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

An in-depth understanding of immune escape mechanisms in cancer is likely to lead to innovative advances in immunotherapeutic strategies. However, much remains unknown regarding these mechanisms and how they impact immunotherapy resistance. Using several preclinical tumor models as well as clinical specimens, we identified a mechanism whereby CD8+ T cell activation in response to programmed cell death 1 (PD-1) blockade induced a programmed death ligand 1/NOD-, LRR-, and pyrin domain–containing protein 3 (PD-L1/NLRP3) inflammasome signaling cascade that ultimately led to the recruitment of granulocytic myeloid-derived suppressor cells (PMN-MDSCs) into tumor tissues, thereby dampening the resulting antitumor immune response. The genetic and pharmacologic inhibition of NLRP3 suppressed PMN-MDSC tumor infiltration and significantly augmented the efficacy of anti–PD-1 antibody immunotherapy. This pathway therefore represents a tumor-intrinsic mechanism of adaptive resistance to anti–PD-1 checkpoint inhibitor immunotherapy and is a promising target for future translational research.

Curing HIV infection will require the elimination of a reservoir of infected CD4+ T cells that persists despite HIV-specific cytotoxic T cell (CTL) responses. Although viral latency is a critical factor in this persistence, recent evidence also suggests a role for intrinsic resistance of reservoir-harboring cells to CTL killing. This resistance may have contributed to negative outcomes of clinical trials, where pharmacologic latency reversal has thus far failed to drive reductions in HIV reservoirs. Through transcriptional profiling, we herein identified overexpression of the prosurvival factor B cell lymphoma 2 (BCL-2) as a distinguishing feature of CD4+ T cells that survived CTL killing. We show that the inducible HIV reservoir was disproportionately present in BCL-2hi subsets in ex vivo CD4+ T cells. Treatment with the BCL-2 antagonist ABT-199 was not sufficient to drive reductions in ex vivo viral reservoirs when tested either alone or with a latency-reversing agent (LRA). However, the triple combination of strong LRAs, HIV-specific T cells, and a BCL-2 antagonist uniquely enabled the depletion of ex vivo viral reservoirs. Our results provide rationale for novel therapeutic approaches targeting HIV cure and, more generally, suggest consideration of BCL-2 antagonism as a means of enhancing CTL immunotherapy in other settings, such as cancer.

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.

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.

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.

Systemic sclerosis (SSc) is an autoimmune fibrotic disease whose pathogenesis is poorly understood and lacks effective therapies. We undertook quantitative analyses of T cell infiltrates in the skin of 35 untreated patients with early diffuse SSc and here show that CD4+ cytotoxic T cells and CD8+ T cells contribute prominently to these infiltrates. We also observed an accumulation of apoptotic cells in SSc tissues, suggesting that recurring cell death may contribute to tissue damage and remodeling in this fibrotic disease. HLA-DR–expressing endothelial cells were frequent targets of apoptosis in SSc, consistent with the prominent vasculopathy seen in patients with this disease. A circulating effector population of cytotoxic CD4+ T cells, which exhibited signatures of enhanced metabolic activity, was clonally expanded in patients with systemic sclerosis. These data suggest that cytotoxic T cells may induce the apoptotic death of endothelial and other cells in systemic sclerosis. Cell loss driven by immune cells may be followed by overly exuberant tissue repair processes that lead to fibrosis and tissue dysfunction.

Immunosuppression continues to be a necessary component of transplantation, despite its association with a multitude of adverse effects. Numerous efforts have been made to circumvent the need for immunosuppression by using various techniques to achieve donor hyporesponsiveness. In this issue of the JCI, Morath et al. take this endeavor forward. Prior to transplantation, the researchers infused recipients with donor-modified immune cells and achieved immunologic hyporesponsiveness. This successful phase I trial also provides a possible avenue for achieving transplantation without the requisite immunosuppression.

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.

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.

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.

