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"Ingrid Bergman: In Her Own Words" is the latest example of what we'll have to start calling primary-source documentaries: nonfiction films that avail themselves of their subjects' personal home movies, video, audio, scrapbooks, diaries, grocery receipts, to-do lists, and so forth. Last year we had "Amy," an Oscar-nominated film that derived its strength from a friend's home videos of Amy Winehouse in her youth, and "Listen to Me Marlon," an eerie resurrection of Marlon Brando using the audio diaries he kept for decades.
Bergman, too, appears to have documented her life from one end to the other — is that why she became a movie star? Because in a sense she already was one? Directed by Stig Björkman and with major input from the actress's grown children, "Ingrid Bergman: In Her Own Words" makes the case that Bergman saw herself and her loved ones through the lens of a camera and the frame of a screen, and she treated life as her very own adventure film. Daughter Pia Lindstrom argues in one heady interview segment that Bergman's intense relationship with her own father — he was a widower, Ingrid his only surviving child — was defined and strengthened by the 16mm home movies he took of their life together. It also meant she had a tendency to fall in love with men on the other side of the camera: war photographer Robert Capa, directors Victor Fleming and Roberto Rossellini.
We see those early home movies in Björkman's film and they're immensely touching. Using diary excerpts from adolescence onward and passages from letters Bergman wrote to friends — read on the soundtrack by actress Alicia Vikander ("The Danish Girl") — "Ingrid Bergman: In Her Own Words" follows its subject from early success in Swedish theater and films to Hollywood and producer David O. Selznick in 1939. The documentary includes her studio screen test, in color, with a chalkboard that reads "NO MAKEUP." Bergman is so naturally ravishing that the film seems lit from within.
She was passionate and ambitious; outwardly shy and inwardly confident. Shortly after arriving in Hollywood, Bergman wrote a friend "Last night a man at the table said to me 'You'll never be an actress. You're too tall.' I said to myself, 'He knows nothing about me.' " Her years in Hollywood included the apotheosis of "Casablanca," of course, but also an Oscar for "Gaslight," a peak Hitchcock film with Cary Grant ("Notorious"), and a quixotic Joan of Arc epic for producer Walter Wanger. Lindstrom remarks that her mother had had a Joan of Arc obsession since childhood, perhaps moved by the notion of "a young girl who hears voices saying she'll go do wonderful things."
"Joan of Arc" was a flop, in part because Bergman had already left her husband Petter, Lindstrom's father, for Rossellini by the time it came out. She gave birth to a son, Roberto, and later twin girls, Ingrid and Isabella, and America reeled from the scandal. The actress was denounced on the floor of the US Senate, and Bergman decamped to Europe, where another wave of home movies capture the growing brood at play. Eventually, Bergman returned to America for "Anastasia" and a second Oscar, was abandoned by Rossellini, married a Swedish theatrical producer, and worked steadily until her death in 1982 at 67.
"I have seen so much, yet it is never enough. . . . I have never understood the kind of happiness I was longing for." So wrote Bergman in a letter and that restlessness was integral to the charm that streamed from her and to the damage she caused. You could even say the two were inextricable. The grown children, interviewed, speak with a mixture of awe and rue: she was delightful to be with, she was never around. "I missed her a lot," says daughter Ingrid. "I'm going to have as much fun as her," Isabella recalls thinking (and she did). "Why didn't you want to live with us?," Pia wonders with an adult's recollection of primal hurt before shrugging that "the reality is that children aren't all that interesting."
At times "Ingrid Bergman: In Her Own Words" isn't all that interesting — at times you really do feel you're watching someone else's home movies and your attention starts to wander. But in its occasionally over-gentle way, the documentary testifies to the ego necessary to be a great star and to live a great life. And it has the temerity to suggest that it might be worth it — both for the person living the life and for everyone watching, near and far.
★ ★ ★
Ingrid Bergman: In Her Own Words
Directed by Stig Björkman. Written by Björkman, Dominika Daubenbüchel, and Stina Gardell. Starring Ingrid Bergman, Isabella Rossellini, Pia Lindstrom, the voice of Alicia Vikander. At Kendall Square. 114 minutes. Unrated (as G: adult behavior in all its contradictions).
Ty Burr can be reached at firstname.lastname@example.com. Follow him on Twitter @tyburr.


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Welcome to PWInsiderXtra's live coverage of PFL Challenger Series 2023, Week 7, which is taking place live from Universal Studios in Orlando, Florida with Impa Kasanganay and Osama ElSeady headlining.
Here is the full card for tonight's event:
The Contract Is Awarded To: Impa Kasanganay
Impa Kasanganay def. Osama ElSeady by KO via strikes (4:15, R1)
Taylor Johnson def. Trey Williams by TKO via strikes (1:20, R1)
Billy Elekana def. Tristan Overvig by unanimous decision (30-27, 30-27, 30-27)
Roland Dunlap def. Monte Morrison by unanimous decision (29-27, 29-27, 29-27)
Follow David Tees on all his platforms via https://linktr.ee/samuraitees

subset: commoncrawl


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Wedding Hair Looks


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Mirror to America
The Autobiography of John Hope Franklin
- $11.99
- $11.99
Publisher Description
John Hope Franklin lived through America's most defining twentieth-century transformation, the dismantling of legally protected racial segregation. A renowned scholar, he has explored that transformation in its myriad aspects, notably in his 3.5-million-copy bestseller, From Slavery to Freedom. Born in 1915, he, like every other African American, could not help but participate: he was evicted from whites-only train cars, confined to segregated schools, threatened—once with lynching—and consistently subjected to racism's denigration of his humanity. Yet he managed to receive a Ph.D. from Harvard; become the first black historian to assume a full professorship at a white institution, Brooklyn College; and be appointed chair of the University of Chicago's history department and, later, John B. Duke Professor at Duke University. He has reshaped the way African American history is understood and taught and become one of the world's most celebrated historians, garnering over 130 honorary degrees. But Franklin's participation was much more fundamental than that.
From his effort in 1934 to hand President Franklin Roosevelt a petition calling for action in response to the Cordie Cheek lynching, to his 1997 appointment by President Clinton to head the President's Initiative on Race, and continuing to the present, Franklin has influenced with determination and dignity the nation's racial conscience. Whether aiding Thurgood Marshall's preparation for arguing Brown v. Board of Education in 1954, marching to Montgomery, Alabama, in 1965, or testifying against Robert Bork's nomination to the Supreme Court in 1987, Franklin has pushed the national conversation on race toward humanity and equality, a life long effort that earned him the Presidential Medal of Freedom, the nation's highest civilian honor, in 1995. Intimate, at times revelatory, Mirror to America chronicles Franklin's life and this nation's racial transformation in the twentieth century, and is a powerful reminder of the extent to which the problem of America remains the problem of color.
At 90, Franklin recalls his extraordinary life. Born in the Oklahoma territory in 1915 and descended from slaves, he studied at Harvard, taught at some of the nation's most prestigious universities, served on committees for FDR and Bill Clinton, published seminal histories of blacks in America and received the Presidential Medal of Freedom for his work in civil rights. Franklin strove to evade the draft in WWII after being treated shamefully by the draft board when he tried to enlist, and did research for Thurgood Marshall in Brown v. Board of Education. Every aspect of Franklin's life has been influenced by the institutionalized racism he's experienced since he was six, when he was forced off a train for sitting in a car reserved for whites. Yet Franklin relates this all in dry, flat prose steeped in minutiae. The larger aspects of his life are glossed over; missing entirely is the emotional response to the ubiquitous racism. Nor does Franklin contextualize his experiences (e.g., in 1945, he refused to move to the back of the bus, but he fails to juxtapose this event with the Rosa Parks incident 10 years later). This disappointing autobiography fails to depict Franklin as the trailblazing iconoclast he was and is. Photos.


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Medical-Grade ECG Now Available for Consumer Wearable Devices as B-Secur Launches ECG Development Kit
September 17, 2021
B-Secur launched an electrocardiogram (ECG) hardware and software development kit designed to help technology companies fast-track the development of their ECG devices.
Heart health ECG monitoring technology company, B-Secur currently works with consumer and medical device companies, who have access to B-Secur's team of engineers on customized solutions.
Per the company, B-Secur has led these companies to develop a full solution stack to accelerate ECG development. Due to the COVID-19 global pandemic, the market demand for ECG monitoring has increased.
The ECG Development Kit will provide access to development integration of B-Secur's FDA Cleared Heartkey technology for smaller consumer wearable device makers.
B-Secur has developed an end-to-end signal chain and this kit, which features a suite of tools and guides designed to help fast-track device makers' ECG development.
B-Secur's ECG Development Kit includes an electrode guide, electrode development test jig, hardware design guide, HeartKey software library of algorithms (in user ID, wellness and health), software guide, and HeartKey signal analysis app. In addition to a dedicated training workshop, users of the kit can also access 24-hour expert support.
The launch of the "ECG Everywhere" Development Kit by B-Secur comes at an important time for cardiovascular disease (CVD), which is the No. 1 cause of death globally with an estimated 17.9 million people dying from the disease each year, representing 32% of all global deaths, according to the World Health Organization.
According to the company, the COVID-19 pandemic caused irreparable cardiac damage and arrhythmias in people with no underlying heart issues, making heart health and remote monitoring a key priority for patients, clinicians, and health service providers around the world. Developed and optimized for everyday devices, HeartKey provides the flexibility in integration, truly enabling "ECG Everywhere."
B-Secur's ECG Development Kit is currently available for license directly via the B-Secur global sales team.
For more information, visit: https://www.b-secur.com


