Accept your self-improvement!

Nitrozac had to undergo an emergency endodontic procedure, *ouch*, so she is off for a few days to let her recover. We'll be back with a new smile soon, in the meantime, here's one of our fave retros...

Contes de fées aux enfants - Dodo le mouton et le landau mystérieux.

Contes de fées aux enfants - Frédéric la grenouille et Elias l'éléphant.

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A little old lady walks into Bank of America and asks to open a savings account. The new accounts receptionist first thinks this is strange, probably because everyone is leaving them for credit unions now. At any rate, the accounts person asks her how much she wanted to deposit to open the account, and the […]

The post Getting Bank of America By The Balls appeared first on Funny & Jokes.

A wealthy Catholic man travels to the Vatican City to see the Bishop of Rome in person, and hopes to meet this leader of the worldwide Catholic Church. Wearing his finest suit, he prays to God that he might be able to meet the Holy Father. During the morning’s Papal procession, he manages to work […]

The post From Riches to Rags appeared first on Funny & Jokes.

A young couple was on their way to get married when they were involved in a fatal car accident. It was really bad, like something from a Quentin Tarantino movie. At any rate, they soon found themselves standing in front of the pearly gates of heaven staring at St. Peter himself. Upset, but wanting to […]

The post Getting Married in Heaven appeared first on Funny & Jokes.

Date: April 25, 2020

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

Today, we’d like to say: 

To all coronavirus helpers, thank you.
 

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

 

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

Location: Global

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

Date: April 28, 2020

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

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

Our 2017 Doodle game celebrating Cricket!

 

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

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

Location: Global

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The post New Arrivals: Top Fishing Sunglasses You Can Try this 2020 appeared first on Ocean Blue Fishing Adventures.

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

Посол Алексей Ерхов в статье, опубликованной в турецком издании по случаю Дня Победы, призвал тех, кто пытается переписывать историческую правду, извлечь правильные уроки из истории Второй мировой войны. В противном случае, по его мнению, мы можем столкнуться с риском снова пережить эту катастрофу.

Levodopa-induced dyskinesia (LID) poses a significant health care challenge for Parkinson’s disease (PD) patients. Amantadine is currently the only drug proven to alleviate LID. Although its efficacy in treating LID is widely assumed to be mediated by blockade of N-methyl-D-aspartate (NMDA) glutamate receptors, our experiments demonstrate that at therapeutically relevant concentrations, amantadine preferentially blocks inward-rectifying K+ channel type 2 (Kir2) channels in striatal spiny projection neurons (SPNs) — not NMDA receptors. In so doing, amantadine enhances dendritic integration of excitatory synaptic potentials in SPNs and enhances — not antagonizes — the induction of long-term potentiation (LTP) at excitatory, axospinous synapses. Taken together, our studies suggest that the alleviation of LID in PD patients is mediated by diminishing the disparity in the excitability of direct- and indirect-pathway SPNs in the on state, rather than by disrupting LTP induction. This insight points to a pharmacological approach that could be used to effectively ameliorate LID and improve the quality of life for PD patients.

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

Whether mutations in cancer driver genes directly affect cancer immune phenotype and T cell immunity remains a standing question. ARID1A is a core member of the polymorphic BRG/BRM-associated factor chromatin remodeling complex. ARID1A mutations occur in human cancers and drive cancer development. Here, we studied the molecular, cellular, and clinical impact of ARID1A aberrations on cancer immunity. We demonstrated that ARID1A aberrations resulted in limited chromatin accessibility to IFN-responsive genes, impaired IFN gene expression, anemic T cell tumor infiltration, poor tumor immunity, and shortened host survival in many human cancer histologies and in murine cancer models. Impaired IFN signaling was associated with poor immunotherapy response. Mechanistically, ARID1A interacted with EZH2 via its carboxyl terminal and antagonized EZH2-mediated IFN responsiveness. Thus, the interaction between ARID1A and EZH2 defines cancer IFN responsiveness and immune evasion. Our work indicates that cancer epigenetic driver mutations can shape cancer immune phenotype and immunotherapy.

