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Philadelphia man scales down 19-storey building to escape fire
Dramatic detail emerges on French commando raid in Burkina
French special forces carried out the raid under cover of dark over the night of Thursday-Friday, supported by USA intelligence and troops from France's Bar...
Venezuela's Guaido Would Probably Accept U.S. Military Intervention if Proposed: Paper
He narrated the drama in real time on Twitter, while images of the incident also circulated on social media. "Democrats, keep up the fight!" tweeted Zambrano...
Huawei CFO Is on the Move to Her Bigger $10 Million Mansion
Meng Wanzhou , 47, the daughter of Huawei Technologies Co Ltd's billionaire founder Ren Zhengfei , was arrested at Vancouver's airport in December on a usa...
Pope Francis Issues Church Law Governing Sex Abuse Reporting And Investigation
In addition, by June 2020, each diocese must set up "stable and easily accessible systems for submission of reports" by the public, although the design of such ...
Chelsea Manning released after spending 62 days in prison
The former US Army intelligence analyst was released because the grand jury's term had ended. "Today marked the expiration of the term of the grand jury, and ...
Beltway Analysts Ponder, Why Subpoena Donald Trump Jr.?
Sen. Richard Burr (R-NC) announced on Wednesday that he has subpoenaed Donald Jr.to appear before the committee he chairs as part of its continuing investigatio...
European elections 2019: Vote for Brexit parties 'a waste'
Britain's opposition Labour Party leader Jeremy Corbyn speaks at the launch of Labour's European election campaign in Kent, Britain, May 9, 2019. The Brit...
Taliban attack aid group office in Afghan capital, kills 5
The assault, claimed by the Taliban, targeted Counterpart International , which has offices near those of the Afghan attorney general, Rahimi said. At least ...
Federal Bureau of Investigation chief: No evidence of illegal spying on Trump campaign
At a hearing last week, he described "spying" as a "good English word" encompassing "all forms of covert intelligence operations" and said he wouldn't back away...
All modes of severe weather possible Wednesday in Green Country
Happy Thursday! Model guidance is all over the place in terms of when storms will begin and when they will end today . Radar estimates of 4 to 5 inches of ra...
United States to Impose New Sanctions on Iran 'Very Soon'
It was unclear, the official said , what the objective was for the missiles being on the Iranian boats and that it was possible they could be fired from the ...
Donald Trump 'Surprised' Richard Burr Subpoenaed Donald Trump Jr
Two people familiar with the subpoena tell The Associated Press that lawmakers want to ask the younger Trump about his 2017 testimony regarding its probe into...
USA seizes cargo ship from North Korea, accuses Pyongyang of violating sanctions
The court filing says payments for improvements to the Wise Honest were done via US banks, also in violation of sanctions. The sanctions aim at reducing the...
Facebook Co-Founder: It's Dangerous. Break It Up
Hughes is the latest in a series of prominent entrepreneurs and tech executives to call for stricter regulation of Facebook and other online platforms. "But I'm...
Maduro regime detains Guaido's VP, US calls for his release
On Tuesday, Venezuela's pro-Maduro Constituent Assembly ruled to strip Mr Zambrano and six other opposition politicians of their parliamentary immunity to allow...
Actress Pamela Anderson Visits Assange in London Prison
The Canadian actress and Assange have developed a close relationship over the years and the actress visited the latter on several occasions during the seven y...
Why is Ramadan important to Muslims?
Many Muslim-majority countries curb the sale of alcohol during the month of Ramadan , limiting when it can be sold and to whom. Fasting is aimed at drawing w...
Gov't to Offer Food Aid to N.Korea Despite Missile Provocation
Assuming the North did test a ballistic missile on Saturday, it would have been the North's first such launch since November 2017. It came in the wake of talk...
Congress coined term 'Hindu terror', kept innocents in jail: PM Modi
Raising questions over why the contract related to Rafale was awarded to Ambani, Gandhi asked Modi to come clear on why the fighter jet was purchased at Rs 1,60...
Indian PM conducts aerial survey of areas affected by cyclone Fani
During the NCMC meeting, the Odisha government has informed that power and telecommunication facilities are gradually being restored in the cyclone affected a...
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Learn how to design a logo from client brief to finished design.
Creating logos isn't easy, especially when working with particular clients. And with so many designers out there, differentiating yourself can be difficult.
Knowing how to effectively map out your ideas will be the foundation on which you can craft extraordinary logos and bring something fresh to the table that clients can't refuse. This is how you make clients happy, draw attention to your work, build your client base, and potentially earn more money.
Learn How to Design an Eye-Catching and Effective Logo Every Time.
The most difficult part of working as a designer is being able to generate a logo that a client will be happy with. The key is knowing how to understand a client's expectations, and using the right tools to draft ideas quickly. As a designer, you should also know how to properly position text, and how to choose the right colors and fonts that will represent a business in the best and most accurate way.
This course, containing over 42 lectures and 2.5 hours of content, provides step-by-step instructions on logo design. No logo design experience is required; however, you should have a full or free trial version of Adobe Illustrator, even though you don't need prior knowledge working in this program.
You'll receive a 61-page eBook on how to design logos, as well as information on how to receive a logo design brief from a client. Then you'll learn how to collect reference materials and imagery to sketch out ideas.
Upon completion of this course, you'll understand mind mapping and mood boards, which help you brainstorm logos. You'll know how to create unique symbols, add elements to a word, use geometric shapes and initials, and position text properly.
Students will nail the basics of Illustrator, know where to find free fonts, and create logos in color, black and white, and in different formats. You'll also receive tips on sending ideas to clients, making changes and finalizing a logo, and pricing your work. All of these skills will make you a more valuable designer or allow you to use your creativity to make your own logos.
A 61 page downloadable pdf ebook with warm up exercises and sample logo design project.


See how BlueSnap helped Kidoz, an Andorid app, increase payment conversions by 33% and reach consumers in over 150 countries.
Kidoz is an Android app designed to turn phones, tablets and PCs into a kid-friendly app store filled with videos, apps and online content just for kids. Kidoz aims to help kids learn how to navigate the online world before they can even read and write. parents don't have to worry about their kids stumbling onto inappropriate content like they would if they were browsing the regular app store. Kidoz lets kids learn in a safe and fun way.
Kidoz was facing a number of challenges when it came to online and mobile checkout. They were moving customers all the way along the buying process to the checkout phase and then losing them. The reasons were many- too many fields, currency issues, coupon problems etc. This is where BlueSnap came in.
After making the switch to the BlueSnap payment platform, Kidoz was able to increase payment conversions by 33% and reach consumers in over 150 countries. And these were just two of the many benefits they saw as a result of the integration of BlueSnap's all-in-one payment platform.
" Increase their Kidoz's payment conversions by +33%	"
Double the payment conversion rate for returning through the one-click checkout process.
Increase their geographical reach, now reaching shoppers in over 150 countries.
Save money and time with a single integration to coupons, subscriptions, digital downloads etc.


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Palaces in Istanbul Turkey
On a spot of land at the confluence of the Bosphorus, the Golden Horn and the Marmara Sea, stands Topkapi Palace, a maze of buildings at the center of the Ottoman Empire between the 15th and 19th centuries. In these opulent surroundings the sultans and their court lived and governed. A magnificent wooded garden fills the outer, or first, court. To the right of the second court, shaded by cypress and plane trees, stand the palace kitchens, now galleries exhibiting the imperial collections of crystal, silver and Chinese porcelain. To the left, the Harem, the secluded quarters of the wives, concubines and children of the sultan, charms visitors with echoes of a centuries old intrigue.
Today, the third court holds the Hall of Audience, the Library of Ahmet III, an exhibition of imperial costumes worn by the sultans and their families, the famous jewels of the treasury and a priceless collection of miniatures from medieval manuscripts. In the center of this innermost sanctuary, the Pavilion of the Holy Mantle enshrines the relics of the Prophet Mohammed brought to Istanbul when the Ottomans assumed the caliphate of Islam. (Open every day except Tuesday.)
Built in the mid-19th century by Sultan Abdülmecit I, the facade of Dolmabahçe Palace stretches for 600 meters along the European shore of the Bosphorus. The vast reception salon, with 56 columns, and a huge crystal chandelier weighing four and a half tons and lit by 750 lights never fails to astonish visitors: At one time, birds from all over the world were kept in the Bird Pavilion for the delight of the palace's privileged residents. Atatürk, founder of the Turkish Republic, died in Dolmabahçe on November 10,1938. (Open every day except Monday and Thursday)
In the 19th century, Sultan Abdülaziz built the Beylerbeyi Palace, a fantasy in white marble amid magnolia filled gardens, on the Bosphorus's Asian Shore. Used as the Sultan's summer residence, it was offered to the most distinguished foreign dignitaries during their visits. Empress Eugenie of France was among its residents. (open everyday except Monday and Thursday.)
In addition to the State Pavilions at Yildiz Palace, the compound includes a series of pavilions and a mosque. It was completed by Abdülhamit II at the end of the 19th century. The Sale, the largest and most exquisite of the buildings, reveals the luxury in which the sultans lived and entertained. Set in a huge park of flowers, shrubs and trees gathered from every part of the world, the palace grounds offer one of the most beautiful panoramic views of the Bosphorus. Because of restoration work, only the Sale and park are open to the public. (Open every day except Monday and Thursday.)
The Göksu Palace, also known as Küçüksu, takes its name from the streams which empty into the Bosphorus near the tiny palace. Built by Abdülmecit I in the middle of the 19th century, it was used as a summer residence. (Open every day except Monday and Thursday)
Originally built in the 18th century and later restored by various sultans, the Aynali Kavak Summer Pavilion assumed its name, Mirrored Poplar, when its famed mirrors, a gift from some of the Venetian, were installed in 1718. This palace on the Golden Horn is one of the most beautiful examples of traditional Turkish architecture. (Open every day except Monday and Thursday.)
The 19th century Ihlamur Pavilion is named after the linden trees that grow in its gardens. Now in the heart of metropolitan Istanbul, when it was originally constructed, the pavilion lay in the rolling countryside that surrounded the city. The Merasim Pavilion was used for official ceremonies while the Maiyet Pavilion sheltered the sultan's entourage and on occasions, his harem during their excursions out of the palace confines. (Open every day except Monday and Thursday.)
The Maslak Pavilion on a shady green hill was conceived by Sultan Abdülaziz as hunting lodges and are superb examples of the late l9th century Ottoman decorative style. These are particularly noteworthy. (Open every day except Monday and Thursday.)
The Florya Atatürk Sea Pavilion served as a summer residence for Turkish presidents. Situated in a T-shaped design jutting out onto the Marmara Sea, this building constructed in 1935, serves as a showcase for some of the loveliest examples of early 20th century furnishings. Atatürk was the first president to stay here. (Open weekdays except Monday and Thursday.)

