Help those searching for transportation research on your site. If you have already implemented the TRIDGET (TRID Widget)  on your website or LibGuide, it will now take you to a result list in TRID based on the keyword(s) you entered into the TRIDGET keyword box.It is a widget that can be embedded on your own web platform and allows your customers to initiate a TRID search directly from your site. It is particularly easy to implement in LibGuides: just copy the TRIDGET code/markup into a Media/W...

As demand for air travel grows, airport-related emissions are increasing and airports are challenged to reduce associated environmental impacts. In response, expanded regulatory programs and global climate protection initiatives are being developed that require the aviation industry—including U.S. airports—to implement new, clean technologies and to modify operational practices to reduce emissions. One effective option for reducing the emissions associated with aircraft auxiliary power units (APUs) and d...

Help those searching for transportation research on your site. If you have already implemented the TRIDGET (TRID Widget)  on your website or LibGuide, it will now take you to a result list in TRID based on the keyword(s) you entered into the TRIDGET keyword box.It is a widget that can be embedded on your own web platform and allows your customers to initiate a TRID search directly from your site. It is particularly easy to implement in LibGuides: just copy the TRIDGET code/markup into a Media/W...

The Genetics Society of America (GSA) is pleased to announce the 2020 recipients of its annual awards for distinguished service in the field of genetics. The awardees were nominated and selected by their colleagues and will be recognized with presentations at The Allied Genetics Conference (TAGC), held April 22-26, 2020, in the metro Washington, DC area.

Today I said goodbye to the most amazing, resilient, loving cat in the world. After fighting a myriad of diseases like a champ, her body finally tired

Our Beloved Denver (Big Guy), Thank you for teaching us the true meaning of what love was always meant to be. You were a beautiful dog with a beautiful

My dear, beloved friend, whom I loved more than life itself, is gone. My darling Reggie, the Plymouth Rock rooster, was snatched from my arms by a sudden

Turner, Our boy always loving, playful. We will miss you but, we know it's time. We have held you, given you a thousand kisses, and told you how much

I've been reading these stories about beloved pets who died at such young ages, so I feel very blessed to have had you for 14 years. Thank you very much

Our beautiful 23 year old long haired tabby Sophie died peacefully in my husband's arms this week on 19 June 2013 - my birthday. The pain is unbearable

You were the perfect companion. We did not share your life on earth for very long, just 6 short years. I feel privileged to have been part of your life

It's so hard to believe it has now been a year since you went to Rainbow Bridge. I miss you just as much now as I did the day you passed. You will

Yesterday I lost my best friend. Nine years ago you saved my life and brought me happiness every day since. Selfishly I wanted to keep you around forever

Dude you were the best dog ever and I feel sad that we didn't tell you this every day. Yes, you drove us nuts by stealing the cats food and sleeping on

Jason: It's been one month now since you have gone to Rainbow Bridge. Jason your love was unconditional. You have left my life, but you will never leave

Pixie, you came to us beaten, starved, scared and lonely. No one wanted to take on a rescue Staffordshire Bull Terrier, but we did as company for our

Saffron, you were the most perfect being that I could ever envision. You were my sunshine. I miss you beyond words, my little Spoopa Roopa. How can we

Hey Jason! Just checking to see how you are doing at Rainbow Bridge? Hope you are making friends and being a good boy! I missed you so much my baby,

Jess came to me in June 1999 as a birthday gift. She was beautiful white with some brown and black. She was the best birthday present that I ever got or

Now, before I start this, I want to reassure you all that this is a true story. I'm not making this up. This really happened, and I thank God every night

My Sweet Toby. You were only with us for a short time and was just 15 days shy of 5 months. Why the door had to open when it did, why you ran into the

Khan-li my darling boy you were and always will be the Apple of my Eye, The Love Of My Life My Heart and all that is wonderful. The memories I have of

2 days ago I lost my best friend. Nine years ago you saved my life and stole my heart. You brought me happiness at my lowest point and gave me reason to

My darling, all of Mama's love. You have gone leaving a void in my life. I still hear you sigh, and the patter of your feet up the steps, and the sound

To my beautiful little girl Sassy, I hope wherever you are you are happy and well. I look at your photos that are all around the house and wish you were

Back when T-Mobile and Sprint were trying to gain regulatory approval for their $26 billion merger, executives repeatedly promised the deal would create jobs. Not just a few jobs, but oodles of jobs. Despite the fact that US telecom history indicates such deals almost always trigger mass layoffs, the media dutifully repeated T-Mobile and Sprint executive claims that the deal would create "more than 3,500 additional full-time U.S. employees in the first year and 11,000 more people by 2024."

About that.

