text:
Toll Free: 1-888-928-9744
Published: Apr 4, 2014 | Pages: 66 | Publisher: Technavio | Industry: ICT | Report Format: Electronic (PDF)
About mobile Education m-Education is the ability to provide educational-related content on smartphones and tablets. Educational-related content refers to all the digital learning content provided on personal devices. m-Education service providers deliver learning solutions using the latest tools and technology, providing users with rich media and graphic-based learning. Since this form of learning is cost-effective and helps enhance employees' efficiency and productivity, many educational firms across the globe are replacing the traditional forms of training with m-education to improve their geographical presence. TechNavio's analysts forecast the Global Mobile Education market will grow at a CAGR of 20.65 percent over the period 2013-2018. Covered in this Report The Global Mobile Education market can be divided into seven segments: E-books and E-courses, Game/Simulation-based Tools, LMS/Authoring Tools, Distance Tutoring, Collaboration Tools, Test Preparation, and Assessment. TechNavio's report, the Global Mobile Education Market 2014-2018, has been prepared based on an in-depth market analysis with inputs from industry experts. The report covers the Americas and the EMEA and APAC regions; it also covers the Global Mobile Education market landscape and its growth prospects in the coming years. The report also includes a discussion of the key vendors operating in this market. Key Regions Americas EMEA APAC Key Vendors Amazon Inc. Apple Inc. Barnes & Noble Inc. Blackboard Inc. Other Prominent Vendors Google Inc. Microsoft Corp. Pearson plc Sony Corp. Key Market Driver Increasing Adoption of Smartphones and Tablets. For a full, detailed list, view our report. Key Market Challenge Unstable Global Economic Conditions. For a full, detailed list, view our report. Key Market Trend Emergence of Virtual Classrooms. For a full, detailed list, view our report. Key Questions Answered in this Report What will the market size be in 2018 and what will the growth rate be? What are the key market trends? What is driving this market? What are the challenges to market growth? Who are the key vendors in this market space? What are the market opportunities and threats faced by the key vendors? What are the strengths and weaknesses of the key vendors? You can request one free hour of our analyst's time when you purchase this market report. Details are provided within the report.
Table of Contents
01. Executive Summary 02. List of Abbreviations 03. Scope of the Report 03.1 Market Overview 03.2 Product Offerings 04. Market Research Methodology 04.1 Market Research Process 04.2 Research Methodology 05. Introduction 06. Market Landscape 06.1 Market Overview 06.2 Market Size and Forecast 06.2.1 Market Segmentation by the Type of Services 06.2.2 Global m-Education Hardware Market 06.3 Universities using Mobile Learning Apps 06.4 Government Initiatives 06.5 Five Forces Analysis 07. Geographical Segmentation 07.1 Global m-Education Market by Geographical Segmentation 2013 08. Key Leading Countries 08.1 USA 08.2 Japan 09. Buying Criteria 10. Market Growth Drivers 11. Drivers and their Impact 12. Market Challenges 13. Impact of Drivers and Challenges 14. Market Trends 15. Trends and their Impact 16. Vendor Landscape 16.1 Competitive Scenario 16.2 Market Share Analysis 2013 16.3 Other Prominent Vendors 17. Key Vendor Analysis 17.1 Amazon Inc. 17.1.1 Business Overview 17.1.2 Business Segmentation 17.1.3 Key Information 17.1.4 SWOT Analysis 17.2 Apple Inc. 17.2.1 Business Overview 17.2.2 Business Segmentation 17.2.3 Revenue Segmentation by Geography 17.2.4 Key Information 17.2.5 SWOT Analysis 17.3 Barnes & Noble Inc. 17.3.1 Business Overview 17.3.2 Business Segmentation 17.3.3 Key Information 17.3.4 SWOT Analysis 17.4 Blackboard Inc. 17.4.1 Business Overview 17.4.2 Business Segmentation 17.4.3 Key Information 17.4.4 SWOT Analysis 18. Other Reports in this Series List of Exhibits: Exhibit 1: Market Research Methodology Exhibit 2: Global m-Education Market by Type of Services 2013-2018 (US$ billion) Exhibit 3: Global m-Education Market by Type of Services 2013 Exhibit 4: M-Education Market by Services 2013-2018 (US$ billion) Exhibit 5: Some of the Smartphones Apps for Students and Teachers Exhibit 6: Geographical Segmentation of Global m-Education Market 2013 Exhibit 7: Business Segmentation of Amazon Inc. Exhibit 8: Amazon.com Inc. Geographical Segmentation by Sales Revenue for Nine Months Ended September 30, 2013 Exhibit 9: Amazon.com Inc. Business Segmentation by Sales Revenue for Nine Months Ended September 30, 2013 Exhibit 10: Business Segmentation of Apple Inc. by Products 2013 Exhibit 11: Revenue Segmentation by Geography 2013 Exhibit 12: Business Segmentation of Barnes & Novel Inc. Exhibit 13: Revenue Segmentation by Business Segmentation Exhibit 14: Business Segmentation of Blackboard Inc.
Global fluorotelomers market size is anticipated to be valued at USD 539.3 million by 2020, as per a new research report by Radiant Insights, Inc. Increasing application scope in fire fighting systems owing to growing safety concerns is likely to driRead More...
Global automotive coatings market size is likely to be valued at USD 27.7 billion by 2022; as per a new research report by Radiant Insights, Inc. Vehicle aesthetics, UV radiation and temperature variation protection and enhance durability are certainRead More...
Global electric water heaters market is expected to be valued at USD 29,322.4 million by 2022, as per a new research report by Radiant Insights, Inc. Escalating demand across extensive range of domestic applications is expected to drive demand. EvolvRead More...
Global PP (Polypropylene) nonwoven fabric market size is anticipated to be valued at USD 30.6 billion by 2020, as per a new research report by Radiant Insights, Inc. Growing usage of hygiene products such as incontinence products and baby diapers isRead More...
Global integrated systems market is projected to reach USD 24 billion by 2020, as per a new research report by Radiant Insights, Inc. Increasing need to re-evaluate data center infrastructure is expected to boost the demand. Change in trend from mainRead More...
Get your queries resolved from an industry expert. Request for a free product review before report purchase.
Phone: 1-415-349-0054
Toll Free: 1-888-928-9744
Email: [email protected]
Speak to the report author to design an exclusive study to serve your research needs.
A testimonial for service excellence represented in the form of BBB "A" Accreditation.
Your personal and confidential information is safe and secure.


text:
Wild Atlantic Way
»This year, journey through the Wild Atlantic Way to immerse yourself in the stunning landscape of Ireland.
Great holiday ideas
»Discover a wealth of amazing holiday ideas and activites with our list of things to do. Take your family, friends or someone you love on some great adventures.
Self catering
»Stay in a cosy Irish home away from home and venture out to explore our beautiful scenery.
Search all festivals
»Experience a host of festivals and events taking place around the country this year.
»Start your search for the perfect Irish break now. What's stopping you?
Linear Cycle Routes
Push off from the crossroads in the centre of the village, head north briefly before taking a right just over the bridge, up the Owenkillew Valley, twisting in tandem with the river. A tight patchwork of green fields spreads up the valley floor to the billowing hills above, streams and ditches gurgle back down under the bridges at your wheels. Continue up the valley past Glenhull village and soon you will encounter an ancient standing stone in the field to your right. Time now to sit back in the saddle and prepare for the tough climb up Doraville with Sawel Mountain rising 700m straight ahead. With the hard work done it's time to relax going down through the beautiful Glenelly valley. Squeeze down through Barnes Gap where a short traffic-free section takes you back along the Owenkillew River. Enjoy the view whilst you make your way back to the village of Gortin as the grey stonewalls stretch a skeletal framework over the soft valley slopes.Public roads: On Public RoadGetting to the start: From Omagh, take the Mountjoy Road, off McConnell Place. This roads turns in the Gortin Road (B48).Traffic: This route is on secondry B & C roads in mainly rural areas. Traffic that may be encountered would include cars, vans, farm machinery, and rural buses.
There is a Gold Mine in the Owenkillew Valley opposite the bridge at Glenlark. The Glenelly Valley is the longest valley in the Sperrins.
Cafe, Shop, Public House, and Public Toilets are all available in the village of Gortin. Gortin Accommodation Suite and Activity Centre which opens 9am - 5pm also has Disabled access toilets and Bike Hire, contact 028 8164 8346. On route there are also Public Houses at Glenhull and Scotch Town, and slightly off route there are Public Toilets, Telephone and Public House in the village of Cranagh.
Cycling on well surfaced roads, hilly in some sections.
Sperrins Route cards. See Attachments
Available from Omagh Tourist Information Centre
Push off from the crossroads in the centre of the village, head north briefly before taking a ...
31 Miles (50Km)
This route is over secondary B and C roads which are tarmac. This route also contains some steep climbs. There is also a section of this route which is traffic free.

