Показали игрокам нарезку из динамичных кадров, который хватило на полторы минуты хронометража.

Креативный директор игры Ашраф Измаил решил ответить геймерам и успокоить аудиторию.

Компания обещает бесплатный ремонт устройств и возмещение расходов, если ноутбук уже отремонтировали.

Every cricket follower fervently needs to watch real-time cricket suit. Nothing can change the excitement, delights and excitement of real-time cricket suit. Live cricket suit is of much worry for a fan during any recurring series or competitions. Every cricket… Continue Reading →

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

At Let Grow, a wise mom named Kate Sundquist admits that while her kids were already good at playing, they certainly weren’t good at filling hours and hours of free time, playing by themselves. (Read the piece here.) So she her and boys created a schedule. “While these routines might seem restrictive or even the […]

Contes de fées aux enfants - Octo-Puce la pieuvre et Craby-la-Pince le crabe.

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Do you have a fear of standing alone at your company party with nobody to talk to and no way to break the ice? Have no fear, F&J is here! Here’s a quick and dirty arsenal of one-liner jokes that are sure to make you the life of the party. Rest assured that nobody will […]

The post 11 Crappy One-Liners Sure To Leave You A Loser appeared first on Funny & Jokes.

Date: April 28, 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 Cricket!

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

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

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Arterial cardiovascular events are the leading cause of death in patients with JAK2V617F myeloproliferative neoplasms (MPNs). However, their mechanisms are poorly understood. The high prevalence of myocardial infarction without significant coronary stenosis or atherosclerosis in patients with MPNs suggests that vascular function is altered. The consequences of JAK2V617F mutation on vascular reactivity are unknown. We observe here increased responses to vasoconstrictors in arteries from Jak2V617F mice resulting from a disturbed endothelial NO pathway and increased endothelial oxidative stress. This response was reproduced in WT mice by circulating microvesicles isolated from patients carrying JAK2V617F and by erythrocyte-derived microvesicles from transgenic mice. Microvesicles of other cellular origins had no effect. This effect was observed ex vivo on isolated aortas, but also in vivo on femoral arteries. Proteomic analysis of microvesicles derived from JAK2V617F erythrocytes identified increased expression of myeloperoxidase as the likely mechanism accounting for their effect. Myeloperoxidase inhibition in microvesicles derived from JAK2V617F erythrocytes suppressed their effect on oxidative stress. Antioxidants such as simvastatin and N-acetyl cysteine improved arterial dysfunction in Jak2V617F mice. In conclusion, JAK2V617F MPNs are characterized by exacerbated vasoconstrictor responses resulting from increased endothelial oxidative stress caused by circulating erythrocyte-derived microvesicles. Simvastatin appears to be a promising therapeutic strategy in this setting.

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

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

Elevated pressure in the pancreatic gland is the central cause of pancreatitis following abdominal trauma, surgery, endoscopic retrograde cholangiopancreatography, and gallstones. In the pancreas, excessive intracellular calcium causes mitochondrial dysfunction, premature zymogen activation, and necrosis, ultimately leading to pancreatitis. Although stimulation of the mechanically activated, calcium-permeable ion channel Piezo1 in the pancreatic acinar cell is the initial step in pressure-induced pancreatitis, activation of Piezo1 produces only transient elevation in intracellular calcium that is insufficient to cause pancreatitis. Therefore, how pressure produces a prolonged calcium elevation necessary to induce pancreatitis is unknown. We demonstrate that Piezo1 activation in pancreatic acinar cells caused a prolonged elevation in intracellular calcium levels, mitochondrial depolarization, intracellular trypsin activation, and cell death. Notably, these effects were dependent on the degree and duration of force applied to the cell. Low or transient force was insufficient to activate these pathological changes, whereas higher and prolonged application of force triggered sustained elevation in intracellular calcium, leading to enzyme activation and cell death. All of these pathological events were rescued in acinar cells treated with a Piezo1 antagonist and in acinar cells from mice with genetic deletion of Piezo1. We discovered that Piezo1 stimulation triggered transient receptor potential vanilloid subfamily 4 (TRPV4) channel opening, which was responsible for the sustained elevation in intracellular calcium that caused intracellular organelle dysfunction. Moreover, TRPV4 gene–KO mice were protected from Piezo1 agonist– and pressure-induced pancreatitis. These studies unveil a calcium signaling pathway in which a Piezo1-induced TRPV4 channel opening causes pancreatitis.