Before the ink on the deal was even dry, T-Mobile began shutting down its Metro prepaid business and laying off impacted employees. When asked about the conflicting promises, T-Mobile refused to respond to press inquiries. Now that shutdown has accelerated, with estimates that roughly 6,000 employees at the T-Mobile subsidiary have been laid off as the freshly-merged company closes unwanted prepaid retailers. T-Mobile says the move, which has nothing to do with COVID-19, is just them "optimizing their retail footprint." Industry insiders aren't amused:

"Peter Adderton, the founder of Boost Mobile in Australia and in the U.S. who has been a vocal advocate for the Boost brand and for dealers since the merger was first proposed, figures the latest closures affect about 6,000 people. He cited one dealer who said he has to close 95 stores, some as early as May 1.

In their arguments leading up to the merger finally getting approved, executives at both T-Mobile and Sprint argued that it would not lead to the kind of job losses that many opponents were predicting. They pledged to create jobs, not cut them.

“The whole thing is exactly how we called it, and no one is calling them out. It’s so disingenuous,” Adderton told Fierce, adding that it’s not because of COVID-19. Many retailers in other industries are closing stores during the crisis but plan to reopen once it’s safe to do so."

None of this should be a surprise to anybody. Everybody from unions to Wall Street stock jocks had predicted the deal would trigger anywhere between 15,000 and 30,000 layoffs over time as redundant support, retail, and middle management positions were eliminated. It's what always happens in major US telecom mergers. There is 40 years of very clear, hard data speaking to this point. Yet in a blog post last year (likely to be deleted by this time next year), T-Mobile CEO John Legere not only insisted layoffs would never happen, he effectively accused unions, experts, consumer groups, and a long line of economists of lying:

"This merger is all about creating new, high-quality, high-paying jobs, and the New T-Mobile will be jobs-positive from Day One and every day thereafter. That’s not just a promise. That’s not just a commitment. It’s a fact....These combined efforts will create nearly 5,600 new American customer care jobs by 2021. And New T-Mobile will employ 7,500+ more care professionals by 2024 than the standalone companies would have."

That was never going to happen. Less competition and revolving door, captured regulators and a broken court system means there's less than zero incentive for T-Mobile to do much of anything the company promised while it was wooing regulators. And of course such employment growth is even less likely to happen under a pandemic, which will provide "wonderful" cover for cuts that were going to happen anyway.

Having watched more telecom megadeals like this than I can count, what usually happens is the companies leave things generally alone for about a year to keep employees calm and make it seem like deal critics were being hyperbolic. Then, once the press and public is no longer paying attention (which never takes long), the hatchets come out and the downsizing begins. When the layoffs and reduced competition inevitably arrives, they're either ignored or blamed on something else. In this case, inevitably, COVID-19.

In a few years, the regulators who approved the deal will have moved on to think tank, legal or lobbying positions at the same companies they "regulated." The same press that over-hyped pre-merger promises won't follow back up, because there's no money in that kind of hindsight policy reporting or consumer advocacy. And executives like John Legere (who just quit T-Mobile after selling his $17.5 million NYC penthouse to Giorgio Armani) are dutifully rewarded, with the real world market and human cost of mindless merger mania quickly and intentionally forgotten.

Update used wrong data type, causing Tinder to Spotify to fall over

A change in the Facebook SDK backend managed to crash many popular iOS apps that integrated the code library, used for implementing various Facebook services.…

It's over, Amazon, we have the high ground (and all you had was a high price) says Redmond

Updated Amazon.com has filed a second, secret, appeal against the decision to award Microsoft the Pentagon's $10bn Joint Enterprise Defense Infrastructure (JEDI) cloud contract.…

I've previously argued that going to Mars and trying to live there is a dumb idea for the foreseeable future. Notwithstanding assorted recent comments by Elon Musk this is still true. The best treatment of Musk's proposal for a big trip to Mars comes from The Martian science fiction author Andy Weir in his comments to Ars Technica. I think Weir went too easy the obviously ridiculous low cost estimates made by Musk and didn't address many of the problems with a Mars colony. But he makes excellent points. Read the article if you are interested. I like Weir's point that solar panels weigh too much to cart all the way to Mars. Better to take a nuclear reactor. I've...

The post Unpacking After a Fishing Trip: Why is it so Important? appeared first on Ocean Blue Fishing Adventures.

Levodopa-induced dyskinesia (LID) poses a significant health care challenge for Parkinson’s disease (PD) patients. Amantadine is currently the only drug proven to alleviate LID. Although its efficacy in treating LID is widely assumed to be mediated by blockade of N-methyl-D-aspartate (NMDA) glutamate receptors, our experiments demonstrate that at therapeutically relevant concentrations, amantadine preferentially blocks inward-rectifying K+ channel type 2 (Kir2) channels in striatal spiny projection neurons (SPNs) — not NMDA receptors. In so doing, amantadine enhances dendritic integration of excitatory synaptic potentials in SPNs and enhances — not antagonizes — the induction of long-term potentiation (LTP) at excitatory, axospinous synapses. Taken together, our studies suggest that the alleviation of LID in PD patients is mediated by diminishing the disparity in the excitability of direct- and indirect-pathway SPNs in the on state, rather than by disrupting LTP induction. This insight points to a pharmacological approach that could be used to effectively ameliorate LID and improve the quality of life for PD patients.