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

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

BACKGROUND Neurofibroma/schwannoma hybrid nerve sheath tumors (N/S HNSTs) are neoplasms associated with larger nerves that occur sporadically and in the context of schwannomatosis or neurofibromatosis type 2 or 1. Clinical management of N/S HNSTs is challenging, especially for large tumors, and established systemic treatments are lacking.METHODS We used next-generation sequencing and array-based DNA methylation profiling to determine the clinically actionable genomic and epigenomic landscapes of N/S HNSTs.RESULTS Whole-exome sequencing within a precision oncology program identified an activating mutation (p.Asp769Tyr) in the catalytic domain of the ERBB2 receptor tyrosine kinase in a patient with schwannomatosis-associated N/S HNST, and targeted treatment with the small-molecule ERBB inhibitor lapatinib led to prolonged clinical benefit and a lasting radiographic and metabolic response. Analysis of a multicenter validation cohort revealed recurrent ERBB2 mutations (p.Leu755Ser, p.Asp769Tyr, p.Val777Leu) in N/S HNSTs occurring in patients who met diagnostic criteria for sporadic schwannomatosis (3 of 7 patients), but not in N/S HNSTs arising in the context of neurofibromatosis (6 patients) or outside a tumor syndrome (1 patient), and showed that ERBB2-mutant N/S HNSTs cluster in a distinct subgroup of peripheral nerve sheath tumors based on genome-wide DNA methylation patterns.CONCLUSION These findings uncover a key biological feature of N/S HNSTs that may have important diagnostic and therapeutic implications.FUNDING This work was supported by grant H021 from DKFZ-HIPO, the University Cancer Center Frankfurt, and the Frankfurt Research Funding Clinician Scientist Program.

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.

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

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

BACKGROUND Preclinical experiments have shown that donor blood cells, modified in vitro by an alkylating agent (modified immune cells [MICs]), induced long-term specific immunosuppression against the allogeneic donor.METHODS In this phase I trial, patients received either 1.5 × 106 MICs per kg BW on day –2 (n = 3, group A), or 1.5 × 108 MICs per kg BW on day –2 (n = 3, group B) or day –7 (n = 4, group C) before living donor kidney transplantation in addition to post-transplantation immunosuppression. The primary outcome measure was the frequency of adverse events (AEs) until day 30 (study phase) with follow-up out to day 360.RESULTS MIC infusions were extremely well tolerated. During the study phase, 10 treated patients experienced a total of 69 AEs that were unlikely to be related or not related to MIC infusion. No donor-specific human leukocyte antigen Abs or rejection episodes were noted, even though the patients received up to 1.3 × 1010 donor mononuclear cells before transplantation. Group C patients with low immunosuppression during follow-up showed no in vitro reactivity against stimulatory donor blood cells on day 360, whereas reactivity against third-party cells was still preserved. Frequencies of CD19+CD24hiCD38hi transitional B lymphocytes (Bregs) increased from a median of 6% before MIC infusion to 20% on day 180, which was 19- and 68-fold higher, respectively, than in 2 independent cohorts of transplanted controls. The majority of Bregs produced the immunosuppressive cytokine IL-10. MIC-treated patients showed the Immune Tolerance Network operational tolerance signature.CONCLUSION MIC administration was safe and could be a future tool for the targeted induction of tolerogenic Bregs.TRIAL REGISTRATION EudraCT number: 2014-002086-30; ClinicalTrials.gov identifier: NCT02560220FUNDING Federal Ministry for Economic Affairs and Technology, Berlin, Germany, and TolerogenixX GmbH, Heidelberg, Germany.

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.

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.

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.

