Hello Internet! In This Episode: Erin and Weer’d talk about a defensive gun use that stopped a potential mass shooting, then discuss the assorted nuttery happening in relationship to the COVID-19 quarantine; Loveball returns to the show to talk about what … Continue reading →

Hello Internet! In This Episode: Erin and Weer’d talk about some of the latest restrictions due to the COVID-19 lockdown, and then discuss how it’s affected the latest Magic: the Gathering expansion; David talks about some of the challenges you … Continue reading →

Hello Internet! In This Episode: Erin and Weer’d discuss the increasing desperation of anti-gunners as they react to mass firearm purchases by Americans of all walks of life; Weer’d fisks a stand-up routine by Steve Hofstetter; David tells us how … Continue reading →

Hello Internet! In This Episode: It’s a “Nothing But Weer’d Beard Segments” show, so Erin takes over in order to have some time on-air! Erin and Weer’d discuss certain states relaxing their quarantine, Dick’s Sporting Goods feeling the consequences of … Continue reading →

Hello Internet! In This Episode: Erin and Weer’d discuss the recent spree killing in Canada, and the conspicuous lack of information on it; David talks about gun parts that are great to have around; Weer’d interviews Logan Metesh of High … Continue reading →

Adult On-Road Cyclist Injury in Victoria, 2008/09 to 2017/18: A Report on Ambulance Attendances, Emergency Department Presentations, Hospital Admissions and Deaths , released by Monash University

A 20-year-old man was transported to hospital via ambulance for treatment following a two vehicle collision in Smith’s parish. A police spokesperson said, “Around 11:10am Tuesday, February 4th police, Bermuda Fire & Rescue Service as well as ambulance personnel were dispatched to a reported two vehicle collision at the junction of Middle Road and Verdmont […] (Click to read the full article)

So, you think you know Galileo? A new book out from Simon and Schuster publishing looks at the life and times of one of the most famous astronomers there ever was: Galileo Galilei. Galileo and the Science Deniers by Dr. Mario Livio not only looks at the life and times of the famous astronomer Galileo, but busts some of the most famous myths surrounding Galileo, and looks at his greatest discoveries and tempestuous clash with the Roman Catholic Church and its aftermath. Livio also connects the science denialism of the day, with comparisons to modern clashes between politics and science.

The post Review: Galileo and the Science Deniers by Mario Livio appeared first on Universe Today.

Někteří badatelé tvrdí, že dějiny Židů v Číně začínají již v 6. století před naším letopočtem za dynastie Čou, k tomu však nejsou žádné archeologické či jiné materiální důkazy. Všeobecně se tak počítají počátky židovské přítomnosti až od 8. století našeho letopočtu, za vlády dynastie Tang, kdy do Říše středu dorazily první skupinky obchodníků po Hedvábné stezce a usazovali se podél ní. Dnes od 18 hodin můžete na Facebooku Reflexu sledovat premiéru speciálního hudebního pořadu Židé v říši středu. Dějiny izraleského národa a Číny jsou zajímavě propojené.

Additional new series for the 2020-2021 season will be announced at a later date.

A few weeks ago, the US telecom industry began pushing a bullshit narrative through its usual allies. In short, the claim revolves around the argument that the only reason the US internet still works during a pandemic was because the Trump FCC ignored the public, ignored most objective experts, and gutted itself at the behest of telecom industry lobbyists. The argument first popped up over at AEI, then the Trump FCC, then the pages of the Wall Street Journal, and has since been seen in numerous op-eds nationwide. I'd wager that's not a coincidence, and I'd also wager we'll be seeing a lot more of them.

All of the pieces try to argue that the only reason the US internet works during a pandemic is because the FCC gutted its authority over telecom as part of its "restoring internet freedom" net neutrality repeal. This repeal, the story goes, drove significant investment in US broadband networks (not remotely true), resulting in telecom Utopia (also not true). The argument also posits that in Europe, where regulators have generally taken a more active role in policing things like industry consolidation and telecom monopolies, the internet all but fell apart (guess what: not true).

Usually, like in this op-ed, there's ample insistence that the US broadband sector is largely wonderful while the EU has gone to hell:

"Unlike here, European networks are more heavily regulated. This has led to less investment and worse performance for consumers for years. American consumers are being generally well served by the private sector."

