text:
Does David Rockefeller rule the World? New World Order
Aleksandar Mishkov/ published 3 years ago
Now at age 100, David is the oldest living member of the organization. He is also the oldest living member of the Rockefellers, a family that has financial inputs in many industries and areas
With so many conspiracy theories nowadays, one can always be count as verified and true: David Rockefeller is one of the most powerful people in world. One can even go a step further and say he is the most powerful among powerful people. Through the years, knowingly or not, Rockefeller has admitted that he is part of a secret organization, called the New World Order, which has only one goal in mind: world domination.
The drive of Rockefellers and their friends has always been simple, create a one-world government that combines communism and super capitalism. Now at age 100, David is the oldest living member of the organization. He is also the oldest living member of the Rockefellers, a family that has financial inputs in many industries and areas. In 1968, an American journalist, Jurriaan Meaessen, wrote one of the first repots on the New World Order, stating that the masonry organization is behind several studies including vaccines and mass castration and sterilization. Since then, the organization has evolved and is now one of the more powerful in the world.
Three Quotes Confirming New World Order
Going back to the knowingly and unknowingly states by Rockefeller, we go through three quotes by the billionaire that perfectly sum up his organization.
- We are grateful to the Washington Post, the New York Times, Time Magazine and other great publications whose directors have attended our meetings and respected their promises of discretion for almost forty years. It would have been impossible for us to develop our plan for the world if we had been subjected to the light of publicity during those years.
- Ideological extremists have used my meeting with Castro to blame my family, and claim we rule the American politics and American institutions. They state I am behind a conspiracy and an organization working against the whole world, one world, if you like to call it like that. If that is the claim, then I state I stand guilty. And I am proud to say it, since we are building better global and political structure.
- All we need is the right major crisis and the nations will accept the New World Order.
What is the New World Order Plan?
The plan for world domination started in 1956, when the Rockefeller Brothers founded the "Special Studies Project", a project that laid the blueprint for the organization that is nowadays more public than secret.
The organization had two goals in mind, and both were in the aftermath of the World War II. The New World Order had the same premises as the United Nations, an organization in which elites spin the agenda in a way that can be sold to people they are working in their best interest. The plan has been masterfully explained by redefininggod with excerpts from the project.
There are countless conspiracy theories linked with the New World Order and David Rockefeller. Here are some that have caught the attention of media.
- The 10 Kings Prophecy have been around since the Book of Revelation. According to the prophecy, 10 kings (nations) will rise to power and create a new government. It is entirely the basis of the New World Order. Another fact pointing to this theory is the paper published in 1973 by the Club of Rome, in which the club suggested that the world should be split into 10 regions. Some theorists even believe that the famous G8 group will expand to 10 core nations one day, which will be a signal for Armageddon and end for the live we know it.
- The Majestic 12 is another group that has been linked with the New World Order. The theory suggests that in the 1940s, President Truman created a secret committee which included some of the best scientists. The group kept track of UFOs in America. The organization was kept secret, but over the years, documents and proofs have surfaced. But the fun part is that the Majestic 12 is actually a hoax, created with a sole purpose to keep the attention of the public away from the threat aliens in the government.
- The Bohemian Grove is actually a very real conspiracy theory. The Bohemian Club is located in California, and is the home of artists and leaders from around the world. The club holds meetings once a year, and nobody knows what happens behind closed doors.
- The surveillance theory was also proven by Edward Snowden. According to the theory, the New World Order uses tons of assets for mass surveillance, which is how they examine people worth living in the new world that they will create. Some believe that the group uses bar codes and tracks every movement thanks to the bar codes.
- Last, but not least, there are theories that the New World Order has only one goal in mind, and that is creating the "Posthuman". The goal is to create new breed of superhumans, and alien technology will play a large part in that.
- One theory suggests that the New World Order will trim the world's population to 2 billion, all of which will continue to function as the human race. How the group will achieve the goal is unknown, but if you link their existence and involvement with organizations like the World Health Organization, it is easy to think that the NOW will release a deadly virus.
New World Order in Politician's Speeches
Since the beginning of time, New World Order has been linked with some of the most powerful politicians in the world. It comes as no surprise that some of them have been as open to mention the organization in their speeches. Here are some examples.
- The 'affirmative task' before us is to "create a New World Order – US VP, Joe Biden
- We will succeed in the Gulf. And when we do, the world community will have sent an enduring warning to any dictator or despot, present or future, who contemplates outlaw aggression. The world can therefore seize this opportunity to fulfill the long-held promise of a new world order – where brutality will go unrewarded, and aggression will meet collective resistance – President George W Bush, 1991
- Each of us has the hope to build a New World Order – Former US President Richard Nixon in China, 1972
- We are moving toward a new world order, the world of communism. We shall never turn off that road - Russian President Mikhail Gorbachev, 1987
- In the next century, nations as we know it will be obsolete; all states will recognize a single, global authority. National sovereignty wasn't such a great idea after all – US Deputy Secretary of State Strole Talbot in 1992
- The real truth of the matter is, as you and I know, that a financial element in the larger centers has owned the Government ever since the days of Andrew Jackson – Former US President Franklin Roosevelt in letter in 1993
- Our new world rests on order. The danger is disorder. And in today's world, it can now spread like contagion – UK Prime Minister Tony Blair.
Making an Oscar® statuette
The Oscars are one of the most prestigious awards. Some might say the Golden Globes are more prestigious awards in the movie industry, and some prefer the Oscars.But behind the gla...
Best Independent Film Documentaries
The Bubble Gum King is one of the best documentaries ever made. The documentary follows the life story of Andy Paris. He rose to stardom by starting a bubblegum business. He ...
USA vs. China - BBC Documentary 2016
During his presidential campaign, Donald Trump reminded everyone how China is beating USA in every category. He was raving on and on about how China is the most powerful econ...
Conspiracy +1
Nazi Temple of Doom
The Chiemsee Cauldron, discovered in 2001 at the bottom of Lake Chiemsee in Bavaria is the focus of the Nazi Temple of Doom conspiracy. Decorated with figures, and with a dia...
Personal Triumphs
Meet Betty Cohen – The Woman who made the 90's Awesome
Betty Cohen founded Cartoon Network in 1992, and she brought some of our favorite cartoons to life
Huaxi – Secrets of the Richest Village in China
From the outside, Huaxi is dubbed as a socialist village. But on the inside, it is actually a capitalist corporation, m...
The Mystery of Oak Island? Is there something there?
The privately owned island has much more to offer, but the most famous spot is the location now known as "the Money Pi...
Airbus A350-1000: 335 million euros worth plane takes its first flight
The aircraft took its first flight from Toulouse-Bagnac Airport at 10:42 am local time


Firestone Diamonds plc completed the first sale of diamonds recovered from its Liqhobong Diamond Mine achieving total sale proceeds of US$8.14 million. The company owns 75 percent in the mine and the remainder is held by the Government of Lesotho.
In the sale held in Antwerp from 6 to 10 February 2017 all 75,936 carats offered for sale were sold at an average price of US$107 per carat. There were over 90 companies viewing the goods and more than 38 companies being successful.
The average price per carat achieved was very pleasing, considering that the carats sold were recovered from the predominantly lower quality ore areas and are not necessarily representative of the run of mine ore. As previously announced, the Company will only realise consistent run of mine results post ramp up, when it will have mined ore from across the whole pipe.
The higher quality diamonds were competitively bid for during the sale. The best stone, a 37 carat type 2a internally flawless white stone was sold for well over US$1.0 million. A number of yellow and fancy yellow stones included in the sale also achieved competitive prices, with interest being exceptionally strong in these categories.


A broken wastewater pipe caused the spill. A Charlotte Water crew repaired the pipe.
Charlotte-Mecklenburg Storm Water Services will lift the advisory when bacteria levels return to safe levels for swimming.


If you've ever tried to share an iWork file between Macs and iOS devices via iCloud, you know that it doesn't work very well. The essential problem is that iWork documents on the two platforms use different file formats. This means that when you edit an iWork document on one platform , the matching document on the other platform is not automatically updated to reflect the change. There is no true syncing of iWork documents between platforms.
If you've ever tried to share an iWork file between Macs and iOS devices via iCloud, you know that it doesn't work very well. The essential problem, as I've detailed previously, is that iWork documents on the two platforms use different file formats. This means that when you edit an iWork document on one platform (an iPhone, for example), the matching document on the other platform (a Mac, in this example) is not automatically updated to reflect the change. There is no true syncing of iWork documents between platforms.
Exciting news! This is all about to change...for the better. At Monday's Worldwide Developers Conference keynote, Apple vice president of software engineering Craig Federighi revealed a new feature of OS X 10.8 Mountain Lion: iWork automatic syncing via Documents in the Cloud.
Surprisingly, aside from the Keynote demo, Apple has barely mentioned this coming change. The tech media have similarly not given the new feature the attention I believe it deserves. So here I am to correct this oversight.
In Mountain Lion, you will be able to live update an iWork document across platforms. That is, not only will there be automatic syncing of files, but the syncing can take place even if the same file is simultaneously open on more than one device. About 50 minutes into the keynote, Federighi showed this new feature in action: After editing a Pages document on an iPhone, the same document, already open on a Mac, updated itself on the Mac's display. Very slick!
Although cited as a new feature of Mountain Lion, I assume this live syncing will also require updates to other components before it kicks into gear. It will certainly require new versions of the iWork apps for both the Mac and iOS platforms. It will likely also require changes to the iCloud software and possibly the release of iOS 6.
iOS iWork documents are currently a "restricted" form of the Mac versions, supporting only the subset of iWork features available with the iOS apps. How will this differ in Mountain Lion so as to enable live syncing? Will the Mac versions of iWork apps support two different file types, the "full" Mac format and a restricted iOS-compatible one (with only the latter allowing live syncing)?
Will you be able to simultaneously edit the same iWork file on a Mac and an iOS device? If so, what if two users are involved? How will the apps prevent making changes on one platform that unintentionally overwrite changes being made by the other user on the other platform? Perhaps Apple assumes only one person will share documents between devices in this way, so that overwriting is not an issue. Perhaps live updating will only work in one direction, from iOS device to Mac.
Are there other limitations or potential problems lurking, not apparent in the Keynote demo, that will make this syncing less useful than it appears to be? We'll have to wait and see.
More generally, what about files that can be opened by more than one app? For example, Pages on the Mac can open .rtf documents created in TextEdit. If you save a file to the iCloud Document Library in TextEdit, will that same file be accessible and openable from the iCloud Document Library list in Pages? Things don't work this way now and Apple's description of iCloud in Mountain Lion suggests this won't be changing: "To find an iCloud document, just open its app. The iCloud Document Library shows your iCloud documents for the app." But I see a bit of wriggle room here. One can always hope.
Regardless, based on what Apple demoed on Monday, a long overdue and much welcome improvement to iWork syncing is coming to Mountain Lion.


