The Big Questions series features perspectives from the five recipients of the Department of Energy Office of Science's 2019 Distinguished Scientists Fellows Award describing their research and what they plan to do with the award. Ian Foster is the director of Argonne National Laboratory's Data Science and Learning Division.

Tiny meteorites that fell to Earth 2.7 billion years ago suggest that the atmosphere at that time was high in carbon dioxide, which agrees with current understanding of how our planet's atmospheric gases changed over time.

A couple of months ago, a records request revealed a private surveillance contractor had access to nearly every piece of surveillance equipment owned and operated by the state of Utah. Banjo was the company with its pens in all of the state's ink. Banjo's algorithm ran on top of Utah's surveillance gear: CCTV systems, 911 services, location data for government vehicles, and thousands of traffic cameras.

All of this was run through Banjo's servers, which are conveniently located in Utah government buildings. Banjo's offering is of the predictive policing variety. The CEO claims its software can "find crime" without any collateral damage to privacy. This claim is based on the "anonymization" of harvested data -- a term that is essentially meaningless once enough data is collected.

This partnership is now on the rocks, thanks to an investigation by Matt Stroud and OneZero. Banjo's CEO, Damien Patton, apparently spent a lot of his formative years hanging around with white supremacists while committing crimes.

In grand jury testimony that ultimately led to the conviction of two of his associates, Patton revealed that, as a 17-year-old, he was involved with the Dixie Knights of the Ku Klux Klan. On the evening of June 9, 1990 — a month before Patton turned 18 — Patton and a Klan leader took a semi-automatic TEC-9 pistol and drove to a synagogue in a Nashville suburb. With Patton at the wheel, the Ku Klux Klan member fired onto the synagogue, destroying a street-facing window and spraying bullets and shattered glass near the building’s administrative offices, which were next to that of the congregation’s rabbi. No one was struck or killed in the shooting. Afterward, Patton hid on the grounds of a white supremacist paramilitary training camp under construction before fleeing the state with the help of a second Klan member.

If you're wondering where the state of Utah's due diligence is in all of this, there's a partial explanation for this lapse: the feds, who brought Patton in, screwed up on their paperwork.

Because Patton’s name was misspelled in the initial affidavit of probable cause filed in Brown’s case — an FBI agent apparently spelled Damien with an “o” rather than an “e” — any search of a federal criminal court database for “Damien Patton” would not have surfaced the affidavit.

Now that his past has been exposed, the state of Utah has announced it won't be working with Banjo.

The Utah attorney general’s office will suspend use of a massive surveillance system after a news report showed that the founder of the company behind the effort was once an active participant in a white supremacist group and was involved in the shooting of a synagogue.

The AG's office can only shut down so much of Banjo's surveillance software. Other government agencies not directly controlled by the state AG are making their own judgment calls. The University of Utah is suspending its contract with Banjo, but the state's Department of Public Safety has only gone so far as to "launch a review" of its partnership with the company. City agencies and a number of police departments who have contracts with Banjo have yet to state whether they will be terminating theirs.

And the AG's reaction isn't a ban. The office appears to believe it might be able to work through this.

“While we believe Mr. Patton’s remorse is sincere and believe people can change, we feel it’s best to suspend use of Banjo technology by the Utah attorney general’s office while we implement a third-party audit and advisory committee to address issues like data privacy and possible bias,” Piatt said. “We recommend other state agencies do the same.”

It's refreshing to hear a prosecutor state that it's possible for former criminals to turn their lives around and become positive additions to their communities, but one gets the feeling this sort of forgiveness is only extended to ex-cons who have something to offer law enforcement agencies. Everyone else is just their rap sheet for forever, no matter how many years it's been since their last arrest.

The other problem here is the DA's office's tacit admission it did not take data privacy or possible bias into account before granting Banjo access to the state's surveillance equipment, allowing it to set up servers in government buildings, and giving it free rein to dust everything with its unaudited AI pixie dust.

These are all steps that should have taken place before any of this was implemented, even if the state had chosen to do business with a company with a less controversial CEO. This immediate reaction is the right step to take, but a little proactivity now and then would be a welcome change.

The coronavirus pandemic and its associated lockdown in most countries has forced major changes in the way people live, work and study. Online learning is now routine for many, and is largely unproblematic, not least because it has been used for many years. However, online testing is more tricky, since there is a concern by many teachers that students might use their isolated situation to cheat during exams. One person's problem is another person's opportunity, and there are a number of proctoring services that claim to stop or at least minimize cheating during online tests. One thing they have in common is that they tend to be intrusive, and show little respect for the privacy of the people they monitor.