Anybody who has spent five minutes talking to Comcast customer support -- or tried to get scandal-plagued ISP like Frontier Communications to upgrade rotten DSL lines -- knows this is bullshit. Still, we penned a lengthy post exploring just how full of shit this argument is, and how there's absolutely zero supporting evidence for the claims. The entire house of cards is built on fluff and nonsense, and it's just ethically grotesque to use a disaster to help justify regulatory capture and market failure.

While it's true that the US internet, in general, has held up relatively well during a pandemic, the same can't be said of the so called "last mile," or the link from your ISP's network to your home. Yes, the core internet and most primary transit routes, designed to handle massive capacity spikes during events like the Superbowl, has handled the load relatively well. The problem, as Sascha Meinrath correctly notes here, is sluggish speeds on consumer and business lines that, for many, haven't been upgraded in years:

"Right now, an international consortium of network scientists is collecting 750,000 U.S. broadband speed tests from internet service provider (ISP) customers each day, and we’ve been tracking a stunning loss of connectivity speeds to people’s homes. According to most ISPs, the core network is handling the extra load. But our data show that the last-mile network infrastructure appears to be falling down on the job."

Again, your 5 Mbps DSL line might be ok during normal times, but it's not going to serve you well during a pandemic when your entire family is streaming 4K videos, gaming, and Zooming. And your DSL line isn't upgraded because there's (1) very little competition forcing your ISP to do so, and (2) the US government is filled to the brim with sycophants who prioritize campaign contributions and ISP revenues over the health of the market and consumer welfare. And while there's a contingency of industry-linked folks who try very hard to pretend otherwise, this is a policy failure that's directly tied to mindless deregulation, a lack of competition, and, more importantly, corruption. In short, the complete opposite of the industry's latest talking point.

For years we've been noting how US telcos have refused to repair or upgrade aging DSL lines because it's not profitable enough, quickly enough for Wall Street's liking. Facing no competition and no regulatory oversight, there's zero incentive for a giant US broadband provider to try very hard. Similarly, because our lawmakers and regulators are largely of the captured, revolving door variety, they rubber stamp shitty mergers, turn a blind eye to very obvious industry problems, routinely throwing billions in taxpayer money at monopolies in exchange for fiber networks that are usually only partially deployed -- if they're deployed at all.

Meanwhile, US telcos that have all but given up on upgrading aging DSL lines have helped cement an even bigger Comcast monopoly across vast swaths of America. It's a problem that the telecom sector, Trump FCC, and various industry apologists will ignore to almost comical effect. Also ignored is the fact that this results in US broadband subscribers paying some of the highest prices for broadband in the developed world:

"Numerous studies, including those conducted by the FCC itself, show that broadband pricing is the second-largest barrier to broadband adoption (availability is the first). It’s obvious that if people are being charged a lot for a service, they’re less likely to purchase it. And independent researchers have already documented that poor areas often pay more than rich communities for connectivity. Redlining of minority and rural areas appears to be widespread, and we need accurate pricing data from the FCC to meaningfully address these disparities."

Try to find any instance where Ajit Pai, or anybody in this chorus of telecom monopoly apologists, actually admits that the US broadband market isn't competitive and, as a result, is hugely expensive for businesses and consumers alike. You simply won't find it. What you will find are a lot of excuses and straw men arguments like this latest one, designed to distract the press, public, and policymakers from very obvious market failure. Market failure that was a major problem in normal times, and exponentially more so during a pandemic where broadband is an essential lifeline.

The EARN IT Act is dangerous. It threatens speech on the internet and tech companies' ability to provide secure communications for their users. There may not be anything about encryption in the dry text of the bill, but the threat is there all the same. No one knows what "best practices" the law will demand from online services, but the bill's focus on child porn strongly suggests any platform that "allows" this information to be transmitted using encrypted communications will be targeted by the government.

Bill Barr and Chris Wray have made it clear encryption is the enemy. Both have advocated for encryption backdoors, even if they're both too cowardly to use that term. No one thinks the government and service providers shouldn't do all they can to prevent the sharing of child porn, but undermining encryption isn't the solution. It may shield some child porn producers and consumers from detection, but the government's efforts in this area show encryption hasn't posed much of a problem to investigators and prosecutors.

Encryption protects people who aren't criminals. As Runa Sundvik explains for TechCrunch, targeting encryption via the EARN IT Act also threatens some of the foremost beneficiaries of the First Amendment: journalists.

[T]echnology experts warn the bill not only fails to meet the challenge, it creates new problems of its own. My job is to enable journalists to do their work securely — to communicate with others, research sensitive stories and publish hard-hitting news. This bill introduces significant harm to journalists’ ability to protect their sources.