Cats. Cats are the best, and I can’t seem to settle down in any one place for too long, so my cats (possibly to their dismay) have had to move around with my silly butt. I don’t own a boat that can cross the Pacific Ocean, so that means taking them on a plane. BUT! While it’s no fun for anyone, it’s not really as hard as you think! Really really! My cats are my family, and if you’re here then you probably also have furry family members, and you are worried about flying with them. I’ve both taken my cats in the cabin and had to check them into the pet cargo hold (to my terror), but they not only survived, they are all flourishing wonderfully. While things do happen (and if something happens, raise a ruckus and make sure that whomever hurt your baby knows it), for the most part, flying is actually pretty safe for cats. Not that you want to take them. It’s just that sometimes you have to. So read on for my personal tips on how to make the flight go as smoothly as possible for all of you! Trust me, you’ll want it to be this way. My cats at the vet for their checkups and vaccinations. 1. Do Your Homework. This might seem obvious, but that being said, let’s put it out there anyway. Know your stuff! There are two things that you’re going to need to find out as soon as you decide to fly with your pets:      a) What paperwork does the airline require for me to bring my cat on the plane?      b) What does my arrival location require for me to bring my cat into the country/state? Usually, a) is the easiest part. It’s usually just a health certificate from your vet, issued less than a week before travel. Just book an appointment at your vet for less than a week before departure, and tell them that you’re flying to (wherever). All of my vets, even my one in Japan, either knew what they needed, or looked it up beforehand. Check your airline’s webpage (my absolute favorite for flying with pets is Alaska Air, btw. You can take two in the cabin by yourself, and it’s the only airline I know of that allows this!), and follow the instructions. I keep all of my paperwork with my passport while flying, so that I can show it to the ticketing agent or anyone else that asks (sometimes, nobody has, but at least I had it). In all of the cases where I’ve flown, my plane required a current health certificate to board, and when I left Japan, they required an inspection from the on-site team, which I just asked for when I arrived in Narita. b) can be easy, or it can be hard. In order to enter the US from Japan, I had to check the US Customs website for the country’s official regulations, and Washington State for its regulations.  The US didn’t have any regulations at the time, but Washington state required a health certificate (same as the plane), and current rabies vaccination, both of which I had done within the week before I left. Funny enough, nobody checked my paperwork after I landed, since it was the 4th of July and the Agricultural Inspections office was closed. When I went to Hawaii, it was another story. It was a long, long, long process (more than 6 months) to get all of my testing and paperwork done for Sansa to enter the state, but I did it, kept all of my paperwork in order, and was able to leave the airport in Hawaii with her in my arms without any fuss! There was a lot to do, but I just made sure that I knew what I needed, did it, and had the documentation, and things were pretty smooth sailing afterward! You should always check the official government pages to make sure that you have the correct information. In Hawaii’s case, it can be found here. All of my cats reacted differently to being examined. 2. Get your stuff in order! Once you have your list of things that you need (vaccinations, health checks, etc), then CALL the airline to make your reservations (you always need to call them in order to add pets to your tickets. They usually cost a little bit extra, and try to get them in the cabin if you can). Then, check your airline’s website to find out what kind of carrier you will need, and whether you will need anything else. When I flew to Washington the first time, and to Hawaii, I only had one cat, so I didn’t need any food (I brought some anyway, and a little bowl in my carryon just in case), and a soft-sided carrier that would fit in the dimensions they specified on their websites (it’s usually in the pet section or the carry-on section, and every airline is different). When I flew to Washington again, it was with three cats, so I needed two large hard carriers that met certain criteria for my babies flying underneath, and one soft-sided one for the baby going in the cabin. The website for the airline was very specific, but it was easy to find what I needed at Petco. Check, check, and check. I had my carriers, my paperwork, and I was ready! When your cat isn’t too happy about getting her shots. 