redpajama_set_name: RedPajamaCommonCrawl


Chemical peels use a chemical solution to improve and smooth the texture of the facial skin by removing its damaged outer layers. It is helpful for those individuals with facial blemishes, wrinkles and uneven skin pigmentation. Phenol, trichloroacetic acid (TCA) and alphahydroxy acids (AHAs) are used for this purpose. The precise formula used may be adjusted to meet each patient's needs. Although chemical peel may be performed in conjunction with a facelift, it is not a substitute for such surgery, nor will it prevent or slow the aging process.
Chemical peels are most commonly performed for cosmetic reasons — to enhance your appearance and self confidence. A chemical peel may also remove pre-cancerous skin growths, soften acne facial scars and even control acne. In certain cases, health insurance may cover the peel procedure.
What are Alpha-hydroxy Acids (AHAs)?
(AHAs), such as glycolic, lactic, or fruit acids are the mildest of the peel formulas and produce light peels. These types of peels can provide smoother, brighter-looking skin for people who can't spare the time to recover from a phenol or TCA peel. AHA peels may be used to treat fine wrinkling, areas of dryness, uneven pigmentation and acne. Various concentrations of an AHA may be applied weekly or at longer intervals to obtain the best result. Your doctor will make this decision during your consultation and as the treatment proceeds. An alphahydroxy acid, such as glycolic acid, can also be mixed with a facial wash or cream in lesser concentrations as part of a daily skin care regimen to improve the skin's texture.
(TCA) can be used in many concentrations, but it is most commonly used for medium-depth peeling. Fine surface wrinkles, superficial blemishes and pigment problems are commonly treated with TCA. The results of TCA peel are usually less dramatic than and not as long-lasting as those of a phenol peel. In fact, more than one TCA peel may be needed to achieve the desired result. The recovery from a TCA peel is usually shorter than with a phenol peel.
With a TCA peel, your healed skin will be able to produce pigment as always; the peel will not bleach the skin. However, TCA-peel patients are advised to avoid sun exposure for several months after treatment to protect the newly formed layers of skin. Even though TCA is milder than phenol, it may also produce some unintended color changes in the skin. Trichloroacetic Acid (TCA) can be used in many concentrations, but it is most commonly used for medium-depth peeling. Fine surface wrinkles, superficial blemishes and pigment problems are commonly treated with TCA. The results of TCA peel are usually less dramatic than and not as long-lasting as those of a phenol peel. In fact, more than one TCA peel may be needed to achieve the desired result. The recovery from a TCA peel is usually shorter than with a phenol peel.
Healing is much quicker than with a phenol peel.
Permanent skin lightening and lines of demarcation may occur.
If you would like to schedule a consultation with Long Island plastic surgeon Dr. Elliot Duboys, call (631) 423-1000 today!
How Can I Prepare for My Chemical Peel?
After a thorough and careful evaluation, Dr. Duboys will instruct you on how to prepare for your peel treatment.
Sometimes Retin A – a prescription medication derived from Vitamin A – is used to pre-treat the skin. This thins out the skin's surface layer, allowing the TCA solution to penetrate more deeply and evenly. If your skin won't tolerate Retin-A pre-treatment, an AHA cream may be used instead.
Hydroquinone, a bleaching agent, is sometimes used in conjunction with Retin-A or AHA pre-treatment, especially if you have blotchy skin areas or pigmentation problems. You may have to spend a month or more in the pre-treatment phase before the doctor will schedule your actual peel.
You will need to arrange for someone to drive you home and help you out for a day or two if you are having a phenol or deeper TCA peel. It probably won't be necessary for any extra assistance if you're having an AHA peel or superficial TCA peel.
Where Will My Chemical Peel Be Performed?
Most chemical peels may be safely performed in the office. Dr. Duboys may want you to stay overnight in a facility or hospital if other cosmetic procedures are performed simultaneously.
Anesthesia isn't required for phenol or TCA peels because the chemical solution acts as an anesthetic. However, sedation may be used before and during the procedure to relax you and keep you comfortable. No anesthesia is needed for AHA peels since they cause only a slight stinging sensation during application.
After an AHA peel, it is common to experience some temporary flaking or scaling, redness and dryness of the skin. However, these conditions will disappear as the skin adjusts to treatment. With an AHA peel, the temporary redness, flaking and dryness that you experience will not prevent you from working or engaging in your normal activities. A fresher and improved skin texture will result with continued AHA treatments. Remember, protecting your skin from the sun is also important following these mild acid peels. Ask your doctor to recommend a sunblock with adequate UVA and UVB protection and use it every day.
A TCA peel may also cause significant swelling, depending upon the strength of the peel used. With a TCA peel, the moderate discomfort and mild swelling you may experience will subside within the first week. In about a week to ten days, your new skin will be apparent and you should be healed sufficiently to return to your normal activities. It is best to avoid sun exposure unless you are adequately protected.
If you've had a phenol peel, your face may become quite swollen. Your eyes may even be swollen shut temporarily. You will need someone to help care for you for a day or two. You may also be limited to a liquid diet and advised not to talk very much during the first few days of recovery. With a phenol peel, new skin will begin to form in about seven to ten days. Your face will be very red at first, gradually fading to a pinkish color over the following weeks to months. During this time, it is especially important that you use a sunblock or blotchy, irregular skin coloring may result.
Your new look Improvements from AHA peels may be very subtle at first. You may detect a healthier glow to your skin. With continued treatments, you will notice a general improvement in the texture of your skin.
The results of a TCA peel are usually not as long-lasting as those of phenol peel. However, your skin will be noticeably smoother and fresher-looking. If you're planning a phenol peel, you can expect dramatic improvement in the surface of your skin – fewer fine wrinkles, fewer blemishes and more even-toned skin. Your results will be long-lasting, although not immune to the effects of aging and sun exposure.
All chemical peels carry some uncertainty and risk. A chemical peel is normally a safe procedure when performed by a qualified, experienced plastic surgeon. However, some unpredictability and risks such as infection and scarring, while infrequent, are possible.
In some states, no medical degree is necessary to perform a chemical peel – even the strongest phenol peels. Many states have laws that permit non-physicians to administer certain peel solutions, but regulate the strengths which they can apply. You should be warned that phenol and TCA peels have been offered by inadequately trained practitioners claiming "miracle techniques" to rejuvenate the skin.
During your initial consultation, it is important that you discuss your expectations with your plastic surgeon. Don't hesitate to ask any questions or express any concerns that you may have. Expect your plastic surgeon to explain the planned procedure in detail, including its risks and benefits, the recovery period and the costs. If you have a history of herpes, you should inform your physician prior to the procedure. Remember, medical insurance doesn't usually cover chemical peel treatments unless they are for medical problems.
If you would like to schedule a consultation for a chemical peel, contact our Huntington office today! Call (631) 423-1000 to schedule a consultation with Long Island plastic surgeon Dr. Elliot Duboys.


Type the exact keywords: Start by typing the keywords or phrases on which you want the information. If you are not getting satisfying result, then you may go to next search page and so on.
Type keyword variations: If you are not getting relevant information then use your keywords in different forms or alternatives. Like, if you are looking for digital marketing and not getting ample results, you can search for variations like what is digital marketing, digital marketing agency, marketing digital, etc. You can get a list of keyword variations corresponding to a particular keyword through various tools, like Google AdWords: Keyword Planner, Keyword Tool, Word Tracker, WordStreams, and so on.
Combine two or more keywords together: Suppose you want a freelance content writer for your projects. However, you would prefer if the writer is from your own location (say New Delhi) so that you can have a meeting with him once in a blue moon. Hence, you can go on to type the query: freelance content writer+New Delhi.
Refine it further: Moving on, if you are looking for a content writer in your vicinity with expertise in Information technology domain, then, you can further refine your search and write Freelance content writer+information technology+New Delhi. Likewise, keep using different combinations until you get favorable results.