☆ To see all of the parts in this series, click here ☆ Although it seemed as if my little fangirl heart couldn’t have taken any more, the day after the Nagayan Fanclub event, I went to see the Hyoutei myu for the first time. Just in case you’re reading this and going Huh? What’s a Hyoutei myu??, I can summarize by saying that it’s one in a series of musicals based on The Prince of Tennis. Yes, the manga that I ended up working on a few years later. ???? I was such a fangirl! Before I copy/paste my report on that musical, I want to say that the reason that I’m making this public again (they’re long gone now, and a lot of it was written privately) is because I want to show how much of a “silly,” squealing fangirl I was. I went from fan to insider purely because, later on, I took crazy-sounding chances and worked hard. And I sincerely believe that you, whomever you are, can do the same! By the way, all of this is eventually becoming fodder for an online comic that I’ve been formulating for a long time! No release date, though. I’m still working on Denkiki, this blog, my Youtube channel, and a few other things. And trying to put a new life together for myself. ???? In the meantime, let’s get to it! My friends and I ready for our dreams to come true, and our dreams were to see the Prince of Tennis musical! August 11, 2005 Tenimyu ~ Imperial Match Hyoutei!! This is the most detailed report on a musical that I’ve ever written. I’m going to do my best from now on to do the same each time!! (I did, for years) As Seigaku said, ♪♪DO YOUR BEST DO YOUR BEST!! DO YOUR BEST DO YOUR BEST!!♪♪ So far I’ve went to the opening performance of Hyoutei musical last night and to the second performance, which was tonight. ^^ I waited to write my report until seeing it a second time because I took very detailed notes the second time and added things and clarified things that the other people had seen afterwards! We had a tenimyu conference. =D (a tradition afterwards!!) It was a solid conclusion that cast improved a lot between the first and second performances. I can’t wait to see the last Tokyo performance, this Sunday. My bet is that they’re going to be VERY solid before then!! Oh wow. Deliciousness on a stick!! My overall feelings can be summed up in the chant that Hyoutei led, *clap clap* “Katsu no wa – Hyoutei! Makeru no Sei-gaku!!” 勝つのは氷帝！負けるの青学！！ (‘The winner will be Hyoutei! The loser will be Seigaku!’) Well, let’s start at what happened today before the musical!! Being hungry and having little other choice in the area for food, we went to the convenience store down the block from the musical… first off, I stopped and stared at this guy who was about to cross the road– who looked a lot like Ishibashi! But I couldn’t tell for sure because he’s changed his hair recently according to his picture set. He stared back at me, but it might have been because I was a tall red-headed foreigner wearing a Hyoutei jersey and a short black skirt.. ? LOL I don’t know if it was him, but I think that it was! He turned and looked back, and I think that he recognized me? I think.. maybe.. hmm..! He definitely recognized me yesterday, but that story is at the end of this report~ In the convenience store, while we are browsing the food sections, who do I notice has walked up alongside our aisle, but quite a few of the cast members! From what I remember, it was Yuu (Tezuka), Aiba (Fuji), Adachi (Kikumaru), Konishi (Kawamura), and Araki (Inui). Araki was wearing a cute hat so it took a minute to recognize him, and while most of the boys wandered along next to me without trouble in the aisle that I was in, Adachi stayed well away by the magazines. He was wearing a mask– which likely means that he has a cold!! Poor boy!! I only talked to Yuu– because I feel most comfortable talking to Yuu out of that group… ^^;; err, sorta. I (stupidly) shouted too loudly, “Yuu!!” when he came into my aisle, and of course he couldn’t ignore something like that. ^^;;; I feel a little bad, because I think that he gave me one of those, ‘why are you talking to me?’ looks. It’s not normal for a fan to actually talk to an actor here if they see them. I said, “hisashiburi!!’ (“It’s been a while!”) thinking that it’s been a while since I talked to him at all, to which he replied, “kino mita….” (“I saw you yesterday”)… Oh yeah…….. he’d obviously seen me at demachi yesterday (more later), and I felt kind of stupid and like I’d been really fannish, so I smiled and left him to do his things with the other boys. It wasn’t until later that I realized that I should have wished him good luck. Ah well, next time!! Itte yosh~! I probably acted way too familar, since we aren’t friends or anything, but it’s the way that I’ve always been with anyone that I’m fond of, friends or acquaintences. So it naturally carries off to them, without me even thinking of it. ^^; Ah well… in any case, I wish them all good luck for the future and rest of the performances!! On to the myu itself! (again! lol) Tenimyu ~ Imperial Match Hyoutei!! KENN special guest star. For both of these performances and for tomororw’s two shows also, KENN (Yuuta) is the special St. Rudolph guest star!! After that is Shiozawa for the next 3 days and Shinoda for the last day. I have tickets to shows with both of them (Thu and Sat for Shio, Sun of course for Shino), so I’m going to note the differences in separate posts. ^^ I can’t wait to see the differences!! ^____________________________^ This is my favorite~ I think that this is