subset: commoncrawl


text:
ER Wait Watcher
Which Emergency Room Will See You the Fastest?
Look up an address, city or zip
For example: 874 State Street CT, Chicago, 11216
Important Note on Hospital Location
Our location data comes from Google Maps. If you think a hospital is missing or in the wrong place, let us know.
(205) 838-3122
50 medical park east drive
birmingham, AL 35235
Hospital Type
Acute Care Hospitals
Hospital Owner
Voluntary non-profit - Private
Emergency Dept. Volume
High (40,000 - 59,999 patients a year)
of Patients Would "Definitely Recommend" this Hospital
(Ala. Avg: 71%)
of Patients Would "Definitely Recommend" this Hospital
(Alabama Avg: 71%)
See this hospital's CMS profile page or inspection reports.
Patient Pathways Through This ER
After a patient arrives at the emergency room, they are typically seen by a doctor and then either sent home or admitted to the hospital and taken to a room. A small percentage of patients leave without being seen at all. The chart below shows on average how long each of these pathways take. Lower numbers are better, and all times refer to the average length of time people waited. Find out more »
Taken to room
All wait times are average.
Detailed Quality Measures
Here is a more in depth look at each quality measure, compared to state and national averages for hospitals with high volumes. Experts caution that very small differences between hospitals for a given measure are unlikely to correspond to noticeable differences in the real world.
(to other hospitals with similar emergency-department volumes, when available)
Waiting Time
Average time patients spent in the emergency room before being seen by a doctor.
Time Until Sent Home
Average time patients spent in the emergency room before being sent home.
Left Without
Being Seen
Percentage of patients who left the emergency room without being seen by a doctor.
Time Before Admission
Average time patients spent in the emergency room before being admitted to the hospital.
Data submitted were based on a sample of cases/patients.
Transfer Time
Among patients admitted, additional time they spent waiting before being taken to their room (sometimes referred to as "boarding time.")
Data submitted were based on a sample of cases/patients.
Broken Bone
Average time patients with broken bones had to wait before receiving pain meds.
CT Scan
Percentage of patients who arrived with stroke symptoms and did not receive brain scan results within 45 mins.
No Data Available
The number of cases/patients is too few to report.
Notes: "Average time" refers to the median waiting time (the midpoint of all patients' waiting times). References to "doctor" indicate a doctor, nurse practitioner or physician assistant. CMS reports the CT scan quality measure as the percentage of patients who received a scan within 45 minutes. We have reversed that measure so that all measures follow a "lower is better" pattern.
Data from the Center for Medicare and Medicaid Services, last updated August 2017. Most data was collected between October 2015 and September 2016.
Icons from The Noun Project.
Rating Summary
Rate this Hospital
Visited this emergency room? Tell us more about how your visit went.
Were you harmed? Please complete ProPublica's Patient Harm Questionnaire.
On Friday August 21, my wife was diagnosed at a clinic with a significant UTI and received antibiotics. On Saturday she was worse and in extreme pain. She was brought to the ER by ambulance. After taking urine and blood samples, the doctor (let's call him Doctor W) told her that her infection was SIGNIFICANT. He prescribed a different antibiotic and told her to come back the next day (Sunday) if not improved because something might be going on besides the infection.
The next evening my wife was even worse, and in extreme pain. Following THEIR ADVICE, we returned to the ER, where we waited an hour and 20 minutes for her to be seen! When the (different) doctor came in (let's call him Doctor B.) he told my wife that one day was not enough time for her (as he put it) VERY MILD UTI. He was VERY dismissive even though she was in massive pain. In fact, he was just short of actually YELLING at her! I asked if he was saying that BOTH her primary doctor and their own doctor from the previous day were wrong and he nodded yes.
Resigned, we left and the next morning(Monday) she was even worse. I took her back to her primary care physician who diagnosed her with a very bad E Coli infection! She was hospitalized for several days and cared for by staff wearing protective garments. After she came home she was attached to a pic line for 10 more days.
I am glad we did not listen to the ER "Doctor B." because my wife might very well have died otherwise, this PER the doctors who cared for her in the hospital! His rudeness, while not excusable, takes second place to his dismissive mis-diagnosis which ignored two other physician opinions AND lab results! I will never return to that ER and recommend strongly that you choose any other option available to you.
The people up front were very good and quick as well as the xray nurse and one male nurse in the room. The female nurse and doctor acted like it was no big deal and I shouldn't be there. The doctor said I had a slight fracture and the female nurse was very rude. They didn't give me any good information and basically tried to rush me out of there. I got another opinion at a different doctor the next day. I had broken both bones in my ankle and tore every ligament. They said they couldn't believe this was unnoticed at previous hospital. I appreciate all the people that did there best to help me and did so with a great attitude, but for the couple people that didn't it ruined my whole experience, as well as waisted my time!


text:
JavaScript 를 사용할 수 없습니다.일부 콘텐츠가 정상적으로 작동하지 않을 가능성이 있습니다.
Full-time Non-tenure Track English Lecturer
The School of Language EducationGyeongsang National University (GNU), Jinju, the Republic of Korea
The School of Language Education (SLE) at Gyeongsang National University is currently recruiting resourceful, culturally sensitive, academic professionals seeking creative input within a diverse ESL programs. Responsibilities include teaching up to 372 teaching hours per semester in GNU's general English program for undergraduate students or SLE's conversational English programs for students and adults; contributing to and participating in curriculum and program development, textbook writing, e-testing and assessment, student advising and support activities.
• Possible nationalities
: American, Canadian, British, South Republic African, Ireland, New Zealand, Australian
• BA diploma from a reputably accredited university(at least)
• Only for those who are currently residing in Korea
• Master's or Doctoral degree is an asset.
• Majors on English education, Linguistics or Education is an asset.
• Relevant certificates on English education is an asset.
[Duties & Responsibilities]
• required to teach 372 hours per semester(6 month) - About 20 hours per week
• prepare and deliver classes and collaborate with co-workers to develop the
program content, program delivery, and teaching methodology
• participate actively and contribute meaningfully to work
- group/committee/project/task assignments
• contribute to student evaluation, counseling, and support operations
• contribute to e-testing, assessment design and administration
• contribute to curriculum development and textbook writing
• complete any other responsibilities assigned by administration
- Proofreading works / Kids Camp / Government Funding special courses
[Place of Work]
• Tongyeong Campus(경상남도 통영시 천대국치길 38 경상대학교 해양과학대학)
• Salary commensurate with degree(BA, MA, Ph. D) and major(Education, Linguistics)
• Starts 2,150,000 - 2,300,000 won per month(pre-tax)
• Six-month initial contract, starting from the end of August, which is
renewable upon re-application in accordance with GNU's fiscal year
• paid one-way air ticket.(once completing the contract successfully)
• Furnished accommodation in accordance with GNU Policies
• Paid Vacation(3 weeks per semester)
• Health Insurance, national Pension, severance pay, overtime pay in
accordance with GNU Policies
[Required Documents]
1. Application Form(See attached)
2. Current Curriculum Vitae/Resumé
3. Cover letter with teaching philosophy
4. A sample lesson plan showcasing one of the following; a basic lesson, an intermediate lesson or an advanced lesson
5. Scanned copy of earned credential--degree certificate
6. Recommendation letters from three references are assets
7. Scanned copy of Passport
8. Any additional documentation that you feel is relevant to your application
(Ex. TESOL or ESL certificate)
[To Apply]
Please submit all of the required documents to email@example.com The application deadline is 4 pm of June 15th . Applicants have to do 10 minutes of open lecture(PPT) on the sample lesson focused on a certain level(Basic, Intermediate or Advanced) and 10 minutes of interview(Attendance is mandatory.)
- Open Lecture & Interview : June 21st(2 pm ~)
- Result Notification : June 23rd
For further information contact :
Gwang-Hun Kim
Program Administrator
The School of Language Education, Gyeongsang National University
- Tel: +82-55-772-0728
- Mobile: +82-10-4845-7353
- Email: email@example.com
- Address: SLE(Bldg.#29), Gyeongsang National University Jinju-daero 501, Jinju,
Gyeongsangnam-Do, South Korea 660-701
June 13th, 2017
The School of Language Education
Gyeongsang National University
For more inqueries
- http://www.gnu.ac.kr/program/multipleboard/BoardList.jsp?groupNo=10303
- http://english.gnu.ac.kr/main/


text:
Physician Care Guides are not only your navigators, they are also your advocates.
Did you know your values and goals don't always determine the health care you receive in our current health care system? You may not fully understand your options, or you may not be aware of alternatives. Our Care Guides help ensure that the health care you want is the health care you actually get.


text:
Holy Crap
Since we've opened 2phatgeeks.com in early March of this year, we've seen quite a bit of growth. Today we hit the big one thanks to some kind Stumbler who thumbed up: Two phat geek's simple secrets to a happy marriage.
(Originally, when this post was made, we had 2, 281 views) Now it's 1, 907 for that single post alone, and 2, 126 views in two days. WOW. That's amazing traffic for our little corner of the internet and we thank you from the bottom of our hearts.
In celebration of growth, we've decided to change the layout of 2phatgeeks to a different template from one of our most favorite (among many) designers. This one's called DailyPress and it's by Jai of Blog Oh! Blog fame.
Why'd we change the layout yet again?
Yeah, we know. Three layout changes in nine months or so, must be driving our readers batty! But, there's a reason! While BlueWeed by Blog Oh! Blog is a sweet ass layout, we were finding now that we'd decided to venture out into trying to make a little more money with 2phatgeeks that the arrangement wasn't working. We had one big giant recent post pushing the sidebar, ad spots, blog roll and categories down the page making you, the viewers, have to scroll to the center of the earth to find them. Not fun. So we decided to chose a pretty swanky layout that wouldn't make you guys have to climb Mount Posterest in search of info, and of course, to give our interested advertisers prime real estate.
We love you and want to squeeze you and even call you George.
So in thanks for your patience, your loyalty, and your continued visits to 2phatgeeks.com the first 10 to comment to this post will get themselves a free link in our links page!
We love you guys for sticking with us! Thanks so much!