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We welcome you to search our cemetery records our just browse through an individual cemeteries records. You may search by name, location, or other information. You do not need to have complete information, our system will display all records that contain your search terms.
Didn't find what you were looking for? The records we provide online are incomplete and are provided as a guide to help you discover more. Call our office in the Johnson Building at 217-923-9306 for more information. We accept inquiries by telephone during open hours at the museums. See the homepage for other contact numbers.
Check the Cemetery Listings page for the cemeteries full name and location.
Records database last updated on 6.18.2014
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Records 24351 - 24400
Young, Samuel Y. DRUMMOND d. Nov. 30, 1864 @ 17 yrs 1 mo 2 days (Son of J.M. & M.A.) ( Co I 155 Ill Inf)
Young, Sara Marie NEOGA b. & d. 1899
Young, Sarah LONG POINT WEST Apr. 7, 1832 - Mar. 7, 1903 (Wife of James D.)
Young, Sarah J. DRUMMOND Oct. 24, 1827 - Mar. 9, 1914 (Wife of Robert)
Young, Thelma A. NEOGA 1910 - 1982 (Wife of Edward S.) (Ladies Auxiliary)
Young, W. H. NEOGA Jan. 7, 1829 - Dec. 28, 1900
Young, W. Raymond NEOGA Feb. 8, 1900 - Aug. 19, 1965 (Father) (Cpl. Co.B, 18th Inf., Philippines, WWI)
Young, William NEOGA Oct. 25, 1896 - Jan. 23, 1969
Young, William Newton TOLEDO Aug. 6, 1876 - July 3, 1915
Young, William Taylor TOLEDO 1847 - 1924
Young, Zada Elizabeth NEOGA b. & d. 1910
Younger, Leon B. TOLEDO Aug. 17, 1908 - Aug. 20, 1986 (Navy Veteran)
Youngman, Unknown HARMONY d. Aug. 14, 1909 @ unknown age (Wife of Wm.) (Misc. record)
Zang, Alvirda Jenny P. (Benner) GREENUP 1926 - 2002 (Wife of Paul M.)
Zang, Jason Thomas GREENUP 1974 - 2004 (Son of Thomas & Beatrice Louer) (Army)
Zang, Paul M. GREENUP 1919 - 2001 (Son of Foster & Annie Raffensberger)
Zebrist (?), Laverne JEWETT Apr. 29 - May 6, 1912 (Son of B.F. & Lilly)
Zei, John J. GREENUP July 21, 1916 - Jan. 10, 2000 (Son of Mathias & Augusta Klein)
Zei, Phyllis (Olenick) GREENUP Feb. 6, 1918 - Feb. 14, 2008 (Wife of John J.)
Zei, Sheila GREENUP 1954 - 1955 (Dau. of John & Phyllis)
Zeigler, Elias CONCORD 1827 - 1896 (Father)
Zeigler, Harriett CONCORD 1834 - 1916 (Wife of Elias)
Zeigler, Hazel (Woodburn) LONG POINT EAST Mar. 30, 1907 - Oct. 2, 1942
Zeigler, William H. CONCORD Nov. 1, 1860 - July 4, 1900
Zeiter, Anna MACEDONIA 1876 - 1911 (Wife of David)
Zigler, Barbara S. NEOGA 1950 - _____
Zigler, Larry G. NEOGA 1941 - 1995
Zike, Ada S. (Walker) DRUMMOND Aug. 3, 1884 - Apr. 6, 1907 (Wife of F.P.)
Zike, Allie Inesi DRUMMOND b. 1888 d. Sept., 1902 (Dau. of Harvey) (County record)
Zike, Barbara (Campbell) DRUMMOND No Dates (Wife of John)
Zike, Burd S. DRUMMOND Apr. 21, 1908 - Mar. 27, 1976 (Son of Wm. & M. Stevens)
Zike, Carolyn DRUMMOND 1942-2018 dau of Orval & Lois D (Wheat) Atteberry wife of Jerry Lee Zike
Zike, Carrie J. (Campbell) MONTROSE 1893 -1914 (Wife of F. P.)
Zike, Daisy D. (Plumly) TOLEDO Feb. 14, 1890 - Mar. 29, 1979 (Wife of Joseph)
Zike, Darrell OTHER 1953-2014 Joseph & Ethel (Oakley) Zike
Zike, Donna Bell DRUMMOND 1939 - 1959
Zike, Ettie Irene DRUMMOND 1892-1907 dau of Harvey & Thurza
Zike, Flora Lizzie DRUMMOND 1878-1898 dau of Harvey & Thurza
Zike, Franklin Pierce DRUMMOND b. 1879 d. Jan., 1924 (County record)
Zike, Harvey DRUMMOND 1850 - 1921
Zike, Helen L. DRUMMOND 1910 - 1968
Zike, Henrietta (Mulligan) DRUMMOND 1840-1922 (Wife of James) (Buried on Drake/Curry)
Zike, James DRUMMOND 1931 - 1957
Zike, Jerry L. DRUMMOND Apr. 18, 1937 - Oct. 8, 1992 (Son of Burd & Helen DeMars)
Zike, John DRUMMOND d. May 25, 1902 @ 56 yrs
Zike, Joseph R. TOLEDO d. June 11, 1977 @ 91 yrs (Son of Harvey & Thursa)
Zike, Joseph R. TOLEDO Apr. 1, 1918 - June 16, 1995 (WWII)
Zike, L. E. TOLEDO Mar. 30, 1880 - Jan. 11, 1958
Zike, Mina DRUMMOND d. June 4, 1901 (Dau. of John) (County record)
Zike, Norman DRUMMOND 1933 - 1941 (Son of Roscoe)


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VC Bridge
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Posted on October 27, 2020 by investleafwebservices@gmail.com
Salto emerges from stealth with $27M and unveils solution to transform business app configuration
TEL AVIV, Israel, Oct. 27, 2020 /PRNewswire/ — Salto today emerged from stealth, launching its SaaS solution for business application configuration and announcing $27 million in Series A funding led by Bessemer Venture Partners, Lightspeed Venture Partners and Salesforce Ventures.
Modern companies rely on an increasing number of business applications and services to support their operations, using Customer Relationship Management (CRM), Marketing Automation, HR and Finance platforms such as Salesforce, HubSpot, Marketo and NetSuite. Keeping these business applications' configurations aligned with the company's rapidly evolving business needs is inherently tied to the success of the modern company. But doing so is difficult, and current processes are labor intensive, time consuming, prone to error and highly inefficient. Business operation (BizOps) teams tasked with configuring and managing these services need a robust toolbox, automated procedures and enhanced methodologies to help the company scale and prosper.
This is the challenge veteran Israeli entrepreneurs Rami Tamir, Benny Schnaider and Gil Hoffer decided to tackle with Salto. After their success with previous companies – Pentacom (acquired by Cisco), Qumranet (acquired by Red Hat) and Ravello Systems (acquired by Oracle) – they founded Salto to fundamentally change the way companies configure and manage their business applications.
"We realized the challenges BizOps teams face are very similar to the problems encountered by software and DevOps engineers on a daily basis," said Salto co-founder and CEO Rami Tamir. "So we adapted software development fundamentals and best practices to the BizOps field. There's no need to reinvent the wheel; the same techniques used to make high-quality software can also be applied to keeping control over business applications."
Salto has offered an open source project since early 2020 with an enterprise solution being released today. Essentially, Salto automatically extracts the configuration elements of different business applications (e.g. fields, flows or processes) and translates them to a new declarative language called NaCl ("Not Another Configuration Language"). Using NaCl with Git, the applications' configurations can be collaboratively edited and deployed back to the live business apps, or to a staging environment for testing. "Defining a company's business logic as code can make a fundamental change in the way business applications are delivered," said Tamir. "We like to think about it as 'company-as-code', much in the same way as 'infrastructure-as-code' transformed the way we manage data centers."
With Salto, the different configuration elements are searchable, and major changes can be properly planned, monitored and synchronized across the many business applications a company uses. Configuration changes to multiple business applications can be easily tested, tracked or even rolled back if needed.
While launching its richly-featured enterprise SaaS offering today, an open source version of Salto is also available, staying true to the spirit of modern software development. "We envision an open ecosystem that doesn't lock users into using Salto alone. Similar to other open source software projects, we foresee a thriving community of members adding their own integrations, solutions and reusable code to share with the community," said Tamir.
"Business agility is more important than ever today, and the alignment of external business services to real business needs is increasing in strategic importance," said Alex Kayyal, Partner and Head of International at Salesforce Ventures. "BizOps teams are becoming more and more crucial to the success of companies. With Salto they are empowered to meet the tasks they are charged with, equipped with modernized methodologies and a greatly enhanced toolbox."
Lazer Cohen
SOURCE Salto
https://salto.io/
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Necrotic enteritis in laying hens. Chickens are usually affected either around 25 weeks of age, or around the beginning of egg laying, or during peak egg laying.
The farmer featured in this video didn't want to continue administrating antibiotics to his struggling flock. He wanted to get at the cause of the problem instead of treating symptoms. He discusses how he has worked with Pruex to attempt to solve his problems. He comments on the results he has experienced by doing so.