3. Getting ready for the flight. A week or so before my flight (or days in my last case), I set all of my pet carriers out in the living room and set them up how I was going to have them for the flight — I lined the bottoms with puppy training pads (in case there was an accident in-flight), then a towel for absorbency (in the large hard carriers only), and finally, on top of that, a blanket that I had been using a lot (so that it had our scents on it, and would comfort the cats). I sprayed the interior of all of the carriers with Feliway, and left them out for the cats to get used to them. The carriers sitting out for the curious kitties to explore. They all took turns exploring the carriers, and after a few days, got comfortable with them and would lounge around inside, play with them, and rub up against the sides. This was all in order to reduce the stress of travel on them as much as possible. I continued to spray them with Feliway at least once a day until we left. There is no hard and fast rule on this, but I took away my cats’ food and water the morning of the trip, and waited until just before we left to toss out the litter boxes. There was some satisfaction in being able to stuff those nasty things in a giant garbage bag and haul them to the trash without scooping! Hey, take pleasure while you can– you’re about to undertake something pretty stressful! After I called my Uber, I rounded up the cats one by one and deposited them in their carriers. Nobody was particularly happy about this, but just be patient. Two of my babies at the airport waiting for inspection. All of them were champs! 4. The Flight Be calm, patient, and as rational as possible. I know that it’s pretty scary (terrifying, to me) to let your precious babies our of your sight, but once the porter had helped me to the ticket counters (I actually needed two the last time, and I tipped them very well), I just reminded myself that it would all be over soon, and that the calmer I was, the better the kitties would feel. In order to pass through security, you will need to remove the cats one-by-one from their carriers and hold them while the crew puts your carrier through the scanner, or manually scans by hand (two of mine were too large to fit). Sometimes, they will let you do all of this in a separate room so that the cats are calmer, but there isn’t always one available (it will say that you can do this on most websites, but I wasn’t allowed a separate room the last time and had to hold three wiggly cats in the middle of the airport). BRING A HARNESS FOR THIS. I can’t stress this enough. My cats don’t like harnesses, but I fastened one to them before I brought them out of the carrier, and removed it right after, and it brought me a lot of peace of mind. None of my cats tried to run, but I have heard that some cats do, and you don’t want to take that chance. Look for a harness like this one— thick and really hard to pull out of. Better safe than sorry. I only brought one harness for three cats, since I would only need to take out one cat at a time. By the next morning, everyone was already claiming “our” new bed as their own. And that’s it!  Once you’re on the flight, it’s mostly a waiting game. I honestly am not sure whether the cats or I were more stressed about the trip, and they were certainly shaken and scared when they arrived at our new home. However, within a few days, my cats were all behaving as if they’d never lived anywhere else. They rebound quickly as long as you shower them with love and affection. ???? Well, those are my tips for making the smoothest ride possible! It helps to have litter and litter pans, food, etc, sent to your new place before you arrive, as well, so that everything will be easy to set up for you. Make sure that your kitties are confined to one room for at least a few hours, and let them hide for as long as they need to. They’ll get curious and hungry and come out on their own. I hope this helps someone! If I did it, anyone can! Remember, I took three cats on a flight overseas BY MYSELF! Nobody to even drop my off at the airport but an UberXL driver! =^-^=

