Go-movix.com redirect removal instructions

What is go-movix.com?

When certain browser's settings are set to go-movix.com, it means that there is some browser hijacker installed on it. Go-movix.com is an address of a fake search engine. As a rule, such search engines are promoted by browser hijackers. It is uncommon for users to download and install such apps knowingly, intentionally. Therefore, they are categorized as potentially unwanted applications.

It sizzles on the grill. But does it fizzle in terms of nutrition? That's the question when it comes to the new burgers made of plant-based meat substitutes that are flying off grocery store shelves and restaurant tables.

The production of formate from CO2 is considered an attractive strategy for the long-term storage of solar renewable energy in chemical form.

  So I wrote an op-ed about the recent Macmillan/ebooks kerfuffle for CNN. Here’s how that all worked…. I got...

Six months ago, which feels like roughly an eternity at this point, we discussed how Jerry Seinfeld and others won an absolutely ludicrous copyright suit filed against them by Christian Charles, a writer and director Seinfeld hired to help him create the pilot episode of Comedians In Cars Getting Coffee. What was so strange about the case is that this pilot had been created in 2012, whereas the lawsuit was only filed in 2018. That coincides with Seinfeld inking a lucrative deal with Netflix to stream his show.

It's not the most well known aspect of copyright law, but there is, in fact, a statute of limitations for copyright claims and it's 3 years. The requirement in the statute is that the clock essentially starts running once someone who would bring a copyright claim has had their ownership of a work disputed publicly, or has been put on notice. Seinfeld argued that he told Charles he was employing him in a work-for-hire arrangement, which would satisfy that notice. His lawyers also pointed out that Charles goes completely uncredited in the pilot episode, which would further put him on notice. The court tossed the case based on the statute of limitations.

For some reason, Charles appealed the ruling. Well, now the Court of Appeals has affirmed that lower ruling, which hopefully means we can all get back to not filing insane lawsuits, please.

We conclude that the district court was correct in granting defendants’ motion to dismiss, for substantially the same reasons that it set out in its well-reasoned opinion. The dispositive issue in this case is whether Charles’s alleged “contributions . . . qualify [him] as the author and therefore owner” of the copyrights to the show. Kwan, 634 F.3d at 229. Charles disputes that his claim centers on ownership. But that argument is seriously undermined by his statements in various filings throughout this litigation which consistently assert that ownership is a central question.

Charles’s infringement claim is therefore time-barred because his ownership claim is time-barred. The district court identified two events described in the Second Amended Complaint that would have put a reasonably diligent plaintiff on notice that his ownership claims were disputed. First, in February 2012, Seinfeld rejected Charles’s request for backend compensation and made it clear that Charles’s involvement would be limited to a work-for-hire basis. See Gary Friedrich Enters., LLC v. Marvel Characters, Inc., 716 F.3d 302, 318 (2d Cir. 2013) (noting that a copyright ownership claim would accrue when the defendant first communicates to the plaintiff that the defendant considers the work to be a work-for-hire). Second, the show premiered in July 2012 without crediting Charles, at which point his ownership claim was publicly repudiated. See Kwan, 634 F.3d at 227. Either one of these developments was enough to place Charles on notice that his ownership claim was disputed and therefore this action, filed six years later, was brought too late.

And that should bring this all to a close, hopefully. This seems like a pretty clear attempt at a money grab by Charles once Seinfeld's show became a Netflix cash-cow. Unfortunately, time is a measurable thing and his lawsuit was very clearly late.

I recently travelled to Pittsburgh, USA, to present the paper “From Playing Games to Committing Crimes: A Multi-Technique Approach to Predicting Key Actors on an Online Gaming Forum” at eCrime 2019, co-authored with Ben Collier and Alice Hutchings. The accepted version of the paper can be accessed here. The structure and content of various underground … Continue reading From Playing Games to Committing Crimes: A Multi-Technique Approach to Predicting Key Actors on an Online Gaming Forum →

The platforms, providers, and infrastructures which together make up the contemporary Internet play an increasingly central role in the business of governing human societies. Although the software engineers, administrators, business professionals, and other staff working at these organisations may not have the institutional powers of state organisations such as law enforcement or the civil service, … Continue reading Three Paper Thursday: The role of intermediaries, platforms, and infrastructures in governing crime and abuse →

Multinationals' UK arms pair up to take on Voda and former state-owned telco

Telcos Telefónica and Liberty Global today confirmed plans to join their O2 UK and Virgin Media subsidiaries into one combined entity in a deal analysts branded a "blockbuster merger".…

If you listen closely, you can hear how the creatures' full-throated call increases in volume when you are on holiday

On Call Friday is here! How is your weekend looking? Same as the last one, and the one before that? Never mind – before breaking into the lockdown lagers, join us for another entry in The Register's tales of those brave souls who are On Call.…

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.…

One-year-old company NovaMed has inked a deal with Hong Kong-based DHB Global that will see the start-up medical consultancy transitioning to a producer of healthcare personal protective equipment, or PPE. Under the deal finalised earlier this...