The websites on this list were not designed with education in mind, but which can easily be used for learning purposes — particularly, though not exclusively, for English language development. I only hope that creators of "educational" content can learn from the qualities that make these sites so engaging.
These would be fun clips to to use in any of the video activities I describe in The Best Popular Movies/TV Shows For ESL/EFL.
Five thousand people from Grand Rapids, Michigan came together to create what Roger Ebert has called "the greatest music video ever made." And it is, indeed, pretty amazing. It was shot in one take. Even though the song's lyrics are probably not the best for English Language Learners, the video itself would be a lot of fun.
Show this next video, but only if you don't think your students will be inspired to try some of the stunts themselves!
"Dr. Stanley's House 2" is what is known as a "point-and-click" adventure game. Its "Walkthrough," or instructions on how to win, can be found here. You can my article, Free Online Games Develop ESL Students' Language Skills, to learn how I use these kinds of games as a great language-development exercise.
Inspector Kloo 4 is another fun online video game that offers a great opportunity for English language learning. You can find its walkthrough (instructions on how to win) here.
Inspector Kloo 5 is a fun online video game that offers a great opportunity for English language learning. You can find its walkthrough (instructions on how to win) here.
Check out the illusion in this video. And if you like it, you can find more here.
You might also want to explore the 700 other "The Best…" lists I've compiled.


We spend 60 minutes at the studio capturing you a high quality profile shot. Of course, we will take quite a few images to make sure we get the best angles and if you want more then it is easy to upgrade the package.
1 fully edited image is included.
We spend 90 minutes at the studio capturing you a high quality profile shot. Of course, we will take quite a few images to make sure we get the best angles and if you want more then it is easy to upgrade the package.
3 fully edited images are included.
6 fully edited images are included.


Shortage of intensive care specialists in the United States: recent insights and proposed solutions.
Caring for the critically ill in developing countries: a perspective from India.
What happens to the fluid balance during and after recovering from septic shock?.
O que ocorre com o balanço hídrico durante e após a reversão do choque séptico?
Patient stress in intensive care: comparison between a coronary care unit and a general postoperative unit.
The reality of patients requiring prolonged mechanical ventilation: a multicenter study.
Blood transfusions in septic shock: is 7.0g/dL really the appropriate threshold?.
Transfusões de sangue no choque séptico: 7,0g/dL é mesmo o limite adequado?
Causes of non-adherence to therapeutic guidelines in severe community-acquired pneumonia.
Septic shock: a major cause of hospital death after intensive care unit discharge.
Swallowing rehabilitation of dysphagic tracheostomized patients under mechanical ventilation in intensive care units: a feasibility study.
Therapeutic hypothermia as a bridge to transplantation in patients with fulminant hepatic failure.
Recurrent rhabdomyolysis secondary to hyponatremia in a patient with primary psychogenic polydipsia.


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redpajama_set_name: RedPajamaGithub


text:
Orepukia egmontensis – gatunek pająka z rodziny Cycloctenidae.

Taksonomia
Gatunek ten opisany został po raz pierwszy w 1973 roku przez Raymonda Roberta Forstera i Cecila Louisa Wiltona w czwartej części monografii poświęconej pająkom Nowej Zelandii. Jako miejsce typowe wskazano stoki Egmontu powyżej Startford House.

Morfologia
Holotypowa samica ma karapaks długości 2,5 mm i szerokości 1,6 mm oraz opistosomę (odwłok) 2,8 mm i szerokości 1,9 mm. Karapaks ma w ubarwieniu wyraźny wzór, na który składa się jasna, wąska przepaska, wychodząca spomiędzy oczu pary tylno-środkowej i ciągnąca się do jamki środkowej. Ośmioro oczu rozmieszczonych jest w dwóch rzędach, z których przedni jest prosty. Szczękoczułki ustawione są pionowo i mają po 2 zęby na krawędziach tylnych oraz po 2 większe i grupkę małych ząbków na krawędziach przednich bruzd. Odnóża są obrączkowane. Kolejność par odnóży od najdłuższej do najkrótszej to: IV, I, II, III. Pazurki górne mają 9 ząbków, zaś pazurki dolne 3 ząbki. Opistosoma ma rozjaśnienia w częściach przednio-bocznych, a na środku grzbietu dwie pary ukośnych przepasek i dwa szewrony za nimi. Zaopatrzona jest znacznie szerszy niż długi stożeczek z włoskami rozmieszczonymi w dwóch łatkach.

Występowanie
Gatunek ten jest endemitem Nowej Zelandii, znanym tylko z miejsca typowego w regionie Taranaki na Wyspie Północnej.

Przypisy

Cycloctenidae
Pająki Nowej Zelandii
Gatunki i podgatunki zwierząt nazwane w 1973 roku

redpajama_set_name: RedPajamaWikipedia


text:
SCIplanet Team
SCIplanet Printed
Science Everywhere
Science Communication: The Lifeline for New Generations
By: Hossam Ragab
Education - Communication - Scientists - Training - Youth
Cover Photo © Planetarium Science Center, Biblitoheca Alexandrina.
Science tends to seem mysterious to those who do not make a career of it! While some of us like it, if not love it, many do not, especially as kids. For most of us, science is difficult because of the equations, calculations, and laws, which require much effort to understand and memorize. Yet, what we fail to realize is that the problem has nothing to do with the science itself, but rather how it is presented and explained. It is always about the means used to reach an end; namely, understanding and viewing science from a different perspective. Said perspective is that of enjoyment, exploration, and savoring new things with fresh eyes. From here stemmed a concept known as "science communication", which serves as a lifeline for new generations when it comes to understanding, viewing, and developing passion towards science.
Believe it or not, many great science discoveries did not find their way into the light for long decades due to the absence of a proper means of communication between the discoverer and the people. A case in point is Gregor Mendel's "Plant Hybridization". Mendel published his paper entitled "Experiments on Plant Hybridization", but we did not recognize its importance until the following century. Similarly, it was many years after the death of Alexander Fleming that the discovery of penicillin was given due importance.
Now, in the third millennium, with the technologies available, questions are all around us. Children are eager to know and understand everything around them; they pose numerous questions. We, adults, however, usually cannot give them clear answers without going into scientific details.
Photo © Planetarium Science Center, Biblitoheca Alexandrina.
As such, there have been several attempts to simplify the sciences over the years, eventually leading to what is known as "science communication". It is a means to simplifying science for non-specialized people in an appealing manner, whether in an amusing way, as a play, or using state-of-the-art exhibits or shows. All around the world, there are people specialized in science communication, working in both scientific and non-scientific newspapers and magazines. Their aim is to simplify everyday astronomical, physical, or chemical phenomena (to name some) and raise awareness about them; and to correct faulty scientific principles, and change the culture of science understanding.
Science communication also aims to connect scientific researchers to different groups, particularly children and youth, to build scientist–audience relationships, unlike how matters were in old times. The advancement of media and the emergence of social media networks, such as Facebook and Twitter among others, have contributed to activating science and making it visible for all, not just those interested in it to begin with, but also those far from it.
Researchers believe that science communication is about using skills, media, and activities properly to produce reactions to the sciences that people are concerned with. Examples include raising awareness about new scientific issues, such as global warming and environmental pollution. The joy lurks in presenting science as art and entertainment, and in volunteering to communicate science through different ways. Last but not least, it is also joyful to help the audience form their own opinions, make or correct their decisions, understand the sciences and their applications.
Now, let me introduce you to some specialists in the field. Dutch astrophysicist Walter Hendrik Gustav Lewin obtained his PhD in nuclear physics in 1965, and served as Professor of Physics at Massachusetts Institute of Technology (MIT), 1966–2009. Lewin explains physics in a wonderful manner that allows listeners to play and interact with physics, and attracts followers. Lewin has several publications and received several awards. In 2011, he presented a series of science episodes entitled Nova broadcasted on American PBS channel, as well as other TV shows.
Also, we cannot skip the genius scientist, engineer, comedian, and science communicator William Sanford Nye who studied Engineering in Cornwell University, and was a student of Carl Sagan*. Nue started his life as a mechanical engineer and was known as the "Science Guy", as he presented a popular show entitled "Bill Nye the Science Guy", 1993–1998; he acted as a science promoter and facilitator in media.
Last but not least, there is the American scientist, astronomer, writer, and TV shows presenter Neil deGrasse Tyson who revived the Cosmos TV show previously presented by his tutor Carl Sagan; he also presented some episodes of the Nova TV show. Currently, Tyson is a researcher in the Department of Astrophysics at the American Museum of Natural History, and is Director of the Museum's planetarium.
I invite you all to read the article entitled "Science Communication: What Is It?"
to learn more about the history of the field and its pioneers.
Since I worked as a science communicator for two years at the Bibliohtheca Alexandrina Planetarium Science Center, I can describe science communication as a means of survival to current and future generations. It would serve as a clear, simple, and mostly entertaining tool to understand the sciences that we once thought were difficult. As such, I urge parents who would like to invest in their children to search the Internet, television, and science centers for science communication portals, which have become available everywhere now. I also urge the youth who want to understand things around them to search for science communication portals available to them; they simply might become truly passionate about it.
*Carl Sagan is an American astronomer and writer whose writings about natural sciences achieved great success.
Jane Gregory & Steve Miller, Science in Public.
Laura Bowater & Kay Yeoman, Science Communication: A Practical Guide for Scientists.
Sarah Perrault, Communicating Popular Science.
Growing Furniture
The Physics of Shipping in Constricted Waters
Occupational Diseases
Arab Scientists (16)
Botany (21)
Diseases (102)
Gastronomy (43)
Geology (19)
Glaciology (7)
Holidays and Festivals (26)
Hygiene (33)
Inventions (127)
Metals (4)
Nobel Prize (12)
Planets (26)
Policy and Ethics (13)
Scientists (64)
Wastes (14)
Women in Science (37)
Young Scientisits (7)
Zoology (35)
SCIplanet is a bilingual edutainment science magazine published by the Bibliotheca Alexandrina Planetarium Science Center and developed by the Cultural Outreach Publications Unit ...
P.O. Box 138, Chatby 21526, Alexandria, EGYPT
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Published by the Planetarium Science Center (PSC)
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redpajama_set_name: RedPajamaCommonCrawl


of the journal Signal Approaches to Children's Books.
substantial written overview of a year's publishing of poetry for children.
this record covers hundreds of books.
original details: author, illustrator, number of pages and publisher.