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

Treating neuropathic pain is challenging and novel non–opioid-based medicines are needed. Using unbiased receptomics, transcriptomic analyses, immunofluorescence, and in situ hybridization, we found that the expression of the orphan GPCR Gpr160 and GPR160 increased in the rodent dorsal horn of the spinal cord following traumatic nerve injury. Genetic and immunopharmacological approaches demonstrated that GPR160 inhibition in the spinal cord prevented and reversed neuropathic pain in male and female rodents without altering normal pain response. GPR160 inhibition in the spinal cord attenuated sensory processing in the thalamus, a key relay in the sensory discriminative pathways of pain. We also identified cocaine- and amphetamine-regulated transcript peptide (CARTp) as a GPR160 ligand. Inhibiting endogenous CARTp signaling in spinal cord attenuated neuropathic pain, whereas exogenous intrathecal CARTp evoked painful hypersensitivity through GPR160-dependent ERK and cAMP response element–binding protein (CREB). Our findings de-orphanize GPR160, identify it as a determinant of neuropathic pain and potential therapeutic target, and provide insights into its signaling pathways. CARTp is involved in many diseases including depression and reward and addiction; de-orphanization of GPR160 is a major step forward understanding the role of CARTp signaling in health and disease.

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) is caused by loss of repression of the DUX4 gene; however, the DUX4 protein is rare and difficult to detect in human muscle biopsies, and pathological mechanisms are obscure. FSHD is also a chronic disease that progresses slowly over decades. We used the sporadic, low-level, muscle-specific expression of DUX4 enabled by the iDUX4pA-HSA mouse to develop a chronic long-term muscle disease model. After 6 months of extremely low sporadic DUX4 expression, dystrophic muscle presented hallmarks of FSHD histopathology, including muscle degeneration, capillary loss, fibrosis, and atrophy. We investigated the transcriptional profile of whole muscle as well as endothelial cells and fibroadiopogenic progenitors (FAPs). Strikingly, differential gene expression profiles of both whole muscle and, to a lesser extent, FAPs, showed significant overlap with transcriptional profiles of MRI-guided human FSHD muscle biopsies. These results demonstrate a pathophysiological similarity between disease in muscles of iDUX4pA-HSA mice and humans with FSHD, solidifying the value of chronic rare DUX4 expression in mice for modeling pathological mechanisms in FSHD and highlighting the importance FAPs in this disease.

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.

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.

BACKGROUND Mirabegron is a β3-adrenergic receptor (β3-AR) agonist approved only for the treatment of overactive bladder. Encouraging preclinical results suggest that β3-AR agonists could also improve obesity-related metabolic disease by increasing brown adipose tissue (BAT) thermogenesis, white adipose tissue (WAT) lipolysis, and insulin sensitivity.METHODS We treated 14 healthy women of diverse ethnicities (27.5 ± 1.1 years of age, BMI of 25.4 ± 1.2 kg/m2) with 100 mg mirabegron (Myrbetriq extended-release tablet, Astellas Pharma) for 4 weeks in an open-label study. The primary endpoint was the change in BAT metabolic activity as measured by [18F]-2-fluoro-d-2-deoxy-d-glucose (18F-FDG) PET/CT. Secondary endpoints included resting energy expenditure (REE), plasma metabolites, and glucose and insulin metabolism as assessed by a frequently sampled intravenous glucose tolerance test.RESULTS Chronic mirabegron therapy increased BAT metabolic activity. Whole-body REE was higher, without changes in body weight or composition. Additionally, there were elevations in plasma levels of the beneficial lipoprotein biomarkers HDL and ApoA1, as well as total bile acids. Adiponectin, a WAT-derived hormone that has antidiabetic and antiinflammatory capabilities, increased with acute treatment and was 35% higher upon completion of the study. Finally, an intravenous glucose tolerance test revealed higher insulin sensitivity, glucose effectiveness, and insulin secretion.CONCLUSION These findings indicate that human BAT metabolic activity can be increased after chronic pharmacological stimulation with mirabegron and support the investigation of β3-AR agonists as a treatment for metabolic disease.TRIAL REGISTRATION Clinicaltrials.gov NCT03049462.FUNDING This work was supported by grants from the Intramural Research Program of the NIDDK, NIH (DK075112, DK075116, DK071013, and DK071014).

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.

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. ????  

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.

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.

Video from Thabo Meerkat, transcribed

Welcome to another edition of Digging Up Positivity! This episode is dedicated to the many volunteers that make all those amazing conventions and charities possible. But besides them, we are covering some animation news and other (maybe otter?) tidbits!

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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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Let me talk to you about “Crash” by the Primitives. Except I’m not actually going to be talking about “Crash” by The Primitives. Get me going about music long enough, and I will tell you about how “Crash” is a perfect pop song. Perfect. The chiming, arpeggiated guitars contrasted with the choppy, crunchy guitars; the … Continue reading Crash

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 →

Are you a taxpreparer who is unsatisfied with the quality of Intuit's ProSeries tax software program? I am not a happy user of ProSeries tax software. Choose your tax software carefully. I will be searching for an alternative tax software vendor for the year 2014. Continue reading →

A year ago this month the U.S. Department of Justice announced that the banking giant JPMorgan Chase would avoid criminal charges by agreeing to pay $13 billion to settle claims that it had routinely overstated the quality of mortgages it … 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 →

