig et al. 1995: Table 1)
1997 12th Meeting – Oslo, Norway (Derocher et al. 1998: Table 1)
2001 13th Meeting – Nuuk, Greenland (Lunn et al. 2002: Table 1)
2005 14th Meeting – Seattle, Washington (Aars et al. 2006: Table 1)
2009 15th Meeting – Copenhagen, Denmark (Obbard et al. 2010: Table 1)
2013 Online status update, posted February 14, 2014
As I've pointed out previously, adjustments made to the PBSG status tables that dropped to zero estimates that had formerly been included in the global totals suggested that by 2009, the totals must actually have increased by 2650 to 5700 bears since 2001.
So to make the population estimates comparable over time, we really need to add back in the ballpark estimates for the Queen Elizabeth Islands (which includes any bears residing there and in the Arctic Basin, last estimated at 200 bears), East Greenland (2,000 bears) and the Chukchi Sea (2,000 bears)1, which were dropped in the 2005 and 2009 PBSG assessments, as well as the estimate for the Laptev Sea (800-1200 bears, dropped in 2013, discussed here).
[I did not include adjustments for Barents Sea changes in this graph (as I did previously), to keep the comparison simple and because some people might not agree that the Barents Sea adjustment qualifies as the same kind of change as the dropped estimates]
Figure 3. Graph using figures from the PBSG status tables plus "inaccurate" estimates dropped between 2005 & 2013.
1. Although the estimate for this region is indeed less "scientifically" accurate than those from regions that have been surveyed, it is very clear that large number of bears reside in the Chukchi Sea. For example, Rode and colleagues (Rode et al. 2014) used an estimate of 2,000 for the Chukchi Sea region ("based on extrapolation of den surveys") to argue that the Chukchi and the Southern Beaufort population of bears were of "similar size." PBSG biologists apparently like to have it both ways: ignore the Chukchi estimate when it doesn't suit them (for global estimates) but include it when they need it for statistical work.
Aars, J., Lunn, N. J. and Derocher, A.E. (eds.) 2006. Polar Bears: Proceedings of the 14th Working Meeting of the IUCN/SSC Polar Bear Specialist Group, 20-24 June 2005, Seattle, Washington, USA. Occasional Paper of the IUCN Species Survival Commission 32. IUCN, Gland (Switzerland) and Cambridge (UK). http://pbsg.npolar.no/en/meetings/
Amstrup, S.C. and Wiig, O. (eds.) 1991. Polar Bears: Proceedings of the 10th meeting of the Polar Bear Specialists Group IUCN/SSC, Oct. 25-29, 1988, Sochi, USSR. Gland, Switzerland and Cambridge UK, IUCN. http://pbsg.npolar.no/en/meetings/
Anonymous. 1985. Polar Bears: Proceedings of the 8th meeting of the Polar Bear Specialists Group IUCN/SSC, 15-19 January, 1981, Oslo, Norway. Gland, Switzerland and Cambridge UK, IUCN. http://pbsg.npolar.no/en/meetings/
Derocher, A., Garner, G.W., Lunn, N.J., and Wiig, Ø. (eds.) 1998. Polar Bears: Proceedings of the 12th meeting of the Polar Bear Specialists Group IUCN/SSC, 3-7 February, 1997, Oslo, Norway. Gland, Switzerland and Cambridge UK, IUCN. http://pbsg.npolar.no/en/meetings/
Lunn, N.J., Schliebe, S., and Born, E.W. (eds.). 2002. Polar Bears: Proceedings of the 13th working meeting of the IUCN/SSC Polar Bear Specialists Group, 23-28 June , 2001, Nuuk, Greenland. Gland, Switzerland and Cambridge UK, IUCN. http://pbsg.npolar.no/en/meetings/
Obbard, M.E., Theimann, G.W., Peacock, E. and DeBryn, T.D. (eds.) 2010. Polar Bears: Proceedings of the 15th meeting of the Polar Bear Specialists Group IUCN/SSC, 29 June-3 July, 2009, Copenhagen, Denmark. Gland, Switzerland and Cambridge UK, IUCN. http://pbsg.npolar.no/en/meetings/
Rode, K.D., Regehr, E.V., Douglas, D., Durner, G., Derocher, A.E., Thiemann, G.W., and Budge, S. 2014 [now in print]. Variation in the response of an Arctic top predator experiencing habitat loss: feeding and reproductive ecology of two polar bear populations. Global Change Biology 20(1):76-88. http://onlinelibrary.wiley.com/doi/10.1111/gcb.12339/abstract
Wiig, Ø., Born, E.W., and Garner, G.W. (eds.) 1995. Polar Bears: Proceedings of the 11th working meeting of the IUCN/SSC Polar Bear Specialists Group, 25-27 January, 1993, Copenhagen, Denmark. Gland, Switzerland and Cambridge UK, IUCN. http://pbsg.npolar.no/en/meetings/
This entry was posted in Conservation Status, Population and tagged Chukchi, East Greenland, estimate, graph, Laptev Sea, PBSG, polar bear, polar bear numbers, Polar Bear Specialist Group, population decline, population estimates, population increase, population over time, Queen Elizabeth Islands, Rode, stable population, status tables, timeline. Bookmark the permalink.


At the heart of Gascony, Condom, our village cottages offers 10 wooden chalets in the middle of a park of 4 hectares. In the heart of nature, you will appreciate the calm, the space and the conviviality of this haven of peace.
At disposal on the spot, a room of relaxation and leisure of 110m ² (ideal for the groups) with corner library, games of board, baby-foot, TV ..., a swimming pool 6 * 12 ml, a playground, a ground petanque, table tennis, bikes / mountain bikes and a badminton / volleyball court.
On hire on site: electric bicycles and planchas.
The equestrian center nearby (300m walk) offers unforgettable walks in the paths of the Gers.
From Condom, take the D110 towards Mézin. Go 2.8 kms then turn right following the small wooden signs "Les Chalets".
Thank you to all our holiday makers who leave us great testimonials of their stays at Chalets de Grazimis!
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Thank you for your welcome"
Only 21 days left to enjoy this offer!
Only 23 days left to enjoy this offer!
The site has a room of 110 m², usually reserved for holidaymakers who have and share it at any time during their stay. There is a TV corner with big screen, a reading corner and board games, a ping-pong table, a football table, a launderette and a tourist documentation area.
Ideal for groups or professionals, it has a capacity of 40 to 50 people at the table.
It is equipped with a kitchen with a large gas stove, a fridge with freezer, a dishwasher, and kitchen utensils.
Tables, chairs and dishes are included in the rental.
We work with several caterers who are used to come to deliver or serve on site. We put you in touch with them on request.
Privatize our village of lodging by renting the 8 chalets and we put at your disposal free this room to gather you!
Rental of 2 electric bikes brand KALKHOFF: they are beautiful, light, easy to use, and have 80 km of autonomy (manufacturer data: 120 km).
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For your grilled vegetables, meat or fish, consider renting your Plancha (gas supply with self-locking safety)!
Cleaning option: 50 € for any stay of a week.
€ 30 for short stays.
Breakfast on request, served at the cottage or in the common room.


With the power of your Samsung Galaxy S 4 and the flexibility offered in Android applications development, it can be difficult to imagine that even more capabilities could be in the works. In spite of this, the following are ten features that would improve the usability and value of your Galaxy S 4 phone.
Whether you're using the default wake-up screen or you implemented the Unlock pattern described in Chapter 17, you need to unlock the phone screen to know how many e-mails, texts, voicemails, or updates you have.
The ability to see on the Secure screen how many new e-mails, texts, and voicemails you have waiting would be nice.