Sometime over the summer, I saw a video on Facebook about a little town in Oregon where it’s Halloween all year long. Halloween? OMG YES, I LOVE HALLOWEEN! You’re not the only one dressing up for once, so it really doesn’t feel awkward to let your geek shine! Especially now that “sexy” halloween costumes aren’t the only “cool” option. I mean, as if nerdy costumes were ever less than cool, but I digress. History has been hard to us nerds. Anyways! So, I saw a video for this Halloweentown that made it look really, really cool, and I thought, hey, I have to go!  Guess what? I did! ???? Here is my report.  First off, did you know that this isn’t a Halloween thing, as much as it is a movie set thing?? I had never even heard of the Halloweentown movie until a week before I went, much less that there was an entire series of movies that I guess kids my age grew up with! I was more of an It’s the Great Pumpkin, Charlie Brown and The Worst Witch kid. Side note: holy cow, why is that movie so expensive now?! Maybe because it’s awesome, but still… So, in order to get myself into the mood, I watched Halloweentown the night before. It was cute, but it’ll still never mean to me what it means to people that grew up watching it. Here’s me and Joanne (my traveling companion — she and my cousin used to be an item, but she’s too cool for him now) at the “famous” gates! We let our Ravenclaw banner fly high all weekend! So, we drove from western Washington for about two hours to get to St. Helens, where all of the festivities take place. From the video, which I had bookmarked and is no longer available(!), it looked like this place would be huge and chock-full of Halloween everywhere we looked. Yay! There were events listed including coin hunts and rides in hearses, and because we went on a weekend in October, some of the movie cast would even be there taking photos (for a price)! It sounded really neat, and we planned to stay the night in the closest drivable town, which was 40 minutes away. There were only a few hotels in town and they were all booked up, boo. So, here’s where I want to mention something… St. Helens is a small town on the bank of the Columbia River. Right across from St. Helens, on the opposite bank of the river, is a town called Kalama. You can stand on the riverbank in St. Helens and look at Kalama on the other side. But there is no bridge. Nada. Nothing! So if you want to drive to that town that you can see happening over yonder, you have to either drive all the way up to Longview,  or all the way down to Portland, and then back. So it’s an hour’s DRIVE to cross the river, and you have to go through other cities to do it. WTF. I don’t understand this at all. Who planned these cities?!?! I just had to say something because it still boggles my mind! Alright, whew! Let’s look at some cute photos to feel better. ???? There was a band performing in Town Square, the center of all activity Halloweentown. Here’s the taxi from the movie. And this big steel pumpkin. It didn’t get crowded until night, but it was still hard to get a shot without people all over the place. I didn’t feel like waiting around, so this was the best that I could do. There was one huge parking lot, and this guy was there to welcome us in… Looks like he’d been waiting for quite a while! City Hall was at the front of the Town Square, and in the movie. This woman is apparently the ideal resident. Someone had a drone, and I thought it made for a cool shot. Looking at Mt. Hood in the distance! I’d love to go hiking there in the spring! Well… to be honest, there wasnt’ actually much to do. There were a few food trucks next to town hall selling noms and running charity drives, a haunted house around the corner, a street full of consignment/used goods shops, and a hair salon selling t-shirts and mugs of the event. During the day, there was also a shuttle to take you uptown where you could do a scavenger hunt and win a commemorative coin. It took Joanne and I over an hour to figure out where the shuttle came, even though you could walk the entire downtown area in 5 minutes, because it wasnt’ on any map and none of the shopkeepers or staff that we asked knew where it came to pick up people! Organization points: 0 We did find it, though, around the corner from all of the fuss, and boarded to do the scavenger hunt. I wasn’t really expecting anything, and it basically was a piece of paper asking us to go into 10 of 15 or so listed shops on the street and find a plaque with numbers on it. If we collected ten numbers and then took them to a certain gas station on the way out of town, we’d receive our coin. Alright, well it wasn’t super imaginative, but I get what they were going for. We did get to see some cute local shops (and I saw my second pot store in a town that takes 1-2 minutes to drive through… I’m not sure I could ever live in Oregon, as I despise any kind of smoking). I also found, of all things, local vegan caramel, so I bought it fully aware that I would try not to eat the entire bag, but would probably fail (I finished them all before I went to bed). It was delicious, though! Soft and chewy and so, so buttery….. yum! Well, after the scavenger hunt, we decided to get the car and drive around a little bit because we had run out of things to do and, guess what? According to a map that we picked up in town, apparently the Twilight series was also filmed there, and all of the locations were mapped! Forget Halloweentown (sorry!), I am a sucker for Edward and Bella’s tale of fated love. I’ve visited Forks and La Push, the real towns that the books are set in, but never the actual movie filming locations. This sort of made my weekend! There were also some old cemetaries marked on the map as places to visit. Both of those things will be in my next posts! After having a bit of an adventure, we returned to the town square to check out the nightly festivities. I think, honestly, that just coming at night to St. Helens would have been enough, because when we returned to Town Square it was starting to get packed. Apparently, at night is when the real town comes alive! Although there still wasn’t a lot to do, the atmosphere was really eerie and the throngs were thick enough that we had trouble getting through. There was a pumpkin-lighting ceremony at 7:30, but it started really late, so we abandoned it to go to the adults-only haunted house. I’m on a perpetual quest to find a haunted house that is actually scary, and this one turns adults-only after 7pm, so I was hoping for something great! Here’s the coin that we got for our scavenger hunt. It was plastic, not metal as I’d been hoping for, but it had been a nice afternoon looking in shops that we otherwise would have probably passed by. Jack was hanging out. You can see how thick the crowd was after dark! These girls had on mermaid-sparkle witch hats. I approve! I wonder whether they attended Ilvermorny. I had to have one of these necklaces. Can’t wait to rock them on halloween! I wore it into the haunted house, which was… well, it was very well done. It was probably the best put-together haunted house that I’ve ever visited in America, but I wasn’t scared at all. So, in terms of usual haunted houses, it gets an A+ rating! But on the honestly-scared-o-meter, it doesn’t register at all. This is probably what most people want, so give it a go when you visit, though! I just have really, really high expectations! Oh, and we did get a photo with Marnie’s actress. She was a real sweetie! Sure, I had just watched Halloweentown for the first time the night before, but why not! So that’s our little visit to Halloweentown! Final Verdict: If you’re nearby and a fan of Halloween, it’s definitely worth a stop! It’s only a half-hour’s drive from Portland, so it’s easy to take a little nip up and check out the festivities! It’s definitely kid-appropriate, and probably actually the most fun for the little ones. If you’re a fan of the movies, this place should definitely be on your bucketlist! Don’t plan for a whole day, though. It’s mostly a nighttime thing. See you tomorrow to share my photos from Bella’s!