the best of all of the musicals. Hands down. Hyoutei was…. droolworthy. Hyoutei rocked the world, and they didn’t even show up for a little while. I’ll start at the beginning~ Tenimyu tenimyu tenimyu tenimyu tenimyu yaaay! <—— (me) First, as in all of the musicals, the curtain wa down andthere were suddenly the sounds of sneakers hitting the pavement. Cue the excitement level to rise and everyone to quiet down suddenly. The lights went down, and the curtain raised silently. A spotlight appeared off to the side, and onto the stage walks Sengoku (Wada) from the right, who does a short introduction. “Welcome,” etc. From the other side, lit with another spotlight, Yuuta (Kenn) made his entrance. They noticed each other and started to walk towards the center, but Yuuta suddenly stops as his cell phone goes off — with his ringer being Ore wa ore no namae de!! XDXDXD Wada starts to interrupt him, but his own phone goes off — with his ringer being Oretachi Jimi-su from bukimyu!! ROFLOL!! So hilarious!! They both managed to get off the phones shortly and walk over to each other, and began to argue — Sengoku asks Yuuta ‘So, who is the coolest player?’ Kenn begins right in saying that his buchou is the coolest, just look at him! And up above them on the screen appears a rather dorky shot of Akazawa and Kaneda from an earlier musical! Yuuta was embarrassed, saying, ‘ack!! I didn’t mean to put both of them up there!!’ Sengoku corrected him, saying, ‘My team is really cool’ — ‘Hey, who put that there?!’ Up on the screen had appeared a shot from Bukimyu of the Jimis mid-dance! Definitely NOT cool! XDXDXD In the end, they couldn’t decide who was the coolest, because music started up behind them…. Cue them to run off of stage and the second curtain to raise~ Starting with Fuji, all of Seigaku minus Ryoma took their places among the strong opening beats of the new Seigaku fight song, ♪Do Your Best! They did a long typical number for the kind of song- with lots of group singing and solos, the whole team going all out on their dancing just as they’d done for Bukimyu. Then they gathered in the center and Ryoma (Yanagi) was raised above! The crowd went noticeably more silent, this was the first time that Yanagi would be performing Ryoma on his own again!! How recovered WAS he? Yanagi didn’t move too much during this song, but he did do a bit of posing, and tried his very very best at singing. He still can’t sing well, but he’s obviously working on it. Hard. (So basically, he sounded terrible, but much better than he had at graduation myu!) Throughout the musical, Yanagi did very little dancing, and mostly posing. When he walked, he mostly walked without a limp, but there were a few times when it was noticeable, especially in the second performance. He could mostly manage it though, but he could not manage any kind of turns, as he stumbled slightly pretty much every time he tried. ;__;  Ganbarou Yanagi!! He’s improved a LOT!! Though there’s still a long road ahead, I think, he really seems to be trying hard. Everyone talked about it afterward and felt the same, very very respectful of what he must have to face and what he’s going through. What a strong boy~~ After Do Your Best, the lyrics consisting mostly of the team outlining their strengths and how they would try their hardest, Seigaku exited the stage and it all went dark. When the curtain raised again, the ichinen trio were sitting at desks on the left side of the stage, puzzling over the answers to their english test. Horio kept copying Kachiro, who shouted at him for it, and when they noticed us, they started in on another hilarious song, led by Horio, and beginning with english!! Horio belted out, “Hello, good day, how are you?” while Kachiro and Katsuo start chiming in. Kachiro seems to think that Horio is copying too much, so he stands up on the desk for his next refrain, and very very slashily (to me), Horio offers him a hand down. Then…….. they start a tap dance across stage that somehow incorporates the lyrics “A B C D”!! XDXD They have their usual display of awesome and hilarious dancing and suddenly rush off stage in the middle of the test when they realize that they’re about to miss the tennis team’s ranking tournament!! Most of Seigaku’s ranking matches are glossed over quickly, with the actors coming in and out quickly, pretending to hit a few balls or so. They give special attention to Ryoma vs. Oishi, after which Ryoma is congratulated for becoming a regular again. Next is the most important match, however. Inui vs. Momo and Inui vs. Tezuka. They do both matches at once, by having Inui stand on the right in the background, and Momo on the left in the background, with Tezuka in the front center (like a triangle). There is scary data-like music playing in the background (hard to describe.. it sounds like data). Inui is hitting balls and every other time that he hits a ball either Tezuka or Momo hits it. He finishes the Momo match first, and lo and behold ~ he beats Momo, who is no longer a regular because of it. Momo can’t believe it and stalks off stage. Then the Inu-Tez match is stopped, and the stage is resituated for a proper viewing of the rest of the match. The entire team is talking about how scary data tennis is, and I agree after seeing that. Inui is powerful in the musical! On to the real InuTez match. Inui tells Tezuka that he can break him with data tennis, because data doesn’t lie. In fact, after he counters Tezuka’s zero-shiki drop shot with data, he...