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Key Specifications of Coal Porcelain Pavers Mini Modular Pattern Porcelain Pavers by Elegance by NT Trading:
- Thickness: 3/4″ (20 millimeters)
- Solar Reflectance Index Range:
- Grip: R11 (per DIN 51130)
- Frost Resistance: Compliant with EN ISO 10545-12.
- Surface Hardness (Mohs): 8 (per UNI EN 101).
- Resistance to Deep Abrasion: ≤ 175 mm³ (per EN ISO 10545-6).
- Resistance to Staining: Conforms to standards.
- Bending Strength/Breaking Strength: ≥ 45 N/mm²
- Water Absorption: ≤ 0.2% (per EN ISO 10545-3)
Packaging Information:
- 12″x24″: 1 pallet = L47″xD31″xH29″ = 240 sqft (3 pcs/box)
- 18″x36″: 1 pallet = L47″xD39″xH23″ = 243 sqft (2 pcs/box)
- 24″x24″: 1 pallet = L47″xD31″xH29″ = 240 sqft (2 pcs/box)
Transform your outdoor space with the Coal Porcelain Pavers Mini Modular Pattern Porcelain Pavers from Elegance by NT Trading, located at 220 Goffle Road, Hawthorne, NJ 07506. Our Italian-made pavers are ideal for a variety of applications including pools, patios, facades, rooftops, steps, treads, fireplaces, and SPAs.
Elegance by NT Trading is a leading manufacturer and distributor in Northern New Jersey, specializing in marble, travertine, and porcelain for both interior and exterior areas. We pride ourselves on providing first-quality materials directly from our quarries to ensure the highest standard for our clients.
Our range caters to over 1000 architectural designers, stores, and mason yards, offering an extensive selection of natural stone and porcelain materials including pavers, tiles, copings, veneers, ledgers, mosaics, and large to medium format slabs.
We understand the complexity of shopping for your home. Our team is dedicated to assisting customers from design ideas to curb side delivery. Clients are welcome to visit our three warehouses, located within 20 minutes of each other, to explore our material options and consult with our representatives, available six days a week.
Custom Coping services are available, including custom cut, bullnose, and mitering, with a turnaround time of under two weeks in NJ.
Contact Elegance by NT Trading today for a free sample and elevate your outdoor space with our exquisite OUTDOOR Pavers.
Elegance by NT Trading, a leading porcelain paver supplier, proudly offers an exquisite range of METAL, perfect for those seeking high-end pavers to elevate their outdoor spaces. As experts in paver supply, we specialize in Wholesale Porcelain Pavers for Outdoor use, blending luxury with practicality.
Available at wholesale prices our outdoor patio pavers, are a testament to our commitment to quality and elegance. Ideal for high-traffic areas, these pavers are a top choice for pool decks, driveways, patios, and any commercial setting. Embrace the sophistication of our high-end pavers and transform your exterior into a haven of style and durability.
As a distinguished paver supply company, Elegance by NT Trading ensures that each porcelain paver is crafted to meet the highest standards of durability, flexibility, and resistance. Our porcelain pavers are not just visually appealing; they are engineered to withstand the rigors of high traffic and the chemical exposure of poolside environments.
Incorporating these porcelain pavers into your elegant patio ideas will not only enhance the beauty of your outdoor areas but also provide a safe, non-slip surface, especially in wet conditions. Their non-porous nature makes them easy to clean and maintain, offering a practical yet stylish solution for your outdoor design needs.
Choose Elegance by NT Trading for your Wholesale Porcelain Pavers for Outdoor applications. We offer an alternative to natural stone tiles with added benefits, making our Porcelain Pavers a superior choice for your high-end paving needs.
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Application: Pool, Patio, Facade, Rooftop, Steps, Treads, Fireplace, SPA
Custom Coping: Custom cut, bullnose and mitering of porcelain available under 2 weeks in NJ
Origin of Porcelain Pavers New Modular Pattern : Italy
Service Areas: New Jersey, Connecticut, New York, Long Island, New Hampshire, Rhode Island, Michigan, North Carolina, South Carolina, Texas, Arizona, Virginia, Maryland, Pennsylvania, Florida, Georgia, California, Illinois, Ohio, Nevada.


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Why is kim cattrall not in the new movie
kim cattrall is not beating around the bush: she will never return as samantha, the icon of "sex and the city".
The Upcoming "Queer As Folk" Star Revealed That After Turning Down A Script For The Third "Satc" Movie In 2017, She Wasn't Contacted For The HBO Max Revival Series "And Just Like That," In Which Carrie (Sarah Jessica Parker), Miranda (Cynthia Nixon), and Charlotte (Kristin Davis) enter new phases of their lives.
"The series is basically the third movie. That's how creative it was," Cattrall told Variety in a cover story. "I was never asked to be a part of the reboot. I made my feelings clear after the possible third movie, so I found out like everyone else: on social media."
Cattrall's sex-positive character Samantha was reportedly going to be part of a "heartbreaking" storyline where she would receive unwanted "penis photos" from Miranda's son Brady, then 14 in the timing of the anticipated third movie and now a high school senior in "and so on".
cattrall, who now stars in hulu's sitcom "how i met your father," explained that, ideally, "some kind of event" would have to occur to warrant his appearance in a third movie, let alone one. reset series. And why would that event include a lecherous preteen?
"why can't samantha, owner of your public relations firm? Maybe she had to sell it due to financial problems? 2008 was tough," cattrall speculated about a different plot line for samantha. "some people are still recovering. he had to sell it to a guy who wears a hoodie, and that's the dilemma he has. I mean that's a scenario that was a little bit out of one of my reps' heads, and I thought that was a great idea. that's a conflict instead of a minor child…"
added, however, that "it's a great wisdom to know when enough is enough" when playing a character. "I also didn't want to compromise what the show was for me. the way forward seemed clear," cattrall said. "Everything in me said, 'I'm done. And you can't go against that feeling. I never want to be on a set and I don't want to be there."
Although Cattrall hasn't seen "and so…", the references to Samantha communicating with Carrie via text message (and missing Big's funeral) feel "different from the Samantha I played".
"I came to the conclusion that really the biggest compliment I could get as an actor is unmissable," Cattrall said, before calling it "strange" that the series still relies on his character's presence. "I don't know how to feel about it. it's so finite for me that it doesn't continue".
cattrall went on to say that the "satc" characters didn't really progress. "Everything has to grow, or it dies. I felt like when the series ended, I thought that was smart," Cattrall said. "We are not repeating ourselves. and then the movie to wrap up all the loose ends. and then there is another movie. and then there's another movie?"
cattrall continued, "parts of [samantha] are with me. I played it and I loved it. I finally felt protective of her… I was ready. As hard as it was, and as scary as it is to stand up and not be bullied by the press or the fans or whoever, just say, I'm fine. I'm on this track it was great working with you. I really enjoyed it, but I'm here."
While cattrall shared that she wants to create her own sitcom one day, the star confirmed that she won't be returning to any iterations of "satc."
as showrunner michael patrick king previously said, "you literally can't make an actress play a role." series star sarah jessica parker also stated that there would be too much history between the cast for cattrall to return.
cattrall simply told the variety that he counts his former co-stars as colleagues: "My colleagues are not my friends. It was professional."
So, it looks like Samantha is gone forever. "It's powerful to say no," Cattrall summed up. "I think the original show is really amazing, but that was a different time."
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EXTREME CONTROL – Mastectomy Sports bra
Maximum support and excellent comfort – designed for women after a mastectomy. The materials used in the extreme control prosthesis sports bra are super soft and finished in such a way as to prevent any kind of friction or skin irritation. The prosthesis pockets are made of a hydrophilic terry, which wicks away sweat from the body for an extra comfortable feeling on the skin. The padded straps offer a secure hold and comfort for the wearer.
Anita sweat management technology
* three part cup
* increasing with size range
Outer fabric
- 74% Polyester
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- 4% Elastane
- Delicate wash 40°
- Do not bleach
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- No dry cleaning
Anita Sweat ManagementAnita Sweat Management The interaction of two breathable hi-tech fabrics permits optimum, active "Sweat Management"
Less Movement
Less movement An optimum sports bra can significantly reduce the upward and downward movement of the sensitive breast tissue


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Adin Ross is a YouTuber who has accumulated a net worth of $35 million by 2023. This impressive figure is testament to Ross's success in the digital space, especially through his diverse and engaging content on YouTube. Ross's financial success reflects his ability to capture a global audience, and monetize online presence.
Adin Ross: Who is he?
Adin Ross, born on October 11, 2000 has become a household brand in the world online content creation. Ross is a popular figure in the digital community for his live streams and vlogs that combine gaming content with everyday experiences. His charismatic presence, relatability, and energetic presentation have helped him to attract a large following as an influencer and entertainer.
How has Adin Ross connected with his audience?
Ross's success can be attributed in large part to his authentic approach to content creation. It is his ability to make the viewer feel like a part of Ross's journey that creates a connection. This makes him a popular internet personality.
What makes Adin Ross unique in the content creation arena?
Ross's content is characterized by its diversity and versatility. Ross does not stick to a single niche, but instead explores a variety of topics, including gaming, lifestyle and social commentary. His adaptability has increased his appeal to a wide range of demographics and boosted his influence as YouTuber.
What has Adin Ross's career been like since he was young?
Adin Ross, who is 22 years old brings a youthful exuberance to the content creation process. He has demonstrated remarkable maturity and professionalism despite his youth, earning the respect and trust of a broad audience.
What are the physical attributes of Adin Ros?
Adin Ross is 167 cm tall (5 feet 5 inches), and weighs around 65 kg (143 pounds). Adin Ross's physical stature has been complemented by a dynamic on-screen personality, which is an important part of his appeal and brand.
What do you know about Adin Ross?
Ross's biography as captivating as his videos. His fascination with the Internet's connectivity as a child in California led him to the world of content creation. From a curious child to a content creator with influence, his journey is filled perseverance and passion.
What is Adin Ross's nationality?
Adin Ross is an American citizen, and his content is rooted deeply in the culture of the United States. His influence is felt across the world, demonstrating his ability to connect with and reach an international audience.
How did Adin Ross build his career?
Ross's career path on YouTube is notable for the authentic connection he has with his viewers and strong sense of community. Ross's natural storytelling talent, coupled with his engaging personality, has catapulted to success and made him stand out among content creators.
What makes Adin Ross such a unique storyteller?
Adin's storytelling ability lies in his ability bring viewers into his life, whether he is embarking on an adventure or sharing bits of his everyday life. Adin's sincerity in sharing his experiences makes each video feel personal.
What are the key milestones in Adin's career?
Ross has never shied away, even as his career grew, from collaborating and launching innovative projects. Ross's collaborations with celebrities and other creators have given his content new dimensions, while his business ventures show off his entrepreneurial spirit.
Adin Ross's journey as a young and ambitious YouTuber to becoming a millionaire is inspirational. Ross's ability to connect authentically with different audiences and his entrepreneurial skills have helped him to become a leader in digital content creation. His influence and networth increase with every expansion and adaptation, cementing his position as one of the most powerful forces online.


