On accorde "The World of Art Award" (WAA) aux artistes, aux galeries et aux musées qui poursuivent les "meilleures pratiques" dans l'art et la culture. Cette concurrence cherche à attirer dies artistes, galeries, les musées qui redéfinissent des normes de l'excellence d'art. Ceux qui défie des trends et des tendances existantes dans l'art et la culture.

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! 

 

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

 

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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:

 

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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

Date: May 8, 2020

As COVID-19 continues to impact communities around the world, people and families everywhere are spending more time at home. In light of this, we’re launching a throwback Doodle series looking back at some of our popular interactive Google Doodle games!

Stay and play at home with today’s featured throwback: 

Our 2010 Doodle game celebrating PAC-MAN!
 

 

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Help stop the spread of COVID-19 by following these steps.  
 

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Learn more here about the latest ways we’re responding, and how our products can help people stay connected during this time.

Location: Global

Tags:

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

The post The Angler’s Code: What are the Best Practices for a Better Fishing Future? appeared first on Ocean Blue Fishing Adventures.

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.

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.

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.

IL-17–producing RORγt+ γδ T cells (γδT17 cells) are innate lymphocytes that participate in type 3 immune responses during infection and inflammation. Herein, we show that γδT17 cells rapidly proliferate within neonatal lymph nodes and gut, where, upon entry, they upregulate T-bet and coexpress IL-17, IL-22, and IFN-γ in a STAT3- and retinoic acid–dependent manner. Neonatal expansion was halted in mice conditionally deficient in STAT5, and its loss resulted in γδT17 cell depletion from all adult organs. Hyperactive STAT5 mutant mice showed that the STAT5A homolog had a dominant role over STAT5B in promoting γδT17 cell expansion and downregulating gut-associated T-bet. In contrast, STAT5B preferentially expanded IFN-γ–producing γδ populations, implying a previously unknown differential role of STAT5 gene products in lymphocyte lineage regulation. Importantly, mice lacking γδT17 cells as a result of STAT5 deficiency displayed a profound resistance to experimental autoimmune encephalomyelitis. Our data identify that the neonatal microenvironment in combination with STAT5 is critical for post-thymic γδT17 development and tissue-specific imprinting, which is essential for infection and autoimmunity.

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

Infection with the Gram-negative bacterium Helicobacter pylori remains the most important modifiable risk factor for the development of gastric cancer, a leading cause of cancer-related deaths worldwide. How the interactions between H. pylori and its host shape the gastric environment during chronic infection warrants further investigation. In this issue of the JCI, Palrasu et al. used human cell lines and mouse models to provide mechanistic insight into H. pylori’s ability to delay apoptosis in gastric epithelial cells by actively driving the degradation of a proapoptotic factor, SIVA1. Their findings suggest that promoting the survival of gastric epithelial cells has implications not only for H. pylori pathogenesis but for host tumorigenesis.

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.

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.

Hypoxia-inducible factor (HIF) is strikingly upregulated in many types of cancer, and there is great interest in applying inhibitors of HIF as anticancer therapeutics. The most advanced of these are small molecules that target the HIF-2 isoform through binding the PAS-B domain of HIF-2α. These molecules are undergoing clinical trials with promising results in renal and other cancers where HIF-2 is considered to be driving growth. Nevertheless, a central question remains as to whether such inhibitors affect physiological responses to hypoxia at relevant doses. Here, we show that pharmacological HIF-2α inhibition with PT2385, at doses similar to those reported to inhibit tumor growth, rapidly impaired ventilatory responses to hypoxia, abrogating both ventilatory acclimatization and carotid body cell proliferative responses to sustained hypoxia. Mice carrying a HIF-2α PAS-B S305M mutation that disrupts PT2385 binding, but not dimerization with HIF-1β, did not respond to PT2385, indicating that these effects are on-target. Furthermore, the finding of a hypomorphic ventilatory phenotype in untreated HIF-2α S305M mutant mice suggests a function for the HIF-2α PAS-B domain beyond heterodimerization with HIF-1β. Although PT2385 was well tolerated, the findings indicate the need for caution in patients who are dependent on hypoxic ventilatory drive.

