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: April 25, 2020

As COVID-19 continues to impact communities around the world, people are coming together to help one another now more than ever. We’re launching a Doodle series to recognize and honor many of those on the front lines.

Today, we’d like to say: 

To all coronavirus helpers, thank you.
 

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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: covid, Current Event, covid-19, appreciation, helpers, coronavirus

Date: April 27, 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 2017 Doodle game celebrating 50 years of Kids Coding!

 

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Date: May 4, 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 2016 Doodle game celebrating Wilbur Scoville!
 

 

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

The post The Great Pause: A Second Chance to a Better World 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.

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.

BACKGROUND Since December 2019, an outbreak of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) emerged in Wuhan, and is now becoming a global threat. We aimed to delineate and compare the immunological features of severe and moderate COVID-19.METHODS In this retrospective study, the clinical and immunological characteristics of 21 patients (17 male and 4 female) with COVID-19 were analyzed. These patients were classified as severe (11 cases) and moderate (10 cases) according to the guidelines released by the National Health Commission of China.RESULTS The median age of severe and moderate cases was 61.0 and 52.0 years, respectively. Common clinical manifestations included fever, cough, and fatigue. Compared with moderate cases, severe cases more frequently had dyspnea, lymphopenia, and hypoalbuminemia, with higher levels of alanine aminotransferase, lactate dehydrogenase, C-reactive protein, ferritin, and D-dimer as well as markedly higher levels of IL-2R, IL-6, IL-10, and TNF-α. Absolute numbers of T lymphocytes, CD4+ T cells, and CD8+ T cells decreased in nearly all the patients, and were markedly lower in severe cases (294.0, 177.5, and 89.0 × 106/L, respectively) than moderate cases (640.5, 381.5, and 254.0 × 106/L, respectively). The expression of IFN-γ by CD4+ T cells tended to be lower in severe cases (14.1%) than in moderate cases (22.8%).CONCLUSION The SARS-CoV-2 infection may affect primarily T lymphocytes, particularly CD4+ and CD8+ T cells, resulting in a decrease in numbers as well as IFN-γ production by CD4+ T cells. These potential immunological markers may be of importance because of their correlation with disease severity in COVID-19.TRIAL REGISTRATION This is a retrospective observational study without a trial registration number.FUNDING This work is funded by grants from Tongji Hospital for the Pilot Scheme Project, and partly supported by the Chinese National Thirteenth Five Years Project in Science and Technology for Infectious Disease (2017ZX10202201).

The pandemic coronavirus infectious disease (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is rapidly spreading across the globe. In this issue of the JCI, Chen and colleagues compared the clinical and immunological characteristics between moderate and severe COVID-19. The authors found that respiratory distress on admission is associated with unfavorable outcomes. Increased cytokine levels (IL-6, IL-10, and TNF-α), lymphopenia (in CD4+ and CD8+ T cells), and decreased IFN-γ expression in CD4+ T cells are associated with severe COVID-19. Overall, this study characterized the cytokine storm in severe COVID-19 and provides insights into immune therapeutics and vaccine design.

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.

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.

Lamin A is a component of the inner nuclear membrane that, together with epigenetic factors, organizes the genome in higher order structures required for transcriptional control. Mutations in the lamin A/C gene cause several diseases belonging to the class of laminopathies, including muscular dystrophies. Nevertheless, molecular mechanisms involved in the pathogenesis of lamin A–dependent dystrophies are still largely unknown. The polycomb group (PcG) of proteins are epigenetic repressors and lamin A interactors, primarily involved in the maintenance of cell identity. Using a murine model of Emery-Dreifuss muscular dystrophy (EDMD), we show here that lamin A loss deregulated PcG positioning in muscle satellite stem cells, leading to derepression of non–muscle-specific genes and p16INK4a, a senescence driver encoded in the Cdkn2a locus. This aberrant transcriptional program caused impairment in self-renewal, loss of cell identity, and premature exhaustion of the quiescent satellite cell pool. Genetic ablation of the Cdkn2a locus restored muscle stem cell properties in lamin A/C–null dystrophic mice. Our findings establish a direct link between lamin A and PcG epigenetic silencing and indicate that lamin A–dependent muscular dystrophy can be ascribed to intrinsic epigenetic dysfunctions of muscle stem cells.