text:
Espace pour la vie
Main menu
Skip to primary content
Skip to secondary content
Why commit
to biodiversity?
What is biodiversity?
The 1000 Days players
1000 Days for Sedna IV and Space for Life
Our scientific communicators
Marie-Odile Noël
Marie-Ève André
Jade-Anaïs Généreux-Gamache
Daphné Laurier-Montpetit
Marika D'Eschambeault
Jean-Guy Trussart
Sophie Tessier
Évelyne Daigle
Biodiversity research
Our researchers
Behind the scenes at the base Camp
The creators of base camp
The artists and artisan
Become an Ambassador
for the Planet
The Ambassadors' movement
Presentation of the actions
Research Showcase
at Espace pour la vie
Live the experience
Presented until 2015
At the Biodiversity Centre
in the Montreal Botanical Garden
View hours
Summer 2013 rates
Including the Botanical Garden, the Mosaïcultures Internationales and the Insectarium
View rates
Educational activity
Your school at Base Camp
May 19 to June 13, 2014
9:30 a.m. & 11:00 a.m.
Activities at Base Camp
During Gardens of Light,
from September 8 to November 2,
Base Camp is open
from 5 p.m. to 9 p.m.
Latest blog posts (in French)
© All rights reserved
Contact us


text:
Sleepy Bum by RobbieFTTWatch
©2013-2017 RobbieFTT
I could not resist drawing something for butt month, I'm sorry!
I like the jigglypuff print!
Could you make a dry version?
so cute im so jelly
so adorable, cute diaper
Pity; won't get back to the house to draw until Butt Month's over. Guess I missed it. Couldn't be as cute as this, though. ^^
butt month?
It's just a silly little thing started by ~RFSwitched earlier this month so yeah, you have him to blame for all the recent cute
Look at that adorable baby butt! X3
absolutely adorable<3 great work~!
Aww! how cute! Petunia is so adorable!!
Aaaand we just hit the Diapbeetus mark in the cute factor.
Adorable pic! And.....wait, is that Buttons? I think that's Buttons.
Adorable pic! And.....wait, is that Buttons? I think that's Buttons.
This month is turning out to be a cute month for artings!
Cause this isn't cute
No, not at all
Nope *Dies*
No, not at all
Nope *Dies*
Why did you blur the bottom of her diaper?
It's supposed to show that the designs are fading in other words she wet herself.
Too cute for words.
DAWWWW!!! So adorable!!!!!
Eww! Looks like she needs to replace her paci :3
Well, the paci's nipple never touched the ground, so I'd say it's fine. ^^
awe so cute. Looks like someone is going to need a nice diaper change when they wake up if that wetness indicator is any clue.
Dawwws! Sleepy baby.
awwww cute X3 bye bye jigglypuff


text: Although Vico (1668-1744) lived his whole life as an obscure academic in Naples, his New Science is an astonishingly ambitious attempt to decode the history, mythology and law of the ancient world. It argues that the key to true understanding lies in accepting that the customs and emotional lives of the Greeks and Romans, Egyptians, Jews and Babylonians, were utterly different from our own. In examining these huge themes, Vico offers countless fresh insights into topics ranging from physics to (poetic) politics, money to monsters, and family structures to the Flood. Deeply influential since the dawn of Romanticism, the New Science even inspired the framework for Joyce's Ulysses. This new translation makes it clear why this work marked a turning-point in humanist thinking as significant as Newton's contemporary revolution in physics.


text:
coal mining work force
Underground Coal Mine Jobs in IL (Hiring),Illinois ...
IL Underground Coal Mine jobs & employment: search 356 Underground Coal Mine jobs in Illinois on Jobs2Careers.Read More
Workforce WV hosts job fair for miners,WBOY.com: Clarksburg ...
Workforce West ia hosted a job fair for unemployed miners Tuesday. Recruiters from several colleges visited Southern West ia Community and Technical College to give people job opportunities outside the coal industry.Read More
Underground Coal Miners Jobs,Simply Hired
83,405 underground coal miners jobs available. Find your next underground coal miners job and jump-start your career with Simply Hired's job search engine.Read More
Coal mining,Wikipedia, the free encyclopedia
The goal of coal mining is to obtain coal from the ground. Coal is valued for its energy content, and, since the 1880s, has been widely used to generate electricity.Read More
Emerging Workforce Trends in the U.S. Mining Industry
Emerging Workforce Trends in the U.S. Mining Industry By Clifford N. Brandon, III Automated Systems Alliance Inc. January 2012 for The Society for Mining, Metallurgy and ExplorationRead More
coal mining work force
Usibelli Coal Mine, Coal Energy. Coal is Alaska's most abundant energy resource. There is more contained energy in Alaskan coal than in all the combined oil and natural gas in Alaska.Read More
Coal Mining Jobs, Employment in West ia,Indeed.com
21 Coal Mining Jobs available in West ia on Indeed.com. one search. all jobs.Read More
WV Mining Laws and Regulation Updates
Some of the regulations have been processed through several versions to see historical versions of go to our regulation archives page. Note ... WV Board of Coal Mine Health and Safety (2008) Responsibility for Care and Maintenance of Equipment Final Rule: ...Read More
Mining-Regulations Which Contain Standards or Requirements ...
Regulatory Basics Initiative Program Reports in Regulations Bureau of Mining and Reclamation . The evaluation and recommendations in this report are intended to stimulate constructive discussion of how Pennsylvania's environmental requirements can be made more effective.Read More
JSPL suspends work at Australia's oldest coal mine
Jindal Steel and Power Ltd (JSPL) today said it is suspending work at the Australia's oldest coal mine, Russell Vale Colliery, due to "significant financial losses" and "operational difficulties".Read More
History of coal miners,Wikipedia, the free encyclopedia
Coal miners have been hard at work for centuries, but they became increasingly important during the Industrial revolution when coal was burnt on a large scale to fuel stationary and locomotive engines and heat buildings. Owing to coal's strategic role as a primary fuel, coal miners have figured ...Read More
Small-scale Mining in Indonesia,IIED pubs: home page
Work Force 9 Characteristics of Miners 10 SSM Illegal Mining Operational Costs and Revenues 10 ... Coal mining Tin mining Other sectors includes industrial minerals such as zeolite mining, kaolin clay mining, andRead More
NORTH ANTELOPE COAL MINE,Campbell County School District
POWDER RIVER COAL COMPANY GILLETTE, WYOMING NORTH ANTELOPE COAL MINE. This page was created by Samantha Bartow, Lakeview Elementary School. North Antelope Coal Mine opened in 1983.Read More
Coal Mine Health and Safety Act 2002,NSW Legislation
Coal Mine Health and Safety Act 2002 No 129 Status information Currency of version Historical version for 1 January 2012 to 23 June 2013 ... Division 3 Inspections on behalf of work force Subdivision 1 Site check inspectors 157 Site check inspectors 66Read More
Ventilation in Underground Mines,Ventilation,TechnoMine
The best work on the history of mine ventilation I found is by Reed and Taylor: ... Sub-surface and mine ventilation: ventilation design, airflow estimation, fan, ... Timko and Derick of NIOSH and Twentymile Coal Company in Determining the Status of Mine Atmospheres ...Read More
Mining and Geological Engineers : Occupational Outlook ...
Mining and geological engineers design mines for the safe and efficient removal of minerals such as coal and metals for manufacturing and utilities.Read More
U.S. Department of Labor -- History -- The Coal Strike of ...
The Coal Strike of 1902 Turning Point in U.S. Policy. The Federal Government, with the Commissioner of Labor in a fact finding role, acted as a 'neutral' forRead More
coal mining work force
KY Coal Facts,KY Employment,Kentucky Coal Education ; The Kentucky coal mining industry has a current work force of approximately 17,959* people directly employed in coal mining jobs.Read More
Industries at a Glance: Mining (except Oil and Gas): NAICS 212
Industries in the Mining (except Oil and Gas) subsector primarily engage in mining, mine site development, and beneficiating (i.e., preparing) metallic minerals and nonmetallic minerals, including coal.Read More
coal mining work force
Coal and jobs in the United States SourceWatch. In 2006, there were 82,595 people employed in coal mining in the ... Basin), and has dramatically cut its workforce in Appalachia.Read More
coal mining work force,Newest Crusher, Grinding Mill ...
coal mining work force , mining application . Colombian coal workers vote to strike at BOGOTA (Reuters),Colombian coal workers voted on SaturliCGMne to strike over pay and working conditions at the 3 ...Read More
Next Post: Mining Equipment Cost Indices


text:
Any idea can be invested but only if it is backed by a wonderful business concept, efficient team and clear vision. With rising opportunities it is important for an entrepreneur to understand and evaluate himself if he is ready for the funding. To understand better we will address this time crucial aspects like:
• What do investors look for?
• Mapping the start-up life-cycle with Investment needs.
• Different modes of funding available.
• Choosing the right investment for your business.
• Primer on Valuations.
Knowlarity Communications Pvt. Ltd,
Amsoft Business Centre, Unitech Trade Centre, Near Park Plaza, Sector 43, Gurgaon, India – 122001
For more Info & Registration: http://chaiiandelhi.ayojak.com/
Entry Fee: Rs. 750 Limited seats, on first come first serve basis.
For further assistance please contact:
Sunil: firstname.lastname@example.com, Cell No. +91-9650021006


text:
I'm in a hurry to get this photo album done for someone I work with, but finding it a challenge with my wrist in a splint. This is the first page of the book. I used Hello Kitty fort cartridge. The paper is K&C "Snuggle Bug" collection. I will post more as I get them done. Take care,
The colors are washed out in this picture, looks much better in person.=)


text:
Are you planning a summer safari? Outstanding value for money, best safari special in Africa with great saving, no single supplement and 50% discount for kids between 6 – 14 years of age. Botswana safari, Namibia safari, South Africa safari, Malawi safari and Lake getaway, Zambia Victoria Falls and Zimbabwe Safari so don't miss it!
This is a crazy safari deal for those who get in quickly. Choose from six different countries and 23 different camps. Mix and match, save over a third of the price on a five star, fully inclusive (excl Malawi & South Africa where drinks are extra) safari experience.
Ideal for couples, single travellers (as there is no single supplement except again in Malawi & South Africa) and families or groups of friends seeking the ultimate safari in Africa this summer.
We've built an entire page dedicated to this one special and you'll find example itineraries and costings to entice. Get in touch so we can create your dream safari holiday for this summer.
You can travel from 10 November until 20 March 2013 excluding Christmas and New Year Period, 20 Dec – 10 Jan. With unprecedented flexibility in itinerary design, allow Encompass Africa to design your ultimate safari experience.
Summer Safari Specials
- 6 night Botswana Classic from US$2,910 per person fully inclusive or 8 night Botswana Classic with Victoria Falls add on from US$3,925 per person fully inclusive. See full itinerary.
- 6 night Botswana Luxury from US$3,420 per person fully inclusive or 8 night Botswana Luxury with Victoria Falls add on from US$4,435. See full itinerary.
- 9 night Best of Botswana Classic from US$4,446 per person fully inclusive or 11 nights Best of Botswana Classic with Victoria Falls add on from US$5,465 per person fully inclusive. See full itinerary.
- 11 night Best of Botswana & Zimbabwe Classic from US$5,259. See full itinerary.
- 6 night Namibia Adventure from 29,745 Rand per person fully inclusive. See full itinerary.