Increased microvascular permeability to plasma proteins and neutrophil emigration are hallmarks of innate immunity and key features of numerous inflammatory disorders. Although neutrophils can promote microvascular leakage, the impact of vascular permeability on neutrophil trafficking is unknown. Here, through the application of confocal intravital microscopy, we report that vascular permeability–enhancing stimuli caused a significant frequency of neutrophil reverse transendothelial cell migration (rTEM). Furthermore, mice with a selective defect in microvascular permeability enhancement (VEC-Y685F-ki) showed reduced incidence of neutrophil rTEM. Mechanistically, elevated vascular leakage promoted movement of interstitial chemokines into the bloodstream, a response that supported abluminal-to-luminal neutrophil TEM. Through development of an in vivo cell labeling method we provide direct evidence for the systemic dissemination of rTEM neutrophils, and showed them to exhibit an activated phenotype and be capable of trafficking to the lungs where their presence was aligned with regions of vascular injury. Collectively, we demonstrate that increased microvascular leakage reverses the localization of directional cues across venular walls, thus causing neutrophils engaged in diapedesis to reenter the systemic circulation. This cascade of events offers a mechanism to explain how local tissue inflammation and vascular permeability can induce downstream pathological effects in remote organs, most notably in the lungs.

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.

BACKGROUND The live attenuated BPZE1 vaccine candidate induces protection against B. pertussis and prevents nasal colonization in animal models. Here we report on the responses in humans receiving a single intranasal administration of BPZE1.METHODS We performed multiple assays to dissect the immune responses induced in humans (n = 12) receiving BPZE1, with particular emphasis on the magnitude and characteristics of the antibody responses. Such responses were benchmarked to adolescents (n = 12) receiving the complete vaccination program of the currently used acellular pertussis vaccine (aPV). Using immunoproteomics analysis, potentially novel immunogenic B. pertussis antigens were identified.RESULTS All BPZE1 vaccinees showed robust B. pertussis–specific antibody responses with regard to significant increase in 1 or more of the following parameters: IgG, IgA, and memory B cells to B. pertussis antigens. BPZE1–specific T cells showed a Th1 phenotype, and the IgG exclusively consisted of IgG1 and IgG3. In contrast, all aPV vaccines showed a Th2-biased response. Immunoproteomics profiling revealed that BPZE1 elicited broader and different antibody specificities to B. pertussis antigens as compared with the aPV that primarily induced antibodies to the vaccine antigens. Moreover, BPZE1 was superior at inducing opsonizing antibodies that stimulated ROS production in neutrophils and enhanced bactericidal function, which was in line with the finding that antibodies against adenylate cyclase toxin were only elicited by BPZE1.CONCLUSION The breadth of the antibodies, the Th1-type cellular response, and killing mechanisms elicited by BPZE1 may hold prospects of improving vaccine efficacy and protection against B. pertussis transmission.TRIAL REGISTRATION ClinicalTrials.gov NCT02453048, NCT00870350.FUNDING ILiAD Biotechnologies, Swedish Research Council (Vetenskapsrådet), Swedish Heart-Lung Foundation.