Plants are individuals and all have their specific needs. Take time to research what your plant's cultural requirements are. Some indoor plants like to dry out before they are watered. Others require that their soil remain consistently moist. Growing indoor plants is not a science of 'one size fits all'.


My style has usually been really casual and laid back.. sneakers and jeans are generally the base of any outfit I put on. So, every single day that you take the time to go outside and hang your clothes to dry instead of utilizing that energy consuming monster in your laundry space, you are not only saving some considerable cash, you are acquiring your physique and mind outdoors for a handful of minutes exactly where you can be performing a straightforward job and soaking up a little sunshine yourself.
The rack also gives me the capacity to visualize what path my style is going in colour smart, and provides me bearing on the colors I want to use in my upcoming posts. When we are camping, I fill a bucket with a lid with dirty clothes, water and soap and put it in the back of the truck and when I have to dash off to the store, it rolls about and agitates the clothes that have to be cleaned before I get house. Mixing plastic and these thin, wire hangers appear to lead to tangles and mess in closets. These are not to be confused with the less expensive contoured wood hangers which have a curved shape but not the wide shoulder pads.
I consider when men and girls comprehend that they can take care of their good clothes at house, they will feel empowered to wear their good clothes on a normal basis. It really is essential to pick the right detergent for the sort of clothes you're washing. Now that your closet appears great, never let it go back to the way issues used to be. When I 1st did this, I was shocked to uncover that it did not take significantly a lot more time to place clothes away now than it used to. I just grab like items and stash them with the appropriate color.
Clothes Mentor does not guarantee the authenticity of any merchandise to their original brand name, and utilizes the brand names to denote the style of its products. I rarely see clotheslines where I reside – I usually dry clothes on a rack, but inside. You can also purchase a machine that does nothing at all except spin the water out of wet clothes. Clothes Mentor is a reseller of brand name and designer goods, and is not an authorized dealer of the mentioned organizations. I've actually place aside some wire hangers as they are acquiring tougher to come by.
These ideas each and every have a reason for being in my list so that your clothesline dried clothes are handled far more efficiently. Be positive to watch the video of the lady in India beating the water out of her clothes in this manner. Last year, when I mentioned how stiff and rough my baby's line-dried diapers had been, my mom suggested performing what she did for years (soon after my grandma suggested it to her) and throw them in the dryer before hanging them. Nevertheless, I have identified that my clothes dry more quickly and come out of the dryer softer than making use of absolutely nothing at all.


text:
Q: Inject pure Java / Obj-C code in NativeScript App I'm currently developing an App for Android / iOS, and now i'm at the stage to let my users interact with Facebook, and especially send private message to their friends.
Facebook implement a SDK for that, for iOS:
FBSDKSendButton *button = [[FBSDKSendButton alloc] init];
button.shareContent = content;
[self.view addSubview:button];

And for android:
SendButton sendButton = (SendButton)findViewById(R.id.fb_send_button);
sendButton.setShareContent(shareContent);
sendButton.registerCallback(callbackManager, new FacebookCallback<Sharer.Result>() { ... });

But i'm unsure if i can actually use those pieces of code with NativeScript.
Does anyone have any experience with facebook send button and NativeScript or at least could shed a light on whether its possible or not.
Thanks a lot

A: There is something similar done in this NativeScript plugin. It provides Facebook login functionality but I believe that it would be fairly easy to make it fit your needs.

A: I asked a similar question last week and was able to get use the addSubview call to work like this:
var mainView = args.object.getViewById('main-view');
mainView.ios.addSubview(publisher.view);

My XML looks like:
<Page loaded="pageLoaded">
 <StackLayout id="main-view">
 </StackLayout>
</Page>

You'll need an ID on the view you created in your XML, then in the code-behind file in your function, use the args.object.getViewById('yourViewID'); to create a variable and then call viewVariable.ios.addSubview('view-you-want-to-add');.
In my case my framework's publisher object is what I passed to the .ios.addSubview() call.
Full code-behind file as well:
var vmModule = require("./main-view-model");

// moving OpenTok out of the plugin and into code base for dev.
// Will move into a plugin after
var OpenTok = {
    createSession: function(options) {
        var apiKey = 'private';
        var sessionID = 'private';
        var delegate = this;

        // Framework Method
        var session = OTSession.alloc().init();
        return session.initWithApiKeySessionIdDelegate(apiKey, sessionID, delegate);
      },
      createPublisher: function() {
        // Framework Method
        var publisher = OTPublisher.alloc().init();

        return publisher;
      }
};

function pageLoaded(args) {
    var page = args.object;
    var mainView = args.object.getViewById('main-view');
    var token = "private";
    var error = new interop.Reference();
    page.bindingContext = vmModule.mainViewModel;

    var session = OpenTok.createSession();
    // Framework Method
    session.connectWithTokenError(token, error);

    var publisher = OpenTok.createPublisher();
    // Framework Method
    publisher.initWithDelegate(publisher);
    // Native iOS Method
    mainView.ios.addSubview(publisher.view);

    var checkConnectionStatus = setInterval(function(){
      if ( session.sessionConnectionStatus == 1 ) {
          console.log('clear interval');
          clearInterval(checkConnectionStatus);
          // Framework Method
          session.publishError(publisher, null);
      }
    }, 1000);

}

exports.pageLoaded = pageLoaded;

This is my question that might also provide more insight if you're still stuck: Nativescript addSubview