I’ve been to Forks and La Push, where the Twilight book series takes place, but I’ve never been to the actual filming locations from the movies! That’s because while the director wanted to film in Forks, when he came to scout the town he realized there was just not enough infrastructure to support an entire film crew– there were literally not enough places to house and feed all of the people who would be working on the movie, and there was no other large town within driving distance! (Yeah, Forks is really far out there) Enter Halloweento— I mean, St. Helens, Oregon! St. Helens stands in for most of Forks in the movies, and a few places in nearby Portland, Oregon make up most of the rest. I ended up nearby by complete accident, as it was only when I picked up a brochure at Halloweentown that I learned that Bella’s house was just on the other side of town! LUCKY!!!  So, we took a short break to drive over to the locations that were still standing, and made a special detour to Portland because how could we leave the Cullen house behind?! I WANTED TO GO INSIDE SO BADLY! It is a real house with real people that live there, and although they encouraged taking photos from outside (according both to a brochure from City Hall and a sign in front of the house), the inside was off-limits. Honestly, it’s not Bella that I particularly love. I didn’t care for her portrayal by Kristen Stewart (sorry!), or her melancholy, passive attitude in the book. Actually, I didn’t care for Edward, either. It was the idea of a love so strong that forces of  nature were pulling you together. It’s the idea of fitting together so perfectly that you can’t do anything without the other that I am a complete sucker for! I said it on my old Livejournal years ago, but Twilight is just a big Mary Sue anyway, so I like to imagine myself as Bella, with a gorgeous (female) Edward out there waiting for me. ???? Like I said, it’s the love, not the characters themselves. I’ll fight you on this (just kidding). ???? Here is where Edward rescued Bella from some catcallers, complete with the mural that the movie crew painted (!) on the building. And the theater that they drove past, that you can’t really see well in the movie but hey, it was on the map!! This is Jilly’s, which supplied all of the dresses in the shop when Bella went to pick out something with her friends for prom. Oddly enough, they had this sign outside but no actual merchandise inside. Go figure. ???? This place, which is a private house now, was the bookstore where Bella went to find out more information about the Quileute myths. And then, though we only had a little bit of time, we drove over to Portland and checked out Edward’s house. I have to say…. THIS HOUSE WAS GORGEOUS. Whew! I would LOVE to live there. LOVE LOVE LOVE! I would also have loved a tour, but it is a private residence, and therefore we kept our distance. Mmm, but it sure is gorgeous! Twilight brings back a lot of memories for me, and it’s special because I grew up (mostly) in Washington. It’s also not the only book series to claim that there are werewolves living amongst the local residents. The town that I spent most of my childhood in also has a series revolving around it! I’m planning to take a trip over there to see my old friends and photograph all of the wolfy places of interest, so I’ll post about it then! Love ya, and see ya tomorrow!