Seizures often herald the clinical appearance of gliomas or appear at later stages. Dissecting their precise evolution and cellular pathogenesis in brain malignancies could inform the development of staged therapies for these highly pharmaco-resistant epilepsies. Studies in immunodeficient xenograft models have identified local interneuron loss and excess glial glutamate release as chief contributors to network disinhibition, but how hyperexcitability in the peritumoral microenvironment evolves in an immunocompetent brain is unclear. We generated gliomas in WT mice via in utero deletion of key tumor suppressor genes and serially monitored cortical epileptogenesis during tumor infiltration with in vivo electrophysiology and GCAMP7 calcium imaging, revealing a reproducible progression from hyperexcitability to convulsive seizures. Long before seizures, coincident with loss of inhibitory cells and their protective scaffolding, gain of glial glutamate antiporter xCT expression, and reactive astrocytosis, we detected local Iba1+ microglial inflammation that intensified and later extended far beyond tumor boundaries. Hitherto unrecognized episodes of cortical spreading depolarization that arose frequently from the peritumoral region may provide a mechanism for transient neurological deficits. Early blockade of glial xCT activity inhibited later seizures, and genomic reduction of host brain excitability by deleting MapT suppressed molecular markers of epileptogenesis and seizures. Our studies confirmed xenograft tumor–driven pathobiology and revealed early and late components of tumor-related epileptogenesis in a genetically tractable, immunocompetent mouse model of glioma, allowing the complex dissection of tumor versus host pathogenic seizure mechanisms.

The physical integrity of endothelial cells (ECs) lining the blood vessels regulates the inflammatory response. Both innate immunity and inflammatory disorders hinge on the EC-neutrophil interaction. Neutrophil binding, rolling, and migrating along and between ECs is associated with vascular permeability. In this issue of the JCI, Owen-Woods et al. tracked neutrophils in vivo in venules of mouse striated muscle and revealed how endothelial permeability can affect neutrophil trafficking. Strikingly, many neutrophils that migrated between EC junctions were able to rejoin the blood circulation. Further, the chemokine and neutrophil chemoattractant, CXCL1, drove this reverse transendothelial migration (rTEM). This paradigm-shifting study provides a mechanism for distal organ damage as well as an explanation for sepsis-associated acute respiratory distress syndrome.

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.

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.

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.

Brown and beige adipose tissues contain thermogenic fat cells that can be activated by β3-adrenergic receptor agonists. In rodents, such drugs both diminish obesity and improve glucose homeostasis. In this issue of the JCI, O’Mara et al. and Finlin and Memetimin et al. report that chronic administration of the approved β3 agonist mirabegron to human subjects was without effect on body weight or fat mass, but improved several measures of glucose homeostasis. Though the mechanisms mediating these metabolic effects are uncertain, the data suggest that β3 agonists could have therapeutic utility in disorders of glucose homeostasis.

BACKGROUND Beige adipose tissue is associated with improved glucose homeostasis in mice. Adipose tissue contains β3-adrenergic receptors (β3-ARs), and this study was intended to determine whether the treatment of obese, insulin-resistant humans with the β3-AR agonist mirabegron, which stimulates beige adipose formation in subcutaneous white adipose tissue (SC WAT), would induce other beneficial changes in fat and muscle and improve metabolic homeostasis.METHODS Before and after β3-AR agonist treatment, oral glucose tolerance tests and euglycemic clamps were performed, and histochemical analysis and gene expression profiling were performed on fat and muscle biopsies. PET-CT scans quantified brown adipose tissue volume and activity, and we conducted in vitro studies with primary cultures of differentiated human adipocytes and muscle.RESULTS The clinical effects of mirabegron treatment included improved oral glucose tolerance (P < 0.01), reduced hemoglobin A1c levels (P = 0.01), and improved insulin sensitivity (P = 0.03) and β cell function (P = 0.01). In SC WAT, mirabegron treatment stimulated lipolysis, reduced fibrotic gene expression, and increased alternatively activated macrophages. Subjects with the most SC WAT beiging showed the greatest improvement in β cell function. In skeletal muscle, mirabegron reduced triglycerides, increased the expression of PPARγ coactivator 1 α (PGC1A) (P < 0.05), and increased type I fibers (P < 0.01). Conditioned media from adipocytes treated with mirabegron stimulated muscle fiber PGC1A expression in vitro (P < 0.001).CONCLUSION Mirabegron treatment substantially improved multiple measures of glucose homeostasis in obese, insulin-resistant humans. Since β cells and skeletal muscle do not express β3-ARs, these data suggest that the beiging of SC WAT by mirabegron reduces adipose tissue dysfunction, which enhances muscle oxidative capacity and improves β cell function.TRIAL REGISTRATION Clinicaltrials.gov NCT02919176.FUNDING NIH: DK112282, P30GM127211, DK 71349, and Clinical and Translational science Awards (CTSA) grant UL1TR001998.