redpajama_set_name: RedPajamaStackExchange


text:
U.S. DEPARTMENT OF VETERANS AFFAIRS, PORTLAND VA MEDICAL CENTER, PORTLAND, OREGON and AMERICAN FEDERATION OF GOVERNMENT EMPLOYEES, LOCAL 2157, AFL-CIO
U.S. DEPARTMENT OF VETERANS AFFAIRS
PORTLAND VA MEDICAL CENTER
AMERICAN FEDERATION OF GOVERNMENT
EMPLOYEES, LOCAL 2157, AFL-CIO
CHARGING PARTY
Case No. SF-CA-11-0467
OALJ 12-10
Vanessa Lim
For the General Counsel
Dennis Saub
For the Respondent
Leonard Fearn
For the Charging Party
Before: CHARLES R. CENTER
Chief Administrative Law Judge
DECISION ON MOTION FOR SUMMARY JUDGMENT
The Respondent failed to file an answer to the complaint and has not replied to the General Counsel's motion for summary judgment. Because the Respondent has presented no extraordinary circumstances to justify its failure to timely file an answer, I find that the Respondent has not demonstrated good cause, and thus, the General Counsel is entitled to summary judgment pursuant to 5 C.F.R. § 2423.27.
PROCEDURAL STANDARDS
Parties appearing before the Authority are charged with knowledge of all pertinent statutory and regulatory filing requirements, U.S. Envtl. Prot. Agency, Envtl. Research Lab., Narragansett, R.I., 49 FLRA 33, 37 (1994). Section 2423.20(b) of the Federal Labor Relations Authority's (FLRA/Authority) rules and regulations requires that the Respondent file and serve its answer to the complaint within 20 days of the date of service of the complaint, but, in any event, prior to the start of the hearing. Section 2423.27(b) requires responses to motions for summary judgment to be filed within five (5) days after the date of service of the motion.[*]
Standards for Summary Judgment
In considering motions for summary judgment submitted pursuant to §2423.27 of the Authority's regulations, the standards to be applied are those used by United States District Courts under Rule 56 of the Federal Rules of Civil Procedure, Dep't of Veterans Affairs, Veterans Affairs Med. Ctr., Nashville, Tenn., 50 FLRA 220, 222 (1995). Rule 56(c) provides, in pertinent part, that:
The judgment sought shall be rendered forthwith if the pleadings, depositions, answers to interrogatories, and admissions on file, together with the affidavits, if any, show that there is no genuine issue as to any material fact and that the moving party is entitled to a judgment as amatter of law.
Upon review of the General Counsel's motion I have determined that the summary judgment process is appropriate in this case.
On November 22, 2011, the Regional Director of the San Francisco Region of the Authority issued a Complaint and Notice of Hearing alleging that the U.S. Department of Veterans Affairs, Portland VA Medical Center, Portland, Oregon (Agency/Respondent), violated §7116(a)(1) and (5) of the Federal Service Labor-Management Relations Statute (the Statute), by implementing a Physical Medicine and Rehabilitation Service Holiday Coverage Policy without first providing the American Federation of Government Employees, Local 2157 (Charging Party/Union), with notice and an opportunity to negotiate over this change to the extent required by the Federal Service Labor-Management Relations Statute (the Statute).
The complaint, which was served on the Respondent by certified mail, specified that Respondent's answer was to be filed by December 19, 2011, and that a failure to file an answer would constitute an admission of the allegations of the complaint. See 5 C.F.R. § 2423.20(b). A hearing was scheduled for January 26, 2012. The Respondent did not file an Answer or other response to the Complaint.
On January 4, 2012, the General Counsel filed a Motion for Summary Judgment, asserting that by its failure to answer the complaint, the Respondent admitted all of the allegations therein. Since no facts are in dispute, the General Counsel submits that the record demonstrates that the Respondent violated the Statute as alleged. The Respondent did not file an opposition to the motion for summary judgment.
Section 2423.20(b) of the Authority's regulations, provides, in pertinent part:
(b) Answer. Within 20 days after the date of service of the complaint . . .
the Respondent shall file and serve . . . an answer with the Office of Administrative Law Judges. The answer shall admit, deny, or explain each allegation of the complaint. . . . Absent a showing of good cause to the contrary, failure to file an answer or respond to any allegation shall constitute an admission. . . .
The Respondent failed to answer the allegations of the complaint and did not show good cause for its failure. Nor did the Respondent oppose the motion for summary judgment or the remedies requested therein. By its inaction, the Respondent admits the allegations of the complaint pursuant to §2423.20(b) and the motion is unopposed. Accordingly, there are no factual issues in dispute, and it is appropriate to resolve this case by summary judgment. Based on the existing record, I make the following findings of fact, conclusions of law, and recommendations.
FINDINGS OF FACT
1. This unfair labor practice complaint and notice of hearing is issued under 5 U.S.C. §§ 7101-7135 and 5 C.F.R. Chapter XIV.
2. The U.S. Department of Veterans Affairs, Portland VA Medical Center, Portland, Oregon is an agency under 5 U.S.C. § 7103(a)(3).
3. The American Federation of Government Employees, AFL-CIO (AFGE) is a labor organization under 5 U.S.C. § 7103(a)(4), and is the exclusive representative of a nationwide unit of employees appropriate for collective bargaining at the U.S. Department of Veterans Affairs, including employees of Respondent.
4. The American Federation of Government Employees, Local 2157, AFL-CIO (Charging Party) is an agent of the exclusive representative for the purpose of representing certain employees of the Respondent within the unit described in paragraph 3.
5. The charge and amended charge were filed by the Charging Party with the San Francisco Regional Director on July 8, 2011 and November 2, 2011, respectively.
6. Copies of the charges described in paragraph 5 were served on the Respondent.
7. At all times material herein, John E. Patrick occupied the position of Director, Portland VA Medical Center.
8. At all times material herein, Mr. Patrick was a supervisor and/or management official under 5 U.S.C. § 7103(a)(10) and (11) at Respondent.
9. At all times material herein, Mr. Patrick acted on behalf of Respondent.
10. On or about May 31, 2011, Respondent, by Mr. Patrick, and/or others implemented a Physical Medicine and Rehabilitation Service Holiday Coverage Policy without first providing the Charging Party with notice and an opportunity to negotiate over this change to the extent required by the Statute.
11. By the conduct described in paragraph 10, the Respondent committed an unfair labor practice in violation of 5 U.S.C. § 7116(a)(1) and (5).
In failing to file an Answer to the complaint, the Respondent admits that it implemented a change to its holiday coverage policy without first providing the Union with notice and an opportunity to negotiate over this change and in doing so, it violated §7114 (a)(1) and (5) of the Statute.
It is well settled that a change to holiday work scheduling constitutes a change in conditions of employment that requires notice and impact and implementation bargaining prior to implementation of the change when the change is more than de minimis. Dep't of the Treasury, U.S. Customs Serv., Region IV Miami, Fla.,19 FLRA 304 (1985). Having failed to file an Answer or a response to the Motion for Summary Judgment, the Respondent has failed to establish that the change was de minimis.
As a remedy for the Respondent's violation, the General Counsel requests an order to return to the status quo ante along with a cease and desist order to bargain, and that the Respondent post a notice to employees throughout its facilities at the U.S. Department of Veterans Affairs, Portland VA Medical Center, Portland, Oregon, signed by the Director of that facility. While neither of the cases cited by the General Counsel included a status quo ante remedy, such a remedy can be appropriate in a summary judgment decision based upon the failure to file an answer or response to the motion. U.S. Dep't of Def., Def. Distrib. Depot, Anniston, Ala., 61 FLRA 108 (2005).
When an agency has failed to bargain over the impact and implementation of a management decision, the Authority evaluates the appropriateness of a status quo ante remedy using the following factors: (1) whether and when notice was given to the union by the agency concerning the change; (2) whether and when the union requested bargaining;
(3) the willfulness of the agency's conduct in failing to discharge its bargaining obligation; (4) the nature and extent of the adverse impact on unit employees; and (5) whether and to what degree a status quo ante remedy would disrupt or impact the efficiency or effectiveness of the agency's operations. Fed. Corr. Inst., 8 FLRA 604 (1982).
As the Respondent could have raised but did not raise any objection to the request for a status quo ante remedy, the granting of such a remedy in this case is appropriate, as the Respondent admits that it provided no notice or an opportunity to negotiate and has failed to establish that the change had no impact on bargaining unit employees or would cause any disruption or impact the efficiency or effectiveness of agency operations.
Therefore I recommend that the Authority grant the General Counsel's Motion for Summary Judgment and issue the following Order:
Pursuant to §2423.41(c) of the Authority's rules and regulations and §7118(a)(7) of the Federal Service Labor-Management Relations Statute (the Statute), the U.S. Department of Veterans Affairs, Portland VA Medical Center, Portland, Oregon, shall:
1. Cease and desist from:
(a) Implementing the Physical Medicine and Rehabilitation Service Holiday Coverage Policy without first providing the American Federation of Government Employees, Local 2157, AFL-CIO, with advance notice and an opportunity to bargain to the extent required by the Statute.
(b) In any like or related manner, interfering with, restraining, or coercing bargaining unit employees in the exercise of their rights assured by the Statute.
2. Take the following affirmative action in order to effectuate the purposes and policies of the Statute:
(a) Rescind the Physical Medicine and Rehabilitation Service Holiday Coverage Policy implemented on or about May 31, 2011.
(b) Restore the practices and procedures concerning holiday coverage as they existed prior to the implementation of the Physical Medicine and Rehabilitation Service Holiday Coverage Policy on or about May 31, 2011.
(c) Post at the Portland VA Medical Center, where bargaining unit employees are located, copies of the attached Notice on forms to be furnished by the Federal Labor Relations Authority. Upon receipt of such forms, they shall be signed by the Director of the Portland VA Medical Center, and shall be posted and maintained for 60 consecutive days thereafter in conspicuous places, including all bulletin boards and other places where notices to employees are customarily posted. Reasonable steps shall be taken to ensure that such Notices are not altered, defaced, or covered by any other material.
(d) Pursuant to §2423.41(e) of the Authority's rules and regulations, notify the Regional Director, San Francisco Region, Federal Labor Relations Authority, in writing, within 30 days from the date of this Order, as to what steps have been taken to comply.
Issued, Washington, DC, March 8, 2012.
CHARLES R. CENTER
NOTICE TO ALL EMPLOYEES
POSTED BY ORDER OF
THE FEDERAL LABOR RELATIONS AUTHORITY
The Federal Labor Relations Authority has found that the U.S. Department of Veterans Affairs, Portland VA Medical Center, Portland, Oregon, violated the Federal Service Labor-Management Relations Statute (the Statute), and has ordered us to post and abide by this Notice.
WE HEREBY NOTIFY OUR EMPLOYEES THAT:
WE WILL NOT unilaterally implement a Physical Medicine and Rehabilitation Service Holiday Coverage Policy without first providing the American Federation of Government Employees, Local 2157, AFL-CIO, with advance notice and an opportunity to bargain to the extent required by the Statute.
WE WILL NOT in any like or related manner, interfere with, restrain, or coerce bargaining unit employees in the exercise of their rights assured by the Statute.
WE WILL rescind the Physical Medicine and Rehabilitation Service Holiday Coverage Policy implemented on or about May 31, 2011.
(Agency/Respondent)
Dated: ___________________ By: _____________________________________
(Signature) (Title)
This Notice must remain posted for 60 consecutive days from the date of posting, and must not be altered, defaced, or covered by any other material.
If employees have any questions concerning this Notice or compliance with its provisions, they may communicate directly with the Regional Director, San Francisco Regional Office, Federal Labor Relations Authority, whose address is: 901 Market Street, Suite 220, San Francisco, CA 94103, and whose telephone number is: (415) 356-5000.
* In accordance with §2429.21 of the rules and regulations, when the period of time allowed for the filing of papers is seven (7) days or less, intermediate Saturdays, Sundays, and legal holidays are excluded from the computation.