Как сообщают источники, компания Apple ведет переговоры со своим партнером GIS о том, чтобы обновить дисплеи в следующих поколениях iPhone. В частности, речь идет об установке в экраны смартфонов ульт...

Platform: Javascript/HTML5 — Bearing the fruit of thoughtful craftsmanship, Rudowski Brothers gifts us with The Trader of Stories - Chapter 2. After spending nearly a Blossoming in the human city of Bark, Little Willow's life seems fairly ordered. She works as a waitress... Tagged as: adventure, bigoldtreethatdreams, browser, free, game, html5, linux, mac, mobile, mrudowski, narrative, pointandclick, traderofstories

Apple has launched a new web page that brings together links and information about its online services for customers shopping from home during the global health crisis.


Titled "Everything you love about our stores is online," the new catch-all page links from the Apple.com home page and includes details about no-contact delivery options, Apple Specialist help, financing and credit options, Apple Trade In, Apple Card, order status checking, service and support.

The page also links out to "Today at Apple - At home," a series of fun how-to videos to help users get creative during the ongoing stay-at-home measures, and there's a series of category links for customers to explore products on Apple's online store.

Apple has been gradually re-opening its retail stores in countries where lockdowns have eased, although some are operating on limited hours.

Apple CEO Tim Cook last week said that Apple was going to reopen stores in Austria and Australia this week, and Apple's sole Apple Store in Vienna will be reopening on Tuesday, May 5.

We're still waiting to hear exactly when stores in North America will reopen, but Cook also said that Apple is planning to reopen a few stores in the U.S. starting in May. Store openings will be staggered, with Apple evaluating data that includes local guidelines and recommendations before reopening.
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Apple today announced that it will begin reopening its retail stores in Germany on May 11, nearly two months after they were closed due to the global health crisis.


In a statement shared with German website Macerkopf, Apple said the stores will initially be focusing on Genius Bar service and support. Enhanced health and safety measures will be implemented, such as body temperature checks prior to entry, limits on how many customers can be in the store at once, social distancing, and reduced hours of operation.

Apple operates 15 retail stores in Germany and will be posting specific hours of operation for each location on its website.

Apple closed all of its retail stores outside of the Greater China region in mid-March. The company has since started to reopen some locations, including in South Korea, Austria, and Australia. All locations in the United States remain closed.

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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.

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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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Apple's plan to release an updated version of AirPods later this year has been delayed due to the global health crisis, according to the Nikkei Asian Review.


This lines up with a recent report from analyst Ming-Chi Kuo, who said that mass production of third-generation AirPods will begin in the first half of 2021, followed by mass production of second-generation AirPods Pro between the fourth quarter of 2021 and the first quarter of 2022. Kuo also expects Apple's rumored high-end over-ear headphones to enter mass production at some point in mid-2020.

Kuo did acknowledge rumors of new AirPods coming in the second half of 2020, but he said they are "more likely to be the new Beats model." Last month, leaker Jon Prosser claimed that Apple was planning to release so-called "AirPods X" around September or October with a BeatsX-like design for sports and running.

Apple's second-generation AirPods launched in March 2019, while the AirPods Pro were released at the end of October.

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Apple in mid-April reopened Apple Garosugil, its lone store in South Korea, located in the Seoul's Gangnam District.


Apple's South Korea reopening has served as a test ground for further store reopenings, and Apple created an instructional video on reopening practices that's now being shared with other retail employees around the world as they prepare to reopen stores. We're not able to share the video, but it provides a good overview of the measures Apple is putting in place to safely operate retail locations.

Retail employees are following a strict set of guidelines that very heavily emphasize social distancing of two meters (or six feet in the United States). Apple is taking the following measures:

• Prior to when work starts, all employees undergo a health screening complete with a temperature check, with the results logged in a daily spreadsheet.


• Daily briefings are done in the mornings in the Forum area at Apple Stores, with employees making sure to sit at least two meters apart.


• Prior to being allowed in the store, customers are also given a temperature check.


• All ‌Apple Stores‌ are providing hand sanitizer, which customers are encouraged to use.


• Stores are limiting the number of people inside, forming lines with customers waiting at least two meters apart.


• Products purchased by customers or returned after repair are delivered from the back in a relay system, being handed off from employee to employee to allow each person to stay in a separated zone without back and forth.


• Product specialists and Genius Bar staff are positioning themselves across tables away from customers in order to maintain distance.