Strip communications platforms of their encryption and you make it that much easier to expose journalists' sources and snoop on their communications. This isn't an existential threat. It's an actual threat. The FBI has spied on journalists and several successive presidential administrations have made rooting out leakers a priority.

But it does more than harm journalists. It also harms the people they're trying to reach: readers. Encryption protects readers who visit news sites utilizing HTTPS. That's almost all of them at this point. This ensures their connection is shielded from people trying to snoop on their web activity. More importantly, it ensures the sites they reach are legit and the content originating from the journalists the site says it is.

If EARN IT becomes law, whistleblowers and other sources will see their secure options disappear. Tor, Signal, etc. will be considered nothing more than aiders and abettors of criminal activity. Anything secured by encryption will be treated as a virtual dead drop for criminal content.

Protecting children from exploitation is important. But the tradeoff legislators are demanding isn't actually a tradeoff. The American public will receive no net benefit from this tangential attack on encryption. Very often we're first informed about serious government misconduct by journalists. Destroying this outlet works out well for the government so often exposed as untrustworthy, but it does nothing for the governed.

No, you still can't edit tweets

Although editing published tweets still remains strictly verboten on Twitter, the microblogging anger echo chamber intends to prompt English-speaking iPhone-wielding users to double-check content before posting a reply that they might regret.…

Politicos watered down earlier efforts, so data defenders will fight to the end

The small group of policy wonks that forced California’s legislature to rush through privacy legislation two years ago are back – and this time they want a ballot.…

Doesn't play well on iPhones, but bureaucrats rushed it out rather than wait months for perfection. Meanwhile serious bug reports have emerged

Australia’s “COVIDSafe” contact-tracing app was rushed to market in the knowledge it would perform poorly on some devices and without agreements in place to let actual contact-tracers use the data it collects. As a result, no collected data has been used in at least 10 days since its launch.…

Zero-click remote-code exec hole found by Googler, updates emitted

Samsung has patched a serious security hole in its smartphones that can be exploited by maliciously crafted text messages to hijack devices.…

Problems aside, no one is sure how useful phone-based tracking will be

The NHSX, a technology group within the UK government's National Health Service, has released the source code for its Android and iOS COVID-19 coronavirus contact-tracing apps in an effort to allay privacy concerns and improve the code.…

Прямо-таки праздничные скидки.

A review by Medio DeCritici (165). A 2020 Review - Aliens Versus Predator (PC, 1999)

A review by Medio DeCritici (165). A 2020 Review - Aliens vs. Predator (PC, 2010)

For those of you who follow the tweets of @DivaBiotech, you are already familiar with the varied interests and activities of outgoing world traveler and international marketing guru in the area of genomics, Ruby Gadelrab. Ruby is one of my favorite tweeps, keeping me up to date on the personal genomics scene and the latest biotech science news. I asked Ruby to guest post; (read more)

Source: Suzy - Discipline: BioTech

Although CEACAM1 (CC1) glycoprotein resides at the interface of immune liver injury and metabolic homeostasis, its role in orthotopic liver transplantation (OLT) remains elusive. We aimed to determine whether/how CEACAM1 signaling may affect hepatic ischemia-reperfusion injury (IRI) and OLT outcomes. In the mouse, donor liver CC1 null mutation augmented IRI-OLT (CC1-KO→WT) by enhancing ROS expression and HMGB1 translocation during cold storage, data supported by in vitro studies where hepatic flush from CC1-deficient livers enhanced macrophage activation in bone marrow–derived macrophage cultures. Although hepatic CC1 deficiency augmented cold stress–triggered ASK1/p-p38 upregulation, adjunctive ASK1 inhibition alleviated IRI and improved OLT survival by suppressing p-p38 upregulation, ROS induction, and HMGB1 translocation (CC1-KO→WT), whereas ASK1 silencing (siRNA) promoted cytoprotection in cold-stressed and damage-prone CC1-deficient hepatocyte cultures. Consistent with mouse data, CEACAM1 expression in 60 human donor liver biopsies correlated negatively with activation of the ASK1/p-p38 axis, whereas low CC1 levels associated with increased ROS and HMGB1 translocation, enhanced innate and adaptive immune responses, and inferior early OLT function. Notably, reduced donor liver CEACAM1 expression was identified as one of the independent predictors for early allograft dysfunction (EAD) in human OLT patients. Thus, as a checkpoint regulator of IR stress and sterile inflammation, CEACAM1 may be considered as a denominator of donor hepatic tissue quality, and a target for therapeutic modulation in OLT recipients.

