Date: May 4, 2020

Happy US Teacher Appreciation Week!

Today (and everyday!), we honor teachers across the nation, who continue to work tirelessly to shape our future generations, even in the midst of the unprecedented COVID-19 pandemic.

Today’s Doodle was created by Doodler Kevin Laughlin who collaborated with the 54 2020 State Teachers of the Year during their visit to Google this past February. 

Below, Kevin shares more on his experience working with the teachers on today’s Doodle!

I know from firsthand experience how much of a positive impact a teacher can have on a young person's life. I can't express how happy I am to have had the opportunity to be a part of the Teacher Appreciation project this year.

When I met these teachers on campus in February, I was so inspired by their love of teaching and dedication to their students, which I felt each minute I spent with them. As they presented their own Doodle designs, they shared anecdotes about their classrooms, advocated for their students, and spoke passionately about educational equity. 

I am glad to see their work represented in the final Doodle on Google’s homepage today celebrating these often unsung heroes. To every teacher, thank you times infinity! 

Learn more about the many ways Google is celebrating and supporting teachers, in classrooms or at home.

See some of the teacher concepts that inspired today’s Doodle below:

...and all of the concepts from our 54 2020 State Teachers of the Year:

Photos from the Doodle brainstorming session at the 2020 National Teacher of the Year Program

Location: U.S. Virgin Islands, United States

Tags: teachers’ day, National Holiday, education, teaching

---------------------------------------------------[Sat Nov 26 15:25:44 2016]--
From: (S) ease of well-being  (steph)

Subject: Optimism or denial as mental self-defence

A few things recently have given me cause to consider my response to bad things
happening, and my reactions to other people's responses.  First, there's
Trump's election in the US which is undesirable and directly or indirectly
likely to cause some people harm (although I doubt it'll have any effect on me
personally).  I agree that he's not the best or even a good candidate and I
agree that he has incited prejudiced people to show and act on their
prejudices: people are being hurt.  However, I do not like the stream of
articles saying he's a white supremacist or a Nazi or California should secede
or the Electoral College should choose Clinton, or whatever.  Part of this is
doubtless my contrary streak, but part of it is something different.  I observe
that I am semi-consciously adopting a position that `things will turn out all
right' or `it won't be that bad' because countenancing the opposite is not good
for my mental health.

The other thing is some changes in the wider organisation for which I work;
basically there has been a botched reorganisation which has left most people
unhappy and from what I hear from numerous sources with good reason.  This
doesn't currently affect me much and I don't expect it to because of political
realities.  However, even just having the argument with someone closer to the
failing department (and more likely to feel its direct effects) seems to be
followed by my feeling anxious and depressed.  Again, adopting a constructive
positive attitude (which may appear to others pollyannaish, naive, optimistic,
or just in denial) seems to be a defence I've learned here and I suspect it
helps.  But there's more obviously a risk when I'm more involved than I am in
the US case, namely that my optimism will blind me to dangers that will be to
my detriment.

Does my ornery nature come to the rescue, though?  Perhaps because I'm at heart
a bit of a grumpy sod and only respect authorities when I think they deserve it
my tendency to want to probe and prod and query and dig my heels in may
counteract the defensive optimism.  Or alternatively, I'm optimistic in a
different sense: perhaps I just have confidence that I'll win?

Hearing loss caused by the death of sensory hair cells of the inner ear is an unfortunate side effect for many patients treated with aminoglycoside antibiotics or platinum-containing chemotherapy agents. In animal models, induction of heat shock confers substantial otoprotection against aminoglycoside- and cisplatin-induced hair cell death. In this issue of the JCI, Breglio et al. demonstrate that inner ear tissue released exosomes carrying heat shock protein 70 (HSP70) in response to heat stress. HSP70 acted by a paracrine mechanism that engaged the Toll-like receptor 4 (TLR4) on hair cells to protect them from death. Exosomes and the HSP70/TLR4 pathway could thus provide treatment targets for the protection of hair cells from chemically induced death or from other insults, such as noise.

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.