Being back in a cold and rainy climate reminds me of Tokyo. No, seriously. Washington has four seasons, just like Tokyo did, and just like Hawaii didn’t. I suppose that’s what has been making me feel really nostalgic these days. I’m in a place with the weather of Japan, but way less awesome. I have seriously owned around seventeen kajillion books about Japan in my lifetime, and I’ve given away, donated, or sold back almost the same amount. Some of them I bought, some of them were given to me, and I even found one or two. But the thing is that I have moved so many times that the only ones I’ve kept are those that I absolutely, positively, do not want to live without. (Well, maybe I could live without them, but then would I really be living?) Anyays! Right now, I only own three books in English about Japan, and these are them, and here is why I really like them:   1. The Otaku Encyclopedia: An Insider’s Guide to the Subculture of Cool Japan Disclaimer: A friend of mine wrote this, but that’s not why I’m recommending it.  Pat has written a bunch of books and papers, and they’re all great, but this is the one that I wish that every single otaku in the world could have. What is it? It’s seriously a dictionary, but not the kind of dictionary that we used when I was a little kid to look up stuff for our school essays. I never had a dictionary like this. You probably know what Hatsune Miku is, but do you know what a Heta-uma is? How about a kuchi-paku? Guess where you can find all of that information that you didn’t know that you needed to have? In this freaking book. I know a fair amount about Otaku culture. I lived and breathed it in Japan for almost a whole decade. But I didn’t know half of the stuff that Patrick wrote about in his book, and that’s why you need it. Plus, it’s got a lot of color, a cute mascot, and some really cool exclusive interviews. You can even learn about Tenimyu!   2. Tokyo on Foot So. I saw this book in the book store in Japan, even though it’s written in English. Maybe that’s because although there is a story in it, it’s mostly drawings and you don’t need to be able to read to get the gist of it. It was written/drawn by an artist that came to stay in Tokyo while his girlfriend was there for an internship. He spent almost every day of his six months there wandering the city with colored pencils and a pad of paper and drawing what he saw. Not only are his drawings aces, I absolutely love his little comments about places and people and things. Right after I bought this book (years ago), I was so enamored that I tried emulating his style with less than stellar results. Me and colored pencils don’t mix, which kind of makes this book even more cool (somehow)! Part of the reason that I really enjoyed this book was because it made me nostalgic for my own first days in Tokyo. I remembered thinking a lot of the same things. I just wish that I’d been good with colored pencils (and had enough confidence to write a book). You can read about my first year here on my blog, though! Honestly, I don’t think that this book is as much a must-have for otaku as the other two, but if art and impressions of Japan is your thing, I think you will love it as much as I do. I seriously only brought two English-language books back with me when I moved out of Japan, and this was one. The other was an ancient copy of The Mysterious Island that my father got when he was a kid and passed on to me.   3. Tokyo Geek’s Guide Aaaaalright. I was really, really skeptical about this one. I’ve seen a hundred other “guides to Tokyo” for otaku, but I didn’t keep any of them. This one, though? I am not only keeping it forever, I am going to give a copy to any of my friends traveling to Japan on their own to go otaku-shopping. Holy cow, I wish this book had existed when I first moved to Japan, because it covers things that it took me years of living there to find on my own! It’s a bona-fide travel guide, minus all of the generic stuff that you can find in a normal travel guide. It doesn’t focus on hotels or nice restaurants. Instead, it lists maid cafes, anime shops, and AWESOME stuff like Swallowtail (don’t know what that is? You need to get this book and find out because it is awesome!). The book is split into districts of Tokyo, and lists otaku-related info about each area along with detailed maps and how to get to all of these places. It’s kind of big and heavy for a travel guide, but it’s seriously the only one that I’m interested in having with me next time that I travel to Tokyo. There are places in it that I haven’t even been to. Oh, and bonus? There is a whole section in the latter part of the book talking about Geeky festivals like Comicket and JUMP Festa. I REALLY, REALLY WISH THAT THIS HAD BEEN AROUND WHEN I MOVED TO JAPAN. It’s 14 years too late for that, but not too late for my next trip, and not too late for yours! It’s also in full color. If you’re reading this, I think that you will probably want this book. GO BUY IT.   This has absolutely NOT been a paid advertisement. I am just a geeky girl honestly recommending things that she likes to you that she thinks you need. :3 See you again soon la la la!