Grove 42 is a celebration of the Orange; an adult, citrus blend of copper-pot distillates including Bitter Orange, Mandarin, Blood Orange, Lemongrass, Sansho Peppercorn, Ginger & Lemon.
Since it's launch in late 2015, Seedlip has been championed by some of the most celebrated bartenders & Michelin starred Chefs around the globe & today is served in over 16 International cities in restaurants & bars such as Eleven Madison Park, The French Laundry & The Dead Rabbit, to name a few. The company is supported by a team of 60 employees with offices in the UK and most recently, Los Angeles, CA.
The launch of Grove 42 follows a string of innovation within the NA category from Seedlip, including a limited edition dark Seedlip Spirit for The World's 50 Best Restaurants Awards, the world's first ever NOgroni made with 22 different ingredients & a ground-breaking inclusive global bar concept, N o l o by Seedlip, which focused on the ingredients & flavor of a cocktail rather than the alcohol content.


Black 100% Cotton, "Unin-habit-ed NUN" celebrates Nunsense 25th Anniversary.
Featuring HOLIER THAN THOU across the chest and a small NUNSENSE logo.
To order by phone or request express shipping, please call 1-800-Yes Nuns. For orders outside of the USA, we will contact you regarding extra shipping fees when we receive your order.


Copyright © 2017 Mikhail Y. Inyushin et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
The amyloid beta (Aβ) peptide and its deposits in the brain are known to be implicated in the neurodegeneration that occurs during Alzheimer's disease (AD). Recently, alternative theories views concerning both the source of this peptide and its functions have been developed. It has been shown that, as in all other known types of amyloidosis, the production of Aβ originates in blood cells or cells related to blood plasma, from which it can then spread from the blood to inside the brain, with the greatest concentration around brain blood vessels. In this review, we summarize research progress in this new area and outline some future perspectives. While it is still unclear whether the main source of Aβ deposits in AD is the blood, the possibility of blocking the chain of reactions that lead to constant Aβ release from the blood to the brain may be exploited in an attempt to reduce the amyloid burden in AD. Solving the problem of Aβ accumulation in this way may provide an alternative strategy for developing anti-AD drugs.
It is known that Alzheimer's disease (AD) is the most common form of dementia, and it worsens over time. Current treatments cannot stop it from progressing, which emphasizes the desperate need for effective drugs. The hallmark of AD is pathological extracellular deposition of amyloid, which mainly consists of amyloid beta (Aβ) peptide, in the brain tissue of patients, and there is evidence supporting the concept that an imbalance between production and clearance of Aβ peptides is a very early, often initiating, factor in AD (reviewed in: ). The damage to the neurons and internal neuronal tangle formation is only a consequence of this imbalance, in which the action of soluble Aβ peptide oligomers plays a very important role [1–3]. While there has been a gradual accumulation of knowledge about the Aβ pathway, which is driving significant pharmaceutical industry drug research , one of the principal questions that might affect the therapeutic landscape is still unresolved: Where does Aβ peptide production originate?
The prevailing hypothesis is that brain cells are responsible for Aβ peptide overproduction. It is known that both astrocytes [5, 6] and neurons [5, 7] produce and release monomeric Aβ to the extracellular space, which may aggregate and form fibrils if they become concentrated in the micromolar (μM) range [8, 9]. It was shown that cultured human neurons with familiar AD-type mutations may, in only a few weeks, induce robust extracellular deposition of Aβ, including detergent-resistant plaques, in a human neural stem cell-derived three-dimensional (3D) culture system . Neurons in this model have both amyloid precursor protein (APP) and presenilin 1 mutations and thus showed significant increases in the ratio of pathogenic Aβ42 to Aβ40 peptides compared with non-AD control neurons [2, 11]. A specialized gel was added to the culture to retain and accumulate the released Aβ , and this is a necessary element of the model; otherwise the aggregation is absent. Some gel components may be seeding points that start the Aβ plaque formation, because it was shown that peptides favor self-aggregation over cross-seeding with nonhomologous sequences . The process of aggregation and amyloid fibril growth may be facilitated by seeding with preformed β-sheet amyloid resulting from cellular uptake, concentration, and aggregation of Aβ within endosomes/exosomes . After β-sheet formation is initiated, this process resembles the spread of crystallization or prion-like propagation . For example, addition of Aβ seeds and the external Aβ peptide can provoke aggregation in pure neuronal cultures that normally do not produce Aβ plaques without the gel. It was shown that while no Aβ deposition was observed in hippocampal neuronal cultures of postnatal APP transgenic (APP-tg) mice, Aβ deposition emerged when cultures were treated once with brain extract from aged APP-tg mice and the culture medium was continuously supplemented with additional synthetic Aβ . These results confirmed that brain cells could supply enough Aβ to produce not only damaging oligomers but also the aggregated forms present in AD patients.
Recently, an alternative view has been developed. It was proposed that beta amyloidosis is developed from Aβ peptides (or from the Aβ seeds) that spread to the brain from the blood as in other common forms of amyloidosis, such as light-chain immunoglobulin amyloidosis, transthyretin amyloidosis, or reactive systemic amyloidosis. Can Aβ peptide come from blood? Previously, it was shown that platelets have relatively high concentrations of APP, which is mostly contained within alpha granules, and the alpha granule content is liberated upon platelet degranulation [16–20]. Practically all of the APP residing in blood plasma (~7 ng/ml) is thought to derive from platelets . Platelets are also the primary source of Aβ peptide in human blood (~90%) , and this secreted peptide is similar to that found in the senile plaques of AD patients and is similarly increased in vivo by the presenilin 1 and presenilin 2 and APP mutations linked to familial AD . The activated platelets in AD retain greater amounts of APP  while showing more platelet adhesion and thrombus formation . In our recently published work we showed that Aβ peptide can be detected by immunocytochemistry in and around the blood vessels in the brain after experimental thrombosis and that this peptide is released from platelets . We have also shown that during clot formation the density of platelets in the lumen of the thrombotic vessel is significantly increased (more than 300–500 times), thus allowing a massive release of Aβ peptide (directly or cleaved from released APP) at the site of clot formation . It was known previously that microinfarcts are closely related to AD pathology [26–28], and there is a correlation with intracranial vessel arteriosclerosis [29, 30] in which microclots are chronically being formed in brain blood vessels during arteriosclerosis [31, 32].
It seems also that, compared with brain cells, in which APP is known to be bound to the cellular membrane during processing with successive secretases to produce the Aβ peptide, platelets use a somewhat distinct mechanism by releasing full-length APP. As shown by western blots and carboxyl-terminal and amino-terminal APP radioimmunoassay, activated platelets released a sedimentable full-length APP with the carboxyl-terminal epitope as well as a soluble APP lacking the carboxyl-terminal epitope (still containing Aβ, according to its molecular weight) . During platelet degranulation some granules and dense bodies or their contents appear to be extruded into a serpentine system of lipid channels that is continuous with the platelet membrane . It is also known that the material from alpha granules after the release from platelets forms a coating on the surface of the platelet . Recently, specialized extracellular lipid vesicles (exosomes, microvessels, or microparticles) were found be emitted by platelets. These exosomes participate in the processing of many proteins (reviewed in ), but specifically it was shown that β-cleavage occurs in early endosomes, and the products are secreted from the cells in association with exosomes . Interestingly, when platelets contact each other in the clot after aggregation, they change the Aβ production mechanism. It has been shown that platelets at high density secrete mainly Aβ ending at residue 40 (Aβ40) as a final product, while the Aβ42 level is not affected by cell density . Alternatively, brain endothelial cell enzymes can cleave the platelet-released APP, forming Aβ, especially if activated platelets adhere directly to the endothelial cells .
To summarize, previous work has shown that platelets in blood vessels may (1) release full-length APP, (2) simultaneously process the released APP inside microvessels/exosomes (that have lipid membranes), (3) liberate Aβ as a final product, and (4) increase its specific production in case of being densely concentrated, as inside a thrombus. In addition, (5) APP may also be processed by the endothelial cells to generate Aβ.
Recently, the concept of very specialized membrane-bound β-/γ-secretases and the mechanism of APP processing were challenged, and it was suggested instead that there is a multiplicity of these proteins and mechanisms . The available literature supports the possibility that APP processing to produce Aβ occurs upon cleavage in endosomes/exosomes, not in external membranes. It was shown that these microvesicles (microparticles) may contain enzymes of the cathepsin B family, a group of proteolytic enzymes whose cysteine or thiol groups are involved in the cleavage of substrates (, also in the book ed. ). The cysteine protease cathepsin B has been identified as a powerful β-secretase, and its inhibition reduces Aβ production from the precursor APP [42–44].
