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

“When I was 17, I was in a serious accident and had to be home for months. Looking out at our boring backyard, I daydreamed a plan for my life. It became a blueprint.” So writes Holly Korbey in a lovely piece at Let Grow. There are different kinds of daydreaming, of course, and some don’t […]

Already we've hit the $1000 genome and faster and cheaper DNA sequencing is on the way. DNA sequencing is going through a speed-up and cost-cutting rate that is similar to that which computer processors have been going through for decades. While the doubling rate of computer power has slowed quite a bit the rate of decrease in DNA sequencing costs has kept up the pace and, in fact, the rate of decline in DNA sequencing costs suddenly accelerated at the end of 2007 has been going down pretty sharply ever since. The cost decline seemed to halt during 2014 only to plunge in 2015. So why should you care? Really cheap massive amounts of DNA sequencing of cancerous cells will...

Survives another day!

The bartender says “You can’t have that thing in here! Get out!” The guy says “It’s okay, this Alligator is highly trained. Just give me a few seconds and I’ll show you.” The bartender, intrigued, gives him the go-ahead. The man gingerly lifts the alligator up onto a table. By this point, everybody in the […]

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

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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 […]

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Date: May 4, 2020

Happy US Teacher Appreciation Week!

Today (and everyday!), we honor teachers across the nation, who continue to work tirelessly to shape our future generations, even in the midst of the unprecedented COVID-19 pandemic.

Today’s Doodle was created by Doodler Kevin Laughlin who collaborated with the 54 2020 State Teachers of the Year during their visit to Google this past February. 

Below, Kevin shares more on his experience working with the teachers on today’s Doodle!

I know from firsthand experience how much of a positive impact a teacher can have on a young person's life. I can't express how happy I am to have had the opportunity to be a part of the Teacher Appreciation project this year.

When I met these teachers on campus in February, I was so inspired by their love of teaching and dedication to their students, which I felt each minute I spent with them. As they presented their own Doodle designs, they shared anecdotes about their classrooms, advocated for their students, and spoke passionately about educational equity. 

I am glad to see their work represented in the final Doodle on Google’s homepage today celebrating these often unsung heroes. To every teacher, thank you times infinity! 

Learn more about the many ways Google is celebrating and supporting teachers, in classrooms or at home.

See some of the teacher concepts that inspired today’s Doodle below:

...and all of the concepts from our 54 2020 State Teachers of the Year:

Photos from the Doodle brainstorming session at the 2020 National Teacher of the Year Program

Location: U.S. Virgin Islands, United States

Tags: teachers’ day, National Holiday, education, teaching

Date: May 8, 2020

Location: South Korea

Tags: Parents' Day, carnations, flowers, stop-motion, Animation

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Hair cells, the mechanosensory receptors of the inner ear, are responsible for hearing and balance. Hair cell death and consequent hearing loss are common results of treatment with ototoxic drugs, including the widely used aminoglycoside antibiotics. Induction of heat shock proteins (HSPs) confers protection against aminoglycoside-induced hair cell death via paracrine signaling that requires extracellular heat shock 70-kDa protein (HSP70). We investigated the mechanisms underlying this non–cell-autonomous protective signaling in the inner ear. In response to heat stress, inner ear tissue releases exosomes that carry HSP70 in addition to canonical exosome markers and other proteins. Isolated exosomes from heat-shocked utricles were sufficient to improve survival of hair cells exposed to the aminoglycoside antibiotic neomycin, whereas inhibition or depletion of exosomes from the extracellular environment abolished the protective effect of heat shock. Hair cell–specific expression of the known HSP70 receptor TLR4 was required for the protective effect of exosomes, and exosomal HSP70 interacted with TLR4 on hair cells. Our results indicate that exosomes are a previously undescribed mechanism of intercellular communication in the inner ear that can mediate nonautonomous hair cell survival. Exosomes may hold potential as nanocarriers for delivery of therapeutics against hearing loss.