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Evan Jones has been working on some amazing projects, including his 3D printed flywheel delayed rifle chambered in .45-70. Learn all about it and ask him any questions you have!
Check out the sponsor – Vedder Holsters! They make great products and they are awesome enough to support me on this new channel.
Make sure you follow him here:
YouTube: https://www.youtube.com/c/EvanJonesProjects
Twitter: https://twitter.com/_Evan__Jones_
Odysee: https://odysee.com/@Evan_Jones:b


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My London: Elaine Burke, Designer
33-year-old fashion designer Elaine Burke is the founder of Khama; an accessories brand that works with community groups in Malawi. She is also a design consultant for Selfridges, John Lewis, House of Fraser, Whistles and ASOS. Here she chats to The London Word about London markets, live music and loving the East End…
'The East End is my favourite part of London. It is such a vibrant, creative area. My studio is there and I love the markets, especially Roman Road and Columbia Road Flower market on a Sunday.
I love the summer in London. My studio is just beside London Fields with the park and the lido so it is great.
Arriving in London on my own nearly 12 years ago is my most vivid memory; staying in a hostel in Victoria feeling scared and excited!
I think the mix of cultures and the creativity makes London really unique and amazing.
My perfect London day out would probably revolve around food. I love the variety of food London has to offer! I would start with a nice breakfast in the Pavillion in the middle of Victoria Park, then walk down the canal and see what Broadway Market has to offer, and then hop on the train to Hampstead Heath for a walk and then a nice roast dinner in the Holly Bush pub. Then back to the East End to meet with some friends and, if there is time, see some music. There are lots of great venues here and I like lots of different types of music so it is perfect!
I feel most creative in my studio of course! I share a space with lots of other designers and makers so it is a really inspiring place to work.
I love markets but I have never been to Smithfield Market. I heard it is being redeveloped so I should go before this happens.
There are restaurants in East Ham and Upton Park serving incredible South Indian food and seriously cheap.
I know the underground is a quick way of getting around, but I prefer to use the bus or walk if I can!
Learn your trade before you go out on your own and do not be afraid to take risks.
I lived in south London when I first came to London and loved Greenwich Park, the market and the Jazz cafe.
I love to relax in my garden. It is surprisingly peaceful even though it's in the centre of Hackney.
My grandmother was brought up on a farm and was a keen seamstress. She inspired me to start designing and has some similarities to the women I now work with in Malawi, who work in the fields and then come and make products with me to gain some extra income.
Go to Billingsgate Market. It is well worth the early morning to get some great bargains on some amazing fish and meet some of the characters that have stalls there.
I am currently working on finishing the set up of our new workshop in Malawi and I have some interesting new collaborations with designers in London coming up.
Happiness is… being creative and surrounded by loved ones.'


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A Screening of "Black Annie and the Pastor"
As we near the end of Black History month, Towne Street Theatre would like to focus on remembrance to look toward a better Black future. This Sunday, February 26th at 4pm, Towne Street will be hosting a screening in the TST Virtual Salon of the informative, heart wrenching and riveting drama Black Annie and the Pastor written by Tony Robinson. This is a play that exposes the true story of a fateful day in August of 1930 when a mob of more than 10,000 white people dragged two African American teens from their jail cells in Marion, Indiana and lynched them on the local courthouse grounds. Word went out that their bodies were to remain hanging to "send a message." At a time and place where almost 30% of white protestant men belonged to the Ku Klux Klan, Pastor J. E. Johnson and three African American men from nearby Muncie defiantly drove to Marion, retrieved the bodies, and took them to be respectfully prepared for burial.
This play is particularly timely because of the Emmett Till Antilynching Act which was passed by President Biden on March 29 of 2022. This legislation makes lynching a federal hate crime, punishable by up to 30 years in prison. For decades lynching was a very real fear that many African Americans had to face. This article describes how lynching and other forms of violence created a stranglehold around the Black community, prohibiting that community from the American ideal of life, liberty and the pursuit of happiness.
In order to preserve the memory of this historical event and inspire contemplation, Towne Street Theatre will also have a Q & A session after the screening led by Henry Ealy, PhD, retired chair of the American Cultures Department and retired president of the Black Faculty and Staff Association at Los Angeles City College, and Brooke-Renee Kinser Bonnell M.A., academic advisor and adjunct instructor of sociology at Ball State University.
Nancy Cheryll Davis Bellamy, TST's co-founder and artistic director states that "through the powerful storytelling talents of today's African-American writers and performers, TST brings together history and recent steps toward change like the passing of the anti-lynching bill." It is her wish and the wish of Towne Street Theatre that this screening will inspire discussion within the community as well as inspire future generations.
This is another contribute what you can event from TST. Get your tickets here.