Alternatively, platelets have been shown to produce the initial seed of the aggregated Aβ, which can be spread to the brain . It was shown that Aβ stimulates the integrin receptor in platelets, leading to the release of ADP and the protein clusterin, and this protein promoted β-sheet folding and the formation of fibrillar Aβ aggregates. The same authors have also shown that in transgenic AD model mice the antiplatelet agent clopidogrel (an ADP receptor [P2Y1, 2] blocker) reduced the amount of clusterin in the circulation and the incidence of cerebral amyloid angiopathy (CAA) . In a transgenic mouse model of AD, platelets were found to be the major contributors to CAA, which then formed a shield of insoluble Aβ around brain blood vessels . Interestingly, another antiplatelet drug, cilostazol, with a completely different mechanism of action that reduces platelet reactivity and degranulation, also reduced Aβ-induced cognitive deficits associated with Aβ accumulation [47–50], while aspirin, which reduces platelet aggregation but has no effect on degranulation, has no effect . These results suggest that the degranulation of platelets is very important in AD development.
Production of Aβ in both brain and blood is beyond doubt. This fact led us to the hypothesis that both mechanisms of Aβ peptide production are important in the development of AD . As a first step, there must be accumulation (aggregation) of platelets due to the response to some still-unknown septic or aseptic cause. According to this hypothesis, the Aβ peptide converted from APP and released from platelets (Figure 1, red arrows) spreads to the endothelium first and then to the perivascular space (Figure 1, green) and accumulates in the basal lamina. Another flow of Aβ peptide released from brain cells (Figure 1, black arrows) needs to pass the astrocyte barrier to reach the same perivascular space. Both brain- and blood-derived Aβ peptide may overwhelm the capacity of the existing clearance system.
Figure 1: Beta-Amyloid from blood and from brain. Blood vessel lumens are shown in red, while perivascular space with basal lamina are shown in green on the sketch.
Perivascular spaces are present around small as well as large blood vessels, in which case they are also known as Virchow-Robin spaces, forming the glymphatic perivascular system . The main function of the glymphatic system is brain clearance: there is a constant flow along the perivenular and periarterial vascular spaces, from smaller to larger vessels [52, 53], and this flow increases during sleep . The perivascular space extends only a few microns from small vessels (see Figure 1), but in bigger vessels it may extend a few millimeters. It is formed between the astrocytic end-feet enwrapping blood vessels (also known as the glia limitans, and the antibodies against aquaporin 4, the end-feet marker, can delimit its border) and the endothelium. In small vessels the perivascular space is known to be filled with basal lamina, a soft gel that consists of laminin, fibronectin, tenascin, collagens, and proteoglycans, which separates the astrocytic end-feet and endothelium cell layers and does not prevent the passage of macromolecules [55, 56]. In arterioles, the space between the end-foot and the endothelium includes also the smooth muscle cell layer. It is important to note that the accumulation of amyloid deposits follows a decreasing gradient from the inside of the vessel to the brain, not vice versa. It was shown that, during the development of AD angiopathy, amyloid accumulates initially in the perivascular space inside the basal lamina [57–59]. As the disease progresses, amyloid deposits extend into the smooth muscle cell layer in arterioles, leading to its loss. With end-stage disease, amyloid appears to spread to adjacent neuropil-forming dysphoric vessels  and produces complete disruption of the blood-brain barrier. Analyzing this data, it seems that amyloid moves from inside the blood vessel to the brain. Interestingly, amyloid deposits do not accumulate in the venous system. It may be important that elevated blood pressure in arteries drives the Aβ peptide from the lumen to the perivascular space, or alternatively it may be important that cerebral arterial pulsations drive the exchange of Aβ peptide in the perivascular space with fluids in the brain parenchyma . In any case, the flow along the glymphatic system was shown to be very important for amyloid clearance [52, 53]. In a transgenic mouse model (APPswe/PS1dE9), it was shown that thrombotic cerebrovascular lesions induced a rapid transient increase in amyloid plaque burden and amyloid angiopathy in the area immediately surrounding the infarcted area . The authors  suggested that this most probably happens due to interference with amyloid clearance pathways. On the other hand, we showed that thrombosis in wild-type mouse brains produces a massive release of APP from platelets, which is converted to Aβ . These results suggest that both brain-derived and blood-derived Aβ peptide may be important and that platelets are the key players.
These deposits include retinal and lens amyloid accumulation, retinal nerve fiber layer loss, and retinal vascular changes .
Aβ-containing structures as well as epitopes containing APP were described in some cases of inclusion-body myositis, the collection of diseases that are characterized by the vacuoles and filamentous inclusions in muscle fibers [63, 64]. Using electron microscopy, it was found that Aβ-immunoreactive structures were often in proximity to cytoplasmic tubulofilament inclusions (CTFs), but CTFs themselves never contained Aβ immunoreactivity . Also, in some affected muscle cells Aβ-immunoreactive accumulations extended beyond the cell boundary, while in the majority of cases they were localized inside the cell (mainly near the sarcolemma boundary, but also deeply in the interior of the cell). Some Aβ-positive accumulations in the myocytes did not contain amyloid in β-pleated sheets, and this was hypothesized to be an early sign in the development of the myopathy . Later, the fact that Aβ-immunoreactive accumulations can be found mainly inside the myocytes led many authors to the hypothesis that diseased muscle cells have the intrinsic genetic ability to produce augmented quantities of APP and Aβ during myositis (reviewed in ). In contrast, it was shown by the authors of the original discovery that inclusion-containing cells cultured from inclusion-body myositic muscle do not accumulate APP and can be restored to normality and easily innervated . The same group also suggested that, during the course of the disease, the blood might produce Aβ and APP during inclusion-body myositis and all other inflammatory myopathies, as they found that human muscle macrophages express APP and have all the necessary machinery for its production.
While the heart may be affected by many diseases related to protein misfolding in myocardium tissue, new studies have shown that some cases of idiopathic cardiomyopathy are related to AD-associated presenilin gene variants . Also, using modern imaging, proteomics, and echocardiographic methods, it was shown that patients with AD have diastolic dysfunction. Aβ40 and Aβ42 were present in the hearts of many patients with heart problems, but their expression was significantly increased in AD .
Amyloid protein deposit immunoreactivity was described many years ago in and around the endothelium of dermal blood vessels in aged AD patients and controls and was proposed as a marker of the disease in AD patients . But another study found that skin accumulation of Aβ around blood vessels was unrelated to the severity of symptoms in AD patients, occurring also in some healthy subjects . Interestingly, Aβ protein was also detected in the skin of patients with amyotrophic lateral sclerosis but not in controls . In any case, it was very important that Joachim et al., 1989 , pointed out that the source of amyloid deposits in the skin and other organs was probably derived from a common circulating precursor, the blood. We have also shown that Aβ peptide can be found in and around skin blood vessels in mice after the experimental photothrombosis in the skin, as revealed by immunostaining, but not in normal skin . These findings implicate thrombosis-related mechanisms as a probable source of this immunoreactivity.
Aβ in the skin may have implications for the development of vaccine against Aβ to cure AD, as patients with compromised clotting, like thrombophilia, thrombophlebitis, or similar diseases, could have additional inflammation problems. It is known that the development of the ACC-011AD vaccine (Elan-Wyeth Corp.) was halted due to patients developing skin lesions, which were suspected to be cases of blood vessel inflammation .
It is now clear that not only the brain but also other organs can be affected by Aβ, and the amount of deposition in these organs may be related or not to the severity of AD. As proposed by others , AD may be viewed either as a systemic disease or as a metastatic disorder, possibly leading to multiple organ failure.
Amyloid aggregates in AD may be of different types, with different solubilities in conventional solvents or detergents and different resistances to proteolysis. Plaques can be Congo Red-positive misfolded amyloid aggregates between the neurons, which typically have low solubility [4, 74–76], and there can be relatively soluble Aβ aggregates that typically appear as clusters of 10–20 nM ovoid structures . The depositions in close proximity and around arteries (CAA) are also mainly insoluble. The major component of the AD deposits is the Aβ peptide, but there are also minor components that may affect solubility. One of the components, serum amyloid P component (AP), is a normal plasma constituent  produced by liver, and its concentration in blood plasma has been shown to be about 5-fold elevated in AD . Besides its role in AD, AP is also a component of β-sheet-containing plaques in other types of amyloidosis, such as light-chain immunoglobulin amyloidosis or reactive systemic amyloidosis. AP reduces solubility and also prevents proteolysis of amyloid deposits, but since it is not itself an enzyme inhibitor, it is protective only when bound to the deposits . This implies that blood components participate in the formation of many brain amyloid aggregates in AD. Why then is it not possible that the Aβ peptide is itself (at least partially) derived from blood?