Although CEACAM1 (CC1) glycoprotein resides at the interface of immune liver injury and metabolic homeostasis, its role in orthotopic liver transplantation (OLT) remains elusive. We aimed to determine whether/how CEACAM1 signaling may affect hepatic ischemia-reperfusion injury (IRI) and OLT outcomes. In the mouse, donor liver CC1 null mutation augmented IRI-OLT (CC1-KO→WT) by enhancing ROS expression and HMGB1 translocation during cold storage, data supported by in vitro studies where hepatic flush from CC1-deficient livers enhanced macrophage activation in bone marrow–derived macrophage cultures. Although hepatic CC1 deficiency augmented cold stress–triggered ASK1/p-p38 upregulation, adjunctive ASK1 inhibition alleviated IRI and improved OLT survival by suppressing p-p38 upregulation, ROS induction, and HMGB1 translocation (CC1-KO→WT), whereas ASK1 silencing (siRNA) promoted cytoprotection in cold-stressed and damage-prone CC1-deficient hepatocyte cultures. Consistent with mouse data, CEACAM1 expression in 60 human donor liver biopsies correlated negatively with activation of the ASK1/p-p38 axis, whereas low CC1 levels associated with increased ROS and HMGB1 translocation, enhanced innate and adaptive immune responses, and inferior early OLT function. Notably, reduced donor liver CEACAM1 expression was identified as one of the independent predictors for early allograft dysfunction (EAD) in human OLT patients. Thus, as a checkpoint regulator of IR stress and sterile inflammation, CEACAM1 may be considered as a denominator of donor hepatic tissue quality, and a target for therapeutic modulation in OLT recipients.

Organ shortage continues to limit the lives of patients who require liver transplantation. While extending criteria for liver organs provides a needed resource, tissue damage from prolonged ischemic injury can result in early allograft dysfunction and consequent rejection. In this issue of the JCI, Nakamura et al. used a mouse transplantation model with prolonged ex vivo cold storage to explore liver graft protection. The authors found that liver grafts with absent carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) exhibited increased ischemia-reperfusion injury inflammation and decreased function in wild-type recipients. The authors went on to correlate CEACAM1 levels with postreperfusion damage in human liver transplant recipients. Notably, this study identified a potential biomarker for liver transplant donor graft quality.

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.

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.

BACKGROUND Since December 2019, an outbreak of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) emerged in Wuhan, and is now becoming a global threat. We aimed to delineate and compare the immunological features of severe and moderate COVID-19.METHODS In this retrospective study, the clinical and immunological characteristics of 21 patients (17 male and 4 female) with COVID-19 were analyzed. These patients were classified as severe (11 cases) and moderate (10 cases) according to the guidelines released by the National Health Commission of China.RESULTS The median age of severe and moderate cases was 61.0 and 52.0 years, respectively. Common clinical manifestations included fever, cough, and fatigue. Compared with moderate cases, severe cases more frequently had dyspnea, lymphopenia, and hypoalbuminemia, with higher levels of alanine aminotransferase, lactate dehydrogenase, C-reactive protein, ferritin, and D-dimer as well as markedly higher levels of IL-2R, IL-6, IL-10, and TNF-α. Absolute numbers of T lymphocytes, CD4+ T cells, and CD8+ T cells decreased in nearly all the patients, and were markedly lower in severe cases (294.0, 177.5, and 89.0 × 106/L, respectively) than moderate cases (640.5, 381.5, and 254.0 × 106/L, respectively). The expression of IFN-γ by CD4+ T cells tended to be lower in severe cases (14.1%) than in moderate cases (22.8%).CONCLUSION The SARS-CoV-2 infection may affect primarily T lymphocytes, particularly CD4+ and CD8+ T cells, resulting in a decrease in numbers as well as IFN-γ production by CD4+ T cells. These potential immunological markers may be of importance because of their correlation with disease severity in COVID-19.TRIAL REGISTRATION This is a retrospective observational study without a trial registration number.FUNDING This work is funded by grants from Tongji Hospital for the Pilot Scheme Project, and partly supported by the Chinese National Thirteenth Five Years Project in Science and Technology for Infectious Disease (2017ZX10202201).

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.