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A protective and anti-inflammatory role for CD1d-dependent NKT cells (NKTs) has been reported in experimental and human autoimmune diseases. However, their role in arthritis has been unclear, with conflicting reports of CD1d-dependent NKTs acting both as regulatory and disease-promoting cells in arthritis. These differing modes of action might be due to genetic differences of inbred mice and incomplete backcrossing of gene-modified mice. We therefore put special emphasis on controlling the genetic backgrounds of the mice used. Additionally, we used two different murine arthritis models, Ag-induced arthritis (AIA) and collagen-induced arthritis (CIA), to evaluate acute and chronic arthritis in CD1d knockout mice and mice depleted of NK1.1+ cells. CD1d-deficient mice developed more severe AIA compared with wild-type littermates, with a higher degree of inflammation and proteoglycan depletion. Chronic arthritis in CIA was also worse in the absence of CD1d-dependent NKTs. Elevated levels of Ag-specific IFN-γ production accompanied these findings rather than changes in IL-17α. Depletion of NK1.1+ cells supported these findings in AIA and CIA. This report provides support for CD1d-dependent NKTs being suppressor cells in acute and chronic arthritis, likely via inhibition of arthritogenic Th1 cells. These results make CD1d-dependent NKTs an attractive target for therapeutic intervention.
The CD1 protein family comprises Ag-presenting molecules found on the cell surface of mainly hematopoietic-derived cells (1). The human genome encodes five CD1 genes (CD1A-E) with four corresponding proteins (CD1a–d) expressed on the cell surface (2) and a fifth (CD1e) expressed as a soluble form in lysosomal compartments (3). Based on shared sequence homology, the CD1 molecules are divided into groups 1 (CD1a, CD1b, CD1c) and 2 (CD1d) (4). The group 1 CD1 molecules are found in humans but not mice, whereas group 2, CD1d, is found in both species (5).
CD1d-restricted T cell populations have been described by many authors as rather heterogeneous. The most characterized is the invariant NKT cell (iNKT), with reference to their invariant TCR α-chain usage (Vα14-Jα18 in mice and Vα24-Jα18 in humans) and the coexpression of NK markers, specifically NK1.1, on their surface. They have also been named type I CD1d-restricted NKTs (6).
The type I NKTs are further subdivided into CD4+ and CD4−CD8− double-negative (DN) categories in mice, and in humans a population of CD8+ NKTs has been identified (7–9). It is not clear what function the expression of CD4 would have on a non-MHC class II-restricted cell, but it seems these subpopulations have different cytokine-secreting patterns poststimulation. By investigating CD4+ T cells in MHC class II-deficient mice, it was found that CD1d-dependent cells are thymically derived. They exhibit an activated, memory phenotype and add diverse TCR-bearing T cells to the CD1d-restricted population (10, 11). This NKT cell population with a variant TCR had later been referred to as type II CD1d-restricted NKTs (6). The type I NKTs respond strongly to stimulation with the Ag αGalCer (originally derived from a marine sponge) via CD1d in contrast to the type II NKTs (12). This has hindered research on type II NKTs; most of our knowledge today regarding the biological function of CD1d-restricted T cells originates from experiments on type I invariant NKT cell functions. Development of CD1d-restricted NKTs has been shown to be dependent on the expression of CD1d in the thymus; hence, this population is missing in targeted mutant mice lacking expression of CD1d (13–16). CD1d-restricted NKTs have been described as fast, potent cytokine producers; when stimulated in vitro, they rapidly release large quantities of cytokines, including IL-4 and IFN-γ (17–20). These cells have been im-plicated as regulators in inflammatory autoimmunity due to their potential to rapidly secrete cytokines, both in human diseases such as diabetes (21) and multiple sclerosis (22–24), as well as in their animal model counterparts (25–39). But their role in suppressing autoimmune diseases remains disputed, as several conflicting reports point toward a dichotomous influence of NKTs as being both beneficial or detrimental for the host (40, 41).
During the past several years, studies have been published on the role of CD1d-dependent NKTs in experimental arthritis. Some of them have focused on possible therapeutic effects of treatment with αGalCer, whereas others have worked with different knockout (ko) approaches to elucidate the intrinsic role of NKTs in arthritis. Puzzlingly enough, the results from these studies have shown discrepancies, with some results pointing toward a suppressive role for NKTs also in experimental arthritis (42–44) and others suggesting that NKTs are drivers of arthritogenic inflammation (45–48).
Due to the discrepant results from various groups, we investigated further the physiological role of endogenous CD1d-dependent NKTs in controlling versus promoting arthritis by using different means to deplete CD1d-dependent NKTs. We investigated their role in acute joint inflammation utilizing Ag-induced arthritis (AIA) (49) and their role in a chronic arthritis model, collagen-induced arthritis (CIA) (50). Both are frequently used models for the human disease rheumatoid arthritis. We show in this study that CD1d-deficient (CD1d ko) mice, lacking CD1d-dependent NKTs, develop more arthritis in both AIA and CIA compared with wild-type (wt) littermates. Hence it was of interest to clarify whether CD1d-dependent NKTs influenced the immune response via mechanisms affecting the inherited immune homeostasis or whether the regulation was an event occurring during the priming of the Ag-specific immune response. We addressed this by comparing mice genetically lacking CD1d-dependent cells with mice undergoing depletion of NK1.1-expressing cells at the time of arthritis induction. Analysis of splenic cells from CD1d ko versus CD1d ko and wt mice depleted of NK1.1+ cells and nondepleted wt mice revealed that the major differences between groups can be attributed to CD1d-dependent NKTs and not CD1d-independent NKTs. Interestingly, the number of NK cells decreased significantly as a result of NK1.1 depletion both in wt and CD1d ko mice compared with their respective nondepleted groups, suggesting that the arthritis findings reported in this paper are not easily explained by the function of NK cells. Lack of CD1d-dependent NKTs at the time of induction of arthritis in wt and CD1d ko mice worsened the disease course both in AIA and CIA, suggesting that the regulation during the priming phase is important for control of the disease. Interestingly, from a treatment perspective, our results indicate that the lack of CD1d-dependent NKTs also affects severity during disease progression.
Materials and Methods
Animals were kept and bred at the conventional animal facility of the University of Lund, Lund, Sweden and the University of Copenhagen, Copenhagen, Denmark. All animal experiments were done in accordance with the ethical committees in Malmö-Lund, Sweden, and Denmark. CD1d ko mice (13) on a C57BL/6J (B6) background (10-generation backcross) were obtained and further backcrossed to B6 in our animal facility for five generations. These mice were also backcrossed to C57BL/10-H2q (BQ) for >10 generations. Both heterozygote CD1d+/− and homozygote CD1d+/+ littermates were used in the experiments as controls. As no differences were detected between these two groups, they will hereafter be referred to as CD1d wt mice. Animals were sex- and age-matched (14–20 wk) in all experiments.
AIA: induction and clinical evaluation
AIA was induced in the first experiment (Fig. 1A) by s.c. injection of 100 μg methylated BSA (mBSA) (Sigma-Aldrich Chemie, Steinheim, Germany) dissolved in 50 μl PBS (Life Technologies, Paisley, U.K.) and emulsified in CFA (2 mg/ml heat-killed Mycobacterium tuberculosis, strain H37RA) (Difco Laboratories, Detroit, MI) at the base of the tail at days −21 and −14. In addition, 500 ng pertussis toxin (Bordella pertussis; Sigma-Aldrich Chemie) was injected i.p. at days −21 and −14. At day 0, 100 μg mBSA in 25 μl PBS was injected into the left knee joint space. As a control, 25 μl PBS was injected into the right knee. Sizes of the knees were measured daily until day 9 and thereafter three times a week.
As this protocol resulted in severe joint inflammation, we widened the window for the detection of disease increase by applying a milder immunization protocol. Therefore, AIA was further induced using a milder protocol by injecting mBSA in CFA and pertussis toxin (as above) at day −14 only (data in Figs. 1B and 7). At day 0, 50 μg mBSA in 5 μl 0.9% saline solution (saline being less of an irritant than PBS) was injected into the joint space of the left knee. As a control, 5 μl 0.9% saline solution was injected into the right knee. Sizes of the knees were measured daily. Knee joint swelling was measured with an Oditest vernier caliper (H.C. Kröplin, Schluechtern, Germany) and was expressed in millimeters as Δ values between the right and left knee.
CIA: induction and clinical evaluation
For induction of CIA, mice were immunized s.c. at the base of the tail with 100 μg rat collagen type II (rCII) (Chondrex, Redmond, WA) emulsified 1:1 in CFA (Difco Laboratories). Mice were given a booster injection at day 30 with 50 μg rCII emulsified 1:1 in IFA (Difco Laboratories). Clinical scoring was performed as described earlier (51). Briefly, each inflamed toe or knuckle gave one point, whereas an inflamed wrist or ankle counted for five points, resulting in a score of 0–15 (5 toes + 5 knuckles + 1 wrist/ankle) for each paw and 0–60 points for each mouse. The mice were examined one to four times per week for at least 2 mo postimmunization. The following parameters were used in data analysis: frequency of diseased animals was calculated as number of diseased animals divided by total number mice in group; mean score was calculated as the sum of all individual scores on one day divided by group size; area under the curve (AUC) is the sum of each scoring point of one individual covering the whole experimental period. Clinical scoring in all experiments was performed blindly, often by at least two independent investigators.
In vivo NK1.1 cell depletion
To deplete NK1.1+ cells in vivo, mice were injected i.p with 500 μg anti-NK1.1 (PK136, hybridomas originally obtained from Dr. M. Kronenberg, La Jolla Institute for Allergy and Immunology, La Jolla, CA) or isotype-matched control Ab (L243, BD Pharmingen, San Diego, CA) in 500 μl PBS.
Both knee joints were dissected at day 5 of AIA, fixed in 4% formaldehyde for 3 d, and then decalcified in EDTA. The knee joints were then dehydrated and embedded in paraffin, sectioned, and stained with hematoxylin and erythrosine for inflammation evaluation and with Safranin O for scoring of proteoglycan depletion. Six slides per group were stained and three areas per slide were scored. Histology scoring was performed using a scale from 0–3; for inflammation, defined as the influx of inflammatory cells, 0 = no inflammation to 3 = severely inflamed joint; for matrix proteoglycan depletion as reduction of Safranin O staining at cartilage surface: 0 = no abnormalities to 3 = destained/complete loss of staining. Data analysis was done on the mean scores from three areas scored per slide.
Proliferation assay using thymidine incorporation
Single-cell suspensions were prepared from spleens at day 5 of AIA and cultured in DMEM with glutamax-1 (Life Technologies) supplemented with 10% heat-inactivated FCS (PAA Laboratories, Linz, Austria), 0.5% MEM nonessential amino acid (#11140, Life Technologies), 0.16 μM/ml penicillin (Sigma-Aldrich Chemie), and 0.03 μM/ml streptomycin (Sigma-Aldrich Chemie) in 96 flat-bottom plates (Nunc, Roskilde, Denmark) with concentrations of 1 × 106 cells/well. The cells were cultured in duplicate with 25 μg/ml of mBSA (Sigma-Aldrich Chemie) or 10 μg/ml purified protein derivative (PPD; Serum Institute, Copenhagen, Denmark) as positive control or without Ag as negative control. Cells were pulsed with 1 μCi [3H]thymidine per well (Amersham Biosciences, Buckinghamshire, U.K.) after 72 h, harvested after an additional 18-h culture, and counted using a β scintillation counter (Matrix 96 direct β counter, Packard, Meriden, CT) to assay T cell proliferation. Data were expressed as the mean from duplicate wells, and the proliferation ratio was calculated (i.e., β counts from Ag-stimulated cultures divided by background counts from cultures in medium only).
Sandwich cytokine ELISAs
Supernatants from in vitro stimulation of T cells (as described above) were collected after 72 h and assayed for IFN-γ. IFN-γ ELISA was performed using 5 μg/ml capturing Ab R46-A2 and 0.5 μg/ml biotinylated detection Ab, Ani8, (BD Biosciences, San Jose, CA). Ninety-six well plates (FluoroNunc Maxisorp, Nunc) were coated with capturing Ab in coating buffer (pH 9) at 4°C overnight. Plates were blocked with 1% BSA (Sigma-Aldrich Chemie) in PBS (Life Technologies). Samples and recombinant cytokines were added in duplicate and incubated at room temperature before detection Ab was added. Plates were thereafter incubated with europium-avidin (Wallac Oy, Turku, Finland) and washed, and enhancement buffer (Wallac Oy) was added and fluorescence intensity measured as relative luminescence units (RLUs) with a Victor/Wallac (Wallac Oy, Turku, Finland). For washing between incubations, PBS-based ELISA buffer with 0.1% Tween (Sigma-Aldrich Chemie) was used. Data were expressed as the mean from duplicate wells, and the cytokine release ratio was calculated (i.e., RLU from Ag-stimulated cultures divided by background RLU from cultures in medium only).
Cytokine ELISAs for the CIA experiment were performed using sandwich ELISA kits following the manufacturer's instruction manuals: IFN-γ (#551866, BD OptEIA, BD Biosciences); IL-17α (#14-7175-68, eBioscience, San Diego, CA); IL-13 (Duo set #DY413, R&D Systems, Minneapolis, MN), and TNF-α (Ready-SET-Go! mouse TNF-α, #88-7324, eBioscience). As substrate TMB ONE (#4380L, Kem-En-Tec Diagnostics, Taastrup, Denmark) was used, the reactions were stopped with 0.2 M sulfonic acid and plates were read at 450 nm in a photospectrometer (BioTek Instruments, Winooski, VT). KJ-junior software was used, and the concentration was calculated based on the provided recombinant cytokine standards.
FACS staining and sorting of PK136-depleted splenocytes
B6 wt and B6 CD1d ko male mice were injected with 500 μg functional grade PK136 (#16-5941-85, eBioscience); control B6 wt mice and B6 CD1d ko mice received i.p. injections with carrier solution. Spleens were collected 2 d later for FACS analysis. Single-cell suspensions were made, and erythrocytes were lysed with RBC-lysis buffer (#00-4333-57, eBioscience), washed in PBS, and resuspended in FACS buffer (2% BSA, 0.01% sodium azide in PBS); cells were incubated with anti-FcR Ab (2.4G2) for 20 min on ice. Thereafter, splenocytes were incubated with biotinylated, FITC- or PE-labeled Abs. For intracellular staining, cells were fixed and permeabilized using BD Cytofix/Cytoperm (BD Biosciences). All Abs were purchased from BD Pharmingen and were used at 1–5 μg/ml unless stated otherwise. Abs were allowed to bind for 20 min on ice. Abs were PE-Cy5–anti-CD4 (GK1.5), FITC–anti-CD3 (145-2C11), APC–anti-CD8a (53-6.7), PE-anti–IFN-γ (XMG1.1, eBioscience), PE-anti–IL-17a (TC11-18H10), PE–anti-CD49b (DX5), FITC, and PE–anti-NK1.1 (PK136). Dead cells were discriminated in all stainings using the LIVE/DEAD Fixable Dead Cell Stain Kit for 405 nm excitation (L34955, Invitrogen, Carlsbad, CA). Cells were acquired with an FACSAria (BD Biosciences) using the FACSDiva software for acquisition after exclusion of duplets, and FlowJo 8.8.6 (Tree Star, Ashland, OR) was used for further analysis. The experiment was repeated twice with similar results, and hence, the shown data are the summary of these two experiments.
Statistical analysis
All statistical evaluations were done using nonparametric Mann-Whitney U tests or Student unpaired t tests with StatView software and Prism 4 for Macintosh (GraphPad San Diego, CA). FACS data were analyzed using ANOVA with Newman-Keuls multiple comparison test. Values of p < 0.05 were considered significant. Data are shown with respective mean ± SEM.
B6 CD1d ko mice develop more severe acute AIA with higher levels of Ag-specific IFN-γ
To investigate the inflammatory response in the absence of CD1d-dependent NKTs, AIA was induced in B6 CD1d ko mice and their heterozygote and homozygote littermates. Swelling of knee joints was measured, and Δ values of left and right knees were compared between the groups of mice. No difference was detected between heterozygote and homozygote wt littermates, and data from the groups were hence collated and will be referred to as the wt group.
As seen in Fig. 1A, both groups developed knee joint inflammation with an acute phase lasting for ~1 wk, after which the swelling receded in both groups. B6 CD1d ko mice developed significantly more severe acute inflammation compared with their wt littermates (p < 0.001, days 1–7), with almost twice as large Ag-specific swelling of the knee joints as the wt mice. After the acute phase, the extent of joint inflammation subsided and became comparably low in both groups. The experiment was repeated with similar results (Fig. 1B). Histopathological analysis of the knee joints on day 5 supported the clinical observations and revealed a significantly higher degree of inflammation (Fig. 1C, 1D) based on scoring numbers of infiltrating cells (CD1d ko, 2.67 ± 0.4; wt, 1.28 ± 0.5; p < 0.001) and proteoglycan depletion score (CD1d ko, 2.03 ± 0.5; wt, 1.31 ± 0.5; p < 0.05) in affected joints from B6 CD1d ko mice compared with B6 wt. Evident bone destruction was not observed in this milder form of the AIA model at this time point.
Ag-specific T cell responses were investigated using in vitro splenocyte cultures dissected on day 5 post AIA. Data presented in Fig. 2A show that Ag-specific T cells from B6 CD1d ko mice released much higher levels of IFN-γ in response to mBSA compared with T cells from B6 wt mice (Ag-specific IFN-γ release, negative control ratio: CD1d ko, 28 ± 10; wt, 7 ± 2; p < 0.01). However, they did not significantly differ in their proliferation (Fig. 2B), indicating that individual mBSA-specific T cells from B6 CD1d ko mice had a higher capacity to release IFN-γ when re-encountering Ag. Interestingly enough, no difference was observed between B6 CD1d ko and wt mice in regards to T cell response toward PPD (Fig. 2) or Con A (data not shown), suggesting that the elevated T cell IFN-γ release in mice lacking CD1d-dependent NKTs was not due to a general higher activation status of T cells in these mice. Even though IFN-γ has recently been implicated as a regulatory cytokine in arthritis (52), others have shown that IFN-γ worsens CIA and is important for cartilage destruction during immune complex-mediated arthritis (53, 54). Nevertheless, arthritis is commonly believed to be a Th1-driven disease, and hence, IFN-γ is an appropriate marker to investigate T cell effector function in models of arthritis.
The significant increases in joint inflammation, measured by joint swelling and histopathological scoring, and increased Ag-specific effector T cell functions indicate an elevated cellular immune response in B6 CD1d ko mice. This is in agreement with the conclusion that CD1d-dependent regulation is active in the acute inflammation in AIA.
BQ CD1d ko mice have a higher incidence and severity of CIA
To investigate the role of CD1d-dependent NKTs in a chronic arthritis model, we immunized BQ CD1d ko and wt mice with rCII to induce CIA. The B6 and BQ mouse strains differ mainly in the MHC haplotypes, with H-2q strains having been shown to be more susceptible to CIA and hence are more widely used in this chronic model (55). No differences in numbers or phenotype of CD1d-dependent NKTs have been reported for the strains, and our preliminary unpublished data do not support any such differences.
As shown in Fig. 3 and Table I, BQ CD1d ko mice developed arthritis more frequently than wt mice (p < 0.05 over experimental period) and also had significantly higher severity scores (AUC over experimental period: CD1d ko, 54.5 ± 21.5; wt, 3.4 ± 1.4; p = 0.01). Single-cell preparations of splenocytes revealed that the BQ CD1d ko mice had significantly higher numbers of splenocytes (Fig. 3C). The higher disease outcome in the BQ CD1d ko mice was also reflected by the significantly higher Ag-specific IFN-γ production upon in vitro restimulation, shown in Fig. 4. For other measured cytokines (IL-17α, IL-13, and TNF-α), no significant differences in the Ag-specific responses could be detected between the BQ CD1d ko and wt groups.
. | n . | Arthritis Incidence (%) . | Maximum Score [mean (SD)] . | Day of Onset (Affected Mice Only) [mean (SD)] . | Accumulative Score (Until Day 50) [mean (SD)] . |
Strain | |||||
Statistics | p = 0.02a | p = 0.008b | NS | p = 0.01b |
. | n . | Arthritis Incidence (%) . | Maximum Score [mean (SD)] . | Day of Onset (Affected Mice Only) [mean (SD)] . | Accumulative Score (Until Day 50) [mean (SD)] . |
Strain | |||||
Statistics | p = 0.02a | p = 0.008b | NS | p = 0.01b |
Arthritis incidence indicates if the mouse was disease affected during the time course of the experiment. Maximum score indicates the highest scoring value of a mouse during the disease course. Day of onset applies to mice that got disease only (healthy mice are excluded). Accumulative score until day 50 (AUC day 50) is the sum of all scores during the experimental period.
χ2 test.
Mann-Whitney U test.
The observed increased arthritis was hence accompanied by an increased level of Ag-specific IFN-γ production, which supports the conclusion that CD1d-dependent NKTs are not only regulators in the acute joint inflammation in AIA, but also operate in the chronic arthritis model, CIA, by dampening the arthritogenic Th1 response, but without a major influence on Ag-specific Th2 or Th17 responses.
No changes in IL-17+ and IFN-γ+ T cell or NKT subsets in B6 CD1d ko versus PK136 depleted mice
The observations of clinical and immune response differences could be due either to an altered immune homeostasis from the ontogenetic absence of CD1d-dependent NKTs or to immune deviation of the immune response mounted in the presence or absence of CD1d-dependent NKTs. To investigate this further, CD1d-dependent NKTs need to be selectively depleted at the time of immunization for arthritis. As there is currently no superior method available to selectively deplete CD1d-dependent NKTs, we chose to investigate their role in arthritis models using the PK136 Ab (anti-NK1.1 IgG) to deplete NK1.1+ cells. In the B6 mouse, the NK1.1 marker is believed to be expressed by the majority of mature CD1d-dependent NKTs in the periphery (41, 56), and the majority of T cells expressing NK1.1 are CD1d reactive (40). However, classical NK cells also express NK1.1 and have been reported to control the early-onset phase of CIA (57), which could influence the results in such an experiment. Nevertheless, using NK1.1 depletion could further elucidate and verify the findings from the CD1d ko mice. However, as mentioned above, the peripheral immune cell homeostasis could be different between genetically CD1d-deficient mice and NK1.1-depleted mice. Therefore, an FACS analysis of splenocytes was conducted to compare B6 wt male mice and B6 CD1d ko, both injected i.p. with the NK1.1-depleting Ab PK136 (500 μg/mouse), to B6 wt mice and B6 CD1d ko mice receiving only carrier solution (n = 3–6/group). Two days postinjection, single-cell suspensions were made from spleens and stained for FACS analysis. As shown in Fig. 5, the analysis revealed that the percentages of DN (gated on CD3+CD4−CD8−) T cells, single-positive CD4 and CD8 T cells, and the CD4/CD8 ratio were similar among the groups studied. As expected, the main differences among wt and CD1d ko groups were found to be in the NKT population (gated on CD3+NK1.1+), which was also reduced as a result of PK136 treatment. Classical NK cells (gated on DX5+NK1.1+) were, as anticipated, also significantly reduced as a result of NK1.1 depletion in both wt and CD1d ko mice. The percentage of NK cells gated on CD3−NK1.1+ showed similar results: mean ± SD of wt, 7.5 ± 1.4; wt PK136-treated, 0.18 ± 0.05; CD1d ko, 5.1 ± 0.94; and CD1d ko PK136-treated, 0.24 ± 0.41; PK136 treatment in both groups reduces NK cells significantly (p < 0.001).
Interestingly, as shown in Fig. 6, CD4+NKTs (CD3+CD4+NK1.1+), CD8+NKTs (CD3+CD8+NK1.1+), and DN NKTs (CD3+CD4−CD8−NK1.1+) were similarly affected by genetic knockdown of CD1d and depletion using PK136, all resulting in significantly lower populations compared with the untreated wt mice.
IL-17 production has been reported to be associated with iNKTs (58–60). However, Fig. 7A shows that the percentages of IL-17+ cells were not affected by either NK1.1 depletion or CD1d de-ficiency in any of the cell populations analyzed. This is because no differences were observed among the groups in IL-17+CD4+ or IL-17+CD8+ T cells or in any subset of NKTs. Furthermore, there was no evidence that IL-17–producing NK cells were affected by CD1d deficiency or by NK1.1 depletion.
The percentages of IFN-γ+ cells showed a similar pattern as IL-17+. No differences in IFN-γ+ cells were observed in the T cell and NKT subsets or NK cells as a result of genetic modification or NK1.1 depletion (Fig. 7B).
Collectively, the FACS analysis confirms that the major differences among B6 wt, B6 CD1d ko mice, and mice actively depleted of NK1.1 cells are related to the CD1d-dependent NKT subpopulations, including CD4+NKTs, CD8+NKTs, and DN NKTs. Although no major effect on NK cells could be seen as a result of genetic knockdown of the CD1d molecule, NK1.1 depletion significantly reduced but did not diminish NK cells in both B6 wt and B6 CD1d ko mice. No significant differences were detected among the groups in the percentages of IL-17+ and IFN-γ+ CD1d-dependent NKTs, other T cell populations, or NK cells.
In summary, it is noteworthy to highlight that the data show that the main differences found among B6 wt and B6 CD1d ko mice in subpopulations of splenocytes can be attributed to the intrinsic defect in generation of CD1d-dependent NKTs. Depletion of NK1.1+ cells from wt mice using PK136 as compared with CD1d ko mice did, however, result in loss of DN NKTs and NK cells in addition to diminishment of all other NKT subpopulations. No major differences were found in other cell populations when comparing CD1d-deficient and NK1.1-depleted mice, and depletion of NK1.1+ cells in CD1d ko mice showed results comparable to wt mice treated with PK136.
Depletion of NK1.1+ cells prior to AIA induction leads to severe disease and higher Ag-specific inflammatory T cell response
To investigate the effect of depleting NK1.1-expressing cells at the time of AIA induction, B6 wt mice were injected i.p. with depleting Ab 1 d preimmunization and 1 d before knee injection and followed for Ag-specific joint inflammation during the acute phase of the disease. Mice were sacrificed for histopathological evaluation of knee joints and in vitro T cell activation assays.
In concordance with previous observations from B6 CD1d ko mice, B6 wt mice treated with anti-NK1.1 also developed significantly more severe Ag-specific joint swelling when compared with mice receiving control Ab (Fig. 8A). In addition, the acute joint inflammation was associated with significantly higher Ag-specific T cell proliferation and IFN-γ release in NK1.1-depleted mice when splenocytes were restimulated in vitro with mBSA (Fig. 8B, 8C), signifying an elevated inflammatory cellular immune response in NK1.1-depleted mice.
The results indicate that suppression mechanisms operating in AIA in B6 wt mice are absent in the B6 CD1d-deficient mice and that this suppression is mediated by NK1.1+ cells. However, as there were no differences between B6 CD1d ko and B6 wt NK1.1-depleted mice in regard to AIA development, we believe that this can be attributed to the suppressive function of CD1d-dependent NKTs and not other NKT subsets or NK cells. Our results also indicate that the disease-suppressive effects of NKT cells are not due to an intrinsic imprinting during development of the immune system, but that their regulatory functions operate during the priming of a specific immune response and subsequent inflammation.
Depletion of NK1.1+ cells upon arthritis induction leads to more frequent and severe CIA
To confirm these findings in a chronic arthritis model, BQ wt mice were depleted of NK1.1+ cells at the time of immunization (day 0) for CIA and compared with control- treated animals. Both groups developed arthritis (Fig. 9, Table II) with a significantly higher frequency in the NK1.1-depleted group (p < 0.05 over expermental period). Also, diseased animals in the NK1.1-depleted group developed a more severe CIA (AUC over experimental period: NK1.1-depleted, 213 ± 70; control, 87 ± 36; p < 0.05). The experiment was repeated with similar results (data not shown). These results indicate that NK1.1+ cells are not only operative in the acute inflammatory AIA model, but also during the disease progression in a chronic inflammatory CIA model. Again, as similar results were observed when investigating BQ CD1d ko and B6 wt NK1.1-depleted mice in regard to CIA development, this suggests that the suppression is likely operating through CD1d-dependent NKTs.
. | n . | Arthritis Incidence (%) . | Maximum Score [mean (SD)] . | Day of Onset (Affected Mice Only) [mean (SD)] . | Accumulative Score (Until Day 75) [mean (SD)] . |
Strain | |||||
BQ wt, PK136 treated | 13 | 69 | 18 (18.5) | 42 (6.7) | 213 (70) |
BQ wt, control treated | 15 | 53 | 9 (12.9) | 51 (11.5) | 87 (36) |
Statistics | p = 0.05a | NS | NS | p = 0.05b |
. | n . | Arthritis Incidence (%) . | Maximum Score [mean (SD)] . | Day of Onset (Affected Mice Only) [mean (SD)] . | Accumulative Score (Until Day 75) [mean (SD)] . |
Strain | |||||
BQ wt, PK136 treated | 13 | 69 | 18 (18.5) | 42 (6.7) | 213 (70) |
BQ wt, control treated | 15 | 53 | 9 (12.9) | 51 (11.5) | 87 (36) |
Statistics | p = 0.05a | NS | NS | p = 0.05b |
Arthritis incidence indicates if the mouse was disease affected during the time course of the experiment. Maximum score indicates the highest scoring value of a mouse during the disease course. Day of onset applies to mice that got disease only (healthy mice are excluded). Accumulative score until day 75 (AUC day 75) is the sum of all scores during the experimental period.
χ2 test.
Mann-Whitney U test.
Although CD1d-dependent NKTs have been proven to be a small subset of regulatory lymphocytes, it is not clear whether their influence on the immune system always leads to beneficial suppression in autoimmune diseases, and it seems their function can be two-headed, giving both intensification and moderation of the immune response in different reported model systems (40, 41, 61, 62). Their function in arthritis models has also been debated, as several contradictory reports have been published (42–48, 63, 64), indicating both protective and disease-promoting roles of CD1d-dependent NKTs in arthritis.
CD1d-dependent NKTs have been implicated as effector cells in Ab-induced arthritis, as serum transfers to induce arthritis in both Jα281−/− mice and CD1d−/− mice resulted in less ankle swelling compared with wt mice (45–47). Pure Ab-induced arthritis models probably do not include adoptive immune responses, but mainly immune complex-induced inflammation (65), and hence, the suppressive role of CD1d-dependent NKTs described in other models with active adoptive immune responses would not be detected in the Ab-induced arthritis model. In contrast, activation of CD1d-dependent invariant NKTs using αGalCer or its analogs α-C–GalCer and OCH have been reported to protect mice from CIA (42–44), indicting a suppressive role for these cells during the arthritis process involving activation of cellular immune re-sponses. However, also utilizing the CIA model, Jα281−/− mice showed decreased clinical arthritis score compared with wt mice (47, 48). The same has been reported by one of the groups when looking at CIA in CD1d−/− mice (48), whereas the other group has reported similar findings only in Ab-induced arthritis in CD1d−/− mice (47). In contrast to the studies activating CD1d-dependent iNKTs with αGalCer or its analogs, these reports would support the notion that NKTs could function as effector cells in driving arthritic inflammation. However, as it has been shown that the TCR-α locus contains several loci modifying arthritis (66), one needs to take into consideration the effect on the linked genetic regions from the ko construct of the Jα281−/− mice when interpreting these results and whether littermates have been used as control animals in these reports.
Taken together, the above-mentioned studies could indicate that CD1d-dependent NKTs have dual functions in arthritis: during the induction phase working as regulators/suppressors of pathogenic T cells and in the effector phase, in which Ab-mediated destruction is prominent, functioning as disease promoters. In our study, by using both chronic and acute arthritis models (CIA and AIA, respectively), we addressed whether CD1d-dependent NKTs could play different roles during distinct phases of the disease. In addition, we aimed to investigate the impact of the congenital lack of CD1d-dependent NKTs compared with their depletion at the induction phase of arthritis.
In the current study, we report that when utilizing CD1d ko mice, which lack thymic-educated CD1d-dependent NKTs, arthritis was significantly more severe throughout the acute phase of AIA. This was seen as augmented swelling of the joint accompanied with histopathological changes such as elevated inflammation and proteoglycan depletion. Prominent Ag-specific IFN-γ production in CD1d ko mice, a predictive disease-promoting factor, was also elevated, implicating CD1d-dependent NKTs as playing an active role in the suppression of inflammatory processes. This is in close agreement with one of our earlier reports in which CD1d ko mice developed more severe experimental autoimmune encephalomyelitis with higher Ag-specific cytokine production (32). Our findings from the acute arthritis model, AIA, were supported when investigating the role of CD1d-dependent NKTs in chronic CIA in CD1d ko mice. These mice developed significantly more frequent and severe arthritis, indicating that CD1d-dependent NKTs are functioning by suppression of the inflammatory responses during the disease course. It remains to be clarified if this suppression is direct via cell-cell interaction through surface receptor–ligand interaction with arthritogenic T cells, or via modification of APCs, and/or via modification of tissue-specific cells and hence inflammation. Nevertheless, such a suppressive function of CD1d-dependent NKTs could have implications for the prevention of relapses with further joint destruction during chronic relapsing disease courses. This could hold therapeutic potential in arthritis.
Looking from a possible treatment perspective, the role for CD1d-dependent NKTs as suppressors of arthritis would be most relevant after disease onset and establishment. This has been addressed in the past with rather promising results in which αGalCer activation of CD1d-dependent invariant NKTs was re-ported to decrease arthritis, even though it was shown that the protocol for administration was crucial for the outcome (44). Although αGalCer is a very strong activator, it is not a naturally occurring ligand for CD1d-dependent NKTs, and hence results reported in previous studies using such treatment do not address the physiological role of these cells. In addition, it has been suggested that serial exposure to αGalCer could render CD1d-dependent NKTs anergic (67). We instead wanted to investigate if CD1d-dependent NKTs were actors during the course of arthritis development without artificial activation. Moreover, it was of interest to clarify whether our observed CD1d-dependent regulation of arthritis in CD1d ko mice was due to an influence of CD1d-dependent NKTs on the inherited immune homeostasis or rather operated by controlling the priming of the adaptive immune response during disease induction. Hence, we aimed to deplete CD1d-dependent NKTs from adult animals at the time of arthritis induction. According to current knowledge, there is no method available to selectively deplete CD1d-dependent NKTs with stringency. However, it is known that most CD1d-restricted mature NKTs in the periphery express the NK1.1 surface marker (68) and can be depleted by injecting an mAb, PK136. Results from our NK1.1 depletion experiments indicated that the possible suppressive role of CD1d-dependent NKTs in arthritis models was by shaping the adaptive immune responses at onset and thereby controlling the arthritis development. Our observations also suggest that the lack of this subpopulation prevents the control of the disease progression, resulting in stronger disease severity in chronic CIA. However, as the IFN-γ and IL-17α cytokine pattern of the remaining NKT cells before and after PK136 depletion and in CD1d ko mice was unchanged, this suggests that the CD1d-dependent NKTs use other effector mechanisms to change the Ag-specific inflammatory environment, possibly by influencing APCs. The Ag-specific arthritogenic Th1 response was clearly ameliorated by CD1d-dependent NKTs, but without a major influence on Ag-specific Th2 or Th17 responses. Because our current report does not support a role for CD1d-dependent NKTs in suppression of Ag-specific Th17 cells, their function could differ from iNKTs recently reported to prevent development of the Th17 lineage (60).
Classical NK cells also express the NK1.1 marker and have recently been implicated in the regulation of CIA (57). In addition, other NK1.1-expressing cells such as CD1-independent DN NKTs are depleted as a result of PK136 treatment of wt mice, which could influence the results from these experiments. Our FACS results confirm a significant reduction of NK cells in the depletion experiments. In addition, the number of NK cells between CD1d ko mice and wt mice showed no major difference, even though the mice have different disease outcomes. This is suggesting that the arthritis findings reported in this paper are not explained by function of NK cells. In contrast, the CD1d ko experiments and the NK1.1 depletion experiments in wt mice show consistent results regarding arthritis development and Ag-specific IFN-γ production, strengthening the notion that CD1d-dependent NKTs function as suppressors during the development of arthritis. The role of CD1-independent NK1.1-expressing cells in arthritis remains to be clarified, as well as a putative shared alternative function of NK1.1 signaling between CD1-dependent and CD1-independent cells expressing this receptor.
One also needs to take into consideration difficulties in classifying and identifying CD1d-dependent NKTs when interpreting data (e.g., Jα281 ko mice do not lack the same NKT cell population as CD1d ko mice or wt mice depleted with anti-NK1.1 Ab) (69, 70). Jα281 ko mice only lack the invariant type I NKTs, whereas in CD1d ko mice, all CD1d-dependent NKTs are absent. When using the NK1.1-specific depleting Ab, all CD1d-dependent and CD1d-independent NKTs expressing the NK1.1 marker would be depleted in addition to other NK1.1-expressing cells.
Moreover, it is noteworthy to mention that we have in this study used different models of arthritis, used mice with slightly different genetic backgrounds, investigated congenital lack of CD1d-dependent NKTs versus depletion in adult animals, and addressed CD1d-dependent NKT function during an acute joint inflammation and in a later chronic phase—all with consistent results. Our collective data point toward CD1d-dependent NKTs being suppressive cells in arthritis models rather than drivers of inflammation. Our current report is also in line with the findings that CD1d Ag presentation and NKT cell functionality are defective in patients with rheumatoid arthritis (71–73), and the findings point toward CD1d-dependent NKTs as potential therapeutic targets for treatment of chronic arthritis.
We thank Emma Mondoc and Ida Ericsson for excellent help with Ab purification and arthritis scoring.
Disclosures The authors have no financial conflicts of interest.
This work was supported by grants (to S.I.-N.) from The Swedish Rheumatism Association, Börje Dahlins Fond, the Swedish Research Council-Medicine, the Crafoordska Foundation, the G-J Kocks Foundation, the Åke Wiberg Foundation, the Alfred Österlunds Foundation, the Tore Nilson Foundation, Konung Gustaf V's 80 Årsfond, the M. Bergvalls Foundation, the Bibi and Nils Jensen Foundation, and the Danish Research Council-Medicine, and a generous grant from the Lundbeck Foundation, Copenhagen, Denmark.
Abbreviations used in this paper:


text:
As a writer, feedback is constantly important.Lakehead University Free Grammarly Account Login… However it's necessary for any feedback to consider the factors behind the writing, or why the text was written in the top place.
It seems to be making a mindful effort to turn their AI editor into something more human with these customized goals.
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Style (formal or casual).
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Domain (scholastic, business or technical).
Changing these settings helps decide which issues it'll flag or neglect. will also deliver some fantastic insights based on these goals.
Let's discuss some of these settings and why I believe they are so essential.
Audience: Your audience is important when identifying the delivery of your material. Using lingo and extremely technical, industry-specific words can be incredibly beneficial when your audience are professionals in the field. It can be exceptionally disconcerting when they're the general audience.
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Can I use Grammar Tools for free or are they worth buying?
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text:
oil on canvas
96.0 x 106.5 cm
signed lower right: Fred Williams
signed, dated and inscribed with title on artist's label verso
bears inscription on stretcher bar verso: 2
Rudy Komon Gallery, Sydney
Private collection, New South Wales, acquired from the above in 1977
Thence by descent
Private collection, New South Wales, acquired from the above in 2004
Acacias, Arthurs Creek, 1977 is a very singular work in Fred Williams' oeuvre.Rich in all the best we associate with his art, here it is raised to new heights through the interaction of the great landscape traditions of the West and the East as they inspire each other. Williams travelled to China in mid-1976, sketching, viewing, absorbing. Visiting the Imperial Palace, Beijing on 2 June, he noted, 'a great landscape painting … 300 years old – one of the best landscapes I have ever seen'.1 Williams was impressed by 'the extraordinary aura that seems to emanate everywhere from a land so suffused with history'.2 Across the scroll-like unrolling of our landscape, seen both in plan and profile, the creek stretches almost from the top to the very bottom of the canvas itself, embracing vestiges of the serpentine rivers recorded in Williams' China Sketchbook, 1976 (private collection). Now creeks, they plummet waterfall-like in their vertical drop. As Deborah Hart has observed, 'Williams saw that despite the many differences, there were some parallels between Australia and China'.3 She cites the enormous size of both countries and dominance of their landscapes, adding, 'In both places this implies a meditative spaciousness in which the human hustle and bustle is made relative'.4
The small country town of Arthurs Creek is a short distance northeast of Melbourne, not far from where fellow-artist Clifton Pugh lived at 'Dunmoochin', Cottles Bridge. It was at Pugh's place in 1969 where Williams began painting the golden wattle that first enthralled him in the mid-winter of 1969. Returning to the subject later, he wrote in his diary for 24 July 1974: 'It was a superb spot and a delight to paint the Wattles in their natural surrounds'.5
Working from his rainbow palette of the time, in Acacias, Arthurs Creek, 1977, Williams provides us with a banquet of paint and colour. Washes are overladen with an abundance of colours and textures – succulent greens, mauves, pinks, browns and most of all, yellows. All herald the golden wattle and nature's promise of the glory that is spring. Veils and swirls of paint translate into landscape forms or expanses, fields undulate or float, and flats romance verticals as dark-lined tree trunks extend the upward–downward compositional pull – the climbing scene allows both visual ascent and descent. A spill or run of pigment becomes a creek. And all is bathed in an atmosphere both luminous and aqueous as realism and abstraction dwell in harmony.
1. Hart, D., Fred Williams: Infinite Horizons, exhibition catalogue, National Gallery of Australia, Canberra, 2011, p. 151
2. ibid.
3. ibid, p. 154
4. ibid, p. 154
5. The artist quoted in Mollison, J., A Singular Vision: The Art of Fred Williams, exhibition catalogue, Australian National Gallery, Canberra, 1989, p. 175


