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---------------------------------------------------[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

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.

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

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

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).

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.

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.

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 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).

Prenatal alcohol exposure (PAE) affects at least 10% of newborns globally and leads to the development of fetal alcohol spectrum disorders (FASDs). Despite its high incidence, there is no consensus on the implications of PAE on metabolic disease risk in adults. Here, we describe a cohort of adults with FASDs that had an increased incidence of metabolic abnormalities, including type 2 diabetes, low HDL, high triglycerides, and female-specific overweight and obesity. Using a zebrafish model for PAE, we performed population studies to elucidate the metabolic disease seen in the clinical cohort. Embryonic alcohol exposure (EAE) in male zebrafish increased the propensity for diet-induced obesity and fasting hyperglycemia in adulthood. We identified several consequences of EAE that may contribute to these phenotypes, including a reduction in adult locomotor activity, alterations in visceral adipose tissue and hepatic development, and persistent diet-responsive transcriptional changes. Taken together, our findings define metabolic vulnerabilities due to EAE and provide evidence that behavioral changes and primary organ dysfunction contribute to resultant metabolic abnormalities.

The editors of JCI and JCI Insight are revisiting our editorial processes in light of the strain that the COVID-19 pandemic places on the worldwide scientific community. Here, we discuss adjustments to our decision framework in light of restrictions placed on laboratory working conditions for many of our authors.

Brown and beige adipose tissues contain thermogenic fat cells that can be activated by β3-adrenergic receptor agonists. In rodents, such drugs both diminish obesity and improve glucose homeostasis. In this issue of the JCI, O’Mara et al. and Finlin and Memetimin et al. report that chronic administration of the approved β3 agonist mirabegron to human subjects was without effect on body weight or fat mass, but improved several measures of glucose homeostasis. Though the mechanisms mediating these metabolic effects are uncertain, the data suggest that β3 agonists could have therapeutic utility in disorders of glucose homeostasis.

BACKGROUND The live attenuated BPZE1 vaccine candidate induces protection against B. pertussis and prevents nasal colonization in animal models. Here we report on the responses in humans receiving a single intranasal administration of BPZE1.METHODS We performed multiple assays to dissect the immune responses induced in humans (n = 12) receiving BPZE1, with particular emphasis on the magnitude and characteristics of the antibody responses. Such responses were benchmarked to adolescents (n = 12) receiving the complete vaccination program of the currently used acellular pertussis vaccine (aPV). Using immunoproteomics analysis, potentially novel immunogenic B. pertussis antigens were identified.RESULTS All BPZE1 vaccinees showed robust B. pertussis–specific antibody responses with regard to significant increase in 1 or more of the following parameters: IgG, IgA, and memory B cells to B. pertussis antigens. BPZE1–specific T cells showed a Th1 phenotype, and the IgG exclusively consisted of IgG1 and IgG3. In contrast, all aPV vaccines showed a Th2-biased response. Immunoproteomics profiling revealed that BPZE1 elicited broader and different antibody specificities to B. pertussis antigens as compared with the aPV that primarily induced antibodies to the vaccine antigens. Moreover, BPZE1 was superior at inducing opsonizing antibodies that stimulated ROS production in neutrophils and enhanced bactericidal function, which was in line with the finding that antibodies against adenylate cyclase toxin were only elicited by BPZE1.CONCLUSION The breadth of the antibodies, the Th1-type cellular response, and killing mechanisms elicited by BPZE1 may hold prospects of improving vaccine efficacy and protection against B. pertussis transmission.TRIAL REGISTRATION ClinicalTrials.gov NCT02453048, NCT00870350.FUNDING ILiAD Biotechnologies, Swedish Research Council (Vetenskapsrådet), Swedish Heart-Lung Foundation.