• In the forum area, employees sit one cube away from customers they're interacting with.


• Employees are encouraged to communicate with one another through the Talk app to cut down on unnecessary movement within the store.


• Half of the workstations in the back are empty, with employees working at alternating workstations to keep more distance between them.


• Tables have been rearranged to put products on corners to prevent customers from being near one another.


• Products on tables have been reduced.


• Communal tables and couches have been removed from employee break rooms and have been replaced with individual chairs evenly spaced about the room.


• Operating hours are reduced.


• Employees are all wearing face masks.

After opening its South Korea store on April 16, Apple has reopened its sole store in Vienna, Austria, and 21 stores located in Australia. Stores in Germany will begin reopening on May 11, and all of the newly opened locations are following many of the same guidelines listed above to keep both customers and employees safe.

There's no word yet on when Apple retail stores in the United States will start to reopen, but Apple CEO Tim Cook last week said that stores in North America will begin reopening starting in the month of May.

Apple plans to evaluate data and make reopening decisions on a city by city, county by county basis, following local guidelines and recommendations before opening up a store.
This article, "Apple Preparing Retail Employees to Return to Work With Tips From South Korea Reopening" first appeared on MacRumors.com

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Apple will begin reopening its retail stores in the United States next week, reports CNBC, starting with locations in Idaho, South Carolina, Alabama, and Alaska.


Apple plans to limit the number of customers in the store at a time, and temperature checks will be performed at the door. Apple also has a number of other measures in place to keep customers and employees safe, as we outlined this morning.

"We're excited to begin reopening stores in the US next week, starting with some stores in Idaho, South Carolina, Alabama and Alaska. Our team is constantly monitoring local heath data and government guidance, and as soon as we can safely open our stores, we will."

"Our new social distance protocol allows for a limited number of visitors in the store at one time so there may be a delay for walk-in customers. We recommend, where possible, customers buy online for contactless delivery or in-store pick up."

Reopened Apple Stores will operate on reduced hours and will primarily focus on repairs, with Apple encouraging customers to purchase online where possible.

Most stores are not listing hours at this time with the exception of Apple Boise Towne Square, which reopens Monday at 11:00 a.m.

During last week's earnings call, Apple CEO Tim Cook said that Apple planned to start reopening some stores in the United States in May. Store reopenings are done on a city by city, county by county basis, with Apple taking into account local data and guidelines.

Apple has already reopened stores in South Korea, Austria, and Australia, with plans to also reopen stores in Germany next week.
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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.

Subscribe to the MacRumors YouTube channel for more videos.
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!
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On Wednesday, May 1, 2019, Flayrah contributor 2cross2affliction wrote in the article 'Sonic the Hedgehog' ... the movie ... the trailer:

Fun fact: no movie directly adapted from a video game has ever scored as "fresh" on the review aggregate site Rotten Tomatoes. [...] But, a new challenger approaches! [...] The question of whether this movie is going to be any good, perhaps unfairly, has mostly already been answered by the Internet. The answer so far has been no. No. Just no. Okay, maybe Jim Carrey? But otherwise, why? Why the human teeth? Why ten times?

Whoops. Turns out Sonic the Hedgehog somehow, against the odds, is rated Fresh by Rotten Tomatoes, with a score of 64% positive reviews from 175 professional opinions, as of this writing.

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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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Fortnite Battle Royale (or just Fortnite) is a “battle royale” shooter that has been around since 2017, and while its getting a bit long in the tooth, it’s still hanging around and still free to play. Last year, the game finally implemented skill-based matchmaking, which means for casual and new players, it’s never been easier to get into. In many ways, it is comparable to Nintendo properties such as Super Smash Bros. or Mario Kart, taking a more traditionally “hardcore” video game genre and making it more accessible with gimmicky gameplay, goofy items, cartoony visuals and massive amounts of RNG.

Of course, the game isn’t exactly furry in and of itself, but the game makes its money selling cosmetic upgrades to player’s in game characters, and quite a few of them feature either characters in animal costumes, or, more recently, straight up anthropomorphic animals. In the time-honored tradition of clickbait listicals, here is my ranking of those skins.

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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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