We need to mention here that some other minor components of AD deposits definitely come from the brain: it was shown that the synaptic vesicle protein synuclein 1 or its components are visible in AD plaques as well .
6. Why Are Platelets Activated in the AD Brain?
The systemic view of AD may be explained by systemic release of Aβ, but in any case the most severe symptoms are developed in the brain. Why is the brain the target of Aβ release in AD if there is no traumatic thrombosis? And why are only some parts of the brain affected?
It is well known that the different parts of the brain are not affected equally, at least according to the density and distribution of senile plaques and neurofibrillary tangles. During development, the disease primarily affects the entorhinal cortex [82–84], which is a major input and output structure of the hippocampal formation (affected in the next stage of the disease) but is also known to convey olfactory information [85, 86]. It was shown that the olfactory bulb is also definitely affected and may be affected even before the cortex [87, 88]. It was proposed that the olfactory tracts might provide a portal for entry into the brain of any putative pathogenic agent(s) that might be responsible for the induction of senile plaques and/or neurofibrillary tangles . This led to the old theory of an infectious etiology for AD and the association with different brain viruses, bacteria, or prions (reviewed in [89, 90]). The evidence for human transmission of Aβ pathology and CAA after the treatment of children with human cadaver-derived growth hormone was reported, and it was suggested that this was an example of the prion-like spread of AD .
Recently, another explanation has been proposed. It was shown that Aβ release may be a specific defense against septic agents. If such agents are transmitted to the brain, the body responds by releasing Aβ peptide to kill them. If this defense mechanism is somehow compromised, it has been suggested that this may lead to overproduction of the Aβ peptide.
The antimicrobial effect of the Aβ peptide is clearly established. Its activity against different viruses has been shown [92–95] as well as its strong antibiotic activity against both Gram-negative and Gram-positive bacteria and yeast [95–97]. This allows one to suggest that Aβ oligomers are a hitherto-unrecognized antimicrobial agent that functions as a normal component of the innate immune system . Two different mechanisms have been proposed to explain this Aβ function: (i) the trapping of bacteria and (ii) pore-forming antibiotic activity.
(i) It was shown that the development of Aβ protofibrils can prevent pathogen adhesion to host cells, thus explaining the protective effect of Aβ against Salmonella bacterial infection . It was shown that Salmonella bacterial infection of the brains of transgenic 5XFAD mice resulted in rapid seeding and accelerated Aβ deposition, which closely colocalized with the invading bacteria. This evidence led the authors to suggest that any infectious or sterile inflammatory stimuli could drive amyloidosis .
(ii) It has been shown that Aβ peptide oligomers perforate cell membranes and form (at low concentrations) tetrameric channels permeable to K+ ions. At higher concentrations they form giant multilevel Ca++-permeable pores, which are mainly hexamers [98–100]. An excess of Ca++ permeability through these pores leads to cell death, as it induces unrestricted calcium flux into the cell, leading to dyshomeostasis .
There is a similarity of the Aβ peptide oligomer pore-forming effect with that of other peptide antibiotics (e.g., cecropin A or nystatin) that kill target cells by formation of large pores in the membrane [101–103]. This led us to hypothesize that Aβ peptide released from platelets or cleaved from platelet-released APP works effectively as a natural antibiotic during clot formation following injury or platelet degranulation in response to other septic or aseptic (inflammatory) stimuli .
8. What Is a New and Alternative Strategy to Fighting AD?
While the Aβ hypothesis is driving the majority of current research on AD, the development of effective drugs against the disease has stalled. These drugs are directed against Aβ, its precursor APP, or the β- and γ-secretase enzymes from the known Aβ pathway. Knowledge about this pathway is driving significant pharmaceutical industry drug research , and while current drugs help mask the symptoms of AD, they do not treat the underlying disease or delay its progression. None of the Aβ‐targeted phase 3 clinical trials in AD has shown a statistically significant benefit in achieving its prespecified clinical endpoints . Several of these trials against Aβ and γ-secretases had to be halted because of side effects that may not have been target related [104, 105].
Analysis of the literature suggests a new approach that takes into account not only brain-derived but also blood-derived Aβ and proposes that platelets are the key players. We further suggest an alternative strategy in which AD is treated through the reduction (inhibition) of pathologically excessive release of Aβ (through APP) by platelets. A breakthrough AD drug must treat the underlying disease and stop or delay the cell damage that eventually leads to the worsening of symptoms.
It is known that normal or pathological platelet activation may take place after attachment and adhesion events or as the effect of many other activation factors, such as thromboxane A2, the ADP/ATP ratio, thrombin, platelet-activating factor (PAF), collagen, and many others. The activation pathways are usually mediated by specific receptors, some of which are shown in Figure 2. Platelet-activation signaling pathways have been known for many years, and over time it has become clear that there is a complex and sophisticated signaling and amplification network (reviewed in ). The specific pathways that are most important in the pathological activation related to AD are not known, and this needs to be studied.
Figure 2: Activation of different types of receptors induces degranulation of platelets.
In Figure 2, we show a few of the many receptors that activate platelets and their possible relation to AD.
Thromboxane A2 (TxA2) Prostanoid G Protein-Coupled Receptors with Two Alternatively Spliced Isoforms (α and β). TxA2 receptor antagonists have been shown to block iPF2αIII-induced increases in Aβ secretion [107, 108].
Glycoprotein VI (GPVI) Collagen Receptor. Honokiol (extracted from magnolia), a specific antagonist of collagen receptor glycoprotein VI, which is expressed on human platelets , was shown to attenuate Aβ-induced memory impairment, which was attributed to its antioxidant activity .
Proteinase-Activated Receptors (PARs). These members of the G protein-coupled receptor family are usually activated by thrombin in platelets. Activation of PARs may result in AD pathogenesis (reviewed by ).
Purinergic ATP-ADP G Protein-Coupled Receptors (P2X, P2Y). It was shown that clopidogrel (a P2Y1, 2 ADP receptor blocker) significantly reduced the incidence of CAA . Using selective purinergic receptor agonists and antagonists in vitro and in AD animal models it was shown that these receptors represent novel therapeutic targets for the treatment of AD .
Glycoprotein IIb/IIIa Receptors. The progression of dementia in AD patients with fast cognitive decline was shown to be correlated with the levels of activated glycoprotein IIb-IIIa complex and P-selectin .
It is especially interesting that the ADP and TxA2 receptors both signal via the specific G protein Gq. Temporal elimination of Gq greatly inhibits functioning of both these receptors. It was shown that agonists (activating ligands) of retinoid X nuclear hormone receptors (RXRs) bind directly to Gq and very effectively inhibit platelet aggregation, due to dysfunction of the ADP and TxA2 receptors, but only weakly affect functioning of collagen (GP VI) receptors . This is definitely a nongenomic effect because the lack of a nucleus in these cells . On the other hand, it was shown that oral administration of the RXR agonist bexarotene to a mouse model of AD resulted in enhanced clearance of soluble Aβ within hours. The Aβ intraneuronal amyloid deposit area was reduced more than 50% within just 72 hours. Furthermore, bexarotene stimulated the rapid reversal of cognitive, social, and olfactory deficits and improved neural circuit function [115, 116].
Analyzing the literature, we agree with Schmaier  that results concerning APP and Aβ peptide structure and function suggest that AD is in part a thrombohemorrhagic disorder and conclude that platelets and their activation mechanisms are most probably involved. Moreover, these insights give us hope for an alternative strategy in anti-AD drug development focused on newly discovered blood-related pathways of Aβ release and aggregation.
Mikhail Y. Inyushin and Lilia Y. Kucheryavykh designed the study; Mikhail Y. Inyushin, Priscila Sanabria, Legier Rojas, Yuriy Kucheryavykh, and Lilia Y. Kucheryavykh performed the study and analyzed data; Mikhail Y. Inyushin and Legier Rojas wrote the paper.
This research was supported by NIH/NIMHD Grant SC2GM111149 to Mikhail Y. Inyushin, NIH/NIMHD SC2GM102040 Grant to Lilia Y. Kucheryavykh, and NIH/NIMHD Grant 5G12MD007583 to Priscila Sanabria and to Mikhail Y. Inyushin.
G. V. Guillama, L. Y. Kucheryavykh, J. Dávila-Rodríguez et al., "Beta-amyloid peptide in blood clots," in Proceedings of VI Meeting of the Physiol, pp. 7-8, Puerto Rico, 2017.


