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.

Colitis caused by Clostridium difficile infection is a growing cause of human morbidity and mortality, especially after antibiotic use in health care settings. The natural immunity of newborn infants and protective host immune mediators against C. difficile infection are not fully understood, with data suggesting that inflammation can be either protective or pathogenic. Here, we show an essential role for IL-17A produced by γδ T cells in host defense against C. difficile infection. Fecal extracts from children with C. difficile infection showed increased IL-17A and T cell receptor γ chain expression, and IL-17 production by intestinal γδ T cells was efficiently induced after infection in mice. C. difficile–induced tissue inflammation and mortality were markedly increased in mice deficient in IL-17A or γδ T cells. Neonatal mice, with naturally expanded RORγt+ γδ T cells poised for IL-17 production were resistant to C. difficile infection, whereas elimination of γδ T cells or IL-17A each efficiently overturned neonatal resistance against infection. These results reveal an expanded role for IL-17–producing γδ T cells in neonatal host defense against infection and provide a mechanistic explanation for the clinically observed resistance of infants to C. difficile colitis.

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.

The prevalence of nonalcoholic fatty liver disease (NAFLD) is increasing worldwide. Although gene-environment interactions have been implicated in the etiology of several disorders, the impact of paternal and/or maternal metabolic syndrome on the clinical phenotypes of offspring and the underlying genetic and epigenetic contributors of NAFLD have not been fully explored. To this end, we used the liver-specific insulin receptor knockout (LIRKO) mouse, a unique nondietary model manifesting 3 hallmarks that confer high risk for the development of NAFLD: hyperglycemia, insulin resistance, and dyslipidemia. We report that parental metabolic syndrome epigenetically reprograms members of the TGF-β family, including neuronal regeneration–related protein (NREP) and growth differentiation factor 15 (GDF15). NREP and GDF15 modulate the expression of several genes involved in the regulation of hepatic lipid metabolism. In particular, NREP downregulation increases the protein abundance of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) and ATP-citrate lyase (ACLY) in a TGF-β receptor/PI3K/protein kinase B–dependent manner, to regulate hepatic acetyl-CoA and cholesterol synthesis. Reduced hepatic expression of NREP in patients with NAFLD and substantial correlations between low serum NREP levels and the presence of steatosis and nonalcoholic steatohepatitis highlight the clinical translational relevance of our findings in the context of recent preclinical trials implicating ACLY in NAFLD progression.

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.

The mechanisms by which prostate cancer shifts from an indolent castration-sensitive phenotype to lethal castration-resistant prostate cancer (CRPC) are poorly understood. Identification of clinically relevant genetic alterations leading to CRPC may reveal potential vulnerabilities for cancer therapy. Here we find that CUB domain-containing protein 1 (CDCP1), a transmembrane protein that acts as a substrate for SRC family kinases (SFKs), is overexpressed in a subset of CRPC. Notably, CDCP1 cooperates with the loss of the tumor suppressor gene PTEN to promote the emergence of metastatic prostate cancer. Mechanistically, we find that androgens suppress CDCP1 expression and that androgen deprivation in combination with loss of PTEN promotes the upregulation of CDCP1 and the subsequent activation of the SRC/MAPK pathway. Moreover, we demonstrate that anti-CDCP1 immunoliposomes (anti–CDCP1 ILs) loaded with chemotherapy suppress prostate cancer growth when administered in combination with enzalutamide. Thus, our study identifies CDCP1 as a powerful driver of prostate cancer progression and uncovers different potential therapeutic strategies for the treatment of metastatic prostate tumors.

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.

Approximately half of the world’s population is infected with the stomach pathogen Helicobacter pylori. Infection with H. pylori is the main risk factor for distal gastric cancer. Bacterial virulence factors, such as the oncoprotein CagA, augment cancer risk. Yet despite high infection rates, only a fraction of H. pylori–infected individuals develop gastric cancer. This raises the question of defining the specific host and bacterial factors responsible for gastric tumorigenesis. To investigate the tumorigenic determinants, we analyzed gastric tissues from human subjects and animals infected with H. pylori bacteria harboring different CagA status. For laboratory studies, well-defined H. pylori strain B128 and its cancerogenic derivative strain 7.13, as well as various bacterial isogenic mutants were employed. We found that H. pylori compromises key tumor suppressor mechanisms: the host stress and apoptotic responses. Our studies showed that CagA induces phosphorylation of XIAP E3 ubiquitin ligase, which enhances ubiquitination and proteasomal degradation of the host proapoptotic factor Siva1. This process is mediated by the PI3K/Akt pathway. Inhibition of Siva1 by H. pylori increases survival of human cells with damaged DNA. It occurs in a strain-specific manner and is associated with the ability to induce gastric tumor.

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

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

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.

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.

В прошлом месяце, изучая содержание исходного кода бета-версии iOS 13.2, журналисты заметили в нем иконку таинственных беспроводных наушников с резиновыми амбушюрами для шумоизоляции. Новая утечка поз...

Источник из Китая опубликовал фотографию, на которой предположительно запечатлена улучшенная версия AirPods. По сообщению инсайдера, беспроводные наушники получат название AirPods Pro и будут представ...

После череды слухов и утечек компания Apple все же запустила в продажу улучшенную версию своих полностью беспроводных наушников. Новинка получила название AirPods Pro и доступна для предзаказа с офици...

Эксперты из DxOMark протестировали камеры новых смартфонов iPhone 11 Pro и 11 Pro Max, и в результате испытаний новинки от компании Apple оказались недостаточно хороши, чтобы возглавить рейтинг. В общ...