text:
The count of monte cristo:
Posted in the Louisville Forum
1 - 1 of 1 Comments Last updated Nov 1, 2007
"Stand up Against Tyranny"
Since: Aug 07
#1 Nov 1, 2007
The count of monte cristo:
(French: Le Comte de Monte-Cristo) is an adventure novel by Alexandre Dumas, père. It is often considered, along with The Three Musketeers, as Dumas' most popular work. The writing of the work was completed in 1844. Like many of his novels, it is expanded from the plot outlines suggested by his collaborating ghostwriter Auguste Maquet.
The story takes place in France, Italy, islands in the Mediterranean and the Levant during the historical events of 18151838 (from just before the Hundred Days through the reign of Louis-Philippe of France). The historical setting is a fundamental element of the book. It is primarily concerned with themes of justice, vengeance, mercy, and forgiveness, and is told in the style of an adventure story.
Dumas got the idea for The Count of Monte Cristo from a true story, which he found in a memoir written by a man named Jacques Peuchet. Peuchet related the story of a shoemaker named Pierre Picaud, who was living in Paris in 1807. Picaud was engaged to marry a rich woman, but four jealous friends falsely accused him of being a spy for England. He was imprisoned for seven years. During his imprisonment a dying fellow prisoner bequeathed him a treasure hidden in Milan. When Picaud was released in 1814, he took possession of the treasure, returned under another name to Paris and spent ten years plotting his successful revenge against his former friends. The plot of this tale of revenge turns on a acient French legal gizmo called (lettre de cachet) literally meaning, a letter of hiding.
The United States as of 2006 are now using this very same legal devise,that have been utterly discredited and centuries thrown on a shelf. This is not about illegal aliens or foriegn residents-this applys to the citizens of the United States of America. At any moment, the President can-without any evidense, and without following any rules of procedures declare any of us to be a danger,"enemy combatments", a discription for which no legal definition excists. Here is a name I'm sure you all have heard "Jose Paddilla", This American citizen was approaching his 5th year in prison by 2006. His first 21 months, he was NOT informed of the charges against him. The Federal Government who held him in their custody elected to ignore the Habeas Corpus guarentees that are in place in this country when we were British subjects. With Congress passing the Bush screw America and its principles "Military Commisions Act", Congress codified that very practice and tossing a 1000 years of Anglo-Saxon criminal jurisprudense out the window. God Bless the U.S.A.(sigh)
Because not many of us were helping Ole Bin Laden in Afghanistan this may not cause any of your panties to get in a wad.
"To those who scare pease-loving people with phantoms of lost Liberties. My message is this: Your tactics only aid terrorist; for they erode our national unity and diminish our resolve. They give ammunition to America's enemies, and pause to America's friends."
Attourny General John Ashcroft, December 5th, 2001
Having knowledge of what was quoted above, any one who mentions lost liberties is considered by George Bush's Attourney General to be guilty of helping terrorist. As the law was written and signed by Bush anyone can be deprived of Heabus Corpus protections by being held in prison without access to a lawyer, without the right to confront their accusers, without the right to a trial and last but not least without even knowing the charges that are against you. God Bless America
The entire process is closed, secret,not open to the public's view. This reminds me of the Star Chamber court, abolished in England in 1641. Freedom my friends has literally been catapolted backwards centuries. The law proffesors of today will tell you that nothing like this has been known in the west since before King John was forced to sign the Magna Carta in 1215.
Tell me when this thread is updated:Subscribe Now Add to my Tracker
Add your comments below
Louisville Discussions
|Last By
|Vince Gill
|7 hr
|Real truth
|Last Post Wins (Mar '11)
|8 hr
|Trump for President, He will win. watch (Aug '16)
|9 hr
|Common Sense
|Is Cody Lane still in Louisville?
|13 hr
|Lester bolles of the jeractors
|18 hr
|Where to find women who just want to sleep around
|Looking for luv
|Hey, I'm a racist (Dec '11)
|New to louisville
Find what you want!
Search Louisville Forum Now
Copyright © 2017 Topix LLC


text:
CCTV camera work on Upper Hunter Shire Council's sewer pipes is scheduled to take place between Monday 30 January and Friday 10 March 2017 in Aberdeen and Scone to help plan our maintenance, sewer pipe renewal and relining. Works will occur between the hours of 7.30am and 6.00pm by Council's contractor Namits.
Alan Fletcher, Council's Director of Infrastructure Services said this work will assist Council is keeping the sewer mains clear and help protect properties from future sewer system interruptions.
"Work includes the cleaning of sewer mains with designed 'pressure jetting' equipment which is used universally among water authorities.
"This procedure can create an air pocket causing a backflow of water and it can remove water from air traps causing odour to emanate from domestic drainage," Mr Fletcher said.
On weeks beginning Monday 30 January, Monday 6 February, Monday 27 February, and Monday 6 March, work will occur in parts of:
Aberdeen – McAdam Street, Nandowra Street Gundebri Street, Hall Street, Dart Street, McQueen Street, Abercarney Terrace, Moray Street, Segenhoe Road and Graeme Street.
Scone – Gray Street, Main Street, Kelly Street, Park Street, Gundy Road, Waverley Street, Short Street, Dangar Street, Bingle Street, Scott Street, Stafford Street, Little Street, Carlyle Street, Barton Street and Oxford Road.
Effected properties will be advised by letter.
For further information, please contact Andrew Brown, Upper Hunter Shire Council's Engineer of Water and Waste Distribution on 02 6540 1100.
Andrew Brown
Engineer of Water and Waste Distribution
Upper Hunter Shire Council
02 6540 1100
Upper Hunter Shire Council is a local government authority and provides an extensive array of services including health and building; town planning; aged care; sporting and recreational facilities; roads; libraries; garbage collection; airport facilities; saleyards; public venues; water; children, youth and families and tourist information.
PO Box 208
Scone NSW 2337
Phone: 02 6540 1100
Fax: 02 6545 2671
135 Liverpool Street, Scone
34-40 Vennacher Street, Merriwa
47 Mayne Street, Murrurundi
After hours emergencies for roads, bridges, animal control,
water, sewer & landfill
Phone: 02 6540 1199


text:
Team Scorpion's simple job at the Los Angeles Natural History Museum turns deadly when they discover thieves robbing a rare gem exhibit in order to get materials needed to enrich a nuclear bomb.
This is Scorpion and you are watching TVZion
Please wait for 3 seconds, we are loading Scorpion stream.
Please enter captcha to continue to video.
If the above stream is offline (saying We are sorry!),
please click on the "Refresh Link" to get a new streaming link. Don't worry it'll just take a second.


text:
World governments have never seriously invested in the development of safer and sounder energy sources with the goal of replacing dangerous existing ones. Will they now?
sort by best latest
In the long term everything will always revert back to capitalism over ecology. However, whilst the world attention is on the crisis in Japan let's get them to pay attention now.
I have put some very good reasons why they need to take notice of the current plight that I am personally experiencing over here in Japan. If you only read one article on my hub then read the aftermath one because if this does not get addressed sufficiently there is going to be more problems which will echo the devastation of the tsunami on the eastern coast. Not only in Japan but globally.
You can help the HubPages community highlight top quality content by ranking this answer up or down.
I doubt that the worlds government leaders for the most part can do much of anything without having a considerable degree of control over what is being manufactured and why!
Many of us believe that in order for the government or, we the people have the right to control how we as a people produce the goods and services we need and to limit the freedom of private enterprise in order to prevent corporate takeover of our government which we call fasism while at the same time utilizing private enterprises need to be frugle in it's business dealings in order to kept it going and use it's profits to improve upon it's increased production of goods and or services.
That said Energy cartels who some say have bought up many energy inventions in order to keep them off the market as well as the politicians they contribute campaign funds to and the lobbyists they pay are all not willing to give up that money from the increase in the cost of energy we pay for as well as all the taxes the government gets and the profits they bring the energy corporations in order to bring out new technologies that would compete with their current energy production.It's like telling them you need to make less money.How many corporations do you know that are willing to do that?
You can help the HubPages community highlight top quality content by ranking this answer up or down.
This is a really good question and hopefully, some consideration will be made, but I tend to doubt it. It seems that even after Three Mile Island & Chernobyl, all the nuclear industry did was create more "fail-safes", which may address certain issues, but don't speak to the basic dangers of this energy source. Let's face it, the BP spill in the Gulf of Mexico did NOTHING to change the oil industry and the reverberating effects of that tragedy will last for decades. GREED & corruption trump safety and human lives.
You can help the HubPages community highlight top quality content by ranking this answer up or down.


text:
Users interested in Jmicron hw raid manager download generally download:
JMicron HW RAID Manager is a free program that allows you to configure the 4 and 8 Bay Raid. The program has a Basic Mode in which you can see the Raid and Disk Information, the event logs and you can make a simple Raid configuration. It also offers you an Advanced Mode in which you can set the Raid stand by timer and you can encrypt the disk.
Additional suggestions for Jmicron hw raid manager download by our robot:
No exact matches found for "jmicron hw raid manager download". Results for similar searches are shown below.
JMB38X is product family that includes 1394a OHCI and Memory Card Reader.