Sterling! This large star gave the quilt's designer space to use a big palette of colorful fabrics. With its small patchwork pieces and seventeen different fabrics, this quilt is about as 'good as it gets'. The piecework is very precise, and appliqué work on the pillow fold is outstanding. The quilt-work surrounding the star is very nice indeed. Signed and dated by its maker.
A single sheet of soft cream white cotton muslin covers the back of the quilt. The quilting density is good, averaging about 120 linear inches of stitching per square foot. The stitching is very good with about 8 stitches per inch. A high quality quilt.


A.E. Woodward lives in Vacationland with her husband and two children. Between her day job and the pursuance of a master's degree, she wrote her first novel. Her novel Imperfectly Perfect, will be the first book in A Series of Imperfections.


text:
Die Vestur-Skaftafellssýsla ist ein Bezirk im Süden Islands.

Der Bezirk liegt an der Südküste zwischen dem westlichen Teil des Vatnajökull und dem Mýrdalsjökull. Er besteht aus den Gemeinden Skaftárhreppur und Mýrdalshreppur, die sich aus ursprünglich sieben Gemeinden gebildet haben. Vík und Kirkjubæjarklaustur sind die bedeutendsten Orte. Die Vestur-Skaftafellssýsla hat eine Fläche von 7701 km² und liegt im Wahlkreis Suðurkjördæmi.

Sýsla (Island)
Suðurland


Please note, not all new features are available to Basic and Standard Edition customers.
Keep up with your mobile volunteers with the new SMS functionality integrated into CERVIS. Send out SMS blasts for urgent communication and use SMS event reminders to remind busy volunteers about service commitments while on the go. This functionality allows you to connect CERVIS to your existing SMS messaging provider for seamless messaging integration, billing, and account management.
*One-time CERVIS activation fee and Third-party messaging provider (Twilio, CellTrust, or Clickatell) required.
- New system icons create a simplified feel and allow CERVIS users to navigate more easily throughout the system and find what they are looking for. Don't like the new icons? Easily switch back to the old icons by updating the system configuration.
- New rich text editor allows for faster system performance and enhanced compatibility across different browsers, including desktop and mobile, while providing a simplified visual experience.
- Expanding list boxes allow easier viewing and selecting of information in lengthy lists by increasing the size of list boxes to accommodate the entire list set.
- Volunteer self-registration page has been enhanced to provide users with a similar registration experience both before and after logging in.
- Volunteer "Main Menu" has been simplified with easier-to-understand wording, navigation, and consolidated selection options.
- Volunteers are now able to view all of the open service projects they are approved for under the "Service Project Management" section of the Volunteer Main Menu.
- Dedicated spell check has been replaced with native browser spell check. This allows for enhanced speed, increased language support, and greater dictionary customization. This will, however, remove spell check functionality from older browsers that do not support native spell checking.
- Inline Terms & Conditions allow organizations with differing requirements to present terms & conditions directly as text on the volunteer profile creation page as opposed to a link with a popup notice. Configure your desired method with the "Terms & Conditions" options in the system configuration.
Have you ever wanted to ask your volunteers questions in a certain order, but the custom profile questions in CERVIS just weren't in the correct order? Now you can...just update the "Custom Field Order" fields in the system configuration to place the custom fields in any order you need.
Get the information you need, when and where you need it, even if you're not sitting at your desk. Now you can view document and spreadsheet reports from CERVIS directly on your Android or iOS mobile device.
- For anyone that has ever needed to change the event organizer for 50 events or set the event status to "Open" for a big day of service...this one's for you! You are now able to update event attributes for multiple events at the same time through the event management dashboard. Just select the events you want, choose the fields you want to update, provide the new values, and you're all set.
- If you've ever managed a volunteer schedule that includes multiple CERVIS events, then you know that volunteers can sometimes show up and not remember exactly which event they registered for. Now you can print a combined event sign-in sheet for multiple events on a single spreadsheet. With this option, you can sort by volunteer name (or whatever criteria you want), print out a spreadsheet, and have an easy method for staff to help direct uncertain volunteers.
- Do you copy the same events every year, or even every month? The newly added Bulk Event Duplicate functionality within CERVIS will enable you to be more efficient by allowing you to duplicate multiple events at once.
- Quickly export a spreadsheet of full event details for multiple events whenever you need it by utilizing the added "Export Event Details" functionality within CERVIS.
- Tired of having to either update time slots one at a time or all together? With this update, you can now bulk update as many (or as few) time slots as you need to by checking/unchecking the "include in bulk slot update" checkbox for each slot as you are performing a bulk update.
- In addition to the options currently available for bulk updating time slot events, you can now also update slot start time, slot end time, and slot status.
- Do your group leaders need additional access to manage their groups? You can now enable group leaders to access the group management options for their group by updating the "Allow Group Leader(s) to Access Group Management" feature in the system configuration.
- Track information about groups, such as preferences, limitations, or special considerations with the new Group Notes feature available in the Group Management Dashboard.
- Have you ever wished that you could automatically assign a group to a volunteer when they registered for a specific event? Now you can make it happen by updating the "Assign Associated Group" field when updating an event.
If you've ever needed to search for a volunteer who is not assigned to a particular group or who is only assigned to a single interest category, now you have that capability. Navigate to the attribute management section of the Main Dashboard, find the desired attribute (interest, group, skill, etc) you're looking for and click on the appropriate search icon under the "Actions" column.
Volunteer age (calculated off of birth date), Years of Service (calculated off of CERVIS Start Date) and Volunteer Profile Notes have been added to the Volunteer Export Spreadsheet.


If you are unable to provide artwork files, we will happily create your artwork FREE of charge, based on one of our examples or your document or sketch.
We will then process your artwork and a photo-realistic proof is created and emailed to you for your approval.
If you require any changes, please let us know the changes you need and a new photo-realistic proof will be created and emailed to you FREE of charge.
Why do we send an email proof?
1. You have sent the correct artwork to us - you simply wouldn't believe how many customers email the incorrect files or old version to us and they only notice their own error when they have their proof that we email to them.
2. To ensure that no technical glitches have occurred or files have become corrupted.
We email a proof to you to ensure that you are happy with the details on your cards (i.e. that wording and important details like telephone numbers or email addresses are correct) and that you have happy with the overall layout etc.


Anna Mohlman Molgard graduated from Brigham Young University with a degree in Music with an emphasis in Media Music. She enjoys working in many aspects of the music business, particularly creating new works. Inspired by requests for various pieces, she founded Faithsong Publications LLC to provide well-crafted music written for sacred use. She has a gift for listening to the Spirit and strives to allow the Lord to guide her in using her talents to build His kingdom.
Rachel Pettit Mohlman has always loved music. She started writing music as a pre-teen and continues to spend her spare time writing, arranging, playing and performing. She graduated from Brigham Young University with a degree in Music Education with a choral emphasis. She enjoys being a full-time wife and mother (which is why sometimes the music comes slowly. . . where's all that spare time she mentioned?) Don't worry, there will be more coming!


We have her prints all over the house, and our friends still comment on our wedding design. I really, really wanted to have this fabric in my stash so someday I could keep the tradition alive and make something with it for a mini Reeve. I still wear my 5 pairs of her Keds to death (even though the owls are held together with sheer willpower at this point), and I almost bought some of the kids' versions to keep for a day in the future when there was a mini Reeve to wear them. But I felt kind of ridiculous buying girls' shoes for an imaginary child in the future. I do not, however, feel ridiculous buying up this fabric to keep aside for the future.
It's my Christmas present to myself. Long live traditions.


text:
Will Smith And Jada Pinkett Smith To Co-Host Nobel Peace Prize Concert
Wyclef Jean, Toby Keith and Donna Summer to perform
Published at 1:46 am on September 30, 2009
American rap artist and actor Will Smith and his wife, the actress Jada Pinkett Smith, will co-host this year's Nobel Peace Prize Concert in Oslo, organizers said Wednesday.
The Dec. 11 show — a day after the award ceremony — will feature performances by Wyclef Jean, Toby Keith, Donna Summer, Puerto Rican singer Luis Fonsi as well as Amadou&Mariam, a blues and jazz duet from Mali.
"The opportunity to recognize the laureate's contributions to the world peace movement will be an awe-inspiring experience," the Smiths said in a joint statement. "We are both humbled and honored to take part in the Nobel Peace Prize Concert this year."
The winner of the 2009 Nobel Peace Prize is to be announced in Oslo on Oct. 9. The award is always handed out Dec. 10, the anniversary of prize founder Alfred Nobel's death in 1896.
"We're excited to have Will Smith and Jada Pinkett Smith join us as hosts for the Nobel Peace Prize Concert," said Geir Lundestad, secretary of the Norwegian Nobel Committee. "Together they've had a global impact on the arts and philanthropy and will be excellent ambassadors for peace."
Smith, 41, rose to fame in the 1980s as a rapper under the name The Fresh Prince and as the star of a popular television comedy show. His many films include "Men in Black" and "Independence Day."
His wife, 38, is an actress, model and singer-songwriter. Her film career has included roles in the "The Nutty Professor," ''Ali," and "The Matrix Reloaded."
Related Content from AccessHollywood.com:
VIEW THE PHOTOS: Will Smith Handprint Ceremony
PLAY IT NOW: Access Exclusive: Willow Smith Makes Her TV Debut (July 15, 2009)
PLAY IT NOW: Access Extended: 'Seven Pounds' Premiere, Los Angeles
MORE ACCESS ON THESE TOPICS: Jada Pinkett Smith - Will Smith - TV One - Celebrities
Copyright NBCAH - Access Hollywood


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No matter how rudely people treat you, NEVER DEGRADE YOURSELF to their level to treat them the same way.
There is nothing more I dislike is a rude person. Someone who don't know how to talk or treat people. These same people wouldn't want others to treat them the way they are being to others.
When I am treated rudely or spoken to in a rude tone, I have learned to not stoop to their level. I ignore them and keep my distance from them if possible. Their actions could be triggered by a lot of different things within themselves. So in short just remember to treat ones how you would like to be treated. Being rude back won't get you far. Be the Bigger Person!
Enjoy your Saturday! Thanks for stopping by.