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International Journal of Drug Development and Research
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Gene and Cytokines expression of Multiple Sclerosis and its Therapeutic Regimen: A Systemic Review
Parul Srivastava1, Md Ali Mujtaba2*,Manmohan Singhal1
School of Pharmaceutical Sciences, Jaipur National University. Jaipur (Raj.), India-302018
Faculty of Pharmacy, Jamia Hamdard, Hamdard Nagar, New Delhi-110062
Nephrology Department, HGR 25, IMSS, Mexico City, Mexico
Corresponding Author: Md. Ali Mujtaba
Faculty of Pharmacy, Jamia Hamdard,
Hamdard Nagar, New Delhi-110062
E mail: ali_jh82@yahoo.com
Fax: +00-91-11-26051164
Received:	16 June 2012 Accepted: 27 June2012
Citation: Parul Srivastava, Md. Ali Mujtaba*,
Manmohan Singhal "Gene and Cytokines
expression of Multiple Sclerosis and its Therapeutic
Regimen: A Systemic Review", Int. J. Drug Dev. &
Res., July-September 2012, 4(3): 55-66
Copyright: © 2012 IJDDR, Md. Ali Mujtaba et
al. This is an open access paper distributed under the
copyright agreement with Serials Publication, which
permits unrestricted use, distribution, and
reproduction in any medium, provided the original
work is properly cited.
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Multiple sclerosis (MS) is a polygenic disease driven by dysregulation of the immune system leading to an autoimmune response against antigens of cerebral white matter tissue. Experimental autoimmune encephalomyelitis (EAE) is a widely accepted model in vivo for the development of new therapy for the treatment of MS. There are different types of rodent EAE model and immunized with different epitopes for the analysis of gene expression and cytokines response in inflammation, demyelination and degeneration of neurons. The present review aimed to effect of gene and cytokines expression and therapeutic regimen in MS.
Multiple sclerosis, Experimental autoimmune encephalomyelitis, Gene expression, Cytokines
Multiple sclerosis (MS) is a debilitating neurological disease with unknown etiology that has a strong autoimmune component and affecting about two million people worldwide. The inflammatory phase of MS likely involves activation and migration of myelin-reactive T cells across the blood–brain barrier (BBB), resulting in damage to myelin and axons in the central nervous system (CNS) (Wang C et al; 2010)[1] and in MS clinical signs and symptoms are very variable and depend on the parts of the CNS it affects, that is, the brain and spinal cord, and include motor, sensory, autonomic and cognitive disabilities (Vosoughi R et al; 2010). [2] CD4+ T helper cells reactive to myelin, which produce proinflammatory cytokines, such as interferon-E (IFN-E), osteopontin (OPN) and tumour necrosis factor-G (TNF-G), are known to have a leading role. In the complex of Th1/Th2 paradigm, MS and EAE, several experiments support a role for Th 1 responses in promoting of diseases and Th 2 responses in suppressing of disease and the adoptive transfer of myelin-reactive Th 2 cells to immune-deficient mice to induce EAE and eosinophils regarded as Th 2- associated cells also contribute in disease development (Friese MA et al; 2003). [3]
Classification of Multiple Sclerosis
1. Relapsing–remitting (RRMS)
2. Secondary progressive (SPMS)
3. Primary progressive (PPMS)
4. Progressive relapsing (PRMS)
Relapsing–remitting (RRMS)
Almost 80% of MS patients suffered from RRMS disease course, It is the most common phenotype, starts with a single mono- or multi-focal demyelinating episode (clinically isolated syndrome, CIS) with partial or full recovery and about 80% of MS patients suffered from RRMS disease course. In this, similar or varied types of relapses occur in time after initial attack. It is dominated by overt inflammation, demyelination, clinical attacks and the formation of new lesions which appears on MRI; though sub-clinically damage to neurons and axons, gradually diminishing the ability to sustain further events without acquiring disability.
Secondary progressive (SPMS)
It involves slowly progressing phase with or without superimposed relapses (SPMS) and about 50% of patient developed SPMS after 10–15 years disease duration. At this stage of the disease inflammation appears less prominent, and instead the accumulated damage to neurons and axons starts to show itself clinically as neurological progression.
Primary progressive (PPMS)
It is recognized by its progressive course from the outset, with a paucity of inflammation detected in the CNS compared with RRMS and about approximately 15% of MS patients develops PPMS.
Progressive relapsing (PRMS)
It involves relapse-like activity (PRMS) developed over time in about 5% of patients and patients have clinical and radiological evidence of inflammation, but no proven effective treatment (Pedotti R et al; 2003). [4]
Common factor of MS
The cause of this disorder is not known, but there are several factors linked to higher risk of developing the disease:
1) Genetics may play an important role and several alleles have been identified as predisposing factors for the disease, most of them related to the human leukocyte antigen (HLA) system;
2) MS is more prevalent in women than in men, suggesting importance of hormones in its pathophysiology.
3) Psychological stress has been implicated in triggering exacerbations, and some metaanalyses suggest a positive relationship between stressful events and higher risk for relapse and increased risk of new gadoliniumenhancing (Gd+) brain lesions (Perez-Nievas BG et al; 2010). [5]
4) Viral factor causes development or progression of MS, such as human herpes virus-6 (HHV-6) or Epstein Barr Virus (EBV). The bacterium Bordetella pertussis causes whopping cough in humans and produces pertussis toxin (PTx) as its main virulence factor (Weber MS et al; 2010). [6]
Common symptom of MS
A) Visual disturbances, which include eye pain, distortion or loss of vision in one eye, or impairment of color perception.
B) Difficulty in walking or performing tasks that require coordination.
C) Loss of sensation.
D) Fatigue and/or weakness.
E) Loss of bowel or bladder control (Ringold S et al; 2006). [7]
Experimental autoimmune encephalomyelitis (EAE) is currently the most commonly used animal model for the study of MS. This model causes inflammation and demyelination that is similar to the MS and to simulate different disease progressions where clinical symptoms (monophasic fashion), either acute or chronic, or in a relapsing form (Peiris M et al; 2007). [8] It is an inducible model of CD4+ T cell driven demyelination and axon damage. Myelin antigen reactive CD4+ T cells dominate the CNS infiltrate and initiate disease upon adoptive transfer into naive animals (Bettini M et al; 2009). [9]
Cytokines have a key role in the EAE process providing the necessary signals to activate T cell specificity against self-antigens and suggest that the T cells mediating EAE are of the Th1 phenotype, producing IL-2, IFN-E, and TNF-G is related to disease-promoting role, while TGF-M and IL-10 are related to the s recovery of EAE (Castro GM et al; 2004). [10]
In early phase of MS, autoreactive T cell crosses the blood brain barrier (BBB) and are estimated by local antigen presenting cell (APC). This results in release of cytokines such as IFN-E, TNF-G and IL-17 which initiates and perpetuates an inflammatory response by activating microglia and recruiting macrophages and BBB is breached and allow for the influx of more T lymphocytes, additional immune cells and the deposition of humoral components. Subsequently, this process leads to myelin destruction, induction of oligodendrocyte death, axonal degeneration and eventually to the development of severe functional deficits (Wiist S et al; 2008). [11]
Various EAE model for MS
A large number of EAE model exist, each parameter reflecting pathologies observed in CNS of MS patients. With different strains of mice, rats or other mammals and immunizing with different epitopes (peptides, whole proteins or complex mixtures like spinal cord homogenate) to achieve a range of pathological and temporal outcomes (Jones MV et al; 2008). [12]
Different types of EAE
Importantly, by stepwise reduction of the complexity of the antigenic material from crude brain tissue and protein extracts through various central myelin protein such as
i. Myelin basic protein (MBP) such as MBP1-37, MBP1-11, MBP1-9, MBP83-99.
ii. Myelin oligodendrocyte glycoprotein (MOG) such as MOG55-75.
iii. Proteolipid protein (PLP) such as PLP139-151.
iv. Myelin-associated oligodendrocytic (MOG) basic protein and 2´,3´-cyclic nucleotide 3´- phosphodiesterase.
Some of other myelin constituents such as neurofascin NF 155, other are expressed on myelin and axons such as the neuronal membrane protein neurofascin NF 186, the neuronal cytoskeletal protein neurofilament-M and the astrocyte-typical Ca+2binding protein S100M.
Neurofascin NF 186 caused axonal injury without enhancing inflammation and demyelination in MOGEAE. In contrast to MOG-EAE, contactin-2/TAG-1- specific T cells induced inflammatory lesions prefentially in the cerebral cortex and the spinal cord white and gray matter.
Timelines of milestones of the development of increasingly specific EAE models were:
i. Induction of EAE by transfer of total lymph node cells, isolated MBP-specific T cell-line cells or IL-23-dependent PLP-specific CD4+T helper IL-17 cells into naïve rats or mice, respectively, establishing distinct forms of adaptive transfer EAE
ii. Generation of transgenic mice with deletion or over-expression of pathogenetically relevant genes. For examples genes are those encoding T cell receptors (TCRs), major histocompatibility complex (MHC) molecules, cytokines as well as neurotrophic factors and their receptors.
Induction of EAE models in different species
The most common mode of EAE induction is based on the injection of an encephalitogenic peptide, mostly MOG35-55 or PLP139-151, which is emulsified in CFA containing mineral oil and Mycobacterium tuberculosis strains H37RA, followed by intraperitoneal injections of pertussis toxin. The resulting phenotype depends mainly on the antigen source and the genetic background of the animal species and the strains used. For example, PLP139-151 induces a relapsing-remitting EAE in SJL mice, whereas MOG35-55 triggers chronic-progressive EAE in C57BL/6 mice. Crossing of C57BL/6 mice, which over-express MOG-TCR and MOG specific B cells, resulted in a severe form of EAE with inflammatory lesions of optic nerves and spinal cord. MOG-TCR transgenic mice backcrossed to SJL/J background develop a relapsing-remitting form of EAE with episodes altering between optic nerve, cerebellum and spinal cord. All EAE models are directly accessible to investigation of the immune and nervous system, which interact during the pathogenesis of the disease and which are both targeted by established and experimental therapies (Mix E et al; 2010). [13]
Various form of EAE has been induced depending on the immunizing neuroantigen and the redent strain used.
Lewis rat EAE showed a monophasic and selfremitting neuroinflammation in the CNS. Swiss- Jackson Laboratories (SJL) mice and Dark Agouti (DA) rats EAE showed a relapsing and remitting course of the disease.
MOG induced EAE in the C57BL/6 mice showed a chronic progressive course and other EAE model induced in NOD and DBA/1 mice showed a chronic progressive and severe course of secondary progressive/primary progressive form of MS (Donia M et al; 2010). [14]
Behavioural analysis of animals after EAE induction
EAE scoring (Clinical scoring)
Immunized animals are observe daily by measuring their body weight, feed weight and assessing clinical signs of EAE, starting at 7 days post immunization.
Grip strength test
Strength of forelimb and hindlimb are tested for grip strength by using Grip Strength Meter. In Grip strength, grip power of hindlimb primarily and majorly affected and forelimb less affected in EAE induced animals.
Rotarod performance
Rotarod test is used to assess motor co-ordination and balance of animals. Each mouse is placed on stationary rod and start the rotation of rod at 4 rpm and accelerated 4 rpm every 30s. The time and speed at which the mouse falls down from rod is recorded in EAE induced animals.
Open field activity test
Open field activity test is determined by using Open Field Photobeam Activity System. It is used to assess total activity and rearing activity of animals. Mice are placed into the clear plastic chamber for the assessment of interruption of infrared beams. In EAE induced mice, the total activity and rearing activity both are decreased consistently (Jones MV et al; 2008). [12]
Gene Expression Profile of EAE model
Microarray analysis technique is usually used for expression of gene in MS and EAE. Oligonucleotide microarray represents 11000 genes (6000 full-length gene and 5000 expressed sequence tags) which are expressed in inflamed spinal cord of EAE mice at the time of onset and the peak of disease determined by the clinical evaluation of the disease. The oligonucleotide microarray data are generally validated by the use of quantitative RT-PCR method to analyse a subsets of gene either down-regulated or up-regulated. The microarray technique enables to identify differentially express gene with a high degree of validity. Increased expression of genes for extracellular matrix, cell adhesion molecules and molecules involved in cell division, death and transcription, differential regulation of molecule involved in signal transduction, protein synthesis and cell metabolism in inflammation.
Genes are group according to their presumed biological functions and to the fold change in gene expression using normal spinal cord as a baseline (Ibrahim SM et al; 2001). [16]
Neural dysfunction in Spinal Cord during EAE
The protein levels of plasma membrane Ca2+ ATPase 2 (PMCA2), an essential ion pump expressed exclusively in grey matter and involved in Ca2+ extrusion, synapsin IIa and syntaxin 1B, important regulators of vesicular exocytosis decreased coincident with the onset of clinical symptoms and changes in the expression of several other ion pumps, vesicular proteins, mitochondrial enzymes and sodium channels also occurred in disease. Glutamate and Kainic acid significantly reduced PMCA2 mRNA levels. In EAE pathogenesis, suppresses neuronal PMCA2 expression leading to Ca2+ dyshomeostasis at initial clinical phases.
Expression of Glutamate-mediated changes in neuronal dysfunction in EAE symptoms
Intracellular Ca2+ level are often increases often and causes cell dysfunction, injury and death in CNS, including Multiple sclerosis, Ischemia, Alzheimer and Parkinson disease. In EAE, loss of voltagedependent channel-mediated Ca+2 balances depicts defect in mechanism that regulate the Ca+2 entry, extrusion or intracellular sequestration. PMCAs are major pumps modulating Ca2+ extrusion and sarcoplasmic and endoplasmic reticulum Ca2+- activated (SERCA) ATPase isoforms causes sequestration of Ca2+ into the endoplasmic reticulum. PMCA2 expression decreases in early phase, which is followed by a reduction in SERCA2 transcript levels clinical phases. The PMCA gene family encodes four isoforms, causes maintenance of basal Ca2+ levels. PMCA2 is expressed primarily in brain and heart, in a region- and cell-type specific manner and in pathological condition of EAE, glutamate receptors are over stimulated and overload of intracellular Ca2+ level.
Role of Aberrant neurotransmitter exocytosis in EAE
The level of Synapsin and Syntaxins are decreases in EAE. Synapsin and Syntaxins are vesicle protein and exhibit important role for exocytosis in presynaptic terminals in clinical symptom of EAE. Synapsins are required for the tethering of vesicles to each other and to cytoskeletal proteins (actin). It is also essential for the formation, maintenance and regulation of the reserve synaptic pool in the vicinity of the active zone and the decreased level of synapsin causes reduced number of synaptic vesicles distal to the active zone, exhibiting synaptic fatigue. Syntaxins belongs to SNAREs class (soluble N-ethylmaleimide-sensitive factor attachment protein receptor) and essential for the docking and fusion of synaptic vesicles. Vesicleassociated SNAREs (synaptobrevin) and target membrane-associated SNAREs (syntaxins and SNAP-25) induces membrane fusion. The level of syntaxin 1B and SNAP-25 are reduced but reduction in syntaxin 1B occurred at onset of symptoms whereas SNAP-25 at a later clinical stage. The expression of synapsin and SNARE proteins interfere with normal neuronal communication during EAE.
Role of Mitochondria in cellular injury at EAE
Mitochondrial function plays important role in cellular injury due to the increased level of mitochondrial cytochrome c oxidase subunits IV and Vb. Cytochrome C oxidase used as a marker for neuronal metabolic activity, especially in oxidative stress. Elevated level of cytochrome c oxidase express in Alzheimer's disease, following traumatic brain injury and preceding apoptotic death of spinal cord motor neurons after sciatic nerve avulsion and also reflect aberrant energy metabolism and oxidative damage in the spinal cord during EAE.
Role of sodium channel in impulse conduction during EAE
Na+ channel also played an important role in EAE and MS. The expression of Na+ channels decreases that cause impairment of nerve conduction at advanced stages of EAE. Expression of sensory neuron-specific sodium channels in Purkinje cells changes during EAE symptoms (Nicot A et al; 2003). [17]
Role of Vitamin D
Vitamin D play important role in the immune system particular on T cell-medicated immunity. Receptor of Vitamin D is found on the surface of T lymphocyte and macrophage cells and highest concentration is found in the immature immune cells of the thymus and the mature CD+8 T lymphocytes (Deluca HF et al; 2001). [18]
Animal model of Autoimmunity
In autoimmune disease, T cells attacks on self tissue. T cells are thymus-derived cells and subsets of T cells called the T-helper (Th) cells that express CD+4 markers on their surface and also played an important role in EAE and diabetic model to mice. In these models, level of CD+4 T cells are decreased. EAE is mediated by CD+4 T specially Th1 type (IL-2, TNF- G, IFN-E) cells that recognize protein in CNS but suppress the Th2 type (IL-4, IL-10) cells.
Vitamin D and Immune system
Vitamin D regulated Ca+2 homeostasis and causes bone formation and resorption. The active form of vitamin D (1,25-(OH)2D3) affected on the immune system. In EAE, level of vitamin D is decreases and upregulated the Th1 cells by increasing proliferation and cytokine (IL-2, TNF-G, IFN-E) secretion. Vitamin D receptors are found in the nuclease of cells and bound to the (1,25-(OH)2D3) and regulated the transcription of targeted genes. Vitamin D act as transcriptional regulator of Th cell cytokine synthesis as a regulator of STAT 1, 4 or 6, as a regulator of GATA-3 or regulate Th cells differentiation (Cantorna MT; 2000). [19]
Cytokines signaling pathways in EAE and Multiple sclerosis
CD4+ T helper (Th) cells play a critical role in MS and EAE (Experimental Autoimmune encephalomyelitis is an animal model for MS). The major types of Th cell are type 1 helper T (Th 1) cells that produce interleukin (IL-2), tumor necrosis factor-G (TNF-G), IFN-E and type 2 helper T (Th 2) cells that produce IL-4, IL-5, IL-10 and IL-13 and type 3 helper T (Th 3) cells that primarily secrete transforming growth factor-M (TGF-M).
Intracellular signaling mechanisms provide the link between the bindings of the cytokine with its receptor and the effect of the cytokine on cellular function. The Janus kinase and signal transducer and activator of transcription (Jas/STAT) family of transducer/transcription-activating factors play a critical role in the signaling of many cytokine receptors. Cytokine binding to the specific receptors activates the Jas molecule associated with the receptor causing phosphorylation of tyrosine residues. This facilitates binding of STAT proteins to the phosphorylated receptor, which dissociates from the receptor and activates transcription of genes containing specific cis-regulatory STAT-binding sequences.
Role of individual cytokines during demyelinating process in MS and EAE
Cytokines play an important role in the pathogenesis of MS because of altered level of cytokines in the CNS and peripheral mononuclear cells of MS patients.
Interferon-: (IFN-:)
It is produced by T cells and Natural killer cells and causes activation of mononuclear cells, differentiation of T cells to Th1 type, induction of MHC I and MHC II expression and apoyptosis of T and other cells types. IFN-E is expressed in the CNS at the onset of EAE and its expression increases during the peak of disease and decreases during disease remission. Over-expression of IFN-E in the CNS causes progressive demyelinating disease. INF-E has an activating role in inflammation in EAE and MS.
Tumor Necrosis Factor-< (TNF-<)
It is produced by activated mononuclear phagocytic cells, natural killer cells, B cell, activated T cells, astrocytes and microglia in the CNS. TNF-G express Th1 type responses and induced activation of variety of cell types and expression of adhesion molecules, chemokines and cytokine. Role of TNF-G is characterized by significantly increases inflammation and demyelination in EAE and MS. TNF-G has a direct effect on the induction of oligodendrocyte apoptosis and demyelination and also promoted the proliferation and induced cell death of oligodendrocyte progenitor cells.
Interleukin-12 (IL-2)
IL-2 is produced by monocytes and the dendritic cells and express Th1 type responses. Over-expression of IL-12 in the CNS resulted in increased inflammation and cellular infiltrates.
Osteopontin (OPN)
Osteopontin is a pleotrophic cytokine that activates macrophage chemotaxis, promotes Th1 responses and activate B-cells. OPN increases plaque formation in the brain of MS patients.
Interleukin-18 (IL-18)
IL-18 is synthesized as an inactive precursor protein and its level increases in the serum of MS patients.
Interleukin-1 (IL-1)
It is produced by monocytes, macrophages, endothelial cells, B cells and activated T cells and upregulated in the CNS and causes increased neuronal cell death and edema. Neuronal apoptosis and neurotoxic effect appear due to expression of iNOS.
IL-3 is a cytokine growth factor produced by CD+4 T cells and microglia. IL-3 mRNA is up-regulated in the CNS of MS patients. Systemic over-expression of IL-3 in the CNS causes degeneration and vacuolation of neurons.
IL-6 is produced by mononuclear phagocytes, vascular endothelial cells and fibroblast and promoted Th1 cytokines. It is important for the growth and differentiation of B-cell and also upregulated in the CNS during the induction phases of disease.
IL-4 is produced by CD+4 Th2 cells and involved in differentiation and growth of B-cells. IL-4 inhibits the activation of Th1 cells and decreases the production of IL-1 and TNF-G. IL-4 amplifies the Th2 response through activation of the intracellular signaling factor STAT6, which induces transcription of Th2 related genes.
IL-10 is produced by monocytes, macrophages, B cells and Th2 cells. It inhibits the production of IL-1 and TNF-G cytokines by macrophages and also reduces MHC II and co-stimulatory molecules expression.
Transforming growth factor (TGF)
The TGF family of molecules has 2 principal members that is TGF-G and TGF-M. TGF-G is a polypeptide growth factor for epithelial and mesenchymal cells and TGF-M is a growth factor for cell survival. TGF-M is produced by T cells by T cell, activated monocytes, astrocytes and microglia. It inhibits proliferation of T cells, maturation of cytotoxic lymphocytes, natural killer cell and also inhibits the activation of macrophages and activates the pro-inflammatory cytokines (Imitola J et al; 2005). [20]
Therapies for EAE and MS
The goal of MS is to produce a period of stabilization of symptoms and interrupt the progress of disease. There is no current treatment that can alter neurological damage (Hadaway LC; 1985) [21] but only very few therapeutics that are successful in preclinical EAE trials have shown similar efficacy in MS patients. The majority of new treatments are either less effective in MS patients and worsened disease or caused severe adverse events (Friese MA et al; 2006). [3]
At present, the exact cause of MS is still unknown in pre-clinical EAE studies, which involve in multiple immune cell types, target cells and pathways but conventional EAE play an important role as first line animal model system for the development of novel treatment for MS. Gene expression and cytokines levels play an important role in MS. Oligodendrocyte microassay is a technique which are used for detection of gene expression contributing to earlier stage of diseases. It represents 11000 genes (6000 full-length gene and 5000 expressed sequence tags) in inflamed spinal cord of EAE induced animals, 213 genes are regulated differentially and 100 genes are showed consistent differential regulation throughout the disease. Gene expressions are upregulated in inflammation because increased expression of immune related molecules, extracellular matrix, cell adhesion molecules and those molecules which are involved in cell division and transcription. Alteration in cytokine balance also involved in autoimmune disease pathogenesis. Th2 cytokines (IL-4, IL-5, IL- 10 and IL-13) appears to play a protective role in the survival and differentiation of neurons and oligodendrocyte in the CNS during demyelination injury and Th1 cytokines (IL-2, TNF-G AND IFN-E) play a degenerative role in MS patient by the activation of mononuclear cells, differentiation of T cells, B cell class switching and apoptosis of T and other cell types. The future of multiple sclerosis therapy looks bright, but increasingly complex. There are number of agents who are used for the treatment of MS through orally and parenterally and some are in different stages of investigation or awaiting approval by federal agencies. All of these medications have demonstrated partial efficacy along with different side effect profiles.
Neurodegeneration occurs through noninflammatory mechanisms but depend upon prior inflammation. In these case, anti-inflammatory therapies are best prevent the progression of disability in early course of the disease, before the cascade of events that leads to axon degeneration has been irretrievably established. This raises the difficult prospect of exposing well non-disabled young adults to potentially toxic treatments; a decision made all the more complex by the unpredictable nature of multiple sclerosis. Finally, these drugs continue to inform basic science, revealing aspects of the pathogenesis of multiple sclerosis and reminding us of the complexity of the human immune system.
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Tables at a glance
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Perez-Nievas BG, Garcia-Bueno, Madrigal JLM, Leza JC. Chronic immobilisation stress ameliorates clinical score and neuroinflammation in a MOGinduced EAE in Dark Agouti rats: mechanisms implicated. Journal of Neuroinflammation. 2010; 7(60): 1-13.
Weber MS, Benkhoucha M, Lehmann-Horn K, Hertzenberg D, Sellner J, Santiago-Raber ML, Chofflon M, Hemmer B, Zamvil SS, Lalive PH. Repetitive Pertussis Toxin Promotes Development of Regulatory T Cells and Prevents Central Nervous System Autoimmune Disease. PLoS ONE. 2010; 5(12): e16009.
Ringold S, Richard MG. Multiple Sclerosis. The Journal of the American Medical Association. 2006; 296(23): 2880.
Peiris M, Monteith GR, Thomson SJR, Cabot PJ. A model of experimental autoimmune encephalomyelitis (EAE) in C57BL/6 mice for the characterisation of intervention therapies. Journal of Neuroscience Methods. 2007; 163: 245-254.
Bettini M, Rosenthal K, Evavold BD. Pathogenic MOG-reactive CD8+ T cells require MOG-reactive CD4+ T cells for sustained CNS inflammation during chronic EAE. Journal of Neuroimmunology. 2009; 213: 60-68.
Castro GM, Zanin ME, Oliveira DV, Vilella CA, Ashimine R, Zollner RL. Th1 and Th2 cytokine immunomodulation by gangliosides in experimental autoimmune encephalomyelitis. Cytokine. 2004; 26: 155-163.
Wiist S, Brandt J, Tischner D, Kleiman A, Tuckermann JP, Gold R, Liihder F, Reichardt HM. Peripheral T cells are the therapeutic targets of glucocorticoids in experimental autoimmune encephalomyelitis. The Journal of Immunology. 2008; 180: 8434-8443.
Jones MV, Nguyen TT, Deboy CA, Griffin JW, Whartenby KA, Kerr DA, Calabresi PA. Behavioral and pathogical outcomes in MOG 35-55 experimental autoimmune encephalomyelitis. Journal of Neuroimmunology. 2008; 199: 83-93.
Mix E, Meyer-Rienecker H, Hartung H, Zettle UK. Animal models of multiple sclerosis-Potentials and limitations. Progress in Neurobiology. 2010; 92: 386-404.
Donia M, Mangano K, Quattrocchi C, Fagone P, Signorelli S, Magro G, Sfacterias A, Bendtzen K, Nicoletti F. Specific and strain-independent effects of dexamethasone in the prevention and treatment of experimental autoimmune encephalomylelitis in rodents. Scandinavian Journal of Immunology. 2010; 72: 396-407.
Gold R, Linington C, Lassmann H. Understanding pathogenesis and therapy of multiple sclerosis via animal models: 70 years of merits and culprits in experimental autoimmune encephalomyelitis
Ibrahim SM, Mix E, Bottcher T, Koczan D, Gold R, Rolfs A, Thiesen HJ. Gene expression profiling of the nervous system in the murine experimental autoimmune encephalomylelitis. Brain.2001; 124: 1927-1938.
Nicot A, Ratnakar PV, Ron Y, Chen CC, Elkabes S. Regulation of gene expression in experimental autoimmune encephalomyelitis indicates early neuronal dysfunction. Brain. 2003; 126: 398-412.
Deluca HF, Cantorna MT. Vitamin D: its role and uses in immunology. FASEB J. 2001; 15: 2579– 2585.
Cantorna MT. Vitamin D and autoimmunity: Is vitamin D status an environmental factor affecting autoimmune disease prevalence. PSEBM. 2000; 223: 230-233.
Imitola J, Chitnis T, Khoyry SJ. Cytokines in multiple sclerosis: from bench to beside. Pharmacology and Therapeutics. 2005; 106: 163- 177.
Hadaway LC. Immunosupressive treatment of multiple sclerosis. NITA. 1985; 8: 503-505.
Copyright © 2019 All rights reserved. iMedPub LTD Last revised : July 17, 2019