As an article in The Verge explains, some employ humans to watch over students using Zoom video calls. That's reasonably close to a traditional setup, where a teacher or proctor watches students in an exam hall. But there are also webcam-based automated approaches, as explored by Vox:

For instance, Examity also uses AI to verify students' identities, analyze their keystrokes, and, of course, ensure they're not cheating. Proctorio uses artificial intelligence to conduct gaze detection, which tracks whether a student is looking away from their screens.

It's not just in the US that these extreme surveillance methods are being adopted. In France, the University of Rennes 1 is using a system called Managexam, which adds a few extra features: the ability to detect "inappropriate" Internet searches by the student, the use of a second screen, or the presence of another person in the room (original in French). The Vox articles notes that even when these systems are deployed, students still try to cheat using new tricks, and the anti-cheating services try to stop them doing so:

it's easy to find online tips and tricks for duping remote proctoring services. Some suggest hiding notes underneath the view of the camera or setting up a secret laptop. It's also easy for these remote proctoring services to find out about these cheating methods, so they're constantly coming up with countermeasures. On its website, Proctorio even has a job listing for a "professional cheater" to test its system. The contract position pays between $10,000 and $20,000 a year.

As the arms race between students and proctoring services escalates, it's surely time to ask whether the problem isn't people cheating, but the use of old-style, analog testing formats in a world that has been forced by the coronavirus pandemic to move to a completely digital approach. Rather than spending so much time, effort and money on trying to stop students from cheating, maybe we need to come up with new ways of measuring what they have learnt and understood -- ones that are not immune to cheating, but where cheating has no meaning. Obvious options include "open book" exams, where students can use whatever resources they like, or even abolishing formal exams completely, and opting for continuous assessment. Since the lockdown has forced educational establishments to re-invent teaching, isn't it time they re-invented exams too?

Follow me @glynmoody on Twitter, Diaspora, or Mastodon.

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-Album Details- Title: NJBP Concert Archives I ~ANCIENT FESTIVAL~ Publisher: SuperSweep Catalog Number: SRVD-5001 Release Date: July 6th, 2019 Ripped by: Razakin -Info- Recording of the New Japan BGM Philharmonic Orchestra’s Ancient Festival concert, which was full of Yuzo Koshiro goodness from the Scheme to Streets of Rage and Etrian Odyssey, and as a main […]

OED Word of the Day: microfinance, n. The provision of loans and other financial services to low-income individuals and communities for the creation of small businesses…

Limit your exposure!

The post The Great Pause: A Second Chance to a Better World appeared first on Ocean Blue Fishing Adventures.

Whether mutations in cancer driver genes directly affect cancer immune phenotype and T cell immunity remains a standing question. ARID1A is a core member of the polymorphic BRG/BRM-associated factor chromatin remodeling complex. ARID1A mutations occur in human cancers and drive cancer development. Here, we studied the molecular, cellular, and clinical impact of ARID1A aberrations on cancer immunity. We demonstrated that ARID1A aberrations resulted in limited chromatin accessibility to IFN-responsive genes, impaired IFN gene expression, anemic T cell tumor infiltration, poor tumor immunity, and shortened host survival in many human cancer histologies and in murine cancer models. Impaired IFN signaling was associated with poor immunotherapy response. Mechanistically, ARID1A interacted with EZH2 via its carboxyl terminal and antagonized EZH2-mediated IFN responsiveness. Thus, the interaction between ARID1A and EZH2 defines cancer IFN responsiveness and immune evasion. Our work indicates that cancer epigenetic driver mutations can shape cancer immune phenotype and immunotherapy.

Chronic pancreatitis (CP) is considered an irreversible fibroinflammatory pancreatic disease. Despite numerous animal model studies, questions remain about local immune characteristics in human CP. We profiled pancreatic immune cell characteristics in control organ donors and CP patients including those with hereditary and idiopathic CP undergoing total pancreatectomy with islet autotransplantation. Flow cytometric analysis revealed a significant increase in the frequency of CD68+ macrophages in idiopathic CP. In contrast, hereditary CP samples showed a significant increase in CD3+ T cell frequency, which prompted us to investigate the T cell receptor β (TCRβ) repertoire in the CP and control groups. TCRβ sequencing revealed a significant increase in TCRβ repertoire diversity and reduced clonality in both CP groups versus controls. Interestingly, we observed differences in Vβ-Jβ gene family usage between hereditary and idiopathic CP and a positive correlation of TCRβ rearrangements with disease severity scores. Immunophenotyping analyses in hereditary and idiopathic CP pancreases indicate differences in innate and adaptive immune responses, which highlights differences in immunopathogenic mechanisms of disease among subtypes of CP. TCR repertoire analysis further suggests a role for specific T cell responses in hereditary versus idiopathic CP pathogenesis, providing insights into immune responses associated with human CP.