Recently, I’ve found myself thinking more often than not about the past – mistakes I’ve made, where I could have done better, things like that. I think that’s a symptom of unhappiness, really, so yeah… I’m putting a stop to that. It’s a hard and imperfect stop, but I’m not willing to continue to think about things that I can’t change. Instead, I am going to look forward — to my next step and how to make it count! That’s how I’ve been trending, anyway, I hope you can tell! I guess that makes it funny that I roped people into going fossil-hunting with me! Get it? THE PAST. But, I LOVE ANCIENT HISTORY! It’s my first time finding a fossil, and my first time hunting, so I count it as a giant leap forward in this travelogue I call life. :3 Anyways, I found a book in the library about gem hunting in Washington and there was a listing for a site where you could find fossils (!!!!) nearby (!!!!!!!!!!). It’s called Lincoln Creek (there does appear to be a creek somewhere nearby, but it’s not right at the site), and let’s just say that I’ve learned a lot from it, both about fossil hunters (STINGY WITH LOCATIONS) and about fossil hunting itself (by blundering right into it without knowing anything). Thank god there were GPS coordinates in the book, because although I found a lot of reviews on fossil hunting at Lincoln Creek online, as well as a few blurry photos, I couldn’t find any information on how to actually get there or what exactly it looked like. All I had was the GPS coordinates from the book. I know that people want to protect their “stash,” and it comes across as pretty selfish to me, but it really makes it hard to start out as a beginner with only passion to rely on, and I don’t think that being “protective” or “exclusive” is a good way to behave in general. That said, let me help you if you decide to go yourself: – GPS coordinates in Google Maps. – A screencap of the map and the turns I walked to get there. I don’t recommend it, unless you want a really great walk in nature that is also technically trespassing and won’t be disappointed if you find nothing, but if you want to go, go for it and enjoy it all you can! It was only supposed to be a half hour drive or so from my sister’s house to the little logging road that led to the site. But I learned something new that had seriously never once crossed my mind: logging roads can be closed off! There was a gate blocking the main road, so we tried driving for miles in every direction to get in another way, but ALL of those were blocked off, too. There were “no tresspassing, this land belongs to Weyerhaeuser” signs, but we eventually just decided to walk it. I am not sorry at all to say that I have zero respect for companies that clearcut or attempt to think that land can “belong” to them for that purpose. Oh, and they have tried to sue the government to be able to log on lands that contain endangered species. Now, I love paper, but f you, Weyerhaeuser. I’m not at all sorry, and I’d walk these lands again a hundred times if I wanted to. So, we ignored the signs, and walked past the gate all the way to our destination. ALLLLLLLL the two hours. It might not seem like a lot, but we honestly thought that we’d be able to drive right up to the site as it said in the book. Welp, it was an unexpected walk, but super awesome to get back among the trees. Being in the forest and a slow walker anyways, I spent a lot of the time by myself contemplating life and sacred rituals. You know, the usual. Come look at some photos with me, and I’ll tell you a little bit about the journey. ???? When we realized that the road was blocked off, we drove around searching for another way into the deep forest and saw this. You know you’re… oh, wait. It looked like their neighbors a little further down were more my kind of people, though! Here’s my niece, all ready for adventure! I’m pretty sure that these were bear droppings, as they were full of berries. They were also somewhat fresh. There are a lot of bears up here in Western Washington, since there aren’t many settled areas. I never thought for a moment that I’d need to bring bear spray, but I definitely am going to have to buy some for my adventures. :/ It was quite lovely. One of the very few blue, sunny days that we’ve had so far this summer. I won’t be sorry to leave the cold behind, as I’m a desert sprite and being in the cold depletes my magic! But this… it was lovely. There were two clearcut clearings. They made for gorgeous views of the valley, but it was also quite sad. I could feel the souls of all of those trees calling out to me… ???? We delved onto a very overgrown road after over an hour of walking. And there was a huge, recent-looking landslide blocking the path! We weren’t about to turn back, so we picked our way across it. And just a little ways farther, down another overgrown road, this one much more primitive, the fossil site was evident. It was also really, really disappointing. It was exactly where the GPS coordinates said it would be (funny enough, I got better cell signal in the middle of the forest than I do in town), and there was basically a slope of discarded rocks that led up to a little overhang. Oops, I mean a lot overhang. People had dug deep into the cliff, and it looked like the forest above was one hit shy of collapsing in on you. I like adventuring, but I don’t like playing with death. And yet, I still picked for about half an hour, looking for concretions (fossilized crabs in the center of rock balls trapped within the rock, if that makes sense). Supposedly this site was full of them, and there were people online saying that they found 80 within an hour. But we found nothing at all, except for some shells that were indeed trapped in the rock, but looked like any old shell. Fossils, yes, but not really cool. This was supposed to be my “I’m tired and disappointed” face. I guess I shouldn’t have smiled, haha! Guess what, though???? We felt so empty-handed that we decided to see if there was anything in the rock slide, and that’s where I found the concretion!! In the middle of this giant rock that I slowly whittled away at. We must have spent about two hours picking through the debris, and we found a ton more shells, but just that one crab. Still, it’s cool, right? I considered it a win for the day after all, and we decided to get out of there as the sun started to go down. Here’s the slightly-overgrown trail we were on (the panorama makes it look like a circle, but it was a straight path XD). Passed the clearcut areas with the sun much lower in the sky. The fairies started to come out as we entered the wooded paths again in the late afternoon sunlight. We made it home while it was still light out, exhausted and quite sore. Here is my concretion, though! Isn’t it cool? You can barely tell that there was a crab inside when it was formed. I didn’t really know what I was doing, so I think that I didn’t preserve it as well as I could when I cracked it open, but I’m still really proud to have found it. ????   My first fossil. Of many. ????  