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Home EU-Startups Summit 2021
On April 28-30, 2021, we're going to host our annual EU-Startups Summit online! At the event we'll showcase a selection of Europe's hottest startups and come together to learn from some of the most successful European entrepreneurs of our time.
The EU-Startups Summit will gather over 1,500 founders, startup enthusiasts, corporates, angel investors, VCs, and media from across Europe. The three-day virtual event is a great opportunity for networking, and a meeting point for aspiring entrepreneurs and investors who are aiming to build international tech companies. We'll have fireside chats with internationally successful founders, great networking opportunities (AI-based matchmaking, video calls, session chats, etc.), workshops, and an exciting pitch competition with 15 finalists – selected from about 1,000 applicants!
Make sure to secure your Tickets soon!
TICKETS ARE AVAILABLE HERE
Some Impressions from our previous in-person event:
The Speakers
We'll welcome many high-profile speakers (successful entrepreneurs, investors, etc.) on our virtual stage at this year's EU-Startups Summit. Below you'll find some of the speakers we already announced. And here you'll find the current stat of the agenda.
Mette Lykke
Mette Lykke is the CEO of Too Good To Go and former co-founder of Endomondo.
CEO of Unbabel - one Portugal's fastest growing startups leveraging AI and providing real-time, human-quality translations at scale.
Frédéric Mazzella
Frédéric Mazzella is the co-founder and President of BlaBlaCar.
Alice Zagury
CEO of The Family - a European organisation that nurtures Entrepreneurs through Education, Unfair Advantages & Capital.
Oscar Pierre
CEO of Glovo - a Spanish unicorn (over €465 million in funding) which is one of the world's fastest growing on-demand delivery players.
Ann-Christine Roope
CEO of Ethan Partners - a rapidly growing Executive Search company that is based in London and operating internationally.
Carlota Pi
Executive President of Holaluz - a Spanish scale-up that's been revolutionising the energy sector for nearly a decade. Most recently Holaluz did an IPO.
Federico Mattia Dolci
CEO of BOOM - a hyper-growing tech startup from Milan that provides high-quality photographic solutions.
James Jenkins Yates
CEO of Airsorted - the proptech startup is active in 20+ cities and has generated over €115 million in bookings for its hosts
Davide Dattoli
CEO of Talent Garden - the leading European coworking network and educational institute for the digital and tech community.
Florian Gschwandtner
Serial entrepreneur who is also the co-founder and former CEO of Runtastic.
Alexander Limpert
CEO of GuestReady - the tech-enabled short-term rental management company operating in fifteen cities across Europe and Asia.
Ville Simola
CEO of Maria 01- a huge coworking space in Helsinki that set out to become Europe's largest startup campus.
Dustin Figge
CEO of Homelike - which boasts over 50,000 apartments in Germany, Austria, Switzerland, Netherlands, Spain & the UK
CEO of Housfy - a rapidly growing proptech startup that is digitalising the real estate industry.
Andrea Scotti Calderini
CEO of Freeda Media - the #1 global female media brand on Instagram, for engagement and interactions.
Tilo Bonow
CEO of PIABO - the Berlin-based PR agency of choice for challenger brands like N26, Shopify, Tinder and wework.
Azahara Espejo
Head of Business Development Spain at Crowdcube - one of the worlds leading equity crowdfunding platforms.
Phil Libin
Co-founder and CEO of All Turtles, a mission-driven product studio, and mmhmm, a new app created during the pandemic that makes video communication more clear and compelling. Previously he founded Evernote.
Co-founder of Basecamp, creator of Ruby-on-Rails, and author of many best-selling business books
Renaud Visage
Co-founder of Eventbrite, Board Partner at Point Nine Capital, and angel investor.
Co-founder & CEO of the US-based unicorn Sendbird.
Pitch Competition
During the EU-Startups Summit, we'll also have a big pitch competition with 15 of Europe's most exciting early-stage startups. The pre-selected startups are going to pitch their business idea with a 3-minute-presentation in front of our attendees and an expert jury of well known investors. The winning startup team will receive an awesome prize package worth about €78,500 (incl. AWS credits, Spaces credits, Vonage credits, and more). The deadline for applications was on March 15. The finalists can be found here.
Timings & Tickets
The main event will take place on April 28-30, from 10am to 6pm. Compared to many other major tech events, we keep our ticket prices affordable, starting at €169 for startup founders and wantrepreneurs, €349 for investors, and €449/€590 for corporates and service providers. Also, everyone who attends this year's online edition of the EU-Startups Summit will get a 60% discount for next year's in-person event in beautiful Barcelona!
Shareworks by Morgan Stanley provides innovative and intuitive equity solutions that help private and public companies realize the full potential of equity compensation. With flexible solutions to manage your plans your way, insightful reporting that makes informed decisions easy and simple-to-use applications no matter where in the world they're used, we help your workforce feel more connected. Build a culture of ownership and get started now.
Catalonia Trade & Investment is the public agency that works to attract foreign investment to Catalonia, promoting the area as attractive, innovative and competitive business location. Check their offerings and the Catalonia Startup Directory.
Spaces offers creative working environments with a unique entrepreneurial spirit and a great community. Add an international network of mobile workspaces and a full calendar of business events and networking lunches, and you'll see just how Spaces keeps you engaged and open to new possibilities. Originating in Amsterdam, Spaces wants to redefine the way work is done.
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Recent Updates: EU-Startups Summit