Thanks for visiting Free SVG Designs! The purpose of this site is to be a creative resource for you, I hope that you have found something that has inspired and helped you to create something fabulous!
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Good morning my sweet creative friends! HAPPY HAPPY NEW YEAR! I know, I am 4 days late wishing you all that here, but unfortunately I have been sick:( My Mom & I had nasty sinus infections & we are FINALLY feeling better THANK GOD!;) I know, NOT A GOOD time to be sick after this biggest release I've ever had! We are doing TONS better & working really hard to get everything out as soon as we can! I know my Mom gets your orders out in record time, but during releases they will take a little bit longer. KEEP IN MIND that we did sell out at 8:40am on release day so ALOT of orders will NOT go out until I get all the new release back in stock! It is usually a 2 week turn around! Hope this helps for those of you who had questions! I apologize for the inconvenience.
Okay, now onto my cute & QUICK card!;) I really REALLY simple, you can see how I put it together in my video below!
I just LOVE LOVE LOVE my newest release & you can definitely use it for MORE that just Valentines!
I hope you enjoyed my simple card for you today! Have a FABULOUS weekend & AGAIN, THANK YOU ALLLL SO VERY MUCH for making this last release a SUCCESSFUL one! ALSO, THANK YOU for enjoying my products as much as I enjoy designing them ALL for you! See you all back here soon!
P.S. You have until Sunday night, Jan 6th @ midnight to leave your comments for our blog hop! I will announce winners next week! You can start HERE!
Super cute card, love the new release! Glad to hear you are feeling better!
I heart this kard...soo adorable!!!
Emma gosh I hope you and your Mama are doing better 2day! I certainly hope your gang made lots of Starbucks' runs for you and your Mama!! Your card is so darling I love how it looks like a chalkboard thanks for just another brilliant idea of yours. I agree with your Daddy you gals do "run yourselves ragged" I know you whatcha do and we so appreciate you soooooo much!! you and your Mama are 2 in a million!! Take good care and looking 4ward to more amazing valentines and other awesome "Emma" projects.
Love the card! Can't wait for my stamps!
Thanks so much to you and your Mom for mailing them all out!
Very cute card today! Sorry to hear about the sinus infection - those can be the worst! I'm glad you both are feeling better!
No wonder your releases run out fast. Not only because you have great stamp sets but you also have the BEST customer service ever!!! Hope you and your Mom are feeling better. I'm just patiently waiting for the mailman to bring me my stamps :) You're the best.
Kim C says it all! You're the best at it all! I will also add your samples make your products irresistible! Heading over to blow my budget!
Super fun Valentine. Love the colors with brown base!
Thank you for all your hard work. I'm glad I was ready to press "buy" we have a 2 hour difference so 8 for you was 10 am for me I had already had a cup of coffee lol. I was probably your first if not 2 customer on release day.
What an adorable card, Emma! Beautiful!!! Take it easy, and get all the way better!
Love your card. I hope I got my order in on time. Looking forward to recieving my stamps.
Love this card! Glad you and your mom are feeling better. Even with being sick, you guys sure shipped my stuff out quickly!! I got notice that my order is on the way to my house. Can't wait to play with my new stamps and dies.
Really adorable card!! Love all the textures!
Cute card design...like the cardboard. Congratulations on the release...I can't remember what time I ordered so I guess I wait and see.
This is gorgeous Emma!!! LOVE how gorgeous your new release is!!
Got my notice yesterday. Feel better you and Mom. And thanks again.
So glad I was introduced to your blog . LOVE.LOVE.LOVE your designs!
Thanks for taking the time to share and hope you feel better!!!!!
Love the use of the stamp frame and heart. Great card!
Emma ~ Oh look waht you created here!! I LOVE it!! That frame die is so AWESOME to work with ~ I LOVE it!! Oh that embossing folder is one of my FAVS too!! As always Miss Emma ~ ADORE your creations and products!!! Sorry you and Mom are sick but hopefully you two will be back to normal real soon!
Emma, I know I am late watching your video, I'm trying to catch-up myself. I love this card and would love to get a set of the die's. I sure hope that you and your Mom are doing much, much better. Thank you for all you do for us! This is another, glam-tastic craft!