Organ shortage continues to limit the lives of patients who require liver transplantation. While extending criteria for liver organs provides a needed resource, tissue damage from prolonged ischemic injury can result in early allograft dysfunction and consequent rejection. In this issue of the JCI, Nakamura et al. used a mouse transplantation model with prolonged ex vivo cold storage to explore liver graft protection. The authors found that liver grafts with absent carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) exhibited increased ischemia-reperfusion injury inflammation and decreased function in wild-type recipients. The authors went on to correlate CEACAM1 levels with postreperfusion damage in human liver transplant recipients. Notably, this study identified a potential biomarker for liver transplant donor graft quality.

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.

Nerve growth factor (NGF) regulates many aspects of neuronal biology by retrogradely propagating signals along axons to the targets of those axons. How this occurs when axons contain a plethora of proteins that can silence those signals has long perplexed the neurotrophin field. In this issue of the JCI, Li et al. suggest an answer to this vexing problem, while exploring why the Elp1 gene that is mutated in familial dysautonomia (FD) causes peripheral neuropathy. They describe a distinctive function of Elp1 as a protein that is required to sustain NGF signaling by blocking the activity of its phosphatase that shuts off those signals. This finding helps explain the innervation deficits prominent in FD and reveals a unique role for Elp1 in the regulation of NGF-dependent TrkA activity.

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.

Fibroblasts are key effector cells in tissue remodeling. They remain persistently activated in fibrotic diseases, resulting in progressive deposition of extracellular matrix. Although fibroblast activation may be initiated by external factors, prolonged activation can induce an “autonomous,” self-maintaining profibrotic phenotype in fibroblasts. Accumulating evidence suggests that epigenetic alterations play a central role in establishing this persistently activated pathologic phenotype of fibroblasts. We demonstrated that in fibrotic skin of patients with systemic sclerosis (SSc), a prototypical idiopathic fibrotic disease, TGF-β induced the expression of DNA methyltransferase 3A (DNMT3A) and DNMT1 in fibroblasts in a SMAD-dependent manner to silence the expression of suppressor of cytokine signaling 3 (SOCS3) by promoter hypermethylation. Downregulation of SOCS3 facilitated activation of STAT3 to promote fibroblast-to-myofibroblast transition, collagen release, and fibrosis in vitro and in vivo. Reestablishment of the epigenetic control of STAT3 signaling by genetic or pharmacological inactivation of DNMT3A reversed the activated phenotype of SSc fibroblasts in tissue culture, inhibited TGF-β–dependent fibroblast activation, and ameliorated experimental fibrosis in murine models. These findings identify a pathway of epigenetic imprinting of fibroblasts in fibrotic disease with translational implications for the development of targeted therapies in fibrotic diseases.

BACKGROUND Glucose-6-phosphate dehydrogenase (G6PD) deficiency decreases the ability of red blood cells (RBCs) to withstand oxidative stress. Refrigerated storage of RBCs induces oxidative stress. We hypothesized that G6PD-deficient donor RBCs would have inferior storage quality for transfusion as compared with G6PD-normal RBCs.METHODS Male volunteers were screened for G6PD deficiency; 27 control and 10 G6PD-deficient volunteers each donated 1 RBC unit. After 42 days of refrigerated storage, autologous 51-chromium 24-hour posttransfusion RBC recovery (PTR) studies were performed. Metabolomics analyses of these RBC units were also performed.RESULTS The mean 24-hour PTR for G6PD-deficient subjects was 78.5% ± 8.4% (mean ± SD), which was significantly lower than that for G6PD-normal RBCs (85.3% ± 3.2%; P = 0.0009). None of the G6PD-normal volunteers (0/27) and 3 G6PD-deficient volunteers (3/10) had PTR results below 75%, a key FDA acceptability criterion for stored donor RBCs. As expected, fresh G6PD-deficient RBCs demonstrated defects in the oxidative phase of the pentose phosphate pathway. During refrigerated storage, G6PD-deficient RBCs demonstrated increased glycolysis, impaired glutathione homeostasis, and increased purine oxidation, as compared with G6PD-normal RBCs. In addition, there were significant correlations between PTR and specific metabolites in these pathways.CONCLUSION Based on current FDA criteria, RBCs from G6PD-deficient donors would not meet the requirements for storage quality. Metabolomics assessment identified markers of PTR and G6PD deficiency (e.g., pyruvate/lactate ratios), along with potential compensatory pathways that could be leveraged to ameliorate the metabolic needs of G6PD-deficient RBCs.TRIAL REGISTRATION ClinicalTrials.gov NCT04081272.FUNDING The Harold Amos Medical Faculty Development Program, Robert Wood Johnson Foundation grant 71590, the National Blood Foundation, NIH grant UL1 TR000040, the Webb-Waring Early Career Award 2017 by the Boettcher Foundation, and National Heart, Lung, and Blood Institute grants R01HL14644 and R01HL148151.