text:
Lecturer: Prof. Tyler Jacks
OK. I think we'll get started. So we're going to continue our discussion today about viruses, finish talking about influenza, influenza A virus and the flu, and then talk a bit about HIV and AIDS. Do you guys know more about the tutorial session and so on and so forth for next week? Has that been decided yet? OK. So you'll get more information Monday and Wednesday. And I'll also have an office hour, probably a couple of office hours at the end of next week. Most likely, if it doesn't conflict with this tutorial session that's being planned, it will be during this hour from 11:00 probably until 1:00 in this room because it's free since we're usually here. But that may conflict with you guys so we'll have to see. I'll let you know on Monday. So, again, the situation with viruses is an ongoing one. And, actually, one of you brought to my attention an outbreak of polio that's happening now both in Africa and Indonesia. This is actually from today's CNN. om where there's a fear that polio is starting to spread. In this case in Jakarta, in Indonesia. And there's a very extensive reaction to this. There's a great fear that polio will spread. This is an area that is not well protected currently by polio vaccination. And so if you look at this you'll see that they are raising lots of money in order to try to vaccinate with standard polio vaccines, which work extremely well, 5.2 million children, to try to stop the spread of this potential epidemic of polio. It hasn't reached anything near those levels to be that concerned, but in order to protect against that possibility they're going to vaccinate. And, obviously, if you vaccinate, individuals cannot be successfully infected. If they cannot be successfully infected, the virus cannot propagate so they cannot pass it on. So you just close off the infectious cycle in a very small circle of infected individuals. Also, in today's Globe, there was a discussion of a local company that makes vaccines against smallpox. And I've mentioned to you that smallpox is largely eliminated, if not fully eliminated in the world, but there are stocks of smallpox in freezers around the world. And there is a concern that an individual could access smallpox virus or make one because the relevant sequences of the genome of the smallpox virus is known. And so, in theory, you could synthesize your own smallpox virus genome, and thereby create your own smallpox virus and expose now unprotected individuals because we don't get vaccinated currently against smallpox. And so there are companies like this one that are making currently and distributing smallpox vaccines. They distributed 182 million doses in this country alone just in case somebody tried to deliberately release some smallpox. So that's what we can do when we know what we're dealing with. We can create effective vaccines. In this case they're effective, but sometimes we get exposed to stuff that we cannot effectively deal with. And I introduced this to you last time. This was the major flu pandemic from 1918. Some people worried that there might be another pandemic this year because in the off season between 1918 and 1919 when this happened, and 20 to 40 million people died, that's when the Red Sox last won the World Series. [LAUGHTER] So the Armageddon folks thought maybe this was the year, but so far so good. So, as I mentioned last time, this was a major outbreak and a major problem worldwide. But you also should know that influenza is an annual problem. And I, for one, didn't appreciate this. Where there are about 25 thousand deaths per year in the United States. And, of course, to deal with that we make available, especially to the elderly and infirmed immunodeficient flu shots. And flu shots are simply flu vaccines. And I'll tell you a little bit about how they're made towards the end of this section, but they're generally effective in combating against the flu that is going to hit the population that year. And they change every year because, as you'll see, flu changes all the time as well. So it's an annual problem. There are occasional epidemics which you could think of as -- -- population-based infection where many individuals within a particular population are infected. And the virus, in this case, is spreading throughout that population. And there are even more occasional pandemics. And that's a worldwide infection. Where, because of the virulence of the virus and its ability to access different populations and the absence of immunity throughout the worldwide population, lots and lots of people get infected. And that's what happened in 1918. So how do we explain this? How do we explain the occasional epidemics of a virus that we're so familiar with? Flu, as I said, we get every year, lots of people get it every year. And, yet, we seem to be susceptible year after year. So why is that? What causes the resistance to this immunity in small measure and in large measure? And that's what I want to review for you today. So this is the responsible agent. It's a virus, of course. More specifically, it's an enveloped virus, which means it has its own lipid bilayer that it picked up from the host cell. And you'll notice on the outside are things sticking out of the bilayer. These are proteins encoded by the virus which are going to be responsible for binding the virus to the host cell. And also allowing the viral membrane to fuse with the host cell membrane. And you'll see that that's done in the case of flu virus in a slightly different way than for some other viruses. And then inside you have the capsid. And wrapped up in this protein, this helical protein structure are the nucleic acids of the virus. And the nucleic acids of this virus are multiple. That is it's not just one. Oops. It's not just one. It's actually several. So, again, it's called influenza A virus. It's an example of an enveloped virus. And I said you should note the envelope proteins, which are largely encoded by the virus itself. And we call these envelope glycoproteins. Glycoproteins because when they emerge through the sorting pathway of the cell they pick up sugars. And so when they're on the outside of the cell, it's not just protein. There is some sugar there, so glycoproteins. And sometimes the antibodies that we make are directed against the sugar moieties alone or in combination with peptides. So the envelope glycoproteins are important. As I said, it's a segmented RNA genome, which means that there are multiple distinct nucleic acids in the viral particle. And in the case of flu there are eight. The RNA genome is single-stranded. And all of the genome segments are in the minus configuration. So their sequence is the complement to the mRNA. OK? And we talked about the significance of RNA viruses that have a minus strand polarity in the sense that they need to have their own RNA polymerase coming in with the virus in order to help, in order to initiate the replication cycle. So, hopefully, that's familiar from last time. This is a diagram of the virus, and it just makes the same points I just made. So, again, it has a lipid bilayer. It has envelope glycoproteins sticking out from the surface. You'll see that they're important for different things in a moment. Inside that is a nucleocapsid which surrounds the nucleic acids. And you can see that there's a series of nucleic acids that are enclosed within this. And, again, there are eight of them. And they're all minus strand. And, importantly, contained within here is a protein, an RNA dependent RNA polymerase, the yellow dot. And it has to get incorporated with the virus so that when the virus infects it goes in there, too. And it can then act on the RNA genome and convert it into a plus strand, which will then serve both as the RNA for translation, as well as the template for the production of more of the minus strand RNA. OK? So this comes from your book, and it is a summary of the infectious cycle of this virus. I've modified it a little bit because some of the details which I think are important were missing. So you might want to pay attention to this figure as you're reading the section, the relevant section in the book. But this is a typical viral lifecycle. The virus attaches. Remember, the terms that I used last time? The virus attaches. Here one of the viral glycoproteins binds to a protein on the surface of the target cell. That then initiates an internalization process, a penetration process in which the virus gets brought in through an endosome. So it gets brought in through a separate vesicle, an endosome. That vesicle, the endosome then fuses with a lysosome, not shown here. And you may recall that the lysosomes have very low pH. And it's in the context of the low pH that one of the viral glycoproteins changes its shape. And when it changes its shape it allows the viral membrane to fuse with the membrane of the lysosome. So this is a pH-dependant protein conformational change which turns an inner protein into a protein that facilitates fusion. And when that happens, the viral capsid can then slip out into the cytoplasm. It gets unpackaged. The RNA, which is the minus strand RNA gets released. And then it gets acted on by that RNA dependent RNA polymerase that came in and gets converted from minus strand to plus strand. And the plus strand can then do two things. It can get translated into viral proteins, both the glycoproteins that go through the sorting pathway and make it to the membrane, as well as the structural proteins that form the capsid. The structural proteins then join up with the viral RNA segments, now the minus strand RNA segments. They meet at the membrane and then bud off to form a new virus. OK? So this is a standard infectious cycle for this class of viruses. And because it's going to be relevant later, I just want to emphasize a couple of points. Through interactions between the cytoplasmic tail of the envelope glycoprotiens, the capsid proteins coalesce underneath the plasma membrane. And there's an interaction between these proteins and the tails of these proteins which causes the virus to start to bud off the surface of the cell. Now, there are separate interactions with the proteins on the inside of the capsid which bring with them the different viral RNA. So remember there are eight. And there's a rather amazing process by which the eight distinct RNA segments get brought together into the capsid, and then the capsid goes to the membrane and gets budded. So there is a sorting process, which we don't fully understand, that ensures that viruses get at least one copy of each of the genomic segments. And that's necessary because if a virus doesn't have all eight, when it gets into the host cell that it might infect, it's not going to be able to replicate. These RNA segments encode one, or at most two of the viral proteins that are necessary for the infectious cycle that's drawn up there. And you'll see why that's important in a moment. OK. So we get infected, we develop antibodies against the proteins of the virus, and we typically develop them against the glycoproteins that are sitting on the outside. We develop T cells that can recognize virus infected cells and kill them. And yet we keep getting flu. So why is that? How is it that we can, how is it that the virus can overcome this immune resistance? And the answer is that the virus changes. And this is a major problem with all viruses, but it's a particular problem with RNA viruses and a particular problem with flu. So here's a depiction of the virus again. It's got its genomic segments in here. And on the surface it has these glycoproteins. And I'm going to draw a little bit more detail in these glycoproteins now. There are actually two distinct glycoproteins on the surface of the cell. There's one that's called HA and there's another that's called NA. And they carry out different functions. When you get infected, your immune system sees these epitopes sitting on the surface of the virus and you make antibodies against them. And there are three particular places on these proteins where good antibodies can be made inside your body. One of them is here, another one is here, and a third one is here. And different people make different of these antibodies. And these antibodies that are made have a name which is neutralizing or blocking antibodies. They're called that because if you have one of these antibodies, and it will bind to the surface of the viral particle, this virus can now not infect the cell. There's an interference between the, what the hell? Between the glycoproteins on the surface and the receptors to which they bind by the antibody. So they block binding. And if you cannot bind you cannot infect. And this is very efficient. This works. So that's how you can overcome the infection to that particular virus. The problem is that viruses change. During their replication there are mutations. And sometimes these mutations affect the structure of the proteins that are sitting on the surface. So you might imagine the strain here gives rise to variant here which has an HA protein which looks more or less the same, but it has an NA protein which has changed. So now this epitope, which was recognized by antibody three, cannot be recognized by antibody three because it's got a difference sequence. OK? If you were a person who made predominantly antibody three in response to this infection, you would not be susceptible to this virus. So if this one came along next year you'd get the flu. If you were a person who made antibody one or antibody two as your major protective antibody, you'd still be resistant to this. You'd be one of the lucky ones. And because there's heterogeneity within our population, even if these new variants arise, they don't spread all that much because there are enough people in the population who are pretty well protected. So those are low-level spread or low-level epidemics. OK? Now, this process, one day I'm going to figure out how this works. This process of generating variant viruses through this mutational mechanism is called antigenic drift. It's a slow drift of the antigens on the virus. And it happens because the virus is highly mutagenic. And it's true of RNA viruses in general. And there are two reasons why RNA viruses create variants at such high levels. One is that RNA is less stable than DNA. Remember, there's a difference in the structure of RNA versus DNA. There's an extra hydroxyl in the structure of RNA which can cause increased mutation, increased breaks and base substitutions in our RNA molecules compared to DNA molecules. So RNA is inherently less stable than DNA. And also RNA polymerases lack proofreading functions. Which means they have an inherently higher mutation rate. And hopefully, again, this is familiar from our discussions about DNA replication. All polymerases make mistakes but your DNA polymerases have what's called a proofreading function which can recognize the mistakes and correct them. RNA polymerases lack that, and so they make the mistakes and they stay as mistakes. So the mutation rates for RNA polymerases are at least ten fold higher than for DNA polymerases, and in some places even higher still. OK. So that's what's called antigenic shift, sorry, antigenic drift. And it happens all the time and is responsible for why we keep getting mild cases of the flu. But that's not what's responsible for the Spanish flu of 1918. Instead of antigenic drift -- -- these are due to a phenomenon called antigenic shift. Rather than generating subtly different variants, like I've shown up here, this is the process of generating essentially entirely new strains. And it happens in the case of flu all the time. And one of the reasons that it happens is that there are lots and lots of types of flu viruses which are kind of similar that infect other species. There are duck flus, swine flus, horse flus, seal flus that are all caused by versions of this influenza A virus. Similar. Not identical but similar. And sometimes those viruses cross over into the human population. And this is an example of a zoonotic infection -- -- which is an infection from another species into the human population. And actually happens all the time. Many of the new pathogens that arise in the human population arise through zoonotic infection. Now, most viruses that are evolved to grow in the cells of one given species, at the temperature of a given species, will not replicate very well inside human cells. So even if they did infect, they wouldn't reproduce themselves very well. And that would be true of these viruses, too, swine flu virus, bird flu viruses. The problem is, in the case of flu, the human virus is so common and the mechanism of replication of this virus is so complex and amenable to generation of recombinant viruses that we can generate new viral forms. And that's what I want to talk to you about now. So here's an example from not too long ago. This is the collection and culling of a lot of birds somewhere in Asia. I'm not really sure where this was. But there was a concern that a new virus was developing in a bird population and was crossing over into humans. And it caused some deaths. And so to avoid that further they just wiped out some millions of these birds in order to prevent further cross infection. But, again, it's not the presence of the virus, the bird virus or swine virus itself that's the problem. It's the fact that the two viruses, the human virus and the bird virus can recombine to form a dangerous new virus which is rather similar to the human virus but carries some segments of the bird virus. And that's illustrated here, and I'll show you on the board in a second. But basically the idea is that a human virus carrying its eight segments, including the segment for HA and NA infects an animal which also gets infected by a bird virus. So that in the same cell there are the segments for the human virus, as well as the segments for the bird virus. And during this process of the generation of a new viral particle, you can get mixing of the segments so that most of the segments come from the human virus and, therefore, will replicate well in the context of the human cell. But two new segments come in from the bird that encode its HA and NA, a version that's never been seen in the human population. Nobody has antibodies against it so the virus can spread like wildfire. And that's what we believe happened then and we fear continues to happen over time. So, again, imagine a cell which has been infected by two different viruses, the avian virus, in this case it was a duck, as well as the human virus in that given year. In that cell there are going to be lots of different segments of virus RNA, the human ones H1, 2, 3, 4, 5, 6, 7, 8 and so on, as well as the duck ones, duck 1, duck 2 and so on and so forth, duck 7 and duck 8. When the viral capsids coalesce underneath the viral glycoproteins to produce a new virus, they cannot necessarily distinguish between the human and the duck subunits. So there might be human 1, human 2, human 3, duck 4, human 5, duck 6, human 7 and human 8. OK? This then makes a virus which is perfectly able to replicate in human cells because it's got mostly the genes that are optimized for human cells, but it's got new HA and NA forms that have never been seen by the human population. So there is nobody who has antibodies against it. So the virus will spread like crazy. OK? So this is an example of antigenic shift, and it's responsible for these worldwide pandemics. OK. Any questions about flu? One thing I failed to mention, sort of trivial but you probably know, is it spread very well because it can spread in water droplets. If you sneeze on your friends they'll also get the flu. It's a very efficient virus so you don't need very many viral particles to go inside of your respiratory system in order to initiate the infection. And this is another good example. When you have a very active infection inside of you, you start producing lots of the cytokines, that I mentioned last time, like interferons. And, again, it's largely those that are causing the symptoms of the flu, and in large enough quantities can cause death. You can also get secondary infections with bacteria when you're that sick, which can be another reason why folks die. OK. So if there are no other questions about flu, we'll now turn our attention to HIV. And I think HIV is probably fairly familiar as a topic. It's, of course, a major, major worldwide health problem. The initiation of this epidemic goes back a very long way. The first cases were reported in 1975, so about 30 years ago. And so that's considered to be the initiation of this epidemic or pandemic. The first case in the United States is considered to have occurred in 1980. And here's another example. We think that this probably occurred by one of the zoonotic infections. But it happened a long time ago. It happened at least before 1950 because there are samples of individuals who died of unknown causes that have now been tested and can be shown to have HIV sequences by PCR. So whenever this happened, and from whatever species it happened, it happened quite a while ago. Why it then initiated in this epidemic form much later is not so clear. The etiological agent -- -- is a virus called HIV, human immunodeficiency virus. It is a retro virus. And we'll briefly review how it replicated, but I told you more or less how that happens last time. And this was another good example. The syndrome was first discovered in 1975, gained a lot of attention in this country starting in the early 1980s, and the virus was first purified and characterized in 1983. So it didn't take too long to identify the agent and then ultimately sequence its genome. And also to develop tests for the presence of actually not the virus itself. The AIDS test is a test for the presence of antibodies in you that recognize the viral glycoproteins. And this was very important, obviously, in screening populations, screening blood banks and so on for contaminated samples. Now, since this time, in the early 1980s, the situation has, of course, gotten much, much worse. In this country, there are currently -- -- a million people infected with HIV. That's between, you know, one and 300 individuals total. And, amazingly, about 20% of those people don't know it. Worldwide, anybody have any idea how many people are infected with HIV in the world? 40 million. And total about 60 million people have been infected because since the early 1980s, 20 million people have died from this disease. More than 20 million. And the prevalence is remarkable in certain places in the world. In Southern Africa, for example, not the country of South Africa but in the Southern Region of Africa, Saharan Africa, there are 25 million people infected. And in certain countries that's one in four sexually active individuals. Remarkable infection rates. And the effect of this disease and the death that it causes has also had dramatic effects on the population. So that in Zimbabwe, for example, where the life expectancy in 1990 was 52 years old, not a huge number but 52 years old, in 2003, because of AIDS, it's less then 35 years. So it has dramatically affected the lives of people throughout the world. OK. And, as you know, I suspect you know that transmission for this virus occurs through direct contact of contaminated fluids. Sexual contact, which is both homosexual and heterosexual. As well as blood transfusion, direct blood contact, through transfusion, and also needle sharing. And sometimes occasionally organ donation, but that's very, very rare. OK. So people die from AIDS because they develop infections. And we'll talk a bit more about that in a moment. But here's one patient who has developed an infection with a virus, a particular type of herpes virus now called Kaposi's sarcoma virus. That virus then is able to replicate in certain cells of the blood vasculature and cause tumors. These are actually tumors. And this individual will die from a disease called Kaposi's sarcoma, a type of cancer, another example of a virus-associated cancer of humans. And in this country AIDS, as you probably know, has taken over as the leading killer of young male adults. It was not known in the early 1980s, and by 1992, just ten years later had become the major killer of young male adults in this country. And, of course, likewise around the world. So here's the virus. As I said, it's a retrovirus. Retroviruses also are enveloped. They have glycoproteins on the outside, envelope glycoproteins. They have a capsid like all viruses do. They have a genome. The genome is made of RNA. And, as you know, through the retroviral lifecycle, the RNA is converted into a DNA form. We'll go over that next time. And that's accomplished by an enzyme called reverse transcriptase which gets prepackaged with the virus. Again, it has to be there because your cells don't have an RNA dependent RNA polymerase. So this gets prepackaged. The virus then infects cells. And this, again, is a somewhat oversimplification. I'll show you more details in a second. But the virus attaches via glycoproteins on its surface, membrane proteins on the surface of the host cell. In this case it's a familiar protein to you called CD4. That leads to a fusion event. So now at the plasma membrane, which is different from what we saw with flu virus which happened in an internal membrane, at the plasma membrane there's a fusion event. So now the viral membrane fuses with the host cell membrane and the viral capsid can lead into the cytoplasm. There's a little bit of unpackaging that goes on. And then reverse transcriptase, that enzyme that got prepackaged there acts on the viral genome, which is made of RNA and converts it to a DNA form, a double-stranded DNA form which is called a provirus. And that provirus then gets integrated into the host cell genome in a random process, random integration, the host cell genome. This is also accomplished by a pre-packed enzyme called integrase. Once in the genome it gets treated like any old piece of DNA. It gets transcribed into actually multiple different RNAs. They get translated into viral proteins which come together at the plasma membrane and the glycoproteins, the capsid proteins which incorporate the genome, plus the reverse transcriptase, and you make a new particle. OK? So this is more or less the lifecycle. There is some detail that I want to share with you in a moment because it's interesting. This is what it looks like in real life. These are HIV particles budding off the surface of an infected cell. They have a very characteristic electron dense structure. You can actually tell it is HIV from just the way it looks in the electron microscope. And this is an HIV infected T cell. Now, CD4 should have rung a bell that it's one of the proteins on the surface of helper T cells, CD4 positive T cells. That is a major cell of infection for HIV. And here is one such cell infected. And all these little blebs budding off the surface of this cell are viruses getting out. This process actually doesn't itself, the budding process doesn't itself kill the T cell but, nevertheless, T cells, this class of T cells dies. And, actually, that's a critical event in the development of HIV-AIDS, the disease. We'll come to that in a second, but let me first tell you one of the interesting details. The situation is a little more complicated than the figure that I gave you on that slide. There are two glycoproteins on the surface of HIV. One of them is called GP120 for glycoprotein 120. It's linked by a disulfide linkage to another protein called GP41. And we now know that both of these proteins participate in binding and fusion. And on the surface of the infected cell is CD4, as was indicated on that slide. And that is the major viral receptor that is present on helper T cells, CD4 positive T cells. It's also present on macrophages. As well as certain cells in the brain called glial cells. So there are CD4 positive macrophages and glial cells. AIDS-associated dementia, which you may know about, is caused by the destruction of the glial cells in the brain. Now, there's another protein which participates, not so much in the binding but in the fusion event that allows the virus to get in. And this is actually a class of proteins called chemokine receptors. There are actually multiple chemokine receptors on your cells. And, in fact, different HIV forms bind to different of these. But just to simplify, let's say that there is one of these which binds to the GP41 portion. And it's that binding that allows the virus to fuse. If you don't have this you cannot fuse. And, therefore, the cells are not infected. What's interesting about that is two-fold. One, it could represent a therapeutic target. That interaction could be a therapeutic target. But it came to light in an interesting way which was there are people who have been followed a long time who lived in high-risk populations, drug-users or homosexual men with multiple contacts with known HIV infected people who have not themselves gotten HIV. They seem to be naturally resistant to the development of HIV, despite documented exposure to the virus. And they were studied. And when that observation was made it was found that these individuals lack the chemokine receptor. And if you lack the chemokine receptor, you may have CD4 on the surface of your cells but you don't have that critical co-receptor. And so there can be binding but no fusion. So your cells are resistant. So these individuals are naturally resistant to HIV. OK. So HIV infects. It infects a lot of T cells, helper T cells and other cells in the body. Why do you get sick? Well, as I mentioned, people get sick because of the loss, the absence -- During infection, the CD4 positive T cells get eliminated. How exactly they get eliminated, why exactly they get eliminated we don't yet know, but we know that the levels of these cells goes down inside the infected individual. And, as you probably remember, CD4 positive T cells -- -- are required for the development of these cells. So if you don't have CD4 positive T cells you cannot make antibody producing cells. You cannot make functional antibodies. And, to some extent, they're also required for the development of cytotoxic T cells. So that part of the immune system is also compromised. So the virus wipes out these cells and, therefore, the immune system crashes. And that's why it's called AIDS for acquired immunodeficiency. Acquired because it comes through an infectious agent. Immunodeficiency because your immune system crashes. And when your immune system crashes you cannot fight infections. And AIDS patients largely die because they get one or another type of infection. So this is a graph which shows the time course of HIV infection. And it kind of makes the point that T cells go away. Shortly after you are infected, the level of HIV in your blood goes way, way up, as you can see here. It spikes in the first several months after your infection. Some people actually manifest that aspect of the disease. Many don't so they don't know that they have such a high concentration of virus. And, importantly, your body deals with it so you make antibodies, in black. You make anti-HIV antibodies. And, remember, it's these that are detected by the AIDS test. If you've been exposed then you make antibodies. And they stick around so that you know that you've been infected. Likewise, T cells, cytotoxic T cells, CD8 positive T cells go up. And that controls the level of the virus. And it stays low for a while, but after a while, because of the affects on the CD4 positive T cells, the other cells in the immune system are no longer sustained so the B cells start to drop off and the T cells start to drop off. And now you're starting to lose the battle against the HIV, so the levels of HIV go up. And as they go up, you lose more CD4 positive T cells and the situation gets worse and worse. So after a while, usually in the several years out time point, your immune system is now no longer functional and you're very susceptible to opportunistic infections. So AIDS patients will develop infections, and the infections will progress in a way that won't happen in a healthy person. Certain bacterial infections that you would clearly very easily take hold and can cause major problems. Kaposi's sarcoma is caused by infection of this particular virus. AIDS patients are very susceptible to tuberculosis, this particular fungal infection, certain other viral infections. And in aggregate, the exposure to these various infectious agents and the damage that they're causing leads to the death of the patient. OK. So that's bad news. And obviously it's have major and devastating consequences around the world. So what can we do about it? Well, there is some good news here. There are antiviral therapies. Remember that viruses largely use your enzymes. And you cannot make good drugs against your own enzymes for treatment of a viral disease, but I've told you about one viral protein to which you might be able to make drugs. And indeed we have. HIV has an RNA genome that gets converted to a DNA form by an enzyme reverse transcriptase. There have been drugs produced that block that enzyme. And you've probably heard of the drug AZT. There are other drugs like dideoxyinosine and dideoxycytosine that likewise bind to and block the activity of this enzyme. They actually cause chain termination in the same way that DNA sequencing works. And they work because this enzyme is sensitive to these drugs at concentrations where your polymerases are not, so that gives you some selected effect in the treatment of the virus. And these agents, when used singly, work for a while. And then the virus becomes resistant and comes roaring back. How does it become resistant? It becomes resistant through mutation, exactly the way cancer cells become resistant to targeted therapies. Variant forms of HIV arise which have slightly altered reverse transcriptases that now won't bind to AZT or DDI or DDC. And the problem is very, very serious because viruses, RNA viruses in particular are highly mutagenic. They create variant forms at high frequency. An HIV infected person makes ten to the tenth viral particles a day. At a mutation rate of ten to the minus fifth, that would mean ten to the fifth variants of every nucleotide. OK? So variants come up frequently that are resistant to this therapy. Oops. Fortunately, there are alternatives. The viral RNA gets translated into a large polyprotein -- -- which is processed by a viral protease encoded by the virus into different mature proteins. Reverse transcriptase is one of them. The integrase that I mentioned is another. And there are others. This is a viral protein, a viral enzyme. And so, in theory, it's possible to make inhibitors against the protease. And that's been successful. Several companies have made inhibitors that will specifically inhibit the viral protease that work well. They work for a while and then resistant forms arise for exactly the same reason I said. You can create versions of protease which still work but won't bind the drug. OK? So what do you do? Does anybody know what you do to overcome this problem? You put the drugs together. So currently HIV patients, in this country anyway, and hopefully soon around the world will get triple therapy when they're diagnosed. And triple therapy includes two reverse transcriptase inhibitors and one protease inhibitor. Since the development of resistance against each of these agents is independent of the other, to get resistance to all three is the product of the individual frequency. So I said that the frequency of developing resistance to any one is ten to the minus fifth. To be resistant to all three would occur at ten to the minus fifteenth, which is highly, highly unlikely. And so people tend not to develop resistance to all three and, therefore, triple therapy tends to keep the virus in-check for sustained periods of time. As you probably know, this works. The fear is that it is starting not to work. And there are starting to be some resistant forms developing here and they are starting to make their way into the population, so we're going to have to develop even better and more different inhibitors to now combat these variant forms. Before I let you go, the last thing I wanted to mention, and I'll just throw it out there and you can think about it, is that what we'd really like to return to for HIV is what we can do for polio. We'd like to be able to treat people routinely in this country or out in the field in more distant regions with an effective vaccine, which isn't possible today. We don't have one for HIV. You might think about what you would do to make one and why it has been so hard. And I'll touch on that next time.