text:
Generalized epilepsy with febrile seizures plus
"GEFS" redirects here. For the online flight simulator, see GEFS-Online.
"SMEB" redirects here. For the League of Legends player, see Smeb.
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GEFS+
Generalized epilepsy with febrile seizures plus (GEFS+) is a syndromic autosomal dominant disorder where afflicted individuals can exhibit numerous epilepsy phenotypes.[1] GEFS+ can persist beyond early childhood (i.e., 6 years of age). GEFS+ is also now believed to encompass three other epilepsy disorders: severe myoclonic epilepsy of infancy (SMEI), which is also known as Dravet's syndrome, borderline SMEI (SMEB), and intractable epilepsy of childhood (IEC).[2][3] There are at least six types of GEFS+, delineated by their causative gene. Known causative genes are the sodium channel α subunit genes SCN1A, an associated β subunit SCN1B, and a GABAA receptor γ subunit gene, GABRG2 and there is another gene related with calcium channel the PCDH19 which is also known as Epilepsy Female with Mental Retardation.[4] Penetrance for this disorder is estimated at approximately 60%.[5]
2 Pathophysiology
2.1 Type 1
2.4 SCN2A mutations
Individuals with GEFS+ present with a range of epilepsy phenotypes. These include febrile seizures that end by age 6 (FS), such seizures extending beyond age 6 that may include afebrile tonic-clonic, myoclonic, absence, atonic seizures and myoclonic-astatic epilepsy. Individuals may also present with SMEI, characterized by generally tonic-clonic seizures, impaired psychomotor development, myoclonic seizures, ataxia, and poor response to many anticonvulsants.[1][6]
Pathophysiology[edit]
Type 1[edit]
Figure 1. Schematic structure of SCN1B with GEFS+ type 1 mutations shown in red. The single red spot is the C121W mutant at the disulfide bond (black) and the stretch of red the I70_E74del mutation.
GEFS+ type 1 is a subtype of GEFS+ in which there are mutations in SCN1B, a gene encoding a sodium channel β subunit. The β subunit is required for proper channel inactivation. There are two known mutations in SCN1B that lead to GEFS+ (Figure 1). The first and best characterized of these mutations is C121W. This mutation alters a cysteine involved in a disulfide bond in the extracellular N-terminus of the protein. This extracellular region is similar to the cell adhesion molecule contactin and other cell adhesion molecules. It is believed that the disulfide bond disrupted by the C121W mutation is required for the proper folding of this N-terminus motif. Coexpression of SCN1B with sodium channel α subunits in oocytes and other cells results in channels that inactivate more slowly. Expression of C121W mutant along with wild-type α subunits produces current indistinguishable from that through α subunits alone.[5][7] Further investigation of this mutation has indicated that it results in decreased frequency dependent rundown and, thus, likely hyperexcitability when compared to cells expressing the wild-type subunit. This mutation also disrupts the subunit's ability to induce cellular aggregation. The importance of this last fact is unclear, though it is presumed that proper channel aggregation within cells and cell-cell contact are required for normal neuronal function.[8][9]
A second mutation has been found in one kindred with GEFS+ type 1. This mutation is in a splice acceptor site of exon 3. The loss of this acceptor site reveals a downstream cryptic acceptor site and a protein missing 5 amino acids in the N-terminus (I70_E74del). This mutation has not been further characterized.[10]
A second subtype of GEFS+, type 2, is the result of mutations in SCN1A, a gene encoding a sodium channel α subunit. There are currently almost 90 known mutations in the SCN1A gene throughout the entirety of the channel (see table 1). These mutations result in almost any imaginable mutation type in the gene, short of duplications. The results of these mutations are highly variable, some producing functional channels while others result in non-functional channels. Some functional channels result in membrane hyperexcitability while others result in hypoexcitability. Most of the functional mutant channels result in hyperexcitability due to decreased frequency dependent rundown. An example of this is the D188V mutation. A 10 Hz stimulation of wild-type channels causes current to decrease to approximately 70% of maximum whereas the same stimulation of mutant channels results in rundown to 90% of maximum. This is caused by an expedited recovery from inactivation for mutant channels versus wild-type. The D188V mutant, for example, recovers to 90% maximal current in 200ms while wild-type channels are unable to recover to this degree in >1000ms.[11] Some other functional mutations that lead to hyperexcitability do so by other means, such as decreasing the rate of entrance into the slow inactivated state.
Some of the other functional mutations are believed to result in hypoexcitability. The R859C mutation, for example, has a more depolarized voltage dependence of activation, meaning that the membrane must be more depolarized for the channel to open. This mutant also recovers more slowly from inactivation.[12] The nonfunctional channels are believed to produce similar changes in cell excitability. Likewise, many of the nonsense mutations likely result in nonfunctional channels and hypoexcitability, though this has yet to be tested. It is also unclear how this membrane hypoexcitability leads to the GEFS+ phenotype.
Table 1. Summary of mutations found in patients diagnosed with GEFS+ type 2
Functional?
Excitability Prediction
R101Q
N-Terminus [13]
S103G
V144fsX148
D1S1 [13]
G177fsX180
D1S2-S3 [14]
D188V
D1S2-S3 Yes Hyperexcitable [11][15]
S219fsX275
D1S4 [13][16]
G265W
E435X
D1-2 [13]
P707fsX715
Q732fsX749
Y779C
D2S2 Yes Hyperexcitable [6][14]
D2S4 Yes Hypoexcitability [12]
T875M
D2S4 Yes Hyperexcitable* [19][20][21][22][23]
D2S5 No Hypoexcitable [24]
D2S5-6 [17]
W942X
R946fsX953
D958fsX973
G979R
D2S6 No Hypoexcitable [6][14]
L986F
D2S6 No Hypoexcitable [16][25]
N1011I
D2-3 Yes Hyperexcitable [6][14]
K1100fsX1107
L1156fsX1172
W1204R
D2-3 Yes Hyperexcitable [2][23][26]
W1204X
R1213X
L1345P
V1353L
Exon 4 [14][16]
V1428A
S1516X
M1549del
V1611F
P1632S
R1648C
D4S4 Yes Hyperexcitable [24]
R1648H
D4S4 Yes Hyperexcitable [20][22][23][29][30]
I1656M
D4S4 Yes [15][25]
D4S4 Yes Hypoexcitable [25][30][31]
F1661S
D4S4-5 [14][16]
G1674R
D4S4-5 No Hypoexcitable [24]
Y1684C
D4S5 No Hypoexcitable [25][27][28]
A1685D
T1709I
D4S5-6 No Hypoexcitable [6][14]
D1742G
G1749E
D4S6 Yes Hypoexcitable [24]
F1756del
F1765fsX1794
1807delMFYE
C-Terminus [14]
C-Terminus Yes Hyperexcitable [6][14]
W1812G
M1841T
S1846fsX1856
C-Terminus [16][17]
D1886Y
C-Terminus Yes Hyperexcitable [33]
Q1904fsX1945
Results are dependent on experimental paradigm
Patients with GEFS+ type 3 have mutations in the GABRG2 gene, which encodes the GABAA γ2 subunit (figure 2). The first mutation discovered in GABRG2 was K289M, in the extracellular region linking membrane-spanning domains M2 and M3. Oocytes injected with α1, β2, and γ2 subunits produce large GABA inducible currents whereas those injected with K289M mutant instead of wild-type subunits produce currents much smaller (about 10% of wild-type). This abnormal current is not the result of non-incorporation of mutant subunits since mutant containing receptors are still sensitive to benzodiazepines, a property for which functional γ subunits are required. Because of these results, it is believed that the GEFS+ phenotype in these individuals is a result of hyperexcitability.[34]
Concurrent with the previous mutation, a second group found a second mutation in GABRG2 associated with GEFS+. This mutation, R43Q, is located in the one of two benzodiazepine binding-sites located in the extracellular N-terminus. Benzodiazepines, such as Diazepam, potentiate GABA induced current. This potentiation is abolished in cells expressing the R43Q mutant subunit instead of the wild-type γ subunit. This mutation does not affect the subunit's ability to coassemble into function receptors as it still confers resistance to GABA current blockade by zinc. As with the previous mutation, this mutation is expected to result in neuronal hyperexcitability.[35][36]
The final known GEFS+ type 3 mutation is a nonsense mutation, Q351X, located in the intracellular region linking the third and fourth membrane spanning segments. When this mutant subunit is expressed in cells with wild-type α and β subunits it produces non-functional receptors. Since wild-type α and β subunits expressed alone are able to produce GABA inducible current this indicates that the mutation either prevents both coassembly of the mutant and wild-type subunits but also coassembly of the wild-type α and β subunits or prevents proper trafficking of the formed receptor to the membrane. Fusion of GFP onto this mutated subunit has indicated that it is localized to the endoplasmic reticulum instead of the cell membrane. As with other known GEFS+ type 3 mutation, Q351X likely results in neuronal hyperexcitability.[37]
SCN2A mutations[edit]
Figure 3. Schematic structure of SCN2A with GEFS+ associated mutation positions indicated by red dots.
The final type of GEFS+ is caused by mutations in the SCN2A gene, which encodes a sodium channel α subunit. The first associated mutation in this gene is R187W, located on the intracellular region linking membrane spanning units two and three in the first domain (D1S2-S3, figure 3). Patients with this mutation have both febrile and afebrile seizures. Electrophysiological examination of this mutant revealed that it increases the time constant for inactivation, presumably increasing sodium current and leading to hyperexcitability. However, this mutation also yields channels that inactivate at more hyperpolarized potentials relative to wild-type channels, indicative of hypoexcitability. Whether the end result on membrane excitability of this mutation is hyperexcitability or hypoexcitability is, as yet, unclear.[28][38]
The second known mutation in SCN2A associated with GEFS+ is R102X. This mutation is located in the intracellular N-terminus (figure 3) and results in SMEI in patients. The result of this mutation is completely non-functional channels and membrane hypoexcitability. The truncated mutant protein also seems to cause wild-type channels to inactivate at more hyperpolarized potentials, indicating that it also acts in a dominant negative manner.[39]
Management[edit]
Long term management is by use of anticonvulsant medication, principally valproate, stiripentol, topiramate or clobazam.[40] Ketogenic diet has also been found useful in certain cases [41]
Management of breakthrough seizures is by benzodiazepine such as midazolam.
Dravet Syndrome Foundation
International Dravet Epilepsy Action League
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^ a b c d e f g h i j k l m n o p q r s t u v Fukuma G, Oguni H, Shirasaka Y, Watanabe K, Miyajima T, Yasumoto S, Ohfu M, Inoue T, Watanachai A, Kira R, Matsuo M, Muranaka H, Sofue F, Zhang B, Kaneko S, Mitsudome A, Hirose S (2004). "Mutations of neuronal voltage-gated Na+ channel alpha 1 subunit gene SCN1A in core severe myoclonic epilepsy in infancy (SMEI) and in borderline SMEI (SMEB)". Epilepsia. 45 (2): 140–8. doi:10.1111/j.0013-9580.2004.15103.x. PMID 14738421.
^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af ag ah ai aj ak Fujiwara T, Sugawara T, Mazaki-Miyazaki E, Takahashi Y, Fukushima K, Watanabe M, Hara K, Morikawa T, Yagi K, Yamakawa K, Inoue Y (2003). "Mutations of sodium channel alpha subunit type 1 (SCN1A) in intractable childhood epilepsies with frequent generalized tonic-clonic seizures". Brain. 126 (Pt 3): 531–46. doi:10.1093/brain/awg053. PMID 12566275.
^ a b c Wallace R, Scheffer I, Barnett S, Richards M, Dibbens L, Desai R, Lerman-Sagie T, Lev D, Mazarib A, Brand N, Ben-Zeev B, Goikhman I, Singh R, Kremmidiotis G, Gardner A, Sutherland G, George A, Mulley J, Berkovic S (2001). "Neuronal Sodium-Channel α1-Subunit Mutations in Generalized Epilepsy with Febrile Seizures Plus". Am J Hum Genet. 68 (4): 859–65. doi:10.1086/319516. PMC 1275639. PMID 11254444.
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^ a b c d e f Kearney J, Wiste A, Stephani U, Trudeau M, Siegel A, RamachandranNair R, Elterman R, Muhle H, Reinsdorf J, Shields W, Meisler M, Escayg A (2006). "Recurrent de novo mutations of SCN1A in severe myoclonic epilepsy of infancy". Pediatr Neurol. 34 (2): 116–20. doi:10.1016/j.pediatrneurol.2005.07.009. PMID 16458823.
^ a b Annesi G, Gambardella A, Carrideo S, Incorpora G, Labate A, Pasqua A, Civitelli D, Polizzi A, Annesi F, Spadafora P, Tarantino P, Cirò Candiano I, Romeo N, De Marco E, Ventura P, LePiane E, Zappia M, Aguglia U, Pavone L, Quattrone A (2003). "Two novel SCN1A missense mutations in generalized epilepsy with febrile seizures plus". Epilepsia. 44 (9): 1257–8. doi:10.1046/j.1528-1157.2003.22503.x. PMID 12919402.
^ Moulard B, Guipponi M, Chaigne D, Mouthon D, Buresi C, Malafosse A (1999). "Identification of a New Locus for Generalized Epilepsy with Febrile Seizures Plus (GEFS+) on Chromosome 2q24-q33". Am J Hum Genet. 65 (5): 1396–400. doi:10.1086/302621. PMC 1288292. PMID 10521305.
^ a b Escayg A, MacDonald B, Meisler M, Baulac S, Huberfeld G, An-Gourfinkel I, Brice A, LeGuern E, Moulard B, Chaigne D, Buresi C, Malafosse A (2000). "Mutations of SCN1A, encoding a neuronal sodium channel, in two families with GEFS+2". Nat Genet. 24 (4): 343–5. doi:10.1038/74159. PMID 10742094.
^ Alekov A, Rahman M, Mitrovic N, Lehmann-Horn F, Lerche H (2001). "Enhanced inactivation and acceleration of activation of the sodium channel associated with epilepsy in man". Eur J Neurosci. 13 (11): 2171–6. doi:10.1046/j.0953-816x.2001.01590.x. PMID 11422459.
^ a b Spampanato J, Escayg A, Meisler M, Goldin A (2001). "Functional effects of two voltage-gated sodium channel mutations that cause generalized epilepsy with febrile seizures plus type 2". J Neurosci. 21 (19): 7481–90. doi:10.1523/JNEUROSCI.21-19-07481.2001. PMID 11567038.
^ a b c Lossin C, Wang D, Rhodes T, Vanoye C, George A (2002). "Molecular basis of an inherited epilepsy". Neuron. 34 (6): 877–84. doi:10.1016/S0896-6273(02)00714-6. PMID 12086636.
^ a b c d e Rhodes T, Lossin C, Vanoye C, Wang D, George A (2004). "Noninactivating voltage-gated sodium channels in severe myoclonic epilepsy of infancy". Proc Natl Acad Sci USA. 101 (30): 11147–52. Bibcode:2004PNAS..10111147R. doi:10.1073/pnas.0402482101. PMC 503754. PMID 15263074.
^ a b c d e Lossin C, Rhodes T, Desai R, Vanoye C, Wang D, Carniciu S, Devinsky O, George A (2003). "Epilepsy-associated dysfunction in the voltage-gated neuronal sodium channel SCN1A". J Neurosci. 23 (36): 11289–95. doi:10.1523/JNEUROSCI.23-36-11289.2003. PMID 14672992.
^ Escayg A, Heils A, MacDonald B, Haug K, Sander T, Meisler M (2001). "A Novel SCN1A Mutation Associated with Generalized Epilepsy with Febrile Seizures Plus—and Prevalence of Variants in Patients with Epilepsy". Am J Hum Genet. 68 (4): 866–73. doi:10.1086/319524. PMC 1275640. PMID 11254445.
^ a b Ito M, Nagafuji H, Okazawa H, Yamakawa K, Sugawara T, Mazaki-Miyazaki E, Hirose S, Fukuma G, Mitsudome A, Wada K, Kaneko S (2002). "Autosomal dominant epilepsy with febrile seizures plus with missense mutations of the (Na+)-channel alpha 1 subunit gene, SCN1A". Epilepsy Res. 48 (1–2): 15–23. doi:10.1016/S0920-1211(01)00313-8. PMID 11823106.
^ a b c Ito M, Yamakawa K, Sugawara T, Hirose S, Fukuma G, Kaneko S (2006). "Phenotypes and genotypes in epilepsy with febrile seizures plus". Epilepsy Res. 70 (2–3 Suppl): 199–205. doi:10.1016/j.eplepsyres.2005.11.028. PMID 16884893.
^ Baulac S, Gourfinkel-An I, Picard F, Rosenberg-Bourgin M, Prud'homme J, Baulac M, Brice A, LeGuern E (1999). "A Second Locus for Familial Generalized Epilepsy with Febrile Seizures Plus Maps to Chromosome 2q21-q33". Am J Hum Genet. 65 (4): 1078–85. doi:10.1086/302593. PMC 1288241. PMID 10486327.
^ a b Vanoye C, Lossin C, Rhodes T, George A (2006). "Single-channel Properties of Human NaV1.1 and Mechanism of Channel Dysfunction in SCN1A-associated Epilepsy". J Gen Physiol. 127 (1): 1–14. doi:10.1085/jgp.200509373. PMC 2151481. PMID 16380441.
^ Nagao Y, Mazaki-Miyazaki E, Okamura N, Takagi M, Igarashi T, Yamakawa K (2005). "A family of generalized epilepsy with febrile seizures plus type 2-a new missense mutation of SCN1A found in the pedigree of several patients with complex febrile seizures". Epilepsy Res. 63 (2–3): 151–6. doi:10.1016/j.eplepsyres.2004.11.005. PMID 15715999.
^ Pineda-Trujillo N, Carrizosa J, Cornejo W, Arias W, Franco C, Cabrera D, Bedoya G, Ruíz-Linares A (2005). "A novel SCN1A mutation associated with severe GEFS+ in a large South American pedigree". Seizure. 14 (2): 123–8. doi:10.1016/j.seizure.2004.12.007. PMID 15694566.
^ Spampanato J, Kearney J, de Haan G, McEwen D, Escayg A, Aradi I, MacDonald B, Levin S, Soltesz I, Benna P, Montalenti E, Isom L, Goldin A, Meisler M (2004). "A novel epilepsy mutation in the sodium channel SCN1A identifies a cytoplasmic domain for beta subunit interaction". J Neurosci. 24 (44): 10022–34. doi:10.1523/JNEUROSCI.2034-04.2004. PMID 15525788.
^ Baulac S, Huberfeld G, Gourfinkel-An I, Mitropoulou G, Beranger A, Prud'homme J, Baulac M, Brice A, Bruzzone R, LeGuern E (2001). "First genetic evidence of GABA(A) receptor dysfunction in epilepsy: a mutation in the gamma2-subunit gene". Nat Genet. 28 (1): 46–8. doi:10.1038/88254. PMID 11326274.
^ Wallace R, Marini C, Petrou S, Harkin L, Bowser D, Panchal R, Williams D, Sutherland G, Mulley J, Scheffer I, Berkovic S (2001). "Mutant GABA(A) receptor gamma2-subunit in childhood absence epilepsy and febrile seizures". Nat Genet. 28 (1): 49–52. doi:10.1038/88259. PMID 11326275.
^ Marini C, Harkin L, Wallace R, Mulley J, Scheffer I, Berkovic S (2003). "Childhood absence epilepsy and febrile seizures: a family with a GABA(A) receptor mutation". Brain. 126 (Pt 1): 230–40. doi:10.1093/brain/awg018. PMID 12477709.
^ Harkin L, Bowser D, Dibbens L, Singh R, Phillips F, Wallace R, Richards M, Williams D, Mulley J, Berkovic S, Scheffer I, Petrou S (2002). "Truncation of the GABAA-Receptor γ2 Subunit in a Family with Generalized Epilepsy with Febrile Seizures Plus". Am J Hum Genet. 70 (2): 530–6. doi:10.1086/338710. PMC 384926. PMID 11748509.
^ Sugawara T, Tsurubuchi Y, Agarwala K, Ito M, Fukuma G, Mazaki-Miyazaki E, Nagafuji H, Noda M, Imoto K, Wada K, Mitsudome A, Kaneko S, Montal M, Nagata K, Hirose S, Yamakawa K (2001). "A missense mutation of the Na+ channel αII subunit gene Nav1.2 in a patient with febrile and afebrile seizures causes channel dysfunction". Proc Natl Acad Sci USA. 98 (11): 6384–9. doi:10.1073/pnas.111065098. PMC 33477. PMID 11371648.
^ Kamiya K, Kaneda M, Sugawara T, Mazaki E, Okamura N, Montal M, Makita N, Tanaka M, Fukushima K, Fujiwara T, Inoue Y, Yamakawa K (2004). "A nonsense mutation of the sodium channel gene SCN2A in a patient with intractable epilepsy and mental decline". J Neurosci. 24 (11): 2690–8. doi:10.1523/JNEUROSCI.3089-03.2004. PMID 15028761.
^ British National Formulary for Children (May 2014)
^ "Search Results | Great Ormond Street Hospital".
ICD-10: G40.3
OMIM: 604233 609800 607208
MeSH: C565809
Diseases of ion channels
Voltage-gated
CACNA1A
Familial hemiplegic migraine 1
Episodic ataxia 2
Spinocerebellar ataxia type-6
CACNA1C
Timothy syndrome
Brugada syndrome 3
Long QT syndrome 8
Ocular albinism 2
CSNB2A
CACNA1S
Hypokalemic periodic paralysis 1
Thyrotoxic periodic paralysis 1
CACNB2
Ligand gated
RYR1
CPVT1
ARVD2
Sodium channel
SCN1A
GEFS+ 2
Febrile seizure 3A
SCN1B
Hyperkalemic periodic paralysis
Paramyotonia congenita
Potassium-aggravated myotonia
Long QT syndrome 10
Febrile seizure 3B
Paroxysmal extreme pain disorder
Congenital insensitivity to pain
Constitutively active
SCNN1B/SCNN1G
Liddle's syndrome
SCNN1A/SCNN1B/SCNN1G
Pseudohypoaldosteronism 1AR
KCNA1
Familial atrial fibrillation 7
KCNC3
Spinocerebellar ataxia type-13
KCNE1
Jervell and Lange-Nielsen syndrome
KCNH2
Short QT syndrome
KCNQ1
Romano–Ward syndrome
BFNS1
Inward-rectifier
KCNJ1
Bartter syndrome 2
Andersen–Tawil syndrome
KCNJ11
TNDM3
Congenital absence of the vas deferens
CLCN1
Thomsen disease
Dent's disease
Osteopetrosis A2, B4
Vitelliform macular dystrophy
CLCNKB
FSGS2
Mucolipidosis type IV
Connexin
GJA1
Oculodentodigital dysplasia
Hallermann–Streiff syndrome
GJB1
Charcot–Marie–Tooth disease X1
Keratitis–ichthyosis–deafness syndrome
Ichthyosis hystrix
Bart–Pumphrey syndrome
Vohwinkel syndrome)
GJB3/GJB4
Erythrokeratodermia variabilis
Progressive symmetric erythrokeratodermia
Clouston's hidrotic ectodermal dysplasia
Porin
AQP2
Nephrogenic diabetes insipidus 2
See also: ion channels
Retrieved from "https://en.wikipedia.org/w/index.php?title=Generalized_epilepsy_with_febrile_seizures_plus&oldid=883921081"
Channelopathies
Epilepsy types
Wikipedia articles that are too technical from October 2013
All articles that are too technical
Articles needing expert attention from October 2013
Articles that may contain original research from October 2013
All articles that may contain original research