TurboTax’s Anti-Fraud Efforts Under Scrutiny Two former security employees at Intuit — the makers of the popular tax preparation software and service TurboTax – allege that the company has made millions of dollars knowingly processing state and federal tax refunds filed … Continue reading →

Accountants CPA Hartford Connecticut LLC:  This transcript may contain errors. The Willis Report:  And tonight’s stunning accusation against Intuit, the maker of Turbotax, the popular tax preparation software.  Two whistleblowers claim that Intuit knew that criminals used its tax software … Continue reading →

Even though Corporate America has anointed Hillary Clinton as its next President, Senator Bernie Sanders' populist message is already in a week's time raising individual contributions totaling millions of dollars from hundreds of thousands of people! Continue reading →

Sen. Bernie Sanders (I-Vt.) warns not to underestimate him in the 2016 Democratic race for the White House. Sanders, who is formally launching his campaign Tuesday, said he has a strong message. Continue reading →

“Thank you all very much for being here and for all the support that you have given me over the years: as the mayor of this great city, as Vermont’s only congressman and now as a U.S. senator. Thanks also … Continue reading →

Eyewitness News has learned that the Berlin High School football recruiting scandal may have cost Berlin taxpayers tens of thousands of dollars. Continue reading →

"This is supposed to be a political party. In a healthy society, there would be a democratic process in the Democratic Party, by which elected people would be overseeing these issues by making sure there wasn’t just nepotism and insider dealing," Curry says. "That the political party itself — which is supposed to be the progressive party — has become mortgaged to a small group of Washington insiders, who raise money from large corporate PACs, [and] has become just a dead carcass of what it once was, is the most important piece of information that this contretemps over the data files has emphasized. It’s time for progressives in this country to stand up and demand a genuinely democratic process." Continue reading →

With the Republican establishment attempting to stop real estate mogul Donald Trump from receiving the GOP nomination, a new anti-Trump ad produced by the Emergency Committee for Israel alleges that Trump supports dictators. But what about Democratic presidential candidate Hillary Clinton’s record on dictators? Earlier this week, Clinton addressed the annual AIPAC conference, seeking to cast herself as a stronger ally to Israel than Donald Trump. We examine her record on Israel and U.S. foreign relations at large with Pulitzer Prize-winning journalist Glenn Greenwald, co-founder of The Intercept. Continue reading →

Bernie Sanders would have already won this nominating contest if we had received an accurate accounting of the vote. It is deeply troubling the Senator would be sending out surrogates to talk about his allegiance to the Democratic party and Clinton in general in the face of the Party instituting theft against its own constituents. It is no mystery HOW to win. Count the votes and contest fraud. A tough Sane Progressive call out. Continue reading →

Ralph Nader on Campaign 2016 Ralph Nader talked about his upcoming book, Breaking Through Power: It’s Easier Than We Think, as well as the latest developments in the 2016 presidential election. Continue reading →

Bernie Sanders and Jane Sanders are mere actors serving as pressure valves which release from time to time all excess heat emanating from failed policies, scandals, and the worsening economic conditions, so that a catastrophic systems’ collapse can be prevented. They are sheepdogs for Hillary Clinton, preventing progressives from supporting a third party progressive candidate and to herd them back into the corral of the Democratic Party. Continue reading →

"Well, reducing the election to personalities is kind of infantile at this point. The fact is, we live in a system that Sheldon Wolin calls inverted totalitarianism. It’s a system where corporate power has seized all of the levers of control. There is no way to vote against the interests of Goldman Sachs or ExxonMobil or Raytheon." Continue reading →

This is one of the best interviews on American politics ever to be broadcasted. Ralph Nader and Jill Stein discuss our corrupt government and corrupt media controlled by corporations, and explain how we no longer have a democracy but corporate tyranny. Continue reading →

"And you know, we have to stop looking beyond this election cycle and see that this corporate driven ideology, you know, this commodification of the culture, this constant extracting of blood from us as citizens to pay what in essence were private debts of the banks which engaged in casino capitalism, has political consequences. History has taught us that. And Hillary Clinton is only going to further that process." Continue reading →

Questions surrounding Hillary Clinton and the Clinton Foundation continue to grow. On Sunday, Democratic National Committee interim chairperson Donna Brazile defended Clinton’s meetings as secretary of state with Clinton Foundation donors, saying, "When Republicans meet with their donors, with their supporters, their activists, they call it a meeting. When Democrats do that, they call it a conflict." Donna Brazile’s comments come in response to an Associated Press investigation revealing that while Hillary Clinton served as secretary of state, more than half of the private citizens she met with during the reporting period had donated to the Clinton Foundation. The AP investigation comes after a three-year battle to gain access to State Department calendars. The analysis shows that at least 85 of 154 people Hillary Clinton had scheduled phone or in-person meetings with were foundation donors. We speak to Pulitzer Prize-winning journalist Glenn Greenwald of The Intercept. His most recent piece is headlined "Why Did the Saudi Regime and Other Gulf Tyrannies Donate Millions to the Clinton Foundation?" Continue reading →