Компания MediaTek анонсировала свой новый флагманский процессор, который должен составить конкуренцию чипам Qualcomm.

Компания Xiaomi, неожиданно для всех, объявила дату анонса очередного смартфона из линейки Redmi K30.

The post What’s Cooking: Why Bleeding your Fish is Important? appeared first on Ocean Blue Fishing Adventures.

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.

The renaissance of complement diagnostics and therapeutics has introduced precision medicine into a widened field of complement-mediated diseases. In particular, complement-mediated diseases (or complementopathies) with ongoing or published clinical trials of complement inhibitors include paroxysmal nocturnal hemoglobinuria, cold agglutinin disease, hemolytic uremic syndrome, nephropathies, HELLP syndrome, transplant-associated thrombotic microangiopathy, antiphospholipid antibody syndrome, myasthenia gravis, and neuromyelitis optica. Recognizing that this field is rapidly expanding, we aim to provide a state-of-the-art review of (a) current understanding of complement biology for the clinician, (b) novel insights into complement with potential applicability to clinical practice, (c) complement in disease across various disciplines (hematology, nephrology, obstetrics, transplantation, rheumatology, and neurology), and (d) the potential future of precision medicine. Better understanding of complement diagnostics and therapeutics will not only facilitate physicians treating patients in clinical practice but also provide the basis for future research toward precision medicine in this field.

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.

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.

Regenerative pain medicine, which seeks to harness the body’s own reparative capacity, is rapidly emerging as a field within pain medicine and orthopedics. It is increasingly appreciated that common analgesic mechanisms for these treatments depend on neuroimmune modulation. In this Review, we discuss recent progress in mechanistic understanding of nociceptive sensitization in chronic pain with a focus on neuroimmune modulation. We also examine the spectrum of regenerative outcomes, including preclinical and clinical outcomes. We further distinguish the analgesic mechanisms of regenerative therapies from those of cellular replacement, creating a conceptual and mechanistic framework to evaluate future research on regenerative medicine.

Prenatal alcohol exposure (PAE) affects at least 10% of newborns globally and leads to the development of fetal alcohol spectrum disorders (FASDs). Despite its high incidence, there is no consensus on the implications of PAE on metabolic disease risk in adults. Here, we describe a cohort of adults with FASDs that had an increased incidence of metabolic abnormalities, including type 2 diabetes, low HDL, high triglycerides, and female-specific overweight and obesity. Using a zebrafish model for PAE, we performed population studies to elucidate the metabolic disease seen in the clinical cohort. Embryonic alcohol exposure (EAE) in male zebrafish increased the propensity for diet-induced obesity and fasting hyperglycemia in adulthood. We identified several consequences of EAE that may contribute to these phenotypes, including a reduction in adult locomotor activity, alterations in visceral adipose tissue and hepatic development, and persistent diet-responsive transcriptional changes. Taken together, our findings define metabolic vulnerabilities due to EAE and provide evidence that behavioral changes and primary organ dysfunction contribute to resultant metabolic abnormalities.

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.

Welcome, this week it's retro time again! Vitamin Hana wants you to escape from an unusual place - from an oceanarium. Then you get locked in Yomino Kagura's prettily decorated room, and then it's time for No1game 's short adventure... Tagged as: blog, browser, escape, escapemen, free, fuwayura, japanese, no1game, pointandclick, puzzle, rating-g, vitaminhana, weekday-escape, yominokagura

Hi, it's time to have some fun from the past! This Weekday Escape is retro! Vitamin Hana wants you to escape a room - no surprise - but also to redecorate it. Yomino Kagura isn't so demanding, their escape is... Tagged as: blog, browser, esc-forest, escape, escapemen, free, japanese, no1game, pointandclick, puzzle, rating-g, vitaminhana, weekday-escape, yominokagura

A great many people only experience science fiction by what my mother and millions of others referred to as "monster movies". From Frankenstein to Aliens and beyond, the unknown and the unexplored are often our undoing. Bleak Horizons, edited by Tarl Hoch, is a wonderful collection of 15 stories that mix SF and Horror with various levels of anthropomorphic settings and characters. And, full disclosure, one of those stories is mine. Happily, the mix includes more than just blood thirsty monsters and end of the universe scenarios.