Hair cells, the mechanosensory receptors of the inner ear, are responsible for hearing and balance. Hair cell death and consequent hearing loss are common results of treatment with ototoxic drugs, including the widely used aminoglycoside antibiotics. Induction of heat shock proteins (HSPs) confers protection against aminoglycoside-induced hair cell death via paracrine signaling that requires extracellular heat shock 70-kDa protein (HSP70). We investigated the mechanisms underlying this non–cell-autonomous protective signaling in the inner ear. In response to heat stress, inner ear tissue releases exosomes that carry HSP70 in addition to canonical exosome markers and other proteins. Isolated exosomes from heat-shocked utricles were sufficient to improve survival of hair cells exposed to the aminoglycoside antibiotic neomycin, whereas inhibition or depletion of exosomes from the extracellular environment abolished the protective effect of heat shock. Hair cell–specific expression of the known HSP70 receptor TLR4 was required for the protective effect of exosomes, and exosomal HSP70 interacted with TLR4 on hair cells. Our results indicate that exosomes are a previously undescribed mechanism of intercellular communication in the inner ear that can mediate nonautonomous hair cell survival. Exosomes may hold potential as nanocarriers for delivery of therapeutics against hearing loss.

Arterial cardiovascular events are the leading cause of death in patients with JAK2V617F myeloproliferative neoplasms (MPNs). However, their mechanisms are poorly understood. The high prevalence of myocardial infarction without significant coronary stenosis or atherosclerosis in patients with MPNs suggests that vascular function is altered. The consequences of JAK2V617F mutation on vascular reactivity are unknown. We observe here increased responses to vasoconstrictors in arteries from Jak2V617F mice resulting from a disturbed endothelial NO pathway and increased endothelial oxidative stress. This response was reproduced in WT mice by circulating microvesicles isolated from patients carrying JAK2V617F and by erythrocyte-derived microvesicles from transgenic mice. Microvesicles of other cellular origins had no effect. This effect was observed ex vivo on isolated aortas, but also in vivo on femoral arteries. Proteomic analysis of microvesicles derived from JAK2V617F erythrocytes identified increased expression of myeloperoxidase as the likely mechanism accounting for their effect. Myeloperoxidase inhibition in microvesicles derived from JAK2V617F erythrocytes suppressed their effect on oxidative stress. Antioxidants such as simvastatin and N-acetyl cysteine improved arterial dysfunction in Jak2V617F mice. In conclusion, JAK2V617F MPNs are characterized by exacerbated vasoconstrictor responses resulting from increased endothelial oxidative stress caused by circulating erythrocyte-derived microvesicles. Simvastatin appears to be a promising therapeutic strategy in this setting.

Elevated pressure in the pancreatic gland is the central cause of pancreatitis following abdominal trauma, surgery, endoscopic retrograde cholangiopancreatography, and gallstones. In the pancreas, excessive intracellular calcium causes mitochondrial dysfunction, premature zymogen activation, and necrosis, ultimately leading to pancreatitis. Although stimulation of the mechanically activated, calcium-permeable ion channel Piezo1 in the pancreatic acinar cell is the initial step in pressure-induced pancreatitis, activation of Piezo1 produces only transient elevation in intracellular calcium that is insufficient to cause pancreatitis. Therefore, how pressure produces a prolonged calcium elevation necessary to induce pancreatitis is unknown. We demonstrate that Piezo1 activation in pancreatic acinar cells caused a prolonged elevation in intracellular calcium levels, mitochondrial depolarization, intracellular trypsin activation, and cell death. Notably, these effects were dependent on the degree and duration of force applied to the cell. Low or transient force was insufficient to activate these pathological changes, whereas higher and prolonged application of force triggered sustained elevation in intracellular calcium, leading to enzyme activation and cell death. All of these pathological events were rescued in acinar cells treated with a Piezo1 antagonist and in acinar cells from mice with genetic deletion of Piezo1. We discovered that Piezo1 stimulation triggered transient receptor potential vanilloid subfamily 4 (TRPV4) channel opening, which was responsible for the sustained elevation in intracellular calcium that caused intracellular organelle dysfunction. Moreover, TRPV4 gene–KO mice were protected from Piezo1 agonist– and pressure-induced pancreatitis. These studies unveil a calcium signaling pathway in which a Piezo1-induced TRPV4 channel opening causes pancreatitis.

