I thought long and hard about the blog topic today because really, when you think about the subject of "what would I be doing now, if I could be doing something else" well, that's a complicated question.There's the thing you could have been doing if you had chosen a completely different path a long, long time ago. That's totally different from what I would; (read more)

Source: Suzy - Discipline: Research

I walked past the mini-conference room area that AACR set up in the middle of the exhibit hall and my eyes immediately zeroed in on the name of one of my science idols: Elizabeth Blackburn.  She was going to be speaking about careers to young scientists and allow them to ask her questions. I noted the day and time. It wouldn’t matter to me what she was talking about. I would be there. ; (read more)

Source: Suzy - Discipline: Careers

“The most difficult part was persuading our children that they had the freedom to make anything they wanted,” writes mom Anam Ahmed at Let Grow. (Click here!) …Like most kids, my children live prescheduled lives (at least they did in “the time before”). At school, someone tells them when to play outside and when to […]

I realize that sounds kinda nuts — why are we asking PARENTS to show us their KIDS being independent? Who, after all, is better at making videos? Mom or little Ava (who’s 5)? But legally we can’t ask anyone under 13 to do anything. So go document your children doing something new on their own, […]

This flow chart, created by University of Virginia Psychology Professors Jim Coan and Daniel Willingham, is just plain terrific. “Could a child do this alone?” asks the chart. Then let ’em! “Could a child do this with some instruction?” Then let ’em. Etc. etc. Check it out — print it out! — by clicking here. […]

Elon Musk thinks a universal basic income is inevitable. Musk doesn't see plausible alternatives. I hope not. So here's the optimistic scenario: On the one hand, manual and low skilled work will mostly get automated out of existence. So one could imagine why demand for people at lower skill levels and lower levels of cognitive ability could just evaporate. On the other hand, automation will cut costs and boost the wealth of those still employed. Even if the pay of manual laborers is low the goods a manual laborer will need to survive should become very cheap. So any upper class people who can find a use for them might pay them enough to survive. But I see a stronger...

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Date: April 29, 2020

On the fifth day of the Hebrew month of Iyar, Israeli communities worldwide celebrate their Independence Day, known locally as Yom Ha’atzmaut. Today’s Doodle pays tribute to this annual holiday in recognition of the day in 1948 when the State of Israel declared its independence. 

Depicted in the Doodle artwork, the flag of Israel features two blue stripes running horizontally over the white background with the Star of David at its center. Officially adopted in 1948, the same year as independence, the flag will be waved proudly wherever Israeli’s call home. 

Happy Yom Ha’atzmaut, Israel!​

Location: Israel

Tags: national day, National Holiday, independence, history, Israel

The post The Great Pause: A Second Chance to a Better World appeared first on Ocean Blue Fishing Adventures.

---------------------------------------------------[Sat Nov 26 15:25:44 2016]--
From: (S) ease of well-being  (steph)

Subject: Optimism or denial as mental self-defence

A few things recently have given me cause to consider my response to bad things
happening, and my reactions to other people's responses.  First, there's
Trump's election in the US which is undesirable and directly or indirectly
likely to cause some people harm (although I doubt it'll have any effect on me
personally).  I agree that he's not the best or even a good candidate and I
agree that he has incited prejudiced people to show and act on their
prejudices: people are being hurt.  However, I do not like the stream of
articles saying he's a white supremacist or a Nazi or California should secede
or the Electoral College should choose Clinton, or whatever.  Part of this is
doubtless my contrary streak, but part of it is something different.  I observe
that I am semi-consciously adopting a position that `things will turn out all
right' or `it won't be that bad' because countenancing the opposite is not good
for my mental health.

The other thing is some changes in the wider organisation for which I work;
basically there has been a botched reorganisation which has left most people
unhappy and from what I hear from numerous sources with good reason.  This
doesn't currently affect me much and I don't expect it to because of political
realities.  However, even just having the argument with someone closer to the
failing department (and more likely to feel its direct effects) seems to be
followed by my feeling anxious and depressed.  Again, adopting a constructive
positive attitude (which may appear to others pollyannaish, naive, optimistic,
or just in denial) seems to be a defence I've learned here and I suspect it
helps.  But there's more obviously a risk when I'm more involved than I am in
the US case, namely that my optimism will blind me to dangers that will be to
my detriment.

Does my ornery nature come to the rescue, though?  Perhaps because I'm at heart
a bit of a grumpy sod and only respect authorities when I think they deserve it
my tendency to want to probe and prod and query and dig my heels in may
counteract the defensive optimism.  Or alternatively, I'm optimistic in a
different sense: perhaps I just have confidence that I'll win?

LJDW

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.

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

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

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

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.

BACKGROUND The anti–programmed cell death 1 (anti–PD-1) antibody pembrolizumab is clinically active against non–small cell lung cancer (NSCLC). In addition to T cells, human natural killer (NK) cells, reported to have the potential to prolong the survival of patients with advanced NSCLC, also express PD-1. This study aimed to investigate the safety and efficacy of pembrolizumab plus allogeneic NK cells in patients with previously treated advanced NSCLC.METHODS In total, 109 enrolled patients with a programmed death ligand 1 (PD-L1) tumor proportion score (TPS) of 1% or higher were randomly allocated to group A (n = 55 patients given pembrolizumab plus NK cells) or group B (n = 54 patients given pembrolizumab alone). The patients received i.v. pembrolizumab (10 mg/kg) once every 3 weeks and continued treatment until the occurrence of tumor progression or unacceptable toxicity. The patients in group A continuously received 2 cycles of NK cell therapy as 1 course of treatment.RESULTS In our study, patients in group A had longer survival than did patients in group B (median overall survival [OS]: 15.5 months vs. 13.3 months; median progression-free survival [PFS]: 6.5 months vs. 4.3 months; P < 0.05). In group A patients with a TPS of 50% or higher, the median OS and PFS was significantly longer. Moreover, the patients in group A treated with multiple courses of NK cell infusion had better OS (18.5 months) than did those who received a single course of NK cell infusion (13.5 months).CONCLUSIONS Pembrolizumab plus NK cell therapy yielded improved survival benefits in patients with previously treated PD-L1+ advanced NSCLC.TRIAL REGISTRATION ClinicalTrials.gov NCT02843204.FUNDING This work was supported by grants from the National Natural Science Foundation of China (NSFC) – Guangdong Joint Foundation of China (no. U1601225); the NSFC (no. 81671965); the Guangdong Provincial Key Laboratory Construction Project of China (no. 2017B030314034); and the Key Scientific and Technological Program of Guangzhou City (no. 201607020016).

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.

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.

BACKGROUND Glucose-6-phosphate dehydrogenase (G6PD) deficiency decreases the ability of red blood cells (RBCs) to withstand oxidative stress. Refrigerated storage of RBCs induces oxidative stress. We hypothesized that G6PD-deficient donor RBCs would have inferior storage quality for transfusion as compared with G6PD-normal RBCs.METHODS Male volunteers were screened for G6PD deficiency; 27 control and 10 G6PD-deficient volunteers each donated 1 RBC unit. After 42 days of refrigerated storage, autologous 51-chromium 24-hour posttransfusion RBC recovery (PTR) studies were performed. Metabolomics analyses of these RBC units were also performed.RESULTS The mean 24-hour PTR for G6PD-deficient subjects was 78.5% ± 8.4% (mean ± SD), which was significantly lower than that for G6PD-normal RBCs (85.3% ± 3.2%; P = 0.0009). None of the G6PD-normal volunteers (0/27) and 3 G6PD-deficient volunteers (3/10) had PTR results below 75%, a key FDA acceptability criterion for stored donor RBCs. As expected, fresh G6PD-deficient RBCs demonstrated defects in the oxidative phase of the pentose phosphate pathway. During refrigerated storage, G6PD-deficient RBCs demonstrated increased glycolysis, impaired glutathione homeostasis, and increased purine oxidation, as compared with G6PD-normal RBCs. In addition, there were significant correlations between PTR and specific metabolites in these pathways.CONCLUSION Based on current FDA criteria, RBCs from G6PD-deficient donors would not meet the requirements for storage quality. Metabolomics assessment identified markers of PTR and G6PD deficiency (e.g., pyruvate/lactate ratios), along with potential compensatory pathways that could be leveraged to ameliorate the metabolic needs of G6PD-deficient RBCs.TRIAL REGISTRATION ClinicalTrials.gov NCT04081272.FUNDING The Harold Amos Medical Faculty Development Program, Robert Wood Johnson Foundation grant 71590, the National Blood Foundation, NIH grant UL1 TR000040, the Webb-Waring Early Career Award 2017 by the Boettcher Foundation, and National Heart, Lung, and Blood Institute grants R01HL14644 and R01HL148151.

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

Lipid-rich myelin forms electrically insulating, axon-wrapping multilayers that are essential for neural function, and mature myelin is traditionally considered metabolically inert. Surprisingly, we discovered that mature myelin lipids undergo rapid turnover, and quaking (Qki) is a major regulator of myelin lipid homeostasis. Oligodendrocyte-specific Qki depletion, without affecting oligodendrocyte survival, resulted in rapid demyelination, within 1 week, and gradually neurological deficits in adult mice. Myelin lipids, especially the monounsaturated fatty acids and very-long-chain fatty acids, were dramatically reduced by Qki depletion, whereas the major myelin proteins remained intact, and the demyelinating phenotypes of Qki-depleted mice were alleviated by a high-fat diet. Mechanistically, Qki serves as a coactivator of the PPARβ-RXRα complex, which controls the transcription of lipid-metabolism genes, particularly those involved in fatty acid desaturation and elongation. Treatment of Qki-depleted mice with PPARβ/RXR agonists significantly alleviated neurological disability and extended survival durations. Furthermore, a subset of lesions from patients with primary progressive multiple sclerosis were characterized by preferential reductions in myelin lipid contents, activities of various lipid metabolism pathways, and expression level of QKI-5 in human oligodendrocytes. Together, our results demonstrate that continuous lipid synthesis is indispensable for mature myelin maintenance and highlight an underappreciated role of lipid metabolism in demyelinating diseases.

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

It’s release day for my new MM romance! My last release was Christmas 2018, so I’m very excited to finally have a new book for you. When I was in Australia earlier this year, I got hooked on Bondi Rescue, and this (completely fictional!) romance between a trainee and an older, very closeted lifeguard was born. […]

You can grab four steamy and sweet MM holiday romances in one box set for a major discount! This new collection is only $6.99 or you can borrow it in KU. I’m also very excited that these novellas are available in print for the first time! ???? Buy the ebook box set exclusively at Amazon […]

“Looking for a fun and sweet holiday romance with dual POV, some heat, a humorous caper, and a wonderful HEA ending? Look no further!” ~ Gay Book Reviews Fa-la-la-la-la! My new holiday romance is now available to buy or borrow in KU! You’ve got fake boyfriends, bisexual exploration, found family, a single dad in desperate need […]

My figure skating romance has a new (old) title! Misha and Dev’s story was originally two novellas published through Loose Id called Cold War and Holding the Edge. I later combined them into one volume to give you more bang for your buck. To avoid confusion, I called the book The Winning Edge. However, Cold War is frankly just a much better […]

We're still waiting to hear news about Apple Card's performance relative to the major card issuers, but that hasn't stopped Samsung from announcing plans to launch an "innovative" debit card as part of a new mobile-first money management platform the company has been developing over the last year.


Announced on Thursday in a blog post by Samsung Pay vice-president Sang Ahn, the forthcoming debit card is in partnership with finance company SoFi and will be backed by a cash management account.

"In 2020, Samsung Pay will be expanding our service from being a rewarding way to shop and pay, to also being a rewarding way to manage money," writes Ahn. "Over the past year we have been busy developing a mobile-first money management platform. Our vision is to help consumers better manage their money so that they can achieve their dreams and goals. Now more than ever, mobile financial services and money management tools will play an even bigger role in our daily lives while also opening up new possibilities."

The debit card is scheduled to launch this summer. Other than that, Samsung hasn't offered any details on how it will work, but expect it to integrate with Samsung's existing mobile payment system.

Launched in August 2019, ‌Apple Card‌ is a credit card linked to Apple Pay and built into the Wallet app on iPhone. Apple partnered with Goldman Sachs to launch the card, and in October the investment bank hailed it as "the most successful credit-card launch ever." Nine months later, neither Apple nor Goldman Sachs has offered any concrete details on its performance.

During the global health crisis, Apple has introduced an ‌Apple Card‌ Assistance Program that allows ‌‌Apple Card‌‌ holders to skip their March and April payments without incurring interest charges for that billing cycle. For more details on how the card works, check out our comprehensive Apple Card guide.
This article, "Samsung Announces 'Innovative' Debit Card Launching this Summer" first appeared on MacRumors.com

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Apple today announced that it will begin reopening its retail stores in Germany on May 11, nearly two months after they were closed due to the global health crisis.


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

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

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

This article, "Apple Stores in Germany to Begin Reopening May 11 With Enhanced Health and Safety Measures" 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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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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