With the real-life dystopian film that was Trump's inauguration finally behind us, much of the conversation and anticipation around the menswear shows has revolved around how the designers might choose to handle the turbulent political climate.
At Balenciaga this took the form of a coded tribute to everyones favourite socialist-grandpa-next-door, Bernie Sanders, with the brand lifting Bernie's campaign logo design as a motif of the autumn/winter 17 menswear collection. The show featured Democrat-blue and Republican-red jackets, shirts, and big cosy scarves. These garms are perfect for wrapping up warm as we eagerly anticipate a bitterly cold four-year winter under President Trump.


Loughborough CryoSpa is a specialist sports recovery facility that uses a TECO chiller to maintain the water temperature of the ice bath or cryospa at 8.0 degrees Celsius. Ice baths or cryospas, such as this one from CET CryoSpas, are used by top class athletes to help promote recovery from injuries and reduce fatigue.
Those of you were following Wimbledon this year will, perhaps, be aware that many top class players use a cryospa as part of their recovery strategy during training and post-match, indeed Andy Murray has one installed at his home. Six cryospas were recently installed under Centre Court at Wimbledon; Mark was down there at the end of May helping Colin Edgar (Managing Director of CET CryoSpas) to install the cryospas and making sure that the chillers are doing their job. Have a look at our Loughborough CryoSpa Facebook page and you will see interesting posts relating to cryospa use at Wimbledon this year, and Jamie Murray is pictured in one of them. We also have a separate Loughborough CryoSpa website, so please do have a look if you are interested. If you are local to Loughborough, and keen on sports, you might like to try out this facility for yourself, particular if you do strenuous workouts or indulge in marathons. It is just £8 for an individual six-minute session, and £6 per person if two of you wish to share a session (yes, the cryospa can accommodate two people at a time!). You can book a session via our Facebook page or website (for Monday to Friday daytime sessions only), or just call us on 07802 841021. If you have a Twitter account, you can also find lots of interesting tweets about ice baths/cryospas at #chilling4champions.
Lobsters, Penguins and CryoSpas. permalink.