Familial dysautonomia (FD) is the most prevalent form of hereditary sensory and autonomic neuropathy (HSAN). In FD, a germline mutation in the Elp1 gene leads to Elp1 protein decrease that causes sympathetic neuron death and sympathetic nervous system dysfunction (dysautonomia). Elp1 is best known as a scaffolding protein within the nuclear hetero-hexameric transcriptional Elongator protein complex, but how it functions in sympathetic neuron survival is very poorly understood. Here, we identified a cytoplasmic function for Elp1 in sympathetic neurons that was essential for retrograde nerve growth factor (NGF) signaling and neuron target tissue innervation and survival. Elp1 was found to bind to internalized TrkA receptors in an NGF-dependent manner, where it was essential for maintaining TrkA receptor phosphorylation (activation) by regulating PTPN6 (Shp1) phosphatase activity within the signaling complex. In the absence of Elp1, Shp1 was hyperactivated, leading to premature TrkA receptor dephosphorylation, which resulted in retrograde signaling failure and neuron death. Inhibiting Shp1 phosphatase activity in the absence of Elp1 rescued NGF-dependent retrograde signaling, and in an animal model of FD it rescued abnormal sympathetic target tissue innervation. These results suggest that regulation of retrograde NGF signaling in sympathetic neurons by Elp1 may explain sympathetic neuron loss and physiologic dysautonomia in patients with FD.

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.

Approximately half of the world’s population is infected with the stomach pathogen Helicobacter pylori. Infection with H. pylori is the main risk factor for distal gastric cancer. Bacterial virulence factors, such as the oncoprotein CagA, augment cancer risk. Yet despite high infection rates, only a fraction of H. pylori–infected individuals develop gastric cancer. This raises the question of defining the specific host and bacterial factors responsible for gastric tumorigenesis. To investigate the tumorigenic determinants, we analyzed gastric tissues from human subjects and animals infected with H. pylori bacteria harboring different CagA status. For laboratory studies, well-defined H. pylori strain B128 and its cancerogenic derivative strain 7.13, as well as various bacterial isogenic mutants were employed. We found that H. pylori compromises key tumor suppressor mechanisms: the host stress and apoptotic responses. Our studies showed that CagA induces phosphorylation of XIAP E3 ubiquitin ligase, which enhances ubiquitination and proteasomal degradation of the host proapoptotic factor Siva1. This process is mediated by the PI3K/Akt pathway. Inhibition of Siva1 by H. pylori increases survival of human cells with damaged DNA. It occurs in a strain-specific manner and is associated with the ability to induce gastric tumor.

Systemic sclerosis (SSc) is an autoimmune fibrotic disease whose pathogenesis is poorly understood and lacks effective therapies. We undertook quantitative analyses of T cell infiltrates in the skin of 35 untreated patients with early diffuse SSc and here show that CD4+ cytotoxic T cells and CD8+ T cells contribute prominently to these infiltrates. We also observed an accumulation of apoptotic cells in SSc tissues, suggesting that recurring cell death may contribute to tissue damage and remodeling in this fibrotic disease. HLA-DR–expressing endothelial cells were frequent targets of apoptosis in SSc, consistent with the prominent vasculopathy seen in patients with this disease. A circulating effector population of cytotoxic CD4+ T cells, which exhibited signatures of enhanced metabolic activity, was clonally expanded in patients with systemic sclerosis. These data suggest that cytotoxic T cells may induce the apoptotic death of endothelial and other cells in systemic sclerosis. Cell loss driven by immune cells may be followed by overly exuberant tissue repair processes that lead to fibrosis and tissue dysfunction.

The editors of JCI and JCI Insight are revisiting our editorial processes in light of the strain that the COVID-19 pandemic places on the worldwide scientific community. Here, we discuss adjustments to our decision framework in light of restrictions placed on laboratory working conditions for many of our authors.