The thematic group Teaching and Teacher Education studies the contribution of teachers in creating optimal conditions for student learning and ensuring educational effectiveness. In this thematic group, theory advancement focuses on the relations between teachers knowledge, teacher activities, and professional development of teachers. Quality of teaching is studied by relating teaching to students' learning processes and (cognitive, affective, and behavioural) learning outcomes.
ICO researchers within this thematic group use various theoretical perspectives to study teaching. Research from an interpersonal perspective, which studies teaching in terms of the relationship between teacher and students, shows differential effects of teacher influence and proximity on cognitive and affective outcomes, and active learning of students. Results also reveal differences in interventions that are adequate for teachers at the start (where influence is relatively low) and for teachers towards the end (where proximity goes downward) of their career. Research from a learning activities perspective, has contributed to understanding of how teaching influences the learning activities students undertake. It adds to understanding the different ways in which student-regulation and teacher-regulation of learning act upon one another, and how to promote congruence and constructive friction and avoid destructive friction between these two modes of control Studies adopting a personal knowledge perspective, have contributed to insights in the content and the structure of the knowledge and beliefs teachers develop about various pedagogical and didactical aspects related to their practice. Among others, research in this area has improved our understanding of the ways experienced teachers respond to educational innovations, depending on their epistemological beliefs in relation to their conceptions of teaching and learning.


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Qwirkle is an elegant tile game, easy to learn and understand, visually inviting, and increasingly challenging as the game progresses. The game can be played by 2 up to 4 players and an average game takes about 45 minutes to play.
The game consists of 108 wooden blocks and they display one of six shapes (circle, square, diamond, starburst, clover and "x") in one of six colors (blue, red, yellow, green, purple and orange). There is no board, players simply use an available flat surface.
Players begin the game with 6 blocks which they hide from other players. All other tiles go into a big bag that's shaken up to mix everything together. Players take turns, adding to an increasingly complex grid of blocks. To place a block, it must be either of the same color or shape as the adjacent blocks. You can place several blocks, as long as they are in one line without duplicates.
If you are fortunate enough to complete a six tile row, which is called a Qwirkle, you receive 6 extra points.
Players score one point for each block played plus all blocks adjacent. It is possible for a block to score in more than one direction.
The player then refills his hand to 6 blocks and the next player continues.
Tactical maneuvers and well-planned strategy is required to win a game. As more tiles are placed, there are more choices, so the search for the high scoring play becomes more and more complex.
The game offers a risk-award concept. You could get a bunch of points creating a line of five, but lines of five are susceptible for another player to add the sixth tile for a Qwirkle while simultaneously making a new line for even more points of top of the 12 points they're already going to get for the Qwirkle.
The challenge is both visual and logical and complex enough for serious adult competition. The strategy is deep, but accessible.
And there is also enough luck involved that inexperienced players can keep it close with more experienced players.
Another strength of Qwirkle lies in its familiar look. The shapes and colors are easily recognizable and the rules are very simple and quick to learn.
Qwirkle will satisfy anyone who enjoys games like Scrabble, Carcassonne or Ticket To Ride.