I went to a funeral today for a neighbor I hardly knew. She was the face behind the wheel of the mini-van, driving her kids here and there, going to work, waving as she drove by me. I knew her as the nice lady next door. Knew she was involved with her church. Knew she was well liked in the neighborhood. Knew she had a hard-working husband and three beautiful children. And that's about it.
Today, I learned important lessons from this "stranger" next door.
When I heard Jane passed (not her real name), I was dumbfounded. She was only 48 years old. Twelve years ago, she beat breast cancer; sadly and shockingly, she passed away this week from an entirely unrelated cancer. According to her good friend, Jane planned her own funeral, picked the songs, the prayers. Needless to say, I was struck by Jane's bravery. My heart went out to her husband and most especially to her sons and daughter. Such grief at their tender ages is unfathomable to me.
When I entered the church, it was immediately evident that my neighbor was greatly loved. The church was packed with her family and her friends. "Here's a life," I thought. "That touched many." Wherever she is now (and I believe it's Heaven), Jane can be extremely proud of the grace and dignity with which her children conducted themselves today (qualities, I can only surmise, learned from her), and the supportive strength of her husband as he gathered their children into his arms.
In planning her own funeral, Jane was able to "speak" to her family and loved ones on this most difficult day. The first hymn Jane chose was "Be Not Afraid." Be not afraid...I sincerely hope her sons and daughter were able to receive that message in their sorrow. From the eulogy given by Jane's brother, it was apparent that Jane was not afraid. There I was in the pew, surrounded by great sorrow, and what did Jane's brother say? Jane considered her cancer a gift. A gift! That made me sit up and take notice. According to her brother, Jane regarded her illness as a gift reminding her to treasure life's every moment and hold her family close. That's a remarkable attitude. That's faith most of us can only hope for.
Thanks to a touching eulogy, I learned some things about the "stranger" next door today. She was a swimmer, liked to exercise, enjoyed a party, liked to bake, volunteered wherever she thought she could make a difference, loved life, and was a cherished mother, wife, sister, and daughter. But the most important thing I learned wasn't in the eulogy. It was in the "air". Amidst the tears and the sorrow, there was an undercurrent of peace, hope, and - dare I say it? - tender joy at Jane's release into what the faithful believe is new life. Again, I can only surmise this came from Jane, the way she lived her life, the way her life touched others, and how she handled her death. Clearly, Jane was a woman of faith, inspiring others even in her passing.
Though Jane's life only lightly brushed with mine, I'm better for it. And that is the greatest lesson I learned today: we should each strive every day to let our lives favorably touch someone else's. You never know the difference you can make, the subtle inspiration you might impart, the faith you might enrich. In her passing, Jane made a difference in my life, and that my friends, is a gift...from a life well lived.