Lipid-rich myelin forms electrically insulating, axon-wrapping multilayers that are essential for neural function, and mature myelin is traditionally considered metabolically inert. Surprisingly, we discovered that mature myelin lipids undergo rapid turnover, and quaking (Qki) is a major regulator of myelin lipid homeostasis. Oligodendrocyte-specific Qki depletion, without affecting oligodendrocyte survival, resulted in rapid demyelination, within 1 week, and gradually neurological deficits in adult mice. Myelin lipids, especially the monounsaturated fatty acids and very-long-chain fatty acids, were dramatically reduced by Qki depletion, whereas the major myelin proteins remained intact, and the demyelinating phenotypes of Qki-depleted mice were alleviated by a high-fat diet. Mechanistically, Qki serves as a coactivator of the PPARβ-RXRα complex, which controls the transcription of lipid-metabolism genes, particularly those involved in fatty acid desaturation and elongation. Treatment of Qki-depleted mice with PPARβ/RXR agonists significantly alleviated neurological disability and extended survival durations. Furthermore, a subset of lesions from patients with primary progressive multiple sclerosis were characterized by preferential reductions in myelin lipid contents, activities of various lipid metabolism pathways, and expression level of QKI-5 in human oligodendrocytes. Together, our results demonstrate that continuous lipid synthesis is indispensable for mature myelin maintenance and highlight an underappreciated role of lipid metabolism in demyelinating diseases.

Эксперты из DxOMark протестировали камеры новых смартфонов iPhone 11 Pro и 11 Pro Max, и в результате испытаний новинки от компании Apple оказались недостаточно хороши, чтобы возглавить рейтинг. В общ...

If you were to Google the definition of a comedian you would see it defined by Dictionary.com as an entertainer whose act is designed to make an audience laugh. Likewise the New York Times has a comedy critic, Jason Zinoman, who defines comedy in a moment of reflecting on his own career of analyzing them.

This often dictates the form of my column, since while the goal of comedy is to make you laugh, what’s fascinating about the art form — especially these days, when it’s so fragmented and aesthetically diverse — is that there are many ways artists accomplish that goal.

However, if you were to ask one furry who considers himself one, 2 Gryphon, you’d find an entirely different etymology of the word, and what the job of a comic is.

It's the JOB of the comic to bring forth uncomfortable things and question them in a way that makes people think about them.Since that has become "wrong", expect that the Western world will not be laughing as much. https://t.co/EIExUX5W2h— 2, The Ranting Gryphon (@2_gryphon) June 9, 2019

It is this quote that we are going to be over-analysing today. I have broken this down into three main points as to why this definition of the job of a comedian is not only a fundamental misunderstanding of the role, but also a resignation of the foundational principles of comedy.

read more

Erowid Exp113948

On the Young Turks, Cenk Uygur quotes passages from Bob Woodward's book, "The Price of Politics", quoting statements made by President Obama proving that he intends to cut entitlements like social security, medicare, and medicaid. Continue reading →

Is your standard charge for a speech $300,000?  According to an article appearing on the website of the Las Vegas Review-Journal, and a May 31, 2013 email, Clinton’s standard contract usually includes: Round-trip transportation on a chartered private jet “e.g., a Gulfstream … Continue reading →

CNN Brianna Keilar interviews Senator Bernie Sanders on State of the Union May 17 2015. Senator Bernie Sanders says the American people want and deserve a serious debate on the serious issues facing our country today instead of merely the same old, endless 30 second, ad hominem, attack ads. Continue reading →

SANDERS: ... there is more coverage about the political gossip of a campaign, about raising money, about polling, about somebody saying something dumb, or some kid works for a campaign sends out something stupid on Facebook, right? We can expect that to be a major story. But what your job is, what the media's job is, is to say, look, these are the major issues facing the country. We're a democracy. People have different points of view. Let's argue it. Continue reading →

The evidence is adding up that this election is a SHAM! Exit polls do not add up on the Democratic side and regularly predict better results for Bernie than the voting machines are telling us! The mainstream media won't even come close to touching this, and in fact they're even attacking Lee Camp for bringing it up. Don't miss this segment of Redacted Tonight! Continue reading →

we know how politics works in the United States. Whoever—whatever political party gets into government is going to merge with the bureaucracy pretty damn fast. It will be in a position where it has some levers in its hand. And so, as a result, corporate lobbyists will move in to help control those levers. So it doesn’t make much difference in the end. What does make a difference is political accountability, a general deterrence set to stop political organizations behaving in a corrupt manner. Continue reading →