text:
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text:
Q: "Selenium::WebDriver::Error::UnhandledAlertError: unexpected alert open" despite using dismiss_confirm This test fails:
describe 'a confirm modal', :js, driver: :chrome do
  it do
    visit '/test/confirm'
    dismiss_confirm do
      click_link 'Cancel'
    end
  end
end

with a Selenium::WebDriver::Error::UnhandledAlertError: unexpected alert open error.
It fails immediately with this error as soon as it gets to the click_link 'Cancel' line:
An error occurred in an after hook
  Selenium::WebDriver::Error::UnhandledAlertError: unexpected alert open: {Alert text : Are you sure?}
  (Session info: chrome=53.0.2785.101)
  (Driver info: chromedriver=2.21.371461 (633e689b520b25f3e264a2ede6b74ccc23cb636a),platform=Linux 4.4.0-42-generic x86_64) (WARNING: The server did not provide any stacktrace information)
Command duration or timeout: 1 milliseconds: null
Build info: version: '2.53.0', revision: '35ae25b', time: '2016-03-15 17:00:58'
System info: host: '64c23d07d03c', ip: '172.18.0.6', os.name: 'Linux', os.arch: 'amd64', os.version: '4.4.0-42-generic', java.version: '1.8.0_03-Ubuntu'
Driver info: org.openqa.selenium.chrome.ChromeDriver
Capabilities [{applicationCacheEnabled=false, rotatable=false, mobileEmulationEnabled=false, chrome={chromedriverVersion=2.21.371461 (633e689b520b25f3e264a2ede6b74ccc23cb636a), userDataDir=/tmp/.com.google.Chrome.nJ0sj0}, takesHeapSnapshot=true, databaseEnabled=false, handlesAlerts=true, hasTouchScreen=false, version=53.0.2785.101, platform=LINUX, browserConnectionEnabled=false, nativeEvents=true, acceptSslCerts=true, locationContextEnabled=true, webStorageEnabled=true, browserName=chrome, takesScreenshot=true, javascriptEnabled=true, cssSelectorsEnabled=true}]
Session ID: 12b4869246e45555e3456370e74ad536 (org.openqa.selenium.UnhandledAlertException)
  occurred at [remote server] sun.reflect.GeneratedConstructorAccessor31():-1:in `newInstance'

I can see in the Chrome window that it is still waiting for me to press OK or Cancel.
Why is this failing? How do I get it to dismiss the confirm instead of erroring out?
When I step through the code with byebug, I can see that dismiss_modal doesn't even get to the part where it tries to find a modal and dismiss. It errors out immediately when it hits the click_link, which I take it is not supposed to happen (otherwise dismiss_modal would have a rescue block for that):
[229, 238] in /usr/local/bundle/gems/capybara-2.10.1/lib/capybara/selenium/driver.rb
   229:     modal.accept
   230:     message
   231:   end
   232:
   233:   def dismiss_modal(type, options={}, &blk)
=> 234:     yield if block_given?
   235:     modal = find_modal(options)
   236:     message = modal.text
   237:     modal.dismiss
   238:     message
(byebug) s

[3, 12] in /app/spec/features/testing_basics_spec.rb
    3: describe 'a confirm modal', :js, driver: :chrome do
    4:   it do
    5:     visit '/test/confirm'
    6:     byebug
    7:     dismiss_confirm do
=>  8:       click_link 'Cancel'
    9:     end

The selenium server is running in a docker container from the selenium/standalone-chrome-debug image.
The driver is configured with:
Capybara.register_driver :chrome do |app|
  Capybara::Selenium::Driver.new(
    app,
    browser:                :remote,
    url:                    "http://#{ENV['CHROME_WEBDRIVER_HOST']}:4444/wd/hub",
    desired_capabilities:   :chrome
  )
end

It's using current versions of the gems (as far as I know):
  * capybara (2.10.1)
  * selenium-webdriver (2.53.4)

This is the Rails template it is interacting with (app/views/confirm.html.haml):

= link_to 'Cancel', '#', :confirm => 'Are you sure?'

Update: Thanks to @TomWalpole and @SaurabhGaur for suggesting this could be due using an older version of chromedriver.
It looks like I hadn't updated my selenium/standalone-chrome-debug image in a few weeks (though I'm surprised that 5 weeks is so old that it would cause a problem).
Before updating...
selenium/standalone-chrome-debug latest 84d9c94a042a 5 weeks ago         844.8 MB

root@65a9cd48f684:/# chromedriver --version
ChromeDriver 2.21.371461 (633e689b520b25f3e264a2ede6b74ccc23cb636a)

After updating...
selenium/standalone-chrome-debug latest df941c594b0a 2 days ago          865.3 MB

root@6800a351c182:/# chromedriver --version
ChromeDriver 2.24.417424 (c5c5ea873213ee72e3d0929b47482681555340c3)

And it works!

A: When using selenium-webdriver with Chrome it's important to keep chromedriver updated when Chrome updates itself.  In your log it shows chromedriver version of 2.21 but the latest is 2.24 - update that and your problems should go away.


I hope you all have gotten a bit over the shock and aftershock of the finale from Merlin. In US it is still airing; next Saturday the 6th Episode. Which is in my opinion probably the most scariest of them all. The Dark Tower!
So good luck with that guys 😉 For those who had not watched it yet.
So what's new? Well as you may have all noticed, the front page had been updated with our splendid victory at the NTA awards! Colin Morgan was chosen as best male drama performance exceeding Matt Smith and Benedict Cumberbatch! And he deserves it! I've gathered every picture I could find in the net and collected them to one gallery here on Myth and Magic enjoy the NTA Awards Gallery! Can't wait to see his next appearance in "Quirke" which I posted a Colin Morgan's New Gig!
Unfortunately for the series Merlin, they got beaten by Downtown Abbey, which I still find hard to believe…Out of all 4 that was the last one I expected to win to be honest.
Alexander Vlahos has recently received some good critics on his work in privates, which aired the begin of January. We hope to see him soon again in a new production.
Katie McGrath will be appearing in a new TV Series called Dracula which is a VS production! Congrats on the breakthrough Katie! More details on this will follow soon after I've done an article collection to find out all the details.
And Angel Coulby, Anthony Head and Janet Montgomery (Mithian) will be making an appearance in the new series on BBC 2 tomorrow; Dancing on the Edge! Airing at 9pm UK Time.
And now for the updates on the Fanart Galleries!
We welcome two new members, to the fanart Galleries namely sxsllxl's ArtGalleryand Kil_Rain's ArtGallery. Whose galleries has just been added to the page.


The always popular Buckeye Air Fair is back Feb. 9 and 10 from 9 a.m. to 3 p.m. at the Buckeye Municipal Airport, 3000 S. Palo Verde Road.
Join us for a weekend of fun featuring a live, two-hour air show both days at Noon, action packed demonstrations, vintage and military aircraft displays thanks to the Copperstate Fly-In, whose enthusiasts will bring hundreds of aircraft to showcase.
In addition, you can enjoy great food, live entertainment, a Kid's zone both days, plus a Sci-Tech Fest on Saturday, Feb 9.
New this year, you can upgrade your free admission and get an up close view of the airshow with front row seats, light refreshments and private restrooms with the purchase of VIP tickets. One-day VIP tickets are $80.00; Two day tickets are $125.00.
You can also purchase all access Kid's Zone tickets in advance for just $10.00.
Purchase your VIP and/or Kid's Zone tickets online.