text:
- Number 41695
- Friends theme
- Ages 4+
- 111 pieces
- Released 1 January, 2022
- Retired 31 December, 2022
Welcome to Heartlake City Pet Clinic. Mia is bringing in her cat Duo with its hurt leg. Help Mia wheel Duo into the clinic on the cute trolley. Place the cat on the table so the vet can scan it. Give Duo some medicine and place it on the bed for a nap. After a rest Duo feels much better. Take the cat upstairs for a bath, groom it and let it play on the cat gym. Duo's been such a brave kitty!
- 2-storey vet clinic toy teaches building skills while kids enjoy fun animal play
- Comes with 2 mini-dolls and 3 animal toys for kids
- Treatment room is downstairs, with a pet play and grooming area upstairs
- Birthday gift for kids aged 4 and up who love toys that spark imagination play
- Takes up little space so can be left out ready for whenever it's time to play
- Starter Bricks and picture guides help kids aged 4 and up build with ease
- 4+ sets help kids develop skills that will get them all set to start school
- Compatible with LEGO Friends Pet Clinic Ambulance (41694)
- LEGO bricks and pieces connect and pull apart easily every time
- This popular toy is tested to the max to ensure a safe play experience
- Weight: 0.364 kg
- Box Length: 61 mm
- Box Width: 191 mm
- Box Height: 262 mm
- Building instructions