text:
Product is out of stockContact us for terms of delivery
- Full review from MusicTech
The Adam F5 2-Way Active Nearfield Studio Monitor is a nearfield solution for recording, mixing and mastering music, film, video and other scenarios that require vertical studio audio monitoring.
The F5 features an ART tweeter that delivers extended frequency response up to 50 kHz, resulting in pristine, detailed and accurate high frequencies that are well suited for high-resolution audio of 96 and 192 kHz. The tweeter and mid-woofer are independently amplified with 25W amplifiers driving both the mid-woofer and the ART tweeter. There are balanced XLR and unbalanced RCA connections on the rear, along with a power switch and volume control dial.
The F5 Speaker
The F5 is the smaller of the nearfield monitors in the F-series and has been designed for listening environments with somewhat limited space
The F models feature a freshly designed version of Adam's highly acclaimed ART tweeter. Slightly smaller than the X-ART tweeter, it is the next step in their continuous evolution in tweeter design
As the name suggests, the F5 sports a 5" woofer made from carbon fiber and paper, as well as a 25mm voice coil. Despite the size of both the woofer and the cabinet, the F5 is capable of an astounding deep yet tight bass response
Several rear panels controls adjust the monitors to the environment including: two room equalizers for the high (>5 kHz) and the low (<300 Hz) frequencies, as well as a volume knob (-∞ to +6 dB)
|Frequency Response (Hz)
|52 - 50 000
|Watts (each)
|Woofer Size/Type
|5" carbon/paper-midwoofer
|Cabinet Dimensions
|29 x 23 x 18.5
|Weight (kg)
|13.6 (Pair)
Buy bundle & save
ADAM Audio was founded in March 1999 in Berlin by the physicist Klaus Heinz along with electrical engineer Roland Stenz. Since then the company has been developing, manufacturing and distributing professional audio loudspeakers. Refined, modern design and authentic reproduction of sound became main features of young and ambitious company - it was a challenge giants of industry had to face. In a very short period of time Advanced Dynamic Audio Monitors came to be one of the most popular tools for professional monitoring. Even though success paid a visit instantly, ADAM Audio are still exploring and researching the field of acoustics and loudspeakers technology.More Adam Audio products