Alterations in calcium signaling in pancreatic acinar cells can result in pancreatitis. Although pressure changes in the pancreas can elevate cytosolic calcium (Ca2+) levels, it is not known how transient pressure-activated elevations in calcium can cause prolonged calcium changes and consequent pancreatitis. In this issue of the JCI, Swain et al. describe roles for the mechanically activated plasma membrane calcium channels Piezo1 and transient receptor potential vanilloid subfamily 4 (TRPV4) in acinar cells. The authors used genetic deletion models and cell culture systems to investigate calcium signaling. Notably, activation of the Piezo1-dependent TRPV4 pathway was independent of the cholecystokinin (CCK) stimulation pathway. These results elegantly resolve an apparent discrepancy in calcium signaling and the pathogenesis of pancreatitis in pancreatic acinar cells.

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.

Hepatocellular carcinoma (HCC) is clearly age-related and represents one of the deadliest cancer types worldwide. As a result of globally increasing risk factors including metabolic disorders, the incidence rates of HCC are still rising. However, the molecular hallmarks of HCC remain poorly understood. Neuropeptide Y (NPY) and NPY receptors represent a highly conserved, stress-activated system involved in diverse cancer-related hallmarks including aging and metabolic alterations, but its impact on liver cancer had been unclear. Here, we observed increased expression of NPY5 receptor (Y5R) in HCC, which correlated with tumor growth and survival. Furthermore, we found that its ligand NPY was secreted by peritumorous hepatocytes. Hepatocyte-derived NPY promoted HCC progression by Y5R activation. TGF-β1 was identified as a regulator of NPY in hepatocytes and induced Y5R in invasive cancer cells. Moreover, NPY conversion by dipeptidylpeptidase 4 (DPP4) augmented Y5R activation and function in liver cancer. The TGF-β/NPY/Y5R axis and DPP4 represent attractive therapeutic targets for controlling liver cancer progression.

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 The anti–programmed cell death 1 (anti–PD-1) antibody pembrolizumab is clinically active against non–small cell lung cancer (NSCLC). In addition to T cells, human natural killer (NK) cells, reported to have the potential to prolong the survival of patients with advanced NSCLC, also express PD-1. This study aimed to investigate the safety and efficacy of pembrolizumab plus allogeneic NK cells in patients with previously treated advanced NSCLC.METHODS In total, 109 enrolled patients with a programmed death ligand 1 (PD-L1) tumor proportion score (TPS) of 1% or higher were randomly allocated to group A (n = 55 patients given pembrolizumab plus NK cells) or group B (n = 54 patients given pembrolizumab alone). The patients received i.v. pembrolizumab (10 mg/kg) once every 3 weeks and continued treatment until the occurrence of tumor progression or unacceptable toxicity. The patients in group A continuously received 2 cycles of NK cell therapy as 1 course of treatment.RESULTS In our study, patients in group A had longer survival than did patients in group B (median overall survival [OS]: 15.5 months vs. 13.3 months; median progression-free survival [PFS]: 6.5 months vs. 4.3 months; P < 0.05). In group A patients with a TPS of 50% or higher, the median OS and PFS was significantly longer. Moreover, the patients in group A treated with multiple courses of NK cell infusion had better OS (18.5 months) than did those who received a single course of NK cell infusion (13.5 months).CONCLUSIONS Pembrolizumab plus NK cell therapy yielded improved survival benefits in patients with previously treated PD-L1+ advanced NSCLC.TRIAL REGISTRATION ClinicalTrials.gov NCT02843204.FUNDING This work was supported by grants from the National Natural Science Foundation of China (NSFC) – Guangdong Joint Foundation of China (no. U1601225); the NSFC (no. 81671965); the Guangdong Provincial Key Laboratory Construction Project of China (no. 2017B030314034); and the Key Scientific and Technological Program of Guangzhou City (no. 201607020016).