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text:
HomeMaseratiNews
Maserati announces Ghibli sedan and Levante crossover
Maserati announced the names of two of their upcoming models. They will be called the Ghibli and Levante.
Sep 27, 2012 at 4:23pm ET
Following the unveiling of the GranCabrio MC, Maserati announced the names of two of their upcoming models.
First up, the company's crossover will be called the Levante after the "Via Emilia Levante" in Bologna where the Maserati brothers originally envisioned the automaker. The crossover was recently previewed by the Kubang concept and is slated to go on sale in 2014.
Specifications were not released, but the Levante will be based on the Jeep Grand Cherokee and could be offered with petrol and diesel engines.
Maserati also confirmed their entry-level sedan will wear the iconic Ghibli moniker. Set to slot beneath the next-generation Quattroporte, the Ghibli could be based on the Chrysler 300 and powered by a twin-turbo V6 engine with 400 hp (298 kW / 406 PS).


text:
Q: NHibernate - NHibernate.Exceptions.GenericADOException: could not execute query I have the following exception occurring seemingly at random:
    NHibernate.Exceptions.GenericADOException: could not execute query
    [ select businesspr0_.BusinessProcessID as col_0_0_, businesspr0_.ProcessNumber as col_1_0_, businesspr1_.Name as col_2_0_, businesspr0_.DateCreated as col_3_0_, actor2_.DisplayName as col_4_0_, usergroup3_.Name as col_5_0_, processele5_.Name as col_6_0_ from BusinessProcess businesspr0_ inner join BusinessProcess businesspr1_ on businesspr0_.DefinitionID=businesspr1_.BusinessProcessID inner join Actor actor2_ on businesspr0_.ActorCreatedID=actor2_.ActorID left outer join UserGroup usergroup3_ on businesspr0_.UserGroupCreatedID=usergroup3_.UserGroupID left outer join Actor usergroup3_1_ on usergroup3_.UserGroupID=usergroup3_1_.ActorID inner join ActiveElement activeelem4_ on businesspr0_.BusinessProcessID=activeelem4_.BusinessProcessID inner join ProcessElement processele5_ on activeelem4_.ProcessElementID=processele5_.ProcessElementID inner join ProcessEmployees processemp6_ on businesspr0_.BusinessProcessID=processemp6_.BusinessProcessID inner join Actor actor7_ on processemp6_.ActorID=actor7_.ActorID inner join UserInGroups users8_ on actor7_.ActorID=users8_.UserGroupID inner join AppUser user9_ on users8_.UserID=user9_.UserID inner join Actor user9_1_ on user9_.UserID=user9_1_.ActorID where businesspr0_.IsDefinition=0 and (businesspr0_.Finished is null) and @p0=user9_.UserID ]
      Name:userID - Value:32771
    [SQL: select businesspr0_.BusinessProcessID as col_0_0_, businesspr0_.ProcessNumber as col_1_0_, businesspr1_.Name as col_2_0_, businesspr0_.DateCreated as col_3_0_, actor2_.DisplayName as col_4_0_, usergroup3_.Name as col_5_0_, processele5_.Name as col_6_0_ from BusinessProcess businesspr0_ inner join BusinessProcess businesspr1_ on businesspr0_.DefinitionID=businesspr1_.BusinessProcessID inner join Actor actor2_ on businesspr0_.ActorCreatedID=actor2_.ActorID left outer join UserGroup usergroup3_ on businesspr0_.UserGroupCreatedID=usergroup3_.UserGroupID left outer join Actor usergroup3_1_ on usergroup3_.UserGroupID=usergroup3_1_.ActorID inner join ActiveElement activeelem4_ on businesspr0_.BusinessProcessID=activeelem4_.BusinessProcessID inner join ProcessElement processele5_ on activeelem4_.ProcessElementID=processele5_.ProcessElementID inner join ProcessEmployees processemp6_ on businesspr0_.BusinessProcessID=processemp6_.BusinessProcessID inner join Actor actor7_ on processemp6_.ActorID=actor7_.ActorID inner join UserInGroups users8_ on actor7_.ActorID=users8_.UserGroupID inner join AppUser user9_ on users8_.UserID=user9_.UserID inner join Actor user9_1_ on user9_.UserID=user9_1_.ActorID where businesspr0_.IsDefinition=0 and (businesspr0_.Finished is null) and @p0=user9_.UserID]
 ---> System.IndexOutOfRangeException: col_0_0_
       at System.Data.ProviderBase.FieldNameLookup.GetOrdinal(String fieldName)
       at System.Data.SqlClient.SqlDataReader.GetOrdinal(String name)
       at NHibernate.Driver.NHybridDataReader.GetOrdinal(String name)
       at NHibernate.Type.NullableType.NullSafeGet(IDataReader rs, String name)
       at NHibernate.Type.NullableType.NullSafeGet(IDataReader rs, String[] names, ISessionImplementor session, Object owner)
       at NHibernate.Hql.Ast.ANTLR.Loader.QueryLoader.GetResultColumnOrRow(Object[] row, IResultTransformer resultTransformer, IDataReader rs, ISessionImplementor session)
       at NHibernate.Loader.Loader.GetRowFromResultSet(IDataReader resultSet, ISessionImplementor session, QueryParameters queryParameters, LockMode[] lockModeArray, EntityKey optionalObjectKey, IList hydratedObjects, EntityKey[] keys, Boolean returnProxies)
       at NHibernate.Loader.Loader.DoQuery(ISessionImplementor session, QueryParameters queryParameters, Boolean returnProxies)
       at NHibernate.Loader.Loader.DoQueryAndInitializeNonLazyCollections(ISessionImplementor session, QueryParameters queryParameters, Boolean returnProxies)
       at NHibernate.Loader.Loader.DoList(ISessionImplementor session, QueryParameters queryParameters)
       --- End of inner exception stack trace ---
       at DotExe.TiCat.DomainModel.Repository.ProcessModel.BusinessProcessDAO.GetProcessForUserGroups(Int32 userID) in D:\Projects\TiCatRNIDS\DotExe.TiCat4\DotExe.TiCat.DomainModel.Repository\ProcessModel\BusinessProcessDAO.cs:line 98
       at DotExe.TiCat4.UseCaseRepository.TicketProcess.TicketQueues.RefreshQueue() in D:\Projects\TiCatRNIDS\DotExe.TiCat4\DotExe.TiCat4\UseCaseRepository\TicketProcess\TicketQueues.cs:line 128

Odd part is this System.IndexOutOfRangeException: col_0_0_ which I could not figure out why is happening.
I can update post with some xml mapping if necessary.
Tnx
Update:
Mappings and the query throwing ex:
<?xml version="1.0" encoding="utf-8" ?>
<hibernate-mapping xmlns="urn:nhibernate-mapping-2.2" assembly="DotExe.TiCat.DomainModel" namespace="DotExe.TiCat.DomainModel.Process">

  <class name="BusinessProcess" table="BusinessProcess">
    <id name="BusinessProcessID">
      <generator class="hilo"/>
    </id>
    <property name = "Name" length="1024" type="string" not-null ="false" />
    <property name = "Description" length="5000" type="string" not-null ="false" />
    <property name = "ProcessNumber" length="500" type="string" not-null ="false" />
    <property name = "CommentOnSolve" length="5000" type="string" not-null ="false" />
    <property name="IsDefinition" type="bool"/>
    <property name="PlaningTimeToSpend" type="long"/>
    <property name="SpendTime" type="long"/>
    <property name="DateCreated" type="DateTime" not-null="false"/>
    <property name="PlanToStart" type="DateTime" not-null="false"/>
    <property name="PlanToFinish" type="DateTime" not-null="false"/>
    <property name="Started" type="DateTime" not-null="false"/>
    <property name="Finished" type="DateTime" not-null="false"/>
    <property name="CustomerRequestCallBack" type="bool" not-null="false"/>
    <property name="EscalationTimeLimitInPercents" type="int"/>
    <property name="IsEscalated" type="bool"/>
    <property name="IsInfinite" type="bool"/>
    <many-to-one name="WorkingWeek" class="WorkingWeek" column="WorkingWeekID" not-null="false" lazy="false"/>
    <many-to-one name="Priority" class="ProcessPriority" column="PriorityID" not-null="false" lazy="false"/>
    <many-to-one name="UserCreated" class="DotExe.TiCat.DomainModel.Actors.Actor" column="ActorCreatedID" not-null="false" lazy="false"/>
    <many-to-one name="UserSolved" class="DotExe.TiCat.DomainModel.Actors.Actor" column="ActorSolvedID" not-null="false" lazy="false"/>
    <many-to-one name="GroupCreated" class="DotExe.TiCat.DomainModel.Actors.UserGroup" column="UserGroupCreatedID" not-null="false" lazy="false"/>
    <many-to-one name="GroupSolved" class="DotExe.TiCat.DomainModel.Actors.UserGroup" column="UserGroupSolvedID" not-null="false" lazy="false"/>
    <many-to-one name="Definition" class="BusinessProcess" column="DefinitionID" cascade="none" />
    <set name="Elements" lazy="false" cascade="save-update">
      <key column="BusinessProcessID"/>
      <one-to-many class="ProcessElement"/>
    </set>
    <set name="ActiveElements" table="ActiveElement" lazy="false" cascade="save-update">
      <key column="BusinessProcessID"/>
      <many-to-many class="ProcessElement" column="ProcessElementID"/>
    </set>
    <set name="ProcessConsumers" table="ProcessConsumers" lazy="false" cascade="save-update">
      <key column="BusinessProcessID"/>
      <many-to-many class="DotExe.TiCat.DomainModel.Actors.Actor" column="ActorID"/>
    </set>
    <set name="ProcessEmployees" table="ProcessEmployees" lazy="false">
      <key column="BusinessProcessID"/>
      <many-to-many class="DotExe.TiCat.DomainModel.Actors.Actor" column="ActorID"/>
    </set>
    <set name="ProcessSupervisors" table="ProcessSupervisors" lazy="false">
      <key column="BusinessProcessID"/>
      <many-to-many class="DotExe.TiCat.DomainModel.Actors.Actor" column="ActorID"/>
    </set>
    <set name="Flows" lazy="false" cascade="save-update">
      <key column="BusinessProcessID"/>
      <one-to-many class="SequenceFlow"/>
    </set>
    <set name="PriorityTimeRules" lazy="false" cascade="save-update">
      <key column="BusinessProcessID"/>
      <one-to-many class="DotExe.TiCat.DomainModel.BusinessRules.PriorityTimeRule"/>
    </set>
  </class>