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

iFixit hasn't yet done a full teardown of the new Magic Keyboard designed for the new iPad Pro models, but the repair site today partnered with x-ray company Creative Electron to create Magic Keyboard x-rays that give us a view of just what's inside.


The Magic Keyboard uses scissor switch keys instead of butterfly keys, which have now been effectively eliminated from Apple's product lineup. The scissor switch mechanism is clearly visible in the x-ray view, and iFixit calls it the simplest mechanism in the accessory, but the biggest improvement compared to the Smart Keyboard.

Below the keyboard, there are metal plates that iFixit believes are for reinforcing the keyboard's body against bending, and the trackpad is a new design that's different from MacBook trackpads.

There appear to be multiple buttons under the trackpad to capture presses, while the MacBook Trackpads have no buttons and simulate presses with haptic feedback.


There are at least two spring loaded hinge designs at the folding point, featuring both a small coil and a larger coil, plus there are two cables for connecting the Smart Connector to the keyboard for power and data transfer.

Lots and lots of magnets are visible in the x-ray, with the magnets used to hold the Magic Keyboard on the ‌iPad Pro‌. There's a whole ring of tiny magnets around the camera cutout, which iFixit said was a "lot of little polarized bits" to line up, space out, and configure with the ‌iPad Pro‌ components.

According to iFixit, there's more going on in the Magic Keyboard than there is in many laptops, which could explain its price point. Apple charges $299 for the 11-inch Magic Keyboard and $349 for the 12.9-inch version.

This article, "An X-Ray View of Apple's Magic Keyboard for iPad Pro" first appeared on MacRumors.com

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

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

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

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

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

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

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


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

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

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

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

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

Related Guide: "Flexgate" Display Issues Affecting 2016 MacBook Pro and Later
This article, "Apple Faces Class Action Lawsuit Over 'Flexgate' Issue With MacBook Pro Displays" first appeared on MacRumors.com

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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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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!
This article, "Top Stories: New 13" MacBook Pro, WWDC Starts June 22, AirPods Pro Firmware Update, and More" first appeared on MacRumors.com

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


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

What's the Same

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


• Magic Keyboard with reliable scissor switch design


• Force Touch trackpad


• 2 × Thunderbolt 3 ports


• 3.5mm headphone jack


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


• Touch ID


• T2 security chip


• 720p webcam


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


• Bluetooth 5.0


• Three-microphone array with directional beamforming


• Dolby Atmos surround sound

Advantages of Base 13-Inch MacBook Pro

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


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


• Touch Bar


• Slightly better sounding speakers

Advantages of MacBook Air

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


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


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


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

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

Performance

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

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

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

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


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


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


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


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

Takeaways:

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


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

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

Bottom Line

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

For more intensive tasks, the 13-inch MacBook Pro's faster processors and more advanced thermal design will allow you to push the limits more without the fans running obnoxiously. You'll also get the Touch Bar, a brighter and more vibrant display, and slightly better sounding speakers with high dynamic range.
This article, "Base 13-Inch MacBook Pro vs. MacBook Air" first appeared on MacRumors.com

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

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

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

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

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Video from Thabo Meerkat, transcribed

Hey there, and welcome to the April 2020 edition of Digging Up Positivity from a rapidly changing world. But even in these weird times, there are still a lot of positive things to be found!

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Contributors this month include 2cross2affliction, dronon, earthfurst, GreenReaper, and mwalimu.

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As of today, my current job is now the longest one I’ve ever held.

On the Young Turks, Cenk Uygur quotes passages from Bob Woodward's book, "The Price of Politics", quoting statements made by President Obama proving that he intends to cut entitlements like social security, medicare, and medicaid. Continue reading →

After being elected in 2008 on "hope and change", "change you can believe in", and "change the way Washington works", President Obama now says that he cannot change Washington from the inside? Then why should we re-elect him in 2012? Continue reading →

Barack Obama promised to change the way things work in Washington, and after four years, nothing has changed: Corporate money controls President Obama and Congress. We need real change: vote for Rocky Anderson. Continue reading →

Glenn Greenwald predicts over the next four years that "it's all going to get much worse", with President Obama shifting politically more to the right while the Democratic base continues to support him. Continue reading →

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

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

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 →

Is your standard charge for a speech $300,000?  According to an article appearing on the website of the Las Vegas Review-Journal, and a May 31, 2013 email, Clinton’s standard contract usually includes: Round-trip transportation on a chartered private jet “e.g., a Gulfstream … Continue reading →

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

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 →

On April 30, 2015 Ed Schultz, host of The Ed Show, interviews Senator Bernie Sanders on his announcement that he will run for President of the United States in the Democratic Primary. Continue reading →

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

THE AMERICAN PEOPLE IN THIS PARTICULAR MOMENT IN OUR HISTORY MUST MAKE A VERY FUNDAMENTAL DECISION, AND THAT DECISION IS DO WE CONTINUE THE STATUS QUO WHICH INCLUDES A 40-YEAR DECLINE OF OUR MIDDLE CLASS AND A HUGE AND GROWING GAP BETWEEN THE VERY, VERY RICH AND EVERYONE ELSE, OR DO WE FIGHT FOR A BOLD AND MEANINGFUL ECONOMIC AGENDA THAT CREATES JOBS, RAISES WAGES, PROTECTS OUR ENVIRONMENT AND PROVIDES HEALTH CARE FOR EVERY AMERICAN 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 →

Bernie Sanders does not have to win the Iowa primary; however, if the gets 35%, 40%, or 45% of the vote, that would set him up nicely for the New Hampshire primary, next door to his state of Vermont. 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 →

The Vermont Senator and Presidential candidate talks Hillary Clinton, the 2016 race, and an essay he wrote in the 70's about sex. Continue reading →