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

The physical integrity of endothelial cells (ECs) lining the blood vessels regulates the inflammatory response. Both innate immunity and inflammatory disorders hinge on the EC-neutrophil interaction. Neutrophil binding, rolling, and migrating along and between ECs is associated with vascular permeability. In this issue of the JCI, Owen-Woods et al. tracked neutrophils in vivo in venules of mouse striated muscle and revealed how endothelial permeability can affect neutrophil trafficking. Strikingly, many neutrophils that migrated between EC junctions were able to rejoin the blood circulation. Further, the chemokine and neutrophil chemoattractant, CXCL1, drove this reverse transendothelial migration (rTEM). This paradigm-shifting study provides a mechanism for distal organ damage as well as an explanation for sepsis-associated acute respiratory distress syndrome.

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

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

Increased microvascular permeability to plasma proteins and neutrophil emigration are hallmarks of innate immunity and key features of numerous inflammatory disorders. Although neutrophils can promote microvascular leakage, the impact of vascular permeability on neutrophil trafficking is unknown. Here, through the application of confocal intravital microscopy, we report that vascular permeability–enhancing stimuli caused a significant frequency of neutrophil reverse transendothelial cell migration (rTEM). Furthermore, mice with a selective defect in microvascular permeability enhancement (VEC-Y685F-ki) showed reduced incidence of neutrophil rTEM. Mechanistically, elevated vascular leakage promoted movement of interstitial chemokines into the bloodstream, a response that supported abluminal-to-luminal neutrophil TEM. Through development of an in vivo cell labeling method we provide direct evidence for the systemic dissemination of rTEM neutrophils, and showed them to exhibit an activated phenotype and be capable of trafficking to the lungs where their presence was aligned with regions of vascular injury. Collectively, we demonstrate that increased microvascular leakage reverses the localization of directional cues across venular walls, thus causing neutrophils engaged in diapedesis to reenter the systemic circulation. This cascade of events offers a mechanism to explain how local tissue inflammation and vascular permeability can induce downstream pathological effects in remote organs, most notably in the lungs.