BACKGROUND Beige adipose tissue is associated with improved glucose homeostasis in mice. Adipose tissue contains β3-adrenergic receptors (β3-ARs), and this study was intended to determine whether the treatment of obese, insulin-resistant humans with the β3-AR agonist mirabegron, which stimulates beige adipose formation in subcutaneous white adipose tissue (SC WAT), would induce other beneficial changes in fat and muscle and improve metabolic homeostasis.METHODS Before and after β3-AR agonist treatment, oral glucose tolerance tests and euglycemic clamps were performed, and histochemical analysis and gene expression profiling were performed on fat and muscle biopsies. PET-CT scans quantified brown adipose tissue volume and activity, and we conducted in vitro studies with primary cultures of differentiated human adipocytes and muscle.RESULTS The clinical effects of mirabegron treatment included improved oral glucose tolerance (P < 0.01), reduced hemoglobin A1c levels (P = 0.01), and improved insulin sensitivity (P = 0.03) and β cell function (P = 0.01). In SC WAT, mirabegron treatment stimulated lipolysis, reduced fibrotic gene expression, and increased alternatively activated macrophages. Subjects with the most SC WAT beiging showed the greatest improvement in β cell function. In skeletal muscle, mirabegron reduced triglycerides, increased the expression of PPARγ coactivator 1 α (PGC1A) (P < 0.05), and increased type I fibers (P < 0.01). Conditioned media from adipocytes treated with mirabegron stimulated muscle fiber PGC1A expression in vitro (P < 0.001).CONCLUSION Mirabegron treatment substantially improved multiple measures of glucose homeostasis in obese, insulin-resistant humans. Since β cells and skeletal muscle do not express β3-ARs, these data suggest that the beiging of SC WAT by mirabegron reduces adipose tissue dysfunction, which enhances muscle oxidative capacity and improves β cell function.TRIAL REGISTRATION Clinicaltrials.gov NCT02919176.FUNDING NIH: DK112282, P30GM127211, DK 71349, and Clinical and Translational science Awards (CTSA) grant UL1TR001998.

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

☆ 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...

Источники из Японии поделились сведениями, которыми им удалось заполучить относительно нового поколения iPhone SE. Согласно свежим слухам, смартфон будет называться на iPhone SE, а iPhone 9. Напомним...

Play the daily online jigsaw puzzle.

I’ve got a new re-release! The title and cover for Road to the Sun were a little too dreamy and not really indicative of the actiony-suspensey vibe of the plot. Dar Albert designed an awesome new cover, and the brilliant Annabeth Albert (no relation!) suggested the new title. You can borrow in KU for the next three months […]

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


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

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

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

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

We're still waiting to hear exactly when stores in North America will reopen, but Cook also said that Apple is planning to reopen a few stores in the U.S. starting in May. Store openings will be staggered, with Apple evaluating data that includes local guidelines and recommendations before reopening.
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Amazon is taking up to $100 off the Apple Watch Series 5 this week, with prices starting at $299.99 for the 40mm GPS models. Only the Gold Aluminum Case with Pink Sport Band is available at this price. If you order today, the Apple Watch should arrive sometime next week.

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

The Apple Watch Series 5 was released in September 2019 with a new OLED screen that supports an always-on feature, which represents the biggest change to the Series 5 models. The newest Apple Watch is available in 40mm and 44mm sizes, and it has the overall same design as the Series 4 models.

$100 OFF

Apple Watch S5 (40mm, GPS) for $299.99

If you're shopping for a cellular model, there are also a few solid discounts on Amazon for these devices. You can get the Gold Aluminum Case with Pink Sport Band (40mm) for $399.00, down from $499.00. Likewise, the Silver Aluminum Case with White Sport Band (40mm) is $399.00 right now.

For the 44mm cellular models, a solid deal is the Space Gray Aluminum Case with Black Sport Band at $429.00, down from $529.00. You'll find the same price on the Silver Aluminum Case with White Sport Band and the Gold Aluminum Case with Pink Sport Band.

Across the board, these sales are either new low prices on the Apple Watch Series 5, or they're matching previous low prices seen on these models on Amazon. There are a few other deals going on for different Series 5 models as well, including numerous 44mm cellular devices that are about $50 off Apple's original prices. Be sure to head to Amazon to check out the full sale before these prices expire, or the retailer runs out of stock.

Keep up with all of this week's best discounts on Apple products and related accessories in our dedicated Apple Deals roundup.
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The Label's "The_Otherside" is this week's addition to Apple Arcade on the iPhone, iPad, and Apple TV. The game is described as both a turn-based RPG and a strategy board game:

Otherside is a turn based RPG and strategy board game where you will control four survivors who hope to push back the shadowy threat. Make your way through each level solving puzzles, fighting monsters, and destroying the spirit anchors that threaten our dimension.

Do you have what it takes to restore the town back to normal and save the day?

"The_Otherside" is available on the App Store with an Apple Arcade subscription. The service provides iPhone, iPad, Apple TV, and Mac users with access to over 100 games with no in-app purchases or ads for $4.99 per month.
This article, "Apple Arcade's Latest Game Combines Turn-Based RPG With Strategy Board Game" first appeared on MacRumors.com

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


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

What's the Same

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


• Magic Keyboard with reliable scissor switch design


• Force Touch trackpad


• 2 × Thunderbolt 3 ports


• 3.5