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.

Popular journaling app Day One today updated to version 4.13, adding support for trackpad navigation on iPad, a new Day View interface, and other improvements.


This release comes after the launch of iOS and iPadOS 13.4, which added support for trackpads and mice on ‌‌iPad‌‌.

After updating, Day One users on ‌iPad‌ can use various trackpad actions to interact with the app, including two-finger swipe down to dismiss, and two-finger horizontal swipe to open and close the journal drawer.

• How to Use a Bluetooth Mouse or Trackpad With Your iPad

The new Day View offers quicker access to daily entries by tapping on or clicking dates in the calendar or the timeline.

Also in this update, Daily Reminders now include additional information like the number of photos taken and locations visited on a given day, and the Settings pages now provide links to Day One feature documents.

Elsewhere, several bugs have been fixed, including one that caused video thumbnails not to display in the media timeline, and one that prevented photos in the activity feed from showing location or calendar events.

Day One is a free download for iPhone and ‌iPad‌ from the App Store with in-app purchases for premium features. [Direct Link]
This article, "Day One Journaling App Update Adds iPad Trackpad Support, New Day View, and More" first appeared on MacRumors.com

Discuss this article in our forums

The DNC is a one big capitalistic gangbang of Democrats and corporate donors and lobbyists. Guess who is getting screwed? 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 →

IBM Research today opened its second research location on the African continent and announced several new project collaborations in the areas of data driven healthcare, digital urban ecosystems and astronomy.

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's Smarter Cities Challenge program (@CitiesChallenge) will be sending teams of company experts to 16 municipalities around the world through 2016 to help cities with critical issues ranging from jobs creation, transportation, and public safety, to healthcare, revenue, social services, and public works.

ENGIE, a global leader in energy transition, today announced a new initiative with IBM. This nonexclusive, technological and commercial alliance is designed to improve the management of cities by looking at patterns, event correlation, anomaly detection and real-time data across all parts of cities.

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

IBM today announced that it will help deliver a tailored fan experience through the IBM Cloud at Atlanta’s new Mercedes-Benz Stadium, scheduled to open later this month.

IBM today announced that Mammoth Resorts, the leading four-season mountain resort operator in California, is using Watson Customer Engagement solutions on the IBM Cloud to create customized offers that are helping to drive record numbers of visitors to the resort every year.

One morning at the tidepools and chance upon the largest creature on earth.

IBM today announced its intention to acquire Vivant Digital business (Vivant), a boutique digital and innovation agency based here. This acquisition extends the strategy and design expertise of IBM iX, one of the world’s largest digital agencies and global business design partners, with Vivant talent and expertise to accelerate clients’ digital transformations.

IBM today announced a research collaboratory in Singapore, where researchers from IBM intend to collaborate with scientists and engineers from public agencies in Singapore to improve the quality of its urban services. The focus of this research effort will be to use sensor networks to more effectively model, predict and manage the use of natural and physical infrastructure resources – water, transport and energy.  

La enfermedad de Parkinson es un trastorno neurológico degenerativo crónico que afecta a una de cada 100 personas mayores de 60 años. Se estima que más de 5 millones de personas en el mundo tienen Parkinson y el número está aumentando con la población actual que envejece.

PROESAH – asociación civil formada por un grupo de doctores, profesores y alumnos de la Universidad Autónoma de Guerrero-, anunció el día de hoy el lanzamiento de una aplicación llamada LUZi, que utiliza tecnología de Inteligencia Artificial (IA) de IBM para analizar el riesgo obstétrico. El objetivo del proyecto es reducir la mortalidad materna e infantil en las comunidades rurales de Guerrero, México.

Durante la conferencia mundial VMworld® 2016, VMware e IBM anunciaron la disponibilidad de los primeros servicios de nube para industrias que permiten a las organizaciones mover rápida y fácilmente, archivos a la nube. Con más de 500 clientes comprometidos ya, la alianza global entre IBM y VMware está ayudando a más organizaciones a extender sus archivos a la nube en horas, en comparación de semanas o meses.