This isn’t in the photos, but it’s foggy and cold this morning in western Washington. It’s the weirdest summer I’ve ever experienced — foggy, frigid mornings, cool days, and then freezing nights! It’s not very pleasant for a desert creature like myself, but it’s quite nice to sit inside and write in my blog a least. I have to say, it sure is weird, though. It’s August and I wear a sweater or sweatshirt most of the time and then I’m still cold! ^^; There are a few sunny days here and there, though. I get out on those days, into the wilderness and bright blue beyond. Sometimes, I just drive and drive in my still-unnamed yellow bug, and other times I find something that not a lot of people know about. This is about one of them. ^^ I love to wander, to find all of the nooks and crannies of wherever I happen to be. Tourist sites? Well, they’re usually cool and I want to see them, but it’s the little, hidden things off the beaten trail that really get my soul revving. So, Johns River (no apostrophe, it was named back when apostrophes weren’t used on maps) was one of those things. I found out about it by googling and googling, thinking that someone, somewhere, must have written about something other than the two really traveled trails in Grays Harbor. I mean, this area is the gateway to the wild peninsula of Washington, where according to Stephanie Meyer and Patricia Briggs, vampires and werewolves run wild. I also loooooooove mountain meadows. Johns river is not in the mountains, so I suppose that it mostly qualifies as grassland surrounded by trees? It’s just a little concrete path, and it’s not even a mile (0.6 miles one way) long, but with the river on one side and a huge expanse of pasture to the other side, it took my breath away.   Just look at this. Elk supposedly graze around here a lot, and I didn’t see any since I went during midday, but I bet it’s really a sight at sunset. It’s not far, so I will definitely have to come back. Can’t you just imagine little river sprites lounging on the bank, cleaning themselves? And little fairies flitting through the air? I bet this is a really magical place at sunset.   The little shack in the distance is off the trail. It’s supposedly for hunters (YUCK) and photographers. It would make a wonderful place to watch the sprites from. This shack is at the very end of the trail, and the same thing. It’s boring inside. I didn’t see any geldings, but I saw a few mosquitoes and a spider. If you’re lucky enough to have a horse that loves to take you along on its adventures, you can continue. I was wearing shorts, so I didn’t go, because ticks! But I will come back. Yes, I will come back. :3 Road to nowhere. Ignore the buildings. They’re only there for magical curse removal. Here’s a panorama of wildness. I’m feeling really magical today, can’t you tell? I think it’s because I have Daniel Waples playing in the background, and it’s all foggy outside. That reminds me that I want a handpan so badly. I need to find a handpan that I can afford soooooo badly, because I think it’s a music that speaks to my inner essence. Does anyone know what these gorgeous purple flowers are? They’re not lavender. The River People watch over this creek. Be careful to please them. It’s me. Sometimes I wear bright colors, sometimes I wear pastels. I don’t think that a magical being has to stick to  neutrals. (That hand thing is a shaka, a very cool gesture that I learned during my time in Hawaii that means “hang loose.” I like to think that it also means that you should be yourself and follow your instincts.) I think that I’ll go research handpans again. I should write down how much they cost so that I can be sure to stock my Airstream with one when I get it. ???? Here’s to the future! Excelsior! (Is that a good “to infinity, and beyond!!” kind of quote? If not, what should I use instead? I feel like “banzai!” is overused) Oh, and I’ve been arting on my Tumblr lately. I’ve been writing a serial ficiton that is mysterious connected to my soon-to-come comic, Denkiki on my other tumblr. Go check them out!  I’m going to start using my mailing list soon, too, to keep people updated, so stay tuned and I’ll post the link soon! Or make it a popup, I’m not sure. But I want to offer something cool for when people sign up. ???? Chaoness!

В подтверждение ранее появлявшихся слухов компания Apple выпустила обновленную модель MacBook Pro. Ноутбук получил 16-дюймовый дисплей, сохранив при этом форм-фактор модели с диагональю 15 дюймов. Но...

Согласно свежему сообщению от достоверных источников, в конце следующего года компания Apple выпустит новые поколения iPad Pro и MacBook Pro. Главная особенность новинок будет состоять в том, что они ...

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]
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Microsoft plans to add trackpad and mouse support to its Word, Excel, and PowerPoint apps for iPad by the fall, according to TechCrunch and The Verge.

iPadOS 13.4 introduced trackpad and mouse support on all iPad models released in the past four to five years. Keyboards with trackpads include Apple's Magic Keyboard and Brydge's Pro+ for the iPad Pro and Logitech's Combo for the 10.2-inch iPad and the 10.5-inch iPad Air.

When using a trackpad, the cursor displays as a circle on the screen, popping up only when you have a finger on the trackpad. The circle then morphs into various other shapes when hovering over app icons, text fields, or other on-screen elements.

This article, "Microsoft to Add Trackpad Support to Word, Excel, and PowerPoint Apps on iPad" first appeared on MacRumors.com

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Woot is ending the week with a refurbished sale on the 15-inch MacBook Pro, available in multiple storage sizes and colors. The sale starts with the 256GB SSD model (16GB RAM, Intel Core i7) for $1,579.99.

Note: MacRumors is an affiliate partner with Woot. When you click a link and make a purchase, we may receive a small payment, which helps us keep the site running.

For more storage, the 512GB SSD model (16GB RAM, Intel Core i9) is on sale for $1,849.99. Woot's refurbished sales are offering more than $800 in savings when compared to the original prices of these notebooks, which began at $2,399.00 when they launched in May 2019.

Similar to previous Woot sales, each MacBook Pro comes with a One Year Limited Woot Warranty. Each device has been refurbished and is ensured to be in full working condition. When shipped, they are packaged in a generic white box.