text:
Can low testosterone cause melancholy?\n6733
androgenic hormone or testosteronemigh result from numerous factors which includes genetic abnormalities, chronic renal system failing, and anxiety amongst others. Very low volume sexual activity hormone in the body normal to diverse symptoms including depression, decreased sense of properly-simply being, and reduction in attention.
- There are numerous testosterone boosters accessible; a lot of of.
- Treatments for despression symptoms related to low androgenic hormone or testosterone levels.
Depressive disorders and reduced male growth hormone
Research has revealed that men people with lower ranges of androgenic hormone or testosterone generally show warning signs of depressive disorders or depressive signs and symptoms if the individual go to an endocrinologist business office. Same studies have found out that guys diagnosed with decrease amounts of male growth hormone had been constantly getting antidepressant prescription drugs. The exact connection involving major depression and the occasional levels of the sexual intercourse hormonal weren't verified technically. Males with lower levels of androgenic hormone or testosterone will invariably normal to exhaustion, improved frustration, and diminished libido. This kind of signs or symptoms will also be linked with despression symptoms.
Study performed in 2004 by Doctor. Molly Sholes found out that lower levels of male growth hormone is actually a risk factor for depressive disorders. Gentlemen with reduced volume hormonal had been 4 times most likely to be well informed they have got major depression than males with normal variety of male growth hormone. As stated previously, certainly one of several achievable outline involving depressive disorders and periodic levels of male growth hormone might be the discussed signs. Apart from this, male growth hormone encourages the creation of serotonin hormonal agent through the entire body functions. Serotonin bodily hormone is vital in regulating our emotions in the body. Insufficient the sex hormone inside your body prevents the standard manufacture of serotonin resulting in despression symptoms symptoms.
With reduced volume hormonal had
More mature guys have great threats have creating major depression as a consequence of lowered levels of androgenic hormone or testosterone when compared to teenagers. Study signifies that old adults have lessened the capability to absorb serotonin. The explanation for this likelihood may be the serotonin receptors within your body of an growing older adult male are minimizing. It's advocated that treatments for each despression symptoms as well as the very low androgenic hormone or testosterone levels in such people may help in preserving their lives.
Lowered levels of androgenic
Treatment method programs for major depression linked with reduced androgenic hormone or testosterone degrees
Programs for
· The most notable treatment selection for this concern consists of hrt. The bodily hormone replacing therapy might help in repairing the male growth hormone ranges to normal. The amount forms suitable for botox treatment injections include spots, injections, and gels.
· Another treatment method alternatives the management of despression symptoms with antidepressant drugs as recommended throughout the medical doctor or pharmacist.
Management of despression symptoms
· Sufferers could possibly be helped by way of helpful management by means of reassurance. Help can assist in increasing their self confidence and give back a sensation of properly-becoming.
There are several benefits affiliated using this that are regular in origin:
- They aid to boost electricity likewise as potential.
- Your exercise periods are rendered less complicated; so, it truly is seriously excellent for sportsmen.
- Our bodies extra fat could be diminished significantly.
- It truly is much easier to obtain groups of muscles with better numbers of androgenic hormone or testosterone enhanced by natural androgenic hormone or testosterone boosters; for that reason you achieve toned muscles bulk without the need for experiencing exposed to your harmful outcomes of dangerous chemical compounds.
- Your libido is increased.
Your libido is increased
- You will be protected within the unpleasant unwanted effects of steroids and chemical substance centered solutions.
There are many male growth hormone boosters obtainable; a number of of those are standard testosterone boosters through the kind of supplements and holistic solutions. It can be essential that you research properly in front of you decide on one particular by yourself. Right after all, the goods which meets your requirements and with the similar time might take proper care never to bring about any injury to the program is one of the many finest male growth hormone boosters yourself.
Resources : natural male testosterone boosters
- - It's much easier to get muscular tissue with far better levels of male.
- More mature the human race has substantial hazards have building despression symptoms as a.
- Major depression and lower androgenic hormone or testosterone.