The mechanisms by which prostate cancer shifts from an indolent castration-sensitive phenotype to lethal castration-resistant prostate cancer (CRPC) are poorly understood. Identification of clinically relevant genetic alterations leading to CRPC may reveal potential vulnerabilities for cancer therapy. Here we find that CUB domain-containing protein 1 (CDCP1), a transmembrane protein that acts as a substrate for SRC family kinases (SFKs), is overexpressed in a subset of CRPC. Notably, CDCP1 cooperates with the loss of the tumor suppressor gene PTEN to promote the emergence of metastatic prostate cancer. Mechanistically, we find that androgens suppress CDCP1 expression and that androgen deprivation in combination with loss of PTEN promotes the upregulation of CDCP1 and the subsequent activation of the SRC/MAPK pathway. Moreover, we demonstrate that anti-CDCP1 immunoliposomes (anti–CDCP1 ILs) loaded with chemotherapy suppress prostate cancer growth when administered in combination with enzalutamide. Thus, our study identifies CDCP1 as a powerful driver of prostate cancer progression and uncovers different potential therapeutic strategies for the treatment of metastatic prostate tumors.

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.

It’s release day for my new MM romance! My last release was Christmas 2018, so I’m very excited to finally have a new book for you. When I was in Australia earlier this year, I got hooked on Bondi Rescue, and this (completely fictional!) romance between a trainee and an older, very closeted lifeguard was born. […]

You can grab four steamy and sweet MM holiday romances in one box set for a major discount! This new collection is only $6.99 or you can borrow it in KU. I’m also very excited that these novellas are available in print for the first time! ???? Buy the ebook box set exclusively at Amazon […]

“Looking for a fun and sweet holiday romance with dual POV, some heat, a humorous caper, and a wonderful HEA ending? Look no further!” ~ Gay Book Reviews Fa-la-la-la-la! My new holiday romance is now available to buy or borrow in KU! You’ve got fake boyfriends, bisexual exploration, found family, a single dad in desperate need […]

My figure skating romance has a new (old) title! Misha and Dev’s story was originally two novellas published through Loose Id called Cold War and Holding the Edge. I later combined them into one volume to give you more bang for your buck. To avoid confusion, I called the book The Winning Edge. However, Cold War is frankly just a much better […]

Apple today announced that it will begin reopening its retail stores in Germany on May 11, nearly two months after they were closed due to the global health crisis.


In a statement shared with German website Macerkopf, Apple said the stores will initially be focusing on Genius Bar service and support. Enhanced health and safety measures will be implemented, such as body temperature checks prior to entry, limits on how many customers can be in the store at once, social distancing, and reduced hours of operation.

Apple operates 15 retail stores in Germany and will be posting specific hours of operation for each location on its website.

Apple closed all of its retail stores outside of the Greater China region in mid-March. The company has since started to reopen some locations, including in South Korea, Austria, and Australia. All locations in the United States remain closed.

I remember reading somewhere that if the earth was shrunk to the size of a pool ball, or a pool ball expanded to the size of the earth, the earth would be the smoother of the two.

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.

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.

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

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.

At the International Supercomputing Conference in Frankfurt, The Weather Company, an IBM Business, today announced a plan to help improve weather prediction globally via a new collaboration with the University Corporation for Atmospheric Research (UCAR) and the National Center for Atmospheric Research (NCAR), a federally funded research and development center for the atmosphere and Earth’s geospace systems.

IBM today announced that according to results from International Data Corporation (IDC) Worldwide Quarterly Server Tracker®(June, 2017) IBM has achieved market growth by 3x compared with the total Linux server market which grew at +6 percent. The improved performance are the result of success across IBM Power Systems including IBM’s OpenPOWER LC servers and IBM Power Systems running SAP HANA as well as the OpenPOWER-Ready servers developed through the OpenPOWER Foundation.

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.

Walmart, JD.com, IBM, and Tsinghua University National Engineering Laboratory for E-Commerce Technologies announced today they will work together in a Blockchain Food Safety Alliance that will kick off with a collaboration designed to enhance food tracking, traceability and safety in China, to achieve greater transparency across the food supply chain.

IBM today announced that Vissensa, a UK-based managed service provider (MSP), has taken delivery of the IBM Enterprise Cloud System, which will help the company offer new and improved cloud services to its customers.

IBM today announced that Clarient Global LLC (“Clarient”), a joint venture established to transform client data and document management in the financial services industry, has selected VMware Cloud Foundation on IBM Cloud to continue to enhance its existing SoftLayer private cloud implementation for its Clarient Entity Hub platform.

IBM today announced plans to acquire Promontory Financial Group, a global market-leading risk management and regulatory compliance consulting firm. Upon close, the capabilities of Promontory combined with IBM's deep industry expertise and Watson’s cognitive capabilities will directly address the massive operational effort and manual cost of escalating regulation and risk management requirements.

IBM and Hootsuite announced plans to integrate several of their respective cloud and social technologies as well as expertise, to provide Hootsuite clients a fast and reliable social experience.