text:
Meet Your School Counselors
12th grade - Class of 2024
[email protected]
570-323-8411 ext. 60522
Mrs. Susan Hunsinger
10th grade - Class of 2026
[email protected]
570-323-8411 ext. 60521
11th Grade - Class of 2025
[email protected]
570-323-8411 ext. 60524
Mrs. Kaitlin Eck
9th grade - Class of 2027
[email protected]
570-323-8411 ext. 60523
Guidance/Athletics Secretary
*Contact for records requests for current students
570-323-8411 ext. 60528
For transcript requests for WAHS graduates, please contact:
District Service Center at 570-327-5500 or WAHS graduates can request transcripts through Parchment at www.parchment.com.
Course Selection
Course selection for the next school year will begin in February 2024. Counselors will meet individually with students during their English classes. Students should review the course catalog before meeting with their counselor so they know what classes they want to request for next year.
Parents/guardians - students will bring a copy of their course request sheet home for you to review and sign. Please reach out to your student's counselor with any questions.
Below is a copy of the 2023-24 Course Catalog.
Scholarships are made available to students as they are received. We will also make announcements about other local scholarships and awards as they become available. It is important for seniors to make an appointment in guidance and pay close attention to the morning announcements to be aware of opportunities.
2023 WAHS Common Scholarship
The WAHS Common Scholarship Application includes a list of local scholarships administered by the WAHS Counseling office. Please read each scholarship and check the ones that you wish to be considered for (and that you meet the specific qualifications). These are scholarships only available to WAHS seniors and are of amounts greater than $500. Recipients are announced at graduation ceremonies.
Career Path — How to Choose
As soon as you enter high school, everyone starts asking you, "What are your plans for after high school?" For some, the answer comes easily, but for many, they remain uncertain about their plans until 11th or 12th grade. What options do you have? Maybe you will go to college, enlist in the military, get a full-time job, or go to a technical/trade school. Regardless of what you are considering, there are many things you can do now to help make the transition much easier for you!
In addition to discussing your interests with your school counselor, consider what skills you have as well as what type of environment you would want to work in. Do you want to be outside? Working and collaborating with others? Are you willing to move for your career? How do you feel about working with children or the elderly? There are many options available, and new careers are being created every day. If you still aren't sure, consider some of the options below.
Complete an Interest Inventory
- Interest inventories will ask you to respond to a series of questions and, based on your responses, will match your interests to a list of potential careers. Either of these would be a great starting point:
- PA Career Zone - Interest Profiler
- O*NET Interest Profiler
Do I Have to Go to College?
Research from the Pennsylvania Department of Education indicates that by 2025, 60% of Americans will need a post-secondary credential. Since 2011, the US economy has added 11.5 million net new jobs but only 80,000 for those with high school diplomas or less.Consider the following: Seventeen of the fastest growing jobs in the United States require less than a 4-year degree. The second fastest growing job, computer support specialist, requires an associate's degree.
So do you have to go to college? The answer is probably yes, but not a traditional 4-year institution. There are a number of career and technical education programs that might better suit your needs.
As a freshman, it is important that you keep as many options open to you as possible upon graduation. You can keep more options open to you by doing your very best and getting involved in clubs and activities throughout your high school.
College Planning Guide for Parents
Affordable Colleges Online created the following guide to help ease the transition process by addressing the common first-year challenges for parents and their children. The following guide helps parents prepare for the high-school to college transition; explores the financial aid process; discusses concerns about housing and student independence; identifies on-campus resources for students; and offers resources for parents of high school students, college freshman, college students, and graduate school students. Click this link to access the guide: College Planning Guide
WAHS Graduation Requirements
1) Earn 23 credits in grades 9-12.
Subject | Credit |
English Credits | 4.0 (1 Course per year) |
Mathematics Credits | 4.0* (1 Course per year) |
Science Credits | 3.0/4.0** (1 Course per year) |
Social Studies Credits | 3.0/4.0** (1 Course per year) |
Physical Education/Health Credits | 1.5 |
Arts and Humanities Credits | 2.0 |
Electives Credits | 4.5 |
* Any student that completes Calculus I by their Junior year has officially completed their high school math requirements.
** Students have a choice of a swing credit. They have the ability to choose a 4th course of science or social studies, their senior year, to fulfill graduation requirements.
2) Score Proficient or Advanced on the required Keystone Exams.
Career & Technical Education Program Completer Requirements:
1) Earn 23 credits in grades 9-12.
Subject | Credit |
English Credits | 4.0 (1 Course per year) |
Mathematics Credits | 4.0* (1 Course per year) |
Science Credits | 3.0 (1 Course per year) |
Social Studies Credits | 3.0 (1 Course per year) |
Physical Education/Health Credits | 1.5 |
Arts and Humanities Credits | 2.0 |
Electives Credits | 4.5 |
* Any student that completes Calculus I by their Junior year has officially completed their high school math requirements.
College Information
SAT and ACT: Which test should I take?
Which test should I take? Learn more about the differences from the Princeton Review.
SAT Registration deadlines
Parchment Exchange enables high school transcripts to be sent to post-secondary educational institutions electronically.
- This adds speed and simplification to the transcript delivery.
- There is no cost for this service to current high school students.
- All students must create a Parchment account in order to send their transcripts.
Links for general information, quick start, and creating an account are listed below.
Student Services
Williamsport Area School District is aware that our students and their families are all different, and require various levels of support and information to help their children succeed in school and prepare for life after school.
In addition to the services listed below, Williamsport Area High School provides assistance with
- Developmental Services
- Assessment and Intervention
- School Health
- Guidance and Counseling
- School Safety
- Substance Abuse
- Mental Health Issues
- School Social Workers
- Peer Mediation
SAP (Student Assistance Program)
Are you facing a challenging issue? Do you have a friend who is struggling? The SAP team can help.
We are a group of specially-trained teachers, counselors, and administrators who are here to help. Our team deals with mental health problems - like depression and suicidal thoughts. We also provide support to those who may be experimenting with alcohol or other drugs.
Our referral process is STRICTLY CONFIDENTIAL! Referrals can be made by talking to any principal, counselor or teacher. Anonymous referrals can also be made in the library - there is a drop box inside the library's entrance.