Overall my favorite stories in this anthology are Hardwire, Pentangle, and The Ouroboros Plate. My least favorites are 4/13/2060 and Not Like Us. Below is a short review of all the pieces. I think you should snag a copy, if only to read my favorites and have a taste for this genre. However, I also really enjoyed Carmen Miranda's Ghost Is Haunting Space Station 3 so you have every right to question my taste.

read more

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

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 →

Glenn Greenwald predicts over the next four years that "it's all going to get much worse", with President Obama shifting politically more to the right while the Democratic base continues to support him. Continue reading →

Online criminals have been systematically targeting TurboTax, filing fraudulent tax returns of individuals, and diverting their tax refunds to prepaid debit, cards, stealing their personal information, and using and impairing their credit ratings. 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 →

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 →

IBM today announced its Health Cloud and Watson cognitive computing capabilities will support health data entered by customers in iOS apps using Apple's ResearchKit and HealthKit frameworks. The move, which complements IBM’s new Watson Health business unit, will arm medical researchers with a secure, open data storage solution, as well as access to IBM’s most sophisticated data analytics capabilities.

There are several discussion groups on LinkedIn dedicated to Root Cause Analysis in one way or another. I follow a couple of them, but the one I like the most has a serious problem. So, being the dynamic (ha) and proactive (haha) person that I am, I created a new one. This new LinkedIn group […]

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

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

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

The Weather Company, an IBM Business, and PRISA Noticias, one of the world’s leading Spanish-language media groups and owner of EL PAÍS newspaper, announced today a collaboration to combine the most accurate forecasts with one of the Spanish-speaking world’s largest media groups. The Weather Company will provide in-depth weather data and forecasts, as well as tailored content across PRISA properties. In turn, PRISA Noticias will provide locally relevant articles, photos and video content within the Spanish versions of The Weather Channel app and website (weather.com). The collaboration will also enable local marketers to access advanced data-driven advertising solutions from IBM Watson Advertising (formerly The Weather Company’s ad sales business) across both companies’ properties.

The Weather Company, an IBM Business and Rogers Media announced today an agreement to provide weather information and content customized specifically for the Canadian market. With this agreement, The Weather Company will provide in-depth weather data and forecasts, as well as curated content, across Rogers Media properties. In turn, Rogers Media will provide locally relevant articles, photos and video content across the Canadian versions of The Weather Channel app and website (weather.com) to provide residents with the most pertinent information possible. The Weather Company and Rogers Media will also align to enhance advertising across both companies’ properties, with Rogers leveraging its ad sales capabilities to monetize The Weather Channel properties in Canada.

IBM announced today that Mediacorp, Singapore’s largest media company, has completed a digital transformation of its broadcast operations using IBM Hybrid Cloud solutions as part of the move to a new office building in Singapore’s one-north district. The Mediacorp broadcast operations team can now more quickly, seamlessly and efficiently deliver video and audio content to consumers across different platforms, including new mobile apps, interactive televisions and other connected devices.

Como parte de las celebraciones del 90 aniversario de IBM en México, la empresa realizó por primera vez en el país, los días 7 y 8 de octubre en el Campus Tecnológico de IBM en Guadalajara, el festival de hackeo para desarrolladores cognitivos: HackaPalooza.

At the Smarter Cities Forum in Shanghai today, IBM announced a collaboration with South China's largest hospital, Guang Dong Hospital of Traditional Chinese Medicine, to apply new analytics technology to help doctors uncover trends and new knowledge about disease treatment from thousands of anonymous Electronic Medical Records (EMR)The tool will also enable clinicians to perform empirical studies on the efficacy of certain traditional Chinese treatments.

Fleury Medicina e Saúde es el primer socio de la unidad IBM Watson Health en Latinoamérica. Las dos compañías trabajaron juntas para testear y validar la solución Watson for Genomics en Brasil como una potencial herramienta, que provee información para ayudar en la toma de decisiones médicas. De este modo, la alianza busca avances que permitan aumentar la precisión en la medicina personalizada.

IBM realizó por 5ª ocasión en México la edición del concurso de emprendedores: IBM SmartCamp, organizado por el IBM Global Entrepreneur Program. El evento tuvo lugar en las instalaciones del espacio de co-working, CoWdf, de la Ciudad de México, resultando ganadora del primer lugar la startup Apli.jobs, en tanto que el segundo lugar fue otorgado a la startup Bayonet.io.

IBM today launched Express Advantage – a portfolio of affordable business solutions designed especially to meet the performance, usability and pricing needs of medium-sized businesses.