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Speusippos, död 339 f.Kr., var en antik grekisk filosof.

Han var systerson till Platon och efterträdde denne som lärare i Akademeia i Aten (347–339 f.Kr.), och blev således den förste representanten för den så kallade nya akademien. Han verkar ännu mer än Platon under dennes sista tid ha närmat sig pythagoreismen och identifierat idéerna med talen. Han sägs inte ha erkänt det goda som alltings grund, utan som ändamålet för de andliga väsendenas utveckling. Han bedrev även biologiska studier, vars resultat han lade fram i ett större verk om likheter.

Hans efterlämnade skrifter ska genom inköp ha övergått i Aristoteles ägo. Till vår tid är inget bevarat av dem annat än ett elegiskt distikon innehållande en apoteos av Platon.

Källor

Antikens grekiska filosofer
Födda okänt år
Avlidna 330-talet f.Kr.
Män

redpajama_set_name: RedPajamaWikipedia


Gunsynd Motor Inn offers pet-friendly accommodation in Goondiwindi. Free private parking is available on site. Every room at this motel is air conditioned and is fitted with a flat-screen TV with satellite channels.


FAR HILLS, NJ --- After a 19 year absence, the Mars Essex Horse Trials, one of the top equestrian competitions, returns with a weekend of outdoor family-oriented events in the beautiful Somerset County countryside at historic Moorland Farm in Far Hills, NJ, from June 24-25, 2017.
The Mars Essex Horse Trials features "eventing," often referred to as an "equestrian triathlon," a competition that combines the elegance of dressage, the thrill of cross-country and the precision of show jumping; a classic car show; The Farmstand offering fresh farm-to-table food from local markets and specialties from artisan vendors; and The Essex Market offering a wide range of shopping from saddles and riding boots to jewelry and artwork.
A Children's Activity Center, sponsored by The Willow School, will offer a fun and creative diversion for younger spectators and their parents. The Willow School, located in Gladstone, is committed to helping children discover who they are, the joy of learning and the wonder of the environment around them.
Moorland Farm, a picturesque 230-acre property, provides the breathtaking setting for the event's return. It is the home of the annual Far Hills Race Meeting, a series of nationally prestigious steeplechase races held each October.
General Admission is just $10 in advance and includes admission for both days. The Hoopstick Club offers a VIP experience with ringside seating adjacent to the Show Jumping arena and overlooking the exciting water complex with additional vistas of the Cross-Country course; a continental breakfast, lunch or brunch with a full open bar; and a cocktail party with wine, beer, a Hoopstick specialty cocktail and light hors d'oeuvres.
For those looking to maximize their outdoor enjoyment, the hillside area provides tailgaters panoramic views of the entire event. Attendees may bring a picnic lunch or purchase all the fixings at The Farmstand. Tailgating packages include one reserved hillside parking space and four admission tickets each day.
Proceeds from the event will benefit the Greater Newark LifeCamp, which provides an enriching day camp experience for approximately 300 Newark-area youths per day for six weeks during July and August.
"We are excited to bring back this iconic event, not just for horse enthusiasts, but for anyone who enjoys a day out in the country," said Ralph Jones, President of Essex Horse Trials. "Morgan Rowsell has designed a beautiful course for the equestrian competition which allows spectators to view the horses up close. And we'll have great vendors and activities that will provide families with plenty to do as they enjoy the spectacular beauty of Moorland Farm."
Mars, Inc., the original sponsor of the Essex Horse Trials, is returning as the event's title sponsor.
Presenting sponsors are Open Road Auto Group, Peapack-Gladstone Bank, RWJ Barnabas Health, and Running 'S' Equine Veterinary Services.
"I am thrilled by the community's positive reception and excitement of having Essex return," said Guy Torsilieri, chairman of Far Hills Race Meeting Association, past chairman of the Essex Horse Trials and current board member of the new Essex Horse Trials. "This is the next step in growing high-level equestrian events in this area."
For three decades, the Essex Horse Trials was one of the highlights of the equestrian calendar, attracting top American and international competitors as well as thousands of fans who enjoyed its social aspects as well. The trials were originally conceived in 1968 as a competition for less experienced riders and horses.
Throughout the 1970s and 1980s, the event continued to grow. It expanded to a three-day format and eventually moved to the United States Equestrian Team headquarters at Hamilton Farm in Gladstone, where riders competed for positions at both the Olympic Games and World Championships. The event ended on its 30th anniversary in 1998 when some of the USET land was developed.
The 2017 Mars Essex Horse Trials will offer competition at the beginner novice through preliminary levels with riders vying for $25,000 in prize money. Eventing provides a rare opportunity for spectators of all ages and interests, not just in equestrian sports, to witness the unique trust and bond between horse and rider over three distinct areas of competition.
Tickets are available at all Peapack-Gladstone Bank locations and online at www.essexhorsetrials.org.
Mars, Incorporated is a private, family-owned business with more than a century of history, $35 billion in sales, and six diverse business segments producing some of the world's best-loved brands: PEDIGREE®, ROYAL CANIN®, IAMS®, BANFIELD® CESAR® (Petcare); M&M'S®, SNICKERS®, DOVE®, GALAXY®, MARS®, MILKY WAY®, TWIX® (Chocolate); DOUBLEMINT®, EXTRA®, ORBIT®, 5™, SKITTLES® (Wrigley); UNCLE BEN'S®, DOLMIO®, MASTERFOODS®, SEEDS OF CHANGE® (Food); ALTERRA COFFEE ROASTERS™, THE BRIGHT TEA COMPANY™, KLIX® FLAVIA® (Drinks); and COCOAVIA® (Symbioscience). Headquartered in McLean, VA, Mars operates in 421 facilities across 78 countries, where our more than 80,000 Associates -all united by the company's Five Principles of Quality, Efficiency, Responsibility, Mutuality and Freedom -strive every day to create relationships with our stakeholders that deliver growth we are proud of.
For more information about Mars, Incorporated, please visit www.mars.com. Join us on Facebook, Twitter, LinkedIn and YouTube.
Saturday, June 24 --- 8:00 a.m.-8:00 p.m.
Sunday, June 25 --- 8:00 a.m.-4:00 p.m.
All tickets include 2-day admission and free parking.
Children age 14 and under: Free.
VIP Hoopstick Club: $250, includes preferred ringside seating, continental breakfast, lunch or brunch, cocktail party.
Tailgating: $400, includes one reserved hillside parking space and four admission tickets.