You can find even more discounts on new MacBooks by visiting our Best Deals guide for MacBook Pro and MacBook Air. In this guide we track the steepest discounts for the newest MacBook models every week, so be sure to bookmark it and check back often if you're shopping for a new Apple notebook.

This article, "Deals: Refurbished 15-Inch MacBook Pro Notebooks on Sale at Woot From $1,580 ($800+ Off)" first appeared on MacRumors.com

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A nationwide class action lawsuit filed against Apple in Northern California court this week accuses the company of knowingly concealing a defect with a display-related flex cable on recent 13-inch and 15-inch MacBook Pro models.


As discovered by repair website iFixit last year, some MacBook Pro models released in 2016 and 2017 have experienced issues with uneven backlighting caused by a delicate flex cable that can wear out and break after repeated opening and closing of the display. Impacted notebooks can exhibit uneven lighting at the bottom of the screen, which has been described as a "stage light" effect, and the backlighting system can eventually fail entirely.

Since the issue often takes time to manifest, the affected ‌MacBook Pro‌ units can be outside of Apple's one-year warranty period when they start exhibiting symptoms, resulting in an out-of-warranty repair fee of up to $850.

"Imagine spending more than $2,500 on a laptop only for it to fail shortly after the manufacturer's warranty expires," said PARRIS Law Firm attorney R. Rex Parris. "What's even more appalling is Apple requiring customers to spend an additional $600 to $850 to replace the screen."

Apple seemingly fixed the issue by extending the length of the flex cable by 2mm in the 2018 MacBook Pro. It also launched a free repair program in May 2019, but the program only applies to 13-inch MacBook Pro models released in 2016.

iFixit found the 2018 MacBook Pro flex cable on the left to be 2mm longer
The class action lawsuit seeks restitution for all costs attributable to replacing or replacing the affected MacBook Pro units, and calls for Apple to expand its repair program to cover the 15-inch MacBook Pro. The proposed class is defined as all persons within the United States who purchased a 2016 or newer MacBook Pro.

Related Guide: "Flexgate" Display Issues Affecting 2016 MacBook Pro and Later
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For this week's giveaway, we've once again teamed up with Throwboy to offer MacRumors readers a chance to win one of Throwboy's plushes modeled after classic Apple products and icons.


Throwboy makes a whole range of different plush pillow options priced at $30 to $40, with each one designed to look like an Apple product of some kind, including classic Macs, the iPod, the iPhone, and more. Each pillow features detailed embroidery and careful construction to highlight each component and to accurately represent Apple's designs.

The 1998 pillow, for example, is modeled after Apple's original iMac with its bright Bondi Blue design, while the 2001 pillow modeled after the original iPod comes complete with a screen and click wheel embroidery.


The 2007 pillow looks like the original ‌iPhone‌ with black bezels and a silver backing, and the Icon Pillow looks like Apple's classic happy Finder icon.


There's even a rainbow-colored Spinning Wheel Pillow that's designed to look like the dreaded spinning pinwheel that the cursor morphs into when an application is busy.


All of Throwboy's plushes are soft, squishy, huggable, and the perfect accent piece for an Apple fan. Each pillow is the ideal size to be used as a comfortable throw pillow for a couch or a chair. Photos of the pillows in action can be seen on Throwboy's Instagram account.


We have 10 of Throwboy's pillows to give away to MacRumors readers, and each winner will be able to pick their favorite pillow: ‌iMac‌, iPod, classic ‌iPhone‌, Finder Icon, or Spinning Wheel.

To enter to win our ‌giveaway‌, use the Gleam.io widget below and enter an email address. Email addresses will be used solely for contact purposes to reach the winners and send the prizes. You can earn additional entries by subscribing to our weekly newsletter, subscribing to our YouTube channel, following us on Twitter, following us on Instagram, or visiting the MacRumors Facebook page.

Due to the complexities of international laws regarding giveaways, only U.S. residents who are 18 years or older and Canadian residents (excluding Quebec) who have reached the age of majority in their province or territory are eligible to enter. To offer feedback or get more information on the ‌giveaway‌ restrictions, please refer to our Site Feedback section, as that is where discussion of the rules will be redirected.