The middle class needs to vote for Donald Trump in order to oppose the elites, Corporate America, Wall Street, the career politicians, and the media, who have all conspired to destroy the middle class. Donald Trump is the Molotov cocktail, the human hand grenade, that every beaten-down, nameless, forgotten working stiff who used to be part of what was called the middle class can legally throw into the system that stole their lives from them. Continue reading →

Julian Assange says Donald Trump would not be permitted to win. All of the establishment--Wall Street, Corporate America, the elites, the media, career politicians, et al--is united behind Hillary Clinton. Continue reading →

"Trump didn’t hijack the populism, the Democratic Party made a gift of it to him. And he simply accepted it. … that elite … made a decision that in the midst of a global insurrection against political corruption and economic oligarchy that Hillary Clinton’s 'pay to play' politics in global finance capitalism would somehow play better than Bernie Sanders Democratic Socialism. … they ignored every poll they had, all the data they had, and even all the anecdotes they could possibly have accumulated in order to reach the conclusion that Hillary was a stronger candidate than Bernie. … And I remain certain that if anyone other than Clinton - and certainly if you accept for just one moment that when all the polls said the right things by such wide margins for so long they might be right - Bernie Sanders could have won this had he been the nominee, like Roosevelt took out Landon." Continue reading →

Jimmy Dore: The intelligence agencies have been releasing the reports to convince us that we should be upset at Russia because they hacked our election. First of all, who gives a shit if they did? The United States tapped Angela Merkel’s … Continue reading →

Claudia Stauber provides a perfect metaphor of how she felt listening to Bernie Sanders today in Vermont, telling us how much he still fights for us against the 1% and the oligarchs. Continue reading →

NEWS 8 IS YOUR LOCAL ELECTION HEADQUARTERS…. AND TONIGHT…VOODOO ECONOMICS! CHIEF POLITICAL CORRESPONDENT MARK DAVIS TELLING US HOW REPEALING THE STATE INCOME TAX IS THE LATEST HEATED TOPIC BETWEEN THE CANIDATES FOR GOVERNOR.   DEMOCRAT NED LAMONT IS OPENING A … Continue reading →

Шестого мая BRIAN MAY опубликовал видео, как он на коляске передвигается по больнице и подписал это сообщение:

«Проверка реальности! Для меня... Нет, вирус меня пока не поймал — слава Богу. Надеюсь, что вы все в безопасности. Но решение ослабить контроль вовсе не означает, что опасность куда-то уходит. Но я??? Да, я молчал, а причины...

Так же, как и чрезмерное напряжение и беспокойство из-за слишком многих потребностей... Я умудрился порвать ягодичную мышцу в момент чрезмерного садоводческого энтузиазма. Так что внезапно я оказался в больнице, где меня просканировали, чтобы выяснить, насколько сильно я на самом деле повредил себя. Оказалось, что я проделал тщательную работу — это было пару дней назад — и я не смогу какое-то время ходить... Или спать без особой помощи, потому что боль не утихает.

Итак, ребята... Мне нужно немного уйти в сумрак, полностью отдохнуть дома.

Пожалуйста, пожалуйста, не посылайте мне слова сочувствия — мне просто нужно немного исцеляющей тишины на некоторое время. Я вернусь, но мне нужен полный перерыв. ХОРОШО?

Спасибо. Берегите себя там!» #Brian_May #BrianMay

Посмотреть эту публикацию в Instagram

Reality check ! For me. No - the Virus didn’t get me yet - thank God. Hope you’re all keeping extra-safe out there. A decision to relax controls doesn’t suddenly make the danger go away. But me ?? Yes, I’ve been quiet. Reason ? As well as getting over-stretched and harassed by too many demands ... I managed to rip my Gluteus Maximus to shreds in a moment of over-enthusiastic gardening. So suddenly I find myself in a hospital getting scanned to find out exactly how much I’ve actually damaged myself. Turns out I did a thorough job - this is a couple of days ago - and I won’t be able to walk for a while ... or sleep, without a lot of assistance, because the pain is relentless. So, folks ... I need to go dark for a while, getting some complete rest, at home. Please, please don’t send me sympathy - I just need some healing silence for a while. I’ll be back - but I need the complete break. OK ? Thanks. Take care out there. Bri

Публикация от Brian Harold May (@brianmayforreal) 6 Май 2020 в 6:44 PDT

Компания Precision Hydration, помогающая спортсменам избежать обезвоживания, станет партнёром и официальным поставщиком команды Williams.