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Discography collection by long time friends. Everything besides the Still Life album tracks. Essential!
South Carolina's ANTISCHISM remain legend among the peace-punk community for raising the voice of resistance, defiance and hope in the dark years of American hardcore music of the early 1990s. Innovative hardcore with blasting male and female vocal tradeoffs, offbeat guitar attack and throttling drum beats charged with powerful lyrics. Antischism is a singles collection including tracks from the rare All Their Money Stinks of Death 7" EP, End of Time 7" EP, their side of the split Thinning the Herd LP with SUBVERT and various other outtakes and compilation tracks. A complement to their classic Still Life LP, The CD is similar to an ultra limited and long out of print version produced by Clearview records in the mid-1990s, but is now enhanced with new mastering, and layout with all the lyrics presented. The booklet folds out into a mini poster with foil stamped exterior. The art has been culled from their original releases and assembled at Stealworks by John Yates who designed many of the bands original releases. Members of ANTISCHISM went on to play in INITIAL STATE, DAMAD, .FUCKING COM and remain a force in today's hardcore scene in CHRONICLE A.D. , GUYANA PUNCH LINE and KARST
1 Foreign Policy 2:14
2 Scream / Violent World 4:31
3 Salvation Or Annihilation 1:55
4 Flesh Of Another 1:57
5 End Of Time 2:25
6 Big Brother (In Your Bedroom) 2:38
7 Elements Of Oppression 3:43
8 Factory 1:43
9 Roleplay 1:17
10 Lines On A Map 1:46
11 Slaughter 3:15
12 Labels 1:19
13 Freedom At Last 3:50
14 No Hope 2:04
15 Alien Race 1:58
16 Greedy Bastards 2:22
17 Foreign Policy 2:07
18 Salvation Or Annihilation 1:55
19 Flesh Of Another 1:54
20 End Of Time 2:22
21 Big Brother (In Your Bedroom) 2:19
22 Elements Of Oppression 3:37
24 Factory 1:39
26 Where We Stand 1:06
27 Take Your City Back 1:21
28 Scream / Violent World 4:10
29 Sacrifice 0:59
31 Path Of Destruction 1:50
32 Mothers 1:20
34 Fist 2:03
35 Evil God 2:12
This CD is a collection of out of print material from Antischism.
Tracks Taken From:
(1-4) - From The "All Their Money Stinks Of Death" 7" ep.
(5-8) - From The "End Of Time" 7" ep.
(9-13) - From The "In The Face Of Desperation" ep. (Unreleased)
(14-16) - From The "Live In The Studio" 7" ep.
(17-29) - From The "Thinning The Herd" Split LP
(30-31) - From The "End Of Time Plus One" 7" ep.
(32-33) - From The "End Of Time Plus One" (2x7") ep.
+ Original Outakes From The "Still Life" Recording Session.
(34-35) - From Original Demo.
(29) - Originally Written & Performed by Rudimentary Peni.


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Q: What event does the probability ${{n\choose k}\over 6^n}$ describe? The event "getting $k$ times the number $6$ in $n$ dice throws" has probability ${n\choose k}\cdot({1\over 6})^k\cdot({5\over6})^{n-k}$
So what event corresponds to ${{n\choose k}\over 6^n}$ ?

A: Just take two random number from $1$ to $6$, say $1$,$2$.
Throwing a dice $n$ times.
Then the probability to have $k$ $1$ appearing and all remaining are $2$ is $ \frac{{n}\choose{k}}{6^n}$.
Which is an extremely low probabilistic event, since the asymptotic estimate of ${n}\choose{k}$ is at most $2^n$.

redpajama_set_name: RedPajamaStackExchange


text:
Q: ArangoDB Create Graph from edges and documents I have created an edge collection , and I read that the collection should point to documents .
As documents I have created a dcument collection this collection has as a schema :
("Entry","name","reference")
the reference attribute is the key that link the documents to the schema found in the edges document .
How do I make that clear to arangoDB to create the graph ?
I don't see how to do it


text:
Views about abortion among adults who feel a deep sense of wonder about the universe at least once a week by age group
Views about abortion among adults who feel a deep sense of wonder about the universe at least once a week by age group (2014) Switch to: Age distribution among adults who feel a deep sense of wonder about the universe at least once a week by views about abortion
% of adults who feel a deep sense of wonder about the universe at least once a week who say abortion should be…
Learn More: Legal in all/most cases, Illegal in all/most cases


FFSC has a thriving yacht section with cruises in company organised regularly from May to September.
Cruises vary from exploring the delights of our local rivers to longer voyages – usually including one to London and an extended cruise to the Netherlands. We welcome all sizes of boat, both sail and power. Many of our members also cruise independently, using the club as a base to keep in touch. Please see the 2019 Cruising Programme for event details.
Our first event of 2019 is a social one. We are meeting on Saturday 16 March to discuss the 2019 Cruising Programme. So if you would like to be involved in the fine tuning of this year's programme please join us for a meal and a pint at at The Kings Head in Woodbridge, at 7.00pm for 7.30pm.
More information about the cruises will be published in the FFSC Weekly email and on the website. All club members are welcome to join by sea or by road.
For more additional information or to register interest for events please contact Lynda Skelton – see contact information below.


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Washington And The World
The Other Russia Scandal This Week
What you missed while you were obsessing about #ReleaseTheMemo.
By MICHAEL CARPENTER
Michael Carpenter is senior director of the Penn Biden Center for Diplomacy and Global Engagement and a former deputy assistant secretary of defense for Russia, Ukraine, Eurasia.
The Trump administration's stunning decision this week to forgo mandatory sanctions on individuals doing business with Russia's defense and intelligence sectors and its failure to publicly name and shame corrupt Kremlin insiders only underscores its dereliction of duty and disregard for our national security. With fitting symbolism, the administration chose instead to invite the directors of the three Russian intelligence services—the very agencies responsible for carrying out an attack on our election—for an unprecedented joint visit to Washington. To repeat: This is something that has never happened before in American history.
Trump officials falsely argued that sanctions on Russia's defense and intelligence sectors were unnecessary because the mere threat of sanctions was sufficient to deter businesses from doing deals. State Department spokeswoman Heather Nauert claimed, for example, that "foreign governments have abandoned planned or announced purchases of several billion dollars in Russian defense acquisitions."
Perhaps. But aside from the fact that the sanctions, which passed last summer by an overwhelming margin in Congress, were not optional, the evidence suggests Russia's defense industry is not being deterred from entering new markets. Far from it: Russia is currently in talks with Turkey, Saudi Arabia, and Qatar—both traditional U.S. arms purchasers—to supply sophisticated S-400 air defense systems, while Russia's United Aircraft Corporation, a major defense contractor, decided just this month to market new airplanes in Europe and North America. Financial markets also read the administration's decision to forgo sanctions as a green light, with yields on Russian bonds sinking to the lowest point since the 2014 invasion of Crimea.
Regarding the requirement to compile a "Kremlin list" of corrupt officials, the administration decided to take the easy way out, and simply released a list of officials that could easily have been a copy-and-paste job of the Kremlin phone book and the Forbes Top 100 list of Russian oligarchs. No details on corruption were made public, thereby completely defeating the purpose of the report—naming and shaming those enabling bad behavior in Moscow, and thus establishing a basis for future sanctions against them.
Despite having enormous asymmetric power at its disposal, including the power to block all transactions going through the U.S. financial system, this White House has proven completely unwilling to impose meaningful costs on Russia in response to its assault on our institutions. Meanwhile, the Kremlin's war machine is still operating in full swing in Ukraine and Syria while defense-sector revenues support Russia's military modernization, including the development of new systems like treaty-banned intermediate-range cruise missiles that could target U.S. forces and allies in Central Europe and East Asia.
First, we have to wake up to the fact that the United States is a financial superpower and that we have the ability to impose costs on Russia in a way that could permanently change the Kremlin's calculus. In the financial sector, for example, the U.S. market is so vast that any "blocking sanctions" on Russia's banks would have an immediate impact by forcing them to withdraw from international markets. Strangely, the United States has decided to take such sanctions entirely off the table, even as the Kremlin doubles down on election interference efforts across Europe, including the recent Czech presidential elections and the March 4 Italian parliamentary elections. Currently, full blocking sanctions, which block all transactions by entities that do business through the U.S. financial system, have been imposed on exactly one Russian bank, Bank Rossiya, which does not even rank in the top 10 Russian financial institutions.
The Trump administration has ignored and subverted the clear will of Congress—and lawmakers therefore have no choice but to respond. They should consider passing an amendment to the Russia sanctions law specifying that unless the administration certifies that Russia has ceased interfering in our democratic institutions, full blocking sanctions will be applied iteratively to a list of select Russian banks according to a fixed schedule—say, every six months. These sanctions would kick in automatically, and the Treasury Department would be able to waive them only if there were evidence of a serious risk of financial contagion.
The goal of such measures is not to crater Russia's economy but to show that the United States takes an attack on its democracy seriously and will respond with meaningful measures. (The measures the previous administration applied to Russia in December 2016, such as designating Russian Embassy personnel as persona non grata and confiscating Russian diplomatic facilities, were largely symbolic and had no impact on the Kremlin's long-term calculus.) Until the costs of its subversive measures outweigh the benefits, the Kremlin will keep trying to sow chaos and widen the political, social and ideological divisions within our country. Since the president and his team are unwilling to defend us from Russia's efforts to weaken our democracy, Congress must step in.


There's evidence that the revenue loss has stabilized. But there's no sign of growth. Here's why that's bad news for stocks.
Federal Revenues Pro Trader subscribers , click here to download the report.
Try Lee Adler's Wall Street Examiner Federal Revenues Report risk free for 90 days!


Your clients are deeply interested in ensuring the permanence of their most important images. What they likely don't understand are the long-term risks of digital media and why 35-mm film is truly archival.
Here are some tools to assist you in marketing film-based archiving to your clients.
A DIGINEG®PRO counter card to use in your studio or at tradeshows, etc.