Throwboy GiveawayThe contest will run from today (May 8) at 11:00 a.m. Pacific Time through 11:00 a.m. Pacific Time on May 15. The winners will be chosen randomly on May 15 and will be contacted by email. The winners will have 48 hours to respond and provide a shipping address before new winners are chosen.
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Apple's next-generation Apple Watch and watchOS 7 will focus on new mental health capabilities, according to leaker Jon Prosser who recently spoke on the Geared Up podcast. The mention of new ‌Apple Watch‌ features comes towards the end of the podcast.


The next-generation version of the ‌Apple Watch‌, the ‌Apple Watch‌ Series 6, has been rumored to include a blood oxygen sensor, which Prosser says Apple will take advantage of to implement new mental health-related features, such as detecting panic attacks.

What their biggest focus on is right now and I hope it comes this year, it might come next year, but I hope it's coming to WWDC is mental health capabilities. Where they can take the oxygen levels in your blood with your heart rate and determine if you're hyperventilating.

They can identify a panic attack before it happens and warn you on your watch. Especially if you're driving, they'll ask you to pull over and they'll offer breathing exercises once you get pulled over.

Prosser says that while he hopes the feature is released this year, "it might come next year." He also says he hopes for a WWDC unveiling, but if the new feature relies on a blood oxygen sensor in an unreleased version of the ‌Apple Watch‌, it's not likely Apple will unveil the capability until the fall when new ‌Apple Watch‌ models that support it are released.

There is, however, a possibility that it will be revealed at WWDC if older ‌Apple Watch‌ models have a latent ability to detect blood oxygen level, which is not clear at this time, or if the feature does not involve blood oxygen monitoring.

The panic attack detecting rumor was first shared by EverythingApplePro and leaker Max Weinbach back in April, who said that the ‌Apple Watch‌ will also be able to determine when a user is experiencing high levels of stress. Weinbach and EverythingApplePro did not suggest the feature would rely on blood oxygen monitoring, however, and said that it would be available on the ‌Apple Watch‌ Series 4 or later.

Hints that blood oxygen tracking capabilities are coming to a future version of the ‌Apple Watch‌ were found in a leaked version of iOS 14. Blood oxygen monitoring is an important feature because a drop in blood oxygen levels can suggest a serious respiratory or cardiac problem that requires immediate medical attention.

Multiple prior rumors from Bloomberg and other sources have also indicated that the next-generation ‌Apple Watch‌ and watchOS 7 will include sleep tracking features, allowing the ‌Apple Watch‌ to measure sleep quality, length, and other metrics.
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This week saw a couple of big announcements, led by the launch of an update for the 13-inch MacBook Pro line. Most notably, the update brought the improved Magic Keyboard previously introduced on its 16-inch sibling and the MacBook Air, with high-end models also receiving updated processors.

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The second significant announcement this week was that Apple's first all-digital Worldwide Developers Conference will kick off on June 22. Other news this week included a firmware update for the AirPods Pro, an update on Apple's Mini-LED efforts, and more.

Read on below and check out our video above for recaps of all of this week's most important stories!

New 13-Inch MacBook Pro Announced With Magic Keyboard, 10th-Gen Processors, Up to 32GB RAM and 4TB SSD, and More

Apple this week refreshed its 13-inch MacBook Pro lineup, with key features including the same Magic Keyboard as the 16-inch MacBook Pro, up to 80 percent faster Intel graphics than the previous generation, up to 32GB of RAM, up to 4TB of SSD storage, and 6K display support.


First introduced on the 16-inch MacBook Pro last year, the Magic Keyboard features a far more reliable scissor mechanism with 1mm of key travel. After five years, Apple has finally transitioned its entire notebook lineup away from its issue-prone butterfly keyboard.

10th-generation Intel processor options are only available on higher-end models, with the $1,799 configuration proving to be up to 16.5% faster than the $1,299 base model with an older 8th-generation processor.

Apple's Virtual WWDC Event to Kick Off on June 22

Apple has announced that its first-ever online-only WWDC will begin Monday, June 22 via the Apple Developer app and website. The weeklong event will include a virtual keynote, sessions, and labs, with more details to be shared in June. And it's free!


Apple is expected to introduce iOS 14, iPadOS 14, macOS 10.16, tvOS 14, and watchOS 7 at WWDC 2020, with beta testing to take place over the summer.