По информации Autosprint, бывший президент Ferrari Лука ди Монтедземоло может заменить Жана Тодта на посту президента FIA...

We are all keeping our social distance these days, and many of us, other than the superheroes in the medical profession and restocking grocery stores, are spending all of our time in our homes. The delightful ladies of Drunk Austen have thus put together a Virtual JaneCon to be held this weekend, March 28 and…

A fundraising initiative spearheaded by Canadian comic retailers and creators aims to auction off items in order to support their struggling industry.

The post Zdarsky, Fabok, & more ask you to “Be Our Heroes” for Canadian retailers appeared first on The Beat.

Plus more ways to support comics creators and new authors launching their books worldwide while social distancing!

The post Social Distancing Roundup: JOHN WICK Livestream, Neil Gaiman reads CORALINE, and an X-MEN ’92 watchalong appeared first on The Beat.

The Joker 80th Anniversary 100-Page Super Spectacular #1 will feature an all-star creative team including James Tynion IV, Dan Mora, Tom Taylor, and many more

The post PREVIEW: The origin of Punchline is revealed in the JOKER 80TH ANNIVERSARY SPECIAL appeared first on The Beat.

Now that’s a name I haven’t heard in a long time…

The post Heads up: TEMUERA MORRISON will be THE MANDALORIAN’s Boba Fett appeared first on The Beat.

IBM today announced that Faurecia, one of the world’s leading automotive suppliers, has selected IBM Cloud as a support of a major business transformation designed to accelerate digital manufacturing.

IBM Security, Packet Clearing House (PCH) and The Global Cyber Alliance (GCA) today launched a free service designed to give consumers and businesses added privacy and security protection as they access the internet. The new Quad9 Domain Name System (DNS) service helps protect users from accessing millions of malicious internet sites known to steal personal information, infect users with ransomware and malware, or conduct fraudulent activity.

Media in quarantine, live audiences abandoned, presenters self-isolate.

Fake news, conspiracy theories, calls to stay calm. How can the media help contain the deadly spread?

Ad revenue forecasts slashed as regional news become the first media casualties of COVID-19.

The media name and shame people breaking the rules on social distancing and self-isolation.

Pain continues for media industry as local news titles cease printing.

The pad thai recipe you're looking for! Try this simple trick to make a turmeric noodle version.

Continue reading Sunshine Pad Thai (Vegetarian) on 101 Cookbooks

IBM and Stone Ridge Technology today announced a performance milestone in reservoir simulation designed to help improve efficiency and lower the cost of production. Working with NVIDIA, the companies shattered previous published results using one-tenth the power and 1/100th of the space. The news demonstrates the ability of NVIDIA GPUs to simulate one billion cell models in a fraction of the published time, while delivering 10x the performance and efficiency than legacy CPU codes.

IBM and Nutanix today announced a multi-year initiative to bring new workloads to hyperconverged deployments.

IBM announced today a new experimental laboratory for nanotechnology research in Brazil. The NanoLab is part of a $4M investment within the recently upgraded IBM Research-Brazil lab in Rio de Janeiro and will focus on projects related to research in Oil & Gas, Agriculture and Health across Latin America.

IBM and the University of California San Diego have announced a multi-year project to enhance quality of life and independence for aging populations through the new Artificial Intelligence for Healthy Living Center (AIHL), located on the campus of UC San Diego. The groundbreaking center will bring together the technology, artificial intelligence and life sciences knowledge of IBM and UC San Diego to promote critical research and applications in two thematic areas: Healthy Aging and the Human Microbiome.

IBM today announced two significant milestones in making the on-premises IBM Cloud Object Storage System much more accessible for customers with new compliance-enabled vaults and concentrated dispersal mode capabilities.