text:
The Nationalux Research Center says it is making plans to launch what it is billing as the first augmented reality (AR) music service platform utilizing Microsoft Hololens.
Nationalux said the AR music service platform can recognize album covers, posters, QR codes and other images via mobile or Microsoft Hololens. The platform can also analyze the frequency of downloaded or streamed MP3s to deliver a more powerful and spectacular sound compared to previous stereo files.
The platform can upmix the files to various audio signals such as the 5.1-7.1 channel and distinguish the direction, volume and time-lag of the files. In addition, sound can be controlled by a simple touch or a hand motion for various sound effects.
Previous multi-channel audio files can also be delivered or played through the platform.
This technology of 5 million songs
The AR music streaming service platform is scheduled to be launched in August simultaneously on Android, iOS and Hololens, initially with a library of 5 million songs. Customers who use Hololens to access the platform will be able to sign up for sound upgrades and premium benefits.


text:
As COVID-19 began to spread, audiences turned toward CNN for information on the rapidly spreading pandemic.
Just in the U.S., CNN in April saw 173 million unique visitors and March saw 184 million unique visitors. Globally, March registered 259 million unique visitors to CNN Digital properties.
In addition, CNN Digital also surpassed ESPN in March and was only behind YouTube, Facebook, Hulu, Vevo, Yahoo, and Netflix in digital video streams.
CNN was also:
- #1 in global digital news in March 2020
- #1 in U.S. multiplatform visitors in March and April 2020
- #1 in mobile unique visitors in March and April 2020
- #1 in multiplatform video starts in March 2020
- #1 in millennial reach in march and April 2020
- #1 political news source in march and April 2020


text:
The National Consumer Commission (NCC) will release its report on the inquiry conducted into the Vacation Ownership / Timeshare Industry at a media briefing to be held on Thursday 6 December 2018 in Pretoria.
The report will be released as follows:
Date: Thursday 6 December 2018
Time: 11AM – 12PM
Venue: GCIS, Ronnie Mamoepa Media Centre, Tshedimosetso House, corner of Francis Baard & Festival Streets, Hatfield, Pretoria.
NB: There will be a video link to the GCIS Imbizo Centre in Cape Town, situated at 120 Plein Street.
Members of the media are invited to the briefing.


text:
Wednesday Dec 19, 2018
Programme 346, Katie Ashford pt 2 (19-12-18)
Wednesday Dec 19, 2018
Wednesday Dec 19, 2018
Presented and produced by Seán Delaney
Theme music composed and arranged by David Vesey
This week I bring you the second part of my interview with Katie Ashford Deputy Head of Michaela Community School in Wembley Park in London. The wide range of topics we discuss include the following:
- Michaela Community School Building
- The Teach First Programme
- Starting a blog, which led to a job offer
- Personalised Instruction and whole class instruction
- Her blog posts
- A typical day
- Family Lunch (at school)
- What she likes most/least about teaching
- Her ideal English lesson
- What schools are for
- Teachers who had a significant impact on her
- Who inspires her
Katie also referred to Tom Bennett's blog and to books by Daisy Christodoulou and Daniel Willingham.
Version: 20230822


text:
Discover the advanced automation experience with H-Bots
Shaping the Future of Human-Robot Interaction
Our goal at H-Bots is to be a leading force in the field of AI-powered robotics, driving innovation and revolutionizing the way humans and robots interact. Artificial intelligence (AI) has the potential to transform the world of robotics, enabling robots to not only perform tasks autonomously but also to understand, learn, and adapt to their environment in real-time.
Pushing the Boundaries of AI Robotics
We are committed to pushing the boundaries of what is possible with AI robotics. Our team of experts in AI, machine learning, and robotics work tirelessly to develop advanced algorithms, sophisticated sensors, and state-of-the-art hardware to create robots that are smarter, more perceptive, and highly capable
Feel The Power of AI and ML in Automation
At H Bots, we are at the forefront of using Artificial Intelligence (AI) and Machine Learning (ML) to revolutionize automation in the field of robotics. Our cutting-edge robotic solutions are powered by advanced AI and ML algorithms that enable our robots to perform tasks autonomously and adapt to changing environments in real-time.
Empowering The Future
We envision a future where robots and humans can work collaboratively, leveraging each other's strengths to achieve extraordinary results. Our robots are designed to be user-friendly, intuitive, and adaptable, empowering businesses and individuals to leverage the power of robotics without the need for specialised expertise. We aim to democratize access to robotics & automation technology, making it accessible to small and medium-sized enterprises, startups, and catering our services to large scale companies.
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Enhance your manufacturing processes with our robotic automation solutions that optimize efficiency, productivity, and quality.
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Unlocking the Future of Robotics: Choose Innovation with H Bots.
We leverage the latest advancements in artificial intelligence, machine learning, and automation to develop state-of-the-art robotics solutions. We're committed to pushing the boundaries of robotics technology and constantly improving our solutions to stay ahead in the rapidly evolving field of robotics.
Our Industry
We have strategically partnered with to drive innovation and deliver cutting-edge solutions to our clients. These partnerships are based on mutual trust, expertise, and shared values, enabling us to collaborate and leverage each other's strengths to push the boundaries of what's possible in robotics.
S P A Enterprise Services Limited
The University of Warwick
Neural Foundry


text:
August 4, 2010 •
Social Media is the Emerging Question
California's Fair Political Practices Commission just released a report by the Subcommittee on Internet Political Activity saying political ads used on Web sites and social media platforms such as Facebook and Twitter should be regulated the same way ads are on any other medium.
Here are two articles for further reading :
"Social media wrap: California watchdog recommends Internet political campaign regulations," by Craig Howie in the Los Angeles Times on August 2, 2010.
"State panel calls for online political ad rules," by Marisa Lagos in the San Francisco Chronicle on August 3, 2010.
State and Federal Communications, Inc. provides research and consulting services for government relations professionals on lobbying laws, procurement lobbying laws, political contribution laws in the United States and Canada. Learn more by visiting stateandfed.com.


text: Katherine has been working at Ekata for 3 years and is the perfect "mom" to the kids in her van. Being a mom herself she knows exactly how much care mixed with discipline the kids need. Kat raised her kids in the SCV and is the wife of a retired law enforcement officer.


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We continue today with the 5th in our series of videos based on the Annual Trafficking in Persons Report (TIP) published by the US State Department in June 2021.
We look today at how the Irish Government built its capacity to prevent trafficking, where the government fell short in the prevention of trafficking, the efforts taken to raise awareness and prevent labour and sex trafficking, as well as the Trafficking in Person's (TIP) report's priority recommendations to prevent trafficking.
5. Human Trafficking – Prevention in Ireland |
For ease of access all previously published videos are available on this page.
4 Human Trafficking – Law Enforcement in Ireland. |
3. Human Trafficking – Ireland's Trafficking in Persons Report Ranking. |
2. Human Trafficking in the Global Pandemic. |
1. Human Trafficking – What is it? |