Amazon is taking up to $100 off the Apple Watch Series 5 this week, with prices starting at $299.99 for the 40mm GPS models. Only the Gold Aluminum Case with Pink Sport Band is available at this price. If you order today, the Apple Watch should arrive sometime next week.

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

The Apple Watch Series 5 was released in September 2019 with a new OLED screen that supports an always-on feature, which represents the biggest change to the Series 5 models. The newest Apple Watch is available in 40mm and 44mm sizes, and it has the overall same design as the Series 4 models.

$100 OFF

Apple Watch S5 (40mm, GPS) for $299.99

If you're shopping for a cellular model, there are also a few solid discounts on Amazon for these devices. You can get the Gold Aluminum Case with Pink Sport Band (40mm) for $399.00, down from $499.00. Likewise, the Silver Aluminum Case with White Sport Band (40mm) is $399.00 right now.

For the 44mm cellular models, a solid deal is the Space Gray Aluminum Case with Black Sport Band at $429.00, down from $529.00. You'll find the same price on the Silver Aluminum Case with White Sport Band and the Gold Aluminum Case with Pink Sport Band.

Across the board, these sales are either new low prices on the Apple Watch Series 5, or they're matching previous low prices seen on these models on Amazon. There are a few other deals going on for different Series 5 models as well, including numerous 44mm cellular devices that are about $50 off Apple's original prices. Be sure to head to Amazon to check out the full sale before these prices expire, or the retailer runs out of stock.

Keep up with all of this week's best discounts on Apple products and related accessories in our dedicated Apple Deals roundup.
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The Label's "The_Otherside" is this week's addition to Apple Arcade on the iPhone, iPad, and Apple TV. The game is described as both a turn-based RPG and a strategy board game:

Otherside is a turn based RPG and strategy board game where you will control four survivors who hope to push back the shadowy threat. Make your way through each level solving puzzles, fighting monsters, and destroying the spirit anchors that threaten our dimension.

Do you have what it takes to restore the town back to normal and save the day?

"The_Otherside" is available on the App Store with an Apple Arcade subscription. The service provides iPhone, iPad, Apple TV, and Mac users with access to over 100 games with no in-app purchases or ads for $4.99 per month.
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Apple's rumored high-end over-ear headphones may be called "AirPods Studio" and retail for $349, according to Jon Prosser of YouTube channel Front Page Tech.


In keeping with the successful ‌AirPods‌ brand, the rumored "Studio" over-ear headphones would significantly diversify Apple's ‌AirPods‌ lineup, which last added the in-ear AirPods Pro in October 2019. The supposed price of $349 would place "‌AirPods‌ Studio" as a direct competitor to high-end noise-canceling over-ear headphones from Bose and Sony.

Looks like Apple is sticking with the “‌AirPods‌” branding for their new over-ear headphones.

‌AirPods‌ Studio
Codename: B515
$349

— Jon Prosser (@jon_prosser) May 9, 2020

Prosser has previously accurately leaked the April 15 launch date of the new iPhone SE and, most recently, the May 4 launch date of the refreshed 13-inch MacBook Pro.