An in-depth understanding of immune escape mechanisms in cancer is likely to lead to innovative advances in immunotherapeutic strategies. However, much remains unknown regarding these mechanisms and how they impact immunotherapy resistance. Using several preclinical tumor models as well as clinical specimens, we identified a mechanism whereby CD8+ T cell activation in response to programmed cell death 1 (PD-1) blockade induced a programmed death ligand 1/NOD-, LRR-, and pyrin domain–containing protein 3 (PD-L1/NLRP3) inflammasome signaling cascade that ultimately led to the recruitment of granulocytic myeloid-derived suppressor cells (PMN-MDSCs) into tumor tissues, thereby dampening the resulting antitumor immune response. The genetic and pharmacologic inhibition of NLRP3 suppressed PMN-MDSC tumor infiltration and significantly augmented the efficacy of anti–PD-1 antibody immunotherapy. This pathway therefore represents a tumor-intrinsic mechanism of adaptive resistance to anti–PD-1 checkpoint inhibitor immunotherapy and is a promising target for future translational research.

BACKGROUND Preclinical experiments have shown that donor blood cells, modified in vitro by an alkylating agent (modified immune cells [MICs]), induced long-term specific immunosuppression against the allogeneic donor.METHODS In this phase I trial, patients received either 1.5 × 106 MICs per kg BW on day –2 (n = 3, group A), or 1.5 × 108 MICs per kg BW on day –2 (n = 3, group B) or day –7 (n = 4, group C) before living donor kidney transplantation in addition to post-transplantation immunosuppression. The primary outcome measure was the frequency of adverse events (AEs) until day 30 (study phase) with follow-up out to day 360.RESULTS MIC infusions were extremely well tolerated. During the study phase, 10 treated patients experienced a total of 69 AEs that were unlikely to be related or not related to MIC infusion. No donor-specific human leukocyte antigen Abs or rejection episodes were noted, even though the patients received up to 1.3 × 1010 donor mononuclear cells before transplantation. Group C patients with low immunosuppression during follow-up showed no in vitro reactivity against stimulatory donor blood cells on day 360, whereas reactivity against third-party cells was still preserved. Frequencies of CD19+CD24hiCD38hi transitional B lymphocytes (Bregs) increased from a median of 6% before MIC infusion to 20% on day 180, which was 19- and 68-fold higher, respectively, than in 2 independent cohorts of transplanted controls. The majority of Bregs produced the immunosuppressive cytokine IL-10. MIC-treated patients showed the Immune Tolerance Network operational tolerance signature.CONCLUSION MIC administration was safe and could be a future tool for the targeted induction of tolerogenic Bregs.TRIAL REGISTRATION EudraCT number: 2014-002086-30; ClinicalTrials.gov identifier: NCT02560220FUNDING Federal Ministry for Economic Affairs and Technology, Berlin, Germany, and TolerogenixX GmbH, Heidelberg, Germany.

Colitis caused by Clostridium difficile infection is a growing cause of human morbidity and mortality, especially after antibiotic use in health care settings. The natural immunity of newborn infants and protective host immune mediators against C. difficile infection are not fully understood, with data suggesting that inflammation can be either protective or pathogenic. Here, we show an essential role for IL-17A produced by γδ T cells in host defense against C. difficile infection. Fecal extracts from children with C. difficile infection showed increased IL-17A and T cell receptor γ chain expression, and IL-17 production by intestinal γδ T cells was efficiently induced after infection in mice. C. difficile–induced tissue inflammation and mortality were markedly increased in mice deficient in IL-17A or γδ T cells. Neonatal mice, with naturally expanded RORγt+ γδ T cells poised for IL-17 production were resistant to C. difficile infection, whereas elimination of γδ T cells or IL-17A each efficiently overturned neonatal resistance against infection. These results reveal an expanded role for IL-17–producing γδ T cells in neonatal host defense against infection and provide a mechanistic explanation for the clinically observed resistance of infants to C. difficile colitis.

Facioscapulohumeral muscular dystrophy (FSHD) results from expression of the full-length double homeobox 4 (DUX4-FL) retrogene in skeletal muscle. However, even in cases of severe FSHD the presence of DUX4 is barely detectable. In this issue of the JCI, Bosnakovski et al. used an inducible, muscle-specific human DUX4 to reproduce the low-level, sporadic DUX4 expression of human FSHD muscle as well the myopathology seen in human FSHD disease. Notably, dysregulated fibroadipogenic progenitors accumulated in affected muscles, thus providing a mechanism for the replacement of muscle by fibrosis and fat.