  <class name="ProcessElement" table="ProcessElement">
    <id name="ProcessElementID">
      <generator class="hilo"/>
    </id>
    <property name = "Name" length="1024" type="string" not-null ="true" />
    <property name="IsDefinition" type="bool"/>
    <property name="IsState" type="bool"/>

    <many-to-one class="BusinessProcess" name="MemberOf" lazy="false" cascade="save-update" column="BusinessProcessID"/>
    <many-to-one class="ProcessElement" name="Definition" column="DefinitionID"/>

    <joined-subclass name="Activity">
      <key column="ActivityID"/>
      <property name = "Name" length="1024" type="string" not-null ="true" />
      <property name = "Description" length="4000" type="string" not-null ="false" />
      <set name="States" >
        <key column="ActivityID"/>
        <one-to-many class="ActivityState"/>
      </set>

      <joined-subclass name="UserTask" table="UserTask">
        <key column="UserTaskID"/>
        <property name="PlaningTimeToSpend" type="int"/>
        <property name="SpendTime" type="int"/>
        <property name="PlanToStart" type="DateTime" not-null="false"/>
        <property name="PlanToFinish" type="DateTime" not-null="false"/>
        <property name="Started" type="DateTime" not-null="false"/>
        <property name="Finished" type="DateTime" not-null="false"/>
        <set name="Comments">
          <key column="UserTaskID"/>
          <one-to-many class="TaskComment"/>
        </set>
        <set name="UserTaskEmployees">
          <key column="UserTaskID"/>
          <many-to-many class="DotExe.TiCat.DomainModel.Actors.Actor" column="ActorID"/>
        </set>
        <set name="UserTaskSupervisors">
          <key column="UserTaskID"/>
          <many-to-many class="DotExe.TiCat.DomainModel.Actors.Actor" column="ActorID"/>
        </set>
        <set name="Priorities">
          <key column="UserTaskID"/>
          <one-to-many class="UserTaskPriority"/>
        </set>
        <set name="AssignmentRules">
          <key column="UserTaskID"/>
          <one-to-many class="DotExe.TiCat.DomainModel.BusinessRules.AssignmentRule"/>
        </set>
        <many-to-one class="DotExe.TiCat.DomainModel.UseCase.ClientApplicationConfig" name="Application" column="ApplicationConfigID"/>
        <many-to-one class="UserTaskPriority" name="TaskPriority" column="TaskPriorityID"/>
      </joined-subclass>

      <joined-subclass name="SendTask">
        <key column="SendTaskID"></key>
        <many-to-one name="EmailAccount" class="DotExe.TiCat.DomainModel.Config.EmailAccount" column="EmailAccountID" lazy="false"></many-to-one>
        <many-to-one name="Template" class="DotExe.TiCat.DomainModel.Templates.Template" column="TemplateID" lazy="false"></many-to-one>
        <set name="Actors" lazy="false">
          <key column="SendTaskID"></key>
          <many-to-many class="DotExe.TiCat.DomainModel.Actors.Actor" column="ActorID"></many-to-many>
        </set>
        <set name="EmailMessages">
          <key column="SendTaskID"></key>
          <one-to-many class="DotExe.TiCat.DomainModel.Email.EmailMessage"/>
        </set>
      </joined-subclass>
    </joined-subclass>

    <joined-subclass name="Gateway">
      <key column="GatewayID"/>
      <joined-subclass name="ExclusiveGateway">
        <key column="ExclusiveGatewayID"/>
      </joined-subclass>
    </joined-subclass>

    <joined-subclass name="Event">
      <key column="EventID"></key>
      <property name="ExecutionTime" type="DateTime" not-null="false"></property>

      <joined-subclass name="StartEvent">
        <key column="StartEventID"></key>
      </joined-subclass>

      <joined-subclass name="EndEvent">
        <key column="EntEventID"></key>
      </joined-subclass>
    </joined-subclass>
  </class>
  <class name="ActivityState" table="ActivityState">
    <id name="ActivityStateID">
      <generator class="hilo"/>
    </id>
    <property name = "Name" length="1024" type="string" not-null ="true" />
    <property name = "Description" length="4000" type="string" not-null ="false" />
    <many-to-one name="StateOf" class="Activity" column="ActivityID"/>
    <property name="IsEndState" type="bool"/>
    <property name="IsStartState" type="bool"/>
    <property name="IsPauseState" type="bool"/>
    <property name="IsProcessSerializationState" type="bool"/>
  </class>
  <class name="SequenceFlow" table ="SequenceFlow">
    <id name="SequenceFlowID">
      <generator class="hilo"/>
    </id>
    <many-to-one class="ProcessElement" name="Source" column="SourceID" lazy="false" cascade="save-update"/>
    <many-to-one class="ProcessElement" name="Target" column="TargetID" lazy="false" cascade="save-update"/>
    <many-to-one name="Process" class="BusinessProcess" column="BusinessProcessID" cascade="save-update"/>
  </class>
  <class name="UserTaskPriority" table ="UserTaskPriority">
    <id name="UserTaskPriorityID">
      <generator class="hilo"/>
    </id>
    <property name = "Name" length="1024" type="string" not-null ="true" />
  </class>
  <class name="TaskComment" table ="TaskComment">
    <id name="TaskCommentID">
      <generator class="hilo"/>
    </id>
    <property name = "Comment" length="4000" type="string" not-null ="true" />
    <many-to-one name="Task" class="ProcessElement" column="UserTaskID"/>
    <many-to-one name="Actor" class="DotExe.TiCat.DomainModel.Actors.Actor" column="ActorID"/>
    <many-to-one name="Process" class="BusinessProcess" column="BusinessProcessID"/>
    <many-to-one name="Group" class="DotExe.TiCat.DomainModel.Actors.UserGroup" column="UserGroupID"/>
    <property name="CommentTime" type="DateTime" not-null="false" />
  </class>
  <class name="TransitionLog">
    <id name="TransitionLogID">
      <generator class="hilo"/>
    </id>
    <property name="LogDate" type="DateTime"/>
    <property name="TaskStarted" type="DateTime" not-null ="false" />
    <property name="TaskEnded" type="DateTime" not-null ="false" />
    <property name="TimeSpend" type="int" not-null ="false" />
    <set name="SendToActors" table="SendToActorLog" lazy="false">
      <key column="TransitionLogID"/>
      <many-to-many class="DotExe.TiCat.DomainModel.Actors.Actor" column="ActorID"/>
    </set>
    <many-to-one name="Actor" class="DotExe.TiCat.DomainModel.Actors.Actor" column="ActorID" lazy="false"/>
    <many-to-one name="Group" class="DotExe.TiCat.DomainModel.Actors.UserGroup" column="UserGroupID"/>
    <many-to-one name="FromElement" class="ProcessElement" column="FromElementID" lazy="false"/>
    <many-to-one name="ToElement" class="ProcessElement" column="ToElementID"/>
    <many-to-one name="Process" class="BusinessProcess" column="BusinessProcessID"/>
    <many-to-one name="LogType" class="LogType" column="LogTypeID" lazy="false"/>
    <property name="Comment" length="4000" type="string" not-null ="false" />
  </class>
  <class name="LogType">
    <id name="LogTypeID"/>
    <property name = "Name" length="1024" type="string" not-null ="false" />
    <property name = "DisplayName" length="1024" type="string" not-null ="false" />
  </class>

  <class name="ProcessPriority">
    <id name="ProcessPriorityID"/>
    <property name = "Name" length="1024" type="string" not-null ="false" />
    <property name = "DisplayName" length="1024" type="string" not-null ="false" />
  </class>

  <class name="WorkingWeek">
    <id name="WorkingWeekID">
      <generator class="hilo"/>
    </id>
    <property name="MondayFrom" type="DateTime" not-null="true"/>
    <property name="MondayTo" type="DateTime" not-null="true"/>
    <property name="TuesdayFrom" type="DateTime" not-null="true"/>
    <property name="TuesdayTo" type="DateTime" not-null="true"/>
    <property name="WednesdayFrom" type="DateTime" not-null="true"/>
    <property name="WednesdayTo" type="DateTime" not-null="true"/>
    <property name="ThursdayFrom" type="DateTime" not-null="true"/>
    <property name="ThursdayTo" type="DateTime" not-null="true"/>
    <property name="FridayFrom" type="DateTime" not-null="true"/>
    <property name="FridayTo" type="DateTime" not-null="true"/>
    <property name="SaturdayFrom" type="DateTime" not-null="true"/>
    <property name="SaturdayTo" type="DateTime" not-null="true"/>
    <property name="SundayFrom" type="DateTime" not-null="true"/>
    <property name="SundayTo" type="DateTime" not-null="true"/>
    <property name="Is24x7" type="bool"/>
    <property name="Name" type="string" length="256" not-null="true"/>
    <!--<set name="BusinessProcesses" cascade="none" lazy="false">
      <key column="WorkingWeekID"/>
      <one-to-many class="BusinessProcess"/>
    </set>-->

  </class>

</hibernate-mapping>

And the query:
IList<object[]> result =
                        session.CreateQuery(" select bp.BusinessProcessID, bp.ProcessNumber, def.Name as Definition," +
                                            " bp.DateCreated, actor.DisplayName as UserCreated," +
                                            " group.Name as GroupCreated, task.Name as ActiveTask " +
                                            " from BusinessProcess bp " +
                                            " join bp.Definition as def " +
                                            " join bp.UserCreated as actor " +
                                            " left join bp.GroupCreated as group " +
                                            " join bp.ActiveElements as task" +
                                            " join bp.ProcessEmployees as res" +
                                            " join res.Users as users " +
                                            " where bp.IsDefinition = false " +
                                            " and bp.Finished is null" +
                                            " and :userID = users.ActorID").SetParameter("userID", userID).List<object[]>();

A: I've gotten this error when I tried to map a null value to a non-nullable property (i.e. an integer). make sure that either you make sure that the sql value is non-nullable, or just make the c# property nullable (public virtual int? NumberOfPoints { get; set; })

A: I don't know the reason for this. But there is something odd in the mappings: Activity has the property "Name", which is already mapped in the base class. This may lead to index out of range. There are probably more problems around.
Be very careful with sets like "Actors" which are many-to-many and do not specify a table name. There is a high risk of defining another "Actors" set which will get conflicting table definitions.
Unrelated for sure: some sets should be inverse, because there is a reference from the element to the parent.

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