Apple analyst Ming-Chi Kuo expects Apple's over-hear headphones to enter mass production in mid-2020, which may suggest a fall 2020 launch.
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Yes, a cancellation

Yes, a postponed con

Yes, both

No I haven't had any plans altered

While the pandemic has been chipping away at the furry convention scene, other furs have stepped forward to try and give those in the community events to look forward to over the now dormant weekends. This had started with a group of Furnal Equinox members creating a digital replacement for their late March convention called Keep Calm and Carry Con - Furnal Isolation. More have started to spring up this spring.

They can have internet dealers dens, streaming dance competitions, and other staples that conventions are known for. Accessible from the safety of your own home.

Below is a comprehensive list of conventions. Last updated May 2nd, 2020 12:18 ET.

Please feel free to place any not listed here in the comments below and we will look into adding it if it appears legitimate.

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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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As governments restrict gatherings of people, furry conventions are being postponed or canceled. Here's a quick run down of events in April, May, and June and their status as of May 5 17:28 EDT (UTC-4) in response to the COVID-19 pandemic - updates to come.

A new section has been added for past events impacted for historical purposes.

Links go to statements if available, or to their Twitter feed or site. See also: Furry Fandom and the Internet forced back to roots by viral outbreak

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Linda McMahon is running for the US Senate in Connecticut. For twenty (20) years, she ran World Wrestling Entertainment (WWE) with her husband, Vince McMahon. A few years ago, a documentary film examined the WWE's celebration of violence against women. Her campaign doesn't want Connecticut voters to see that film. Watch these excerpts from the film to see why. Continue reading →

Cornel West and Tavis Smiley criticize President Barack Obama for being to the right of even President Richard Nixon. Continue reading →

The Town of Berlin Connecticut continues to raise property taxes in the face of a never-ending recession. The Berlin Property Owners Association has been speaking out against these increases in property taxes. Recorded herein are four speeches by residents of the Town of Berlin at the first Town Council meeting subsequent to the Town Council's approval of an increase in property taxes, resulting from giving raises to virtually all town employees, who are already very well compensated. Continue reading →

William Brighenti, who founded the Berlin Property Owners Association, argued that the town can’t afford a new police headquarters, and police should look to clear space in their current building. He thinks one way to accomplish this is to get rid of tactical gear. Continue reading →

Are you as an employer having trouble paying online your unemployment compensationtaxes with the Connecticut Department of Labor? SNAFU. Continue reading →

Does a stooge prepare your income tax returns? Watch the Three Stooges prepare a tax return and learn from them. Don't be a stooge: hire a CPA to prepare your next tax return! Continue reading →

Are accountants destined to be the anthropologists of the cyber era? Gillian Tett appears to suspect such. 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 →

Democratic presidential candidate Bernie Sanders (I-VT) on Tuesday unveiled a plan to address income inequality by taxing Wall Street speculation and using the money to eliminate college tuition. Continue reading →

Read the text of Senator Bernie Sanders bill to make college tuition free for students and to be financed by a tax on Wall Street speculation. WASHINGTON, May 19 – Sen. Bernie Sanders (I-Vt.) today introduced legislation to make 4-year public colleges and universities tuition free. “We live in a highly competitive global economy. If our economy is to be strong, we need the best educated work force in the world. That will not happen if every year hundreds of thousands of bright young people cannot afford to go to college and if millions more leave school deeply in debt,” Sanders said. Under the legislation, $70 billion a year in assistance – two-thirds from the federal government and one-third from states – would replace what public colleges and universities now charge in tuition and fees. The federal share of the cost would be offset by imposing a tax on Wall Street transactions by investment houses, hedge funds and other speculators. The legislation also would overhaul student loan programs so students and their parents could reduce crushing debt loads which now exceed Americans’ credit card debt. Federal profits on loans would be eliminated, work-study programs expanded and incentives offered for colleges and universities to keep costs down. “We once led the world in the percentage of our people with a college degree, now we are in 12th place.” Sanders said. “Countries like Germany, Denmark, Sweden and many more are providing free or inexpensive higher education for their young people. They understand how important it is to be investing in their youth. We should be doing the same,” he added. Tuition at 4-year public colleges and universities rose by 50 percent in the United States during the past decade. As state governments have cut support for higher education, the burden has shifted to students and their parents. With this spring’s college commencement season underway, the class of 2015 is the most indebted class in American history, according to Mark Kantrowitz, publisher of Edvisors, a website on college costs and financial aid. Continue reading →

Presidential candidate Bernie Sanders says he wants to offer tuition free at public colleges and universities, paid for with a new tax on Wall Street. Ed Schultz and Sanders discuss the senator’s proposal. Continue reading →