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

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

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.
This article, "Deals: Apple Watch Series 5 Models Discounted by Up to $100 on Amazon" 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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Video from Thabo Meerkat, transcribed

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

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The Ursa Majors are ready for votes and the nominees have been revealed. Voting can be found at their website and is open throughout the month of March. Two categories, however, received no nominees due to being an insufficient number of nominations and will not be put up to vote for a winner. Those two categories being Fursuits and Non-Fiction.

If you enjoy film, fiction, art, or any other of the many items that are up for selection as the best of the best for the year of 2019 be sure to vote this month. If you like non-fiction or fursuits, well, you can always be sure to nominate next year.

The nominees are:

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Rick May, best known to furries and non-furries alike as the voice of Peppy Hare in the English version of the game Star Fox 64 passed away April 13, 2020 due to COVID-19. May was born September 21, 1940 (with the full name of Richard J. May), meaning he would have turned 80 later this year. May had also recently suffered a stroke in February, making him even more vulnerable to the disease caused by the novel coronavirus.

May will forever be known as the man who originally uttered the memetic line "Do a barrel roll! (Z or R twice.)" in Star Fox 64, explaining to players how to perform what is technically an aileron roll in order to deflect enemy attacks. May also played the villain of Star Fox 64, Andross. Outside of furry video games, May is probably best known for voicing the Soldier of Team Fortress 2; furries might also recognize his voice behind the villainous Dr. M from the third Sly Cooper game. In addition to voice work for video games, May has had a long history of working both on and for the stage as both a director and actor, beginning with USO shows while stationed in Japan. His part in a Renton, Washington production of Cotton Patch Gospel featured a combination of his voice and stage work, as he used different voices to portray 21 characters in what was reportedly his favorite stage role.

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A great many people only experience science fiction by what my mother and millions of others referred to as "monster movies". From Frankenstein to Aliens and beyond, the unknown and the unexplored are often our undoing. Bleak Horizons, edited by Tarl Hoch, is a wonderful collection of 15 stories that mix SF and Horror with various levels of anthropomorphic settings and characters. And, full disclosure, one of those stories is mine. Happily, the mix includes more than just blood thirsty monsters and end of the universe scenarios.

Overall my favorite stories in this anthology are Hardwire, Pentangle, and The Ouroboros Plate. My least favorites are 4/13/2060 and Not Like Us. Below is a short review of all the pieces. I think you should snag a copy, if only to read my favorites and have a taste for this genre. However, I also really enjoyed Carmen Miranda's Ghost Is Haunting Space Station 3 so you have every right to question my taste.

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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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