text:
PhoneDog's innovative comparison tool can help you save on cell phones and plans. Find the best phone and plan for you today with PhoneDog!
The ASUS ZenFone Zoom is a smartphone that comes with a 5.5-inch IPS LCD display, a 1080x1920 resolution and 403ppi...
Anna Scantlin
22 hours 22 min ago
Beau Hamilton
1 day 17 hours ago
4 days 22 hours ago
1 week 1 day ago
More Featured Articles
More People's Choice
Apple iPhone X
Everything I wanted iPhone X to be!!!!
reviewed by Djtracstar
Samsung Galaxy S8
reviewed by jlrichardsonjr
iPhone X - Beautiful Art
reviewed by Lilcc512
More Reviews
More Videos


text:
The CEO of W.T. Humphrey Group has been appointed to the Rural Infrastructure Authority.
The CEO of W.T. Humphrey Group has been appointed to the Rural Infrastructure Authority.
Steven Wangerin�s appointment by Gov. Pat McCrory was announced Thursday afternoon. He will hold an at-large seat on the board, according to the Governor�s Office.
Wangerin is the chairman of the Jacksonville Onslow Economic Development Board, a former chairman of the Jacksonville-Onslow Chamber of Commerce and studied finance and economics at University of North Carolina at Charlotte.
Wangerin, who said he previously served on the governor�s military affairs commission, said he was excited about the new challenge.
�I think it�s going to be a challenge because it�s a new authority for the state and we�ll be setting new rules and ways to distribute monies to the rural areas of the state for infrastructure and I�m excited about it because ... I have some background between banking and rural infrastructure development to understand the needs,� he said.
Wangerin said he was asked to consider serving on the authority by N.C. Sen. Harry Brown, who was not immediately available for comment, and other area officials.
�It�s hard for me to have any expectations or goals going on because I really don�t know what our charge or mission is ultimately going to be. I think that�s going to be discussed (today),� he said.
Wangerin said he was looking forward to the group�s first meeting.
�It�ll be an interesting swearing in (Friday) afternoon and learning what we are going to be responsible for,� he said late Thursday.
The authority reviews and authorizes grants and loans for rural areas within the state, according to the governor�s office. Members formulate policies for making loans and grants and create ways for the Rural Economic Development Division of the North Carolina Department of Commerce to effectively aid local governments in meeting preliminary project planning costs, as well providing insight into the application and review process.
The group also reviews the efficacy of the programs and submits its ideas for improvement each year.
The authority will meet today, Dec. 6, from 1 to 4 p.m. in the fourth floor boardroom of the Education Building, 301 North Wilmington St., in downtown Raleigh.
Amanda Hickey is the government reporter at The Daily News. She can be reached at email@example.com.


text:
Like a sleepy blue ocean.
Come let me love you.
Post your flight number again!
RobertBlack wrote:So Count Zero is visiting you in Bangcock?
RobertBlack wrote:Why did you open a thread saying you loved Count Zero again?
The Angel of God wrote:Hey you faggot piece of shit asshole. I'm *still* banging poon here. Nothing will ever stop me.
If you want to suck wang, there's no end to that also.
The Angel of God wrote:Do not be a fkn fag, cuz if you do you are playing right into his game, which is faggotry.


text:
Forgot your password? Enter the email address you signed up with and we will send you a link to create a new password.
Your password reset has been submitted to the address provided.
Standard character mark
Edible oil, cooking oil, and nuts which are shelled, roasted or otherwise processed
Business in Newport Beach, CA


text:
Bariatric Surgery Educational Symposium & Training
16 October 2015
Centre Hospitalier Universitaire Notre Dame des Secours
16 October 2015
Centre Hospitalier Universitaire Notre Dame des Secours
President Welcome
The Obesity & Metabolic Surgery Unit at Notre Dame des Secours University Hospital (CHU-NDS) in collaboration with the Faculty of Medicine and Medical Sciences at the Holy Spirit University of Kaslik (USEK) has the pleasure to announce the Bariatric surgery Educational Symposium & Training ''BEST 2015''.
''BEST 2015'' organized for the first time this year, aims to provide attendees with the latest advances and enhancements in the medical and surgical management of clinically severe obesity. I would like to invite you to join us for "BEST 2015" to highlight the importance of a multidisciplinary approach to the surgical treatment of obesity and metabolic disorders.
Looking forward to welcoming you all!!
Dr. Elie Chlela
Head of the Obesity and Metabolic Surgery
Centre Hospitalier Universitaire Notre Dame des Secours
Tailored for:
Obesity Specialists
Online Registration is Closed
Onsite Registration is Available
Looking Forward to Welcome You All !!!
1/ SILS and Revision Bariatric Surgery
2/ Bariatric Surgery: What's New?
3/ Cut or No Cut: Obesity Multidisciplinary Management
4/ Patient Management Post Bariatric Surgery
5/ Updates in Complications' Management Post Bariatric Surgery
50 participants only !!
Priority for practicing hospital dietitians to attend the workshop
Workshop Registration Fees 20$
Symposium Registration Fees Free of Charge
Surgery Program
Dietetics Program
For further information please contact:
SciencePRO s.a.r.l.
Tel: +961 4 723099; Mob: +961 71 208822
email: firstname.lastname@example.com


text:
Entries Tagged with 'Sean Harris'
Creep Release Date: 28 January 2005 (UK) Genre: Horror | Mystery | Thriller Director(s): Christopher Smith Writer(s): Christopher Smith Staring: Franka Potente, Sean Harris, Vas Blackwood The general consensus around the net is that Creep is good, but far from great. And that right there sums up my feelings on the movie. Creep certainly has […](Continue reading…)


text:
Rainbow Juices has officially set the date for their Grand Opening celebration, to be on March 14 from 3:00PM to 10:00PM at their brand new location at 246 E. 3rd St.
The dynamic duo, Dawna Bass and Chrissy Cox will be offering 10 percent off all cleanse sign ups alongside in-house juice specials, ginger shots, and drawings to win cleanses, packages and more.
Come grub and refuel on hors d'oeuvres by Sarah Lim of SOL Food, coffee pour overs, teas and snacks by Wide Eyes Open Palms and kombucha by Jodine and Jay of Fine Feathers Kombucha Co. Sacred Roots Holistic Healing will be sharing their healing expertise and donation based massages will be offered from 3:00PM to 7:00PM.
Live musical performances by Alyssandra Nightswonger, Rene Marino and Alicia Murphy will occur from 4:00 to 7:00PM, DJ SGEtc will play a set with guest rapper Julie Potter from 7:00PM to 10:00PM, and Sirena Serpentina will show off her Tribal Fire Bellydance at 8:30PM.
Chrissy and Dawna encourage guests to attend the festivities for just a little while or stay all day to celebrate their health-conscious small business in downtown Long Beach.