Student developers from all over the world can enter Apple's Swift Student Challenge by creating an interactive scene in Swift Playgrounds that can be experienced in three minutes. Winners will receive an exclusive WWDC20 jacket and pin set. Submissions are open through May 17.

Apple Updates AirPods Pro Firmware to Version 2D15

Apple this week released a new firmware version 2D15 for the AirPods Pro, replacing version 2C54.


In recent months, some AirPods Pro owners have been complaining about reduced noise cancellation and crackling or static sounds, so users have listened for any improvements following the update.

Perhaps proving how subjective sound quality can be, feedback has been decidedly mixed, with some users noticing an improvement, some noticing no change, and some noticing further degradation to noise cancellation.

Apple has offered some help in the form of two new support documents for users to troubleshoot noise cancellation or crackling sound issues.

10 Tips and Tricks for the iPad Pro Magic Keyboard

Have you recently picked up a new Magic Keyboard for the iPad Pro? Here's a list of our favorite tips and tricks that you need to know.


The tips and tricks relate to adjusting the backlight brightness, customizing the cursor's behavior, enabling tap-to-click on the trackpad, other trackpad gestures, accessing the Emoji keyboard, and more.

Apple's Mini-LED Product Roadmap May Have Been Pushed Back to 2021

Disappointed that the new 13-inch MacBook Pro was not the rumored 14-inch model? That may be due to a slight delay in Apple's plans to release a range of new products with Mini-LED backlit displays.

Kuo believes Apple's first Mini-LED products might not launch until 2021. The analyst has previously said these products would include a new 14.1-inch MacBook Pro, 16-inch MacBook Pro, 12.9-inch iPad Pro, and more.


Kuo has previously said that Mini-LED displays will allow for thinner and lighter product designs, while offering many of the same benefits of OLED displays used on the latest iPhones, including good wide color gamut performance, high contrast and dynamic range, and local dimming for truer blacks.

NFC-Based Digital Key Specification Released Ahead of Apple's Rumored CarKey Feature on iPhone

Amid rumors that Apple is working on a digital "CarKey" feature for iPhone, the Car Connectivity Consortium has announced that its NFC-based Digital Key Release 2.0 specification has been finalized and made available to its members, which includes Apple.


"CarKey" will allow an iPhone or Apple Watch to unlock, lock, and start an NFC-compatible vehicle. Just like credit cards and boarding passes, users will be able to add a digital car key to the Wallet app, eliminating the need to use a physical car key or key fob.

MacRumors Newsletter

Each week, we publish an email newsletter like this highlighting the top Apple stories, making it a great way to get a bite-sized recap of the week hitting all of the major topics we've covered and tying together related stories for a big-picture view.

So if you want to have top stories like the above recap delivered to your email inbox each week, subscribe to our newsletter!
This article, "Top Stories: New 13" MacBook Pro, WWDC Starts June 22, AirPods Pro Firmware Update, and More" first appeared on MacRumors.com

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Apple recently updated the 13-inch MacBook Pro, and the $1,299 base model remains a popular alternative to the $999 MacBook Air. To help with your buying decision, read our comparison of the notebooks below.


The differences between the base 13-inch MacBook Pro and the MacBook Air are quite nuanced, with each notebook possessing some unique features.

What's the Same

• 13-inch Retina display with 227 pixels per inch and True Tone support


• Magic Keyboard with reliable scissor switch design


• Force Touch trackpad


• 2 × Thunderbolt 3 ports


• 3.5mm headphone jack


• 256GB of SSD storage standard, configurable up to 2TB


• Touch ID


• T2 security chip


• 720p webcam


• 802.11ac Wi-Fi, also known as Wi-Fi 5


• Bluetooth 5.0


• Three-microphone array with directional beamforming


• Dolby Atmos surround sound

Advantages of Base 13-Inch MacBook Pro

• The display supports the P3 wide color gamut for more vibrant and lifelike colors


• The display is brighter at up to 500 nits vs. 400 nits on MacBook Air


• Touch Bar


• Slightly better sounding speakers

Advantages of MacBook Air

• Up to 11 hours of battery life vs. 10 hours on base 13-inch MacBook Pro


• Weighs slightly less at 2.8 pounds vs. 3.1 pounds for base 13-inch MacBook Pro


• Faster RAM: 3733MHz LPDDR4X vs. 2133MHz LPDDR3 for base 13-inch MacBook Pro


• 6K display support vs. 5K on base 13-inch MacBook Pro

Unlike the MacBook Pro, the MacBook Air also has a gold color option.

Performance

Generally speaking, the MacBook Air remains best suited for lightweight day-to-day tasks like web browsing and creating spreadsheets, while the MacBook Pro is better equipped to handle more intensive tasks like rendering large video files. This is not only because the MacBook Pro has faster processors than the Air, but also because it has a more advanced thermal design for dissipating heat inside the computer.

While the MacBook Air has been updated with Intel's latest 10th-generation processors, the base 13-inch MacBook Pro continues to use older 8th-generation processors. However, the Air uses lower-wattage Y-series chips with lower clock speeds, so the Pro still has faster overall performance, as confirmed by benchmarks.

Geekbench 5 scores for the latest 13-inch MacBook Pro and MacBook Air configurations:

• MacBook Air / 1.1GHz dual-core Core i3: 1,002 single-core and 1,998 multi-core


• MacBook Air / 1.1GHz quad-core Core i5: 1,055 single-core and 2,645 multi-core


• MacBook Air / 1.2GHz quad-core Core i7: 1,102 single-core and 2,843 multi-core


• MacBook Pro / 1.4GHz quad-core Core i5: 927 single-core and 3,822 multi-core


• MacBook Pro / 1.7GHz quad-core Core i7: 1,036 single-core and 3,909 multi-core

Takeaways:

• The base model 13-inch MacBook Pro for $1,299 has up to 91 percent faster multi-core performance than the base model MacBook Air for $999


• If considering the MacBook Air, upgrading to the quad-core Core i5 option is well worth the extra $100, as it is up to 32 percent faster than the base model and more closely rivals the base 13-inch MacBook Pro

Geekbench 5 scores are calibrated against a baseline score of 1,000, which is the score of an Intel Core i3-8100. Higher scores are better, with double the score indicating double the performance. Compare with other Mac benchmarks here.

Bottom Line

If you value portability and up to an extra hour of battery life, and are willing to sacrifice some performance, the MacBook Air is a relatively good value. Just remember to consider spending an extra $100 on the quad-core Core i5 processor option, as the $999 base model is equipped with a particularly sluggish dual-core processor.

For more intensive tasks, the 13-inch MacBook Pro's faster processors and more advanced thermal design will allow you to push the limits more without the fans running obnoxiously. You'll also get the Touch Bar, a brighter and more vibrant display, and slightly better sounding speakers with high dynamic range.
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The internet was seen as a major catalyst for the furry fandom finding one another during the times before we held conventions. During that earlier period in the 1990s, conventions and meets were rare, and finding one another was done mostly through the chat rooms and message boards of the past. There was no bandwidth for video or sharing major animation projects, therefore most of our intimate conversations were textual.

For many younger furries, it was a time that was lost in the annals of a distant history. Instead they found themselves joining in amongst a wave of growing conventions being held in various places around the world on any given weekend. Ones where those in custom fursuits march out in the streets openly rather than feeling a stifling isolation of being cooped up in hotel spaces, with a handful of home made creations, being wary of a hostile media looking for a freak show.

Coming out of 2019, it seemed that the time where furry was just an internet thing was fully behind it. However a series of unfortunate events were in line for 2020, a year that has led humanity to be forced into their rooms by an irate Mother Nature as an easily spread virus has forced governments around the globe to take drastic measures to slow its spread and put strict limits on social gatherings. A situation which has forced both the furry fandom, and the internet that brought it together, back to their roots.

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Animal Crackers (trailer) is a 94-minute computer-animated children's movie. The brainchild of Scott Sava, it caught the early attention of furry fandom at least as far back as 2015. Concept animation showed a guy haphazardly munching on animal-shaped cookies that turned him into the animals. As time went on, Sava brought in financial backers, a co-director (Tony Bancroft, who'd worked on several Disney movies), and a co-writer (Dean Lorey). The finished product premiered at the Annecy Film Festival in 2017... and then vanished.

It turns out that Sava had made the mistake of not securing a distributor ahead of time. With very little bargaining power, it eventually got shown in China in 2018, and some other countries in 2019.

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Disney has announced that it will be producing a new Robin Hood movie.

Yes, that Robin Hood.

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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.

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