It’s no secret that I love Japan. I mean, I really, really love Japan. I felt more at home in Tokyo than I ever have anywhere else, and I think about going back all. the. time. I’m even thinking about it right now. You’re probably reading this right now because, at the very least, some tiny part of you is curious about whether you should do it. It might be the tiiiiiiiniest little part, but I’m sure it’s there. Maybe you don’t want to admit it because it seems pretty impossible, and yeah, I will admit that if you have a job that you don’t want to leave, strong family ties, kids, pets, or no money (among other things), it must seem like a distant what-if that will never happen. Here’s the thing. If you’re really, honestly interested, then make it happen. Because guess what? You freaking can make it happen, and don’t let anybody tell you no. If you’re coming up with a “But…” right now, I’ll stop you right there! “But I have kids/pets…” Figure out how to take them with you, because you can! “But I don’t want to leave my job…” Take a sabbatical for a year, look into transfers to a branch abroad, look for a better job in the same field in Japan, or look into whether this job is really worth giving up on this dream (maybe it isn’t). “But I can’t speak the language…” So? I moved to Japan and didn’t speak a word. Some people learn before they go, some people learn while they’re there (me), and some people never learn (I don’t recommend this). I could go on forever, but the whole world is at your fingers if you really want it! I seriously believe that. It’s not always easy, but if you want something badly enough, don’t you owe it to yourself to at least try? Anyways, let me give you the top reasons why I think that you should give living in Japan a try! 1. Living in a different culture opens your eyes. This especially is true if you immerse yourself in as much of the culture as you can. Make Japanese friends, learn about what people do on a daily basis and what they believe in. Try doing things in ways that are new to you. Try new foods! Mochi is the schiz, by the way! Once you’ve experienced doing new things, it will change how you do things even if you return back home. I will always have a no-shoes policy in my house (it’s so much cleaner!), I absolutely CRAVE a train system (if only!), and I have a newfound respect for walking and cycling. I never did this when I was little, but now, if I can, I walk! 2. You’ll have a fresh start. In your new home in Japan, you won’t have any of the drama that surrounded you in your old one. Thanks to the internet, we can still keep in touch with friends and family, but being a few thousand miles away from them will keep a lot of the drama to a minimum. Take a chance to stretch your wings and see what kind of person you are when you have the freedom to be you without their judgement. Trust me, it takes a weight off being in a new place where nobody knows who you used to be (or who they thought you used to be). Oh, and you know what? I bet that you will love yourself more than you ever did before. 3. Japan is a magical place! Seriously. Cherry blossoms, gorgeous temples and “castles” (I wouldn’t call them castles, but they’re called that nonetheless, and they’re really cool anyway), a rich history filled with Samurai and ninjas (who doesn’t love ninjas?), seasonal treats, and an entire culture that grew up reading manga. How does this not sound like an amazing place to live?!  And no offense to any other country, but Japanese trains come quickly, go almost everywhere, are extremely punctual, and pretty clean, which makes them (Tokyo especially) easily #1 in the world in public transportation. Now that sounds magical to me. 4. Universal Health Care. If you’re American like me, this will make a HUGE difference in your life. Trust me. If you come from pretty much any other 1st world nation, it probably won’t matter as much, though. But at least it’s good! 5. Japan is safer than where you came from. There’s no gun violence. There’s very low crime in general. You can walk in the dead of night in the seediest parts of town, as a woman, alone, and still feel perfectly safe from other people. From earthquakes is another matter, but you’ll get used to them really fast, and Japan is built to withstand all but the biggest. 6. Wa. There is a concept called wa in Japanese society, which essentially promotes practicing peace and harmony in your daily life. Wa is obvious in everything from traditional architecture and decor to the way that people act around each other– courteousness, quiet, and respect are what you expect most from your neighbors. You’re never going to wake up to your neighbors blaring music at 3am having a raucous party. Even drunken people wandering the street are more polite than not (although most of them just sort of stumble home or sit down where they are for the night– but remember, Japan is safe so they only thing they have to worry about is getting chilly). We could all use a little bit of harmony in our lives, and that’s something that Japan taught me to value. I’m surprised that yoga isn’t more popular, since they’re pretty in tune with each other. 7. All the new gadgets, and all of the old culture. Sure, Silicon Valley is where a lot of new apps are coming out, but if you want lots of little weird but useful gadgets to make your life easier (or more interesting), take a stroll through Akihabara. Plus, there are tons of cheap versions of what you’re used to, like large-capacity flash drives and SD cards. And I would be remiss in not mentioning the used electronics! Smartphones! Right next to small neighborhood temples, btw. It’s the only place to find Ayanami Rei in a kimono, wandering the street. The best of both worlds! 8. MANGA AND ANIME EVERYWHERE. This should be your main reason. This should be enough of a reason. Not only is it available everywhere, but events abound. If you wanted, you could go to an anime-related event every weekend of the year. Also, let’s not forget that it’s the only place to see all of the anime movies released in the theater, go to the official events (like Jump Festa, Comicket, World Cosplay Summit, and Anime Japan, among others), and see the musicals, seiyuu radio shows, and stage plays. If this isn’t reason enough, you’re probably in the wrong place. 9. It’s cheaper than you think. I lived in Tokyo, and then I moved back to the US, thinking that because I was living in a place often called “The Most Expensive City In The World,” it would be cheaper here. Nope.. Apartment rents, even in small cities, are at least the price that I was paying in Tokyo (~$600/mo). And try finding that in LA. So far I haven’t had any luck, and especially not in the areas that are actually sort-of-kind-of safe. Food is also about on-par with the US, especially domestic food. Considering that it’s an island, it’s actually really, really cheap. Food in Hawaii cost sometimes 3-4 times what I was able to get it for in Japan. Then, when you factor in healthcare, which is pretty cheap (what you pay for the insurance is based on your income, and then it covers 80% of all your bills — this is a simplification, but generally holds true), and transportation costs (you don’t need a car, therefore no gas, no insurance, no car maintenance fees), it’s downright cheap. Even living in Tokyo. 10. You will never run out of things to do. In nearly a decade, I never ran out of cool things to do. Can you say the same about the city that you live in now? Thought so. Ah man, I kinda feel ready to jump back on a plane and move across the ocean… three cats and all! Somebody hold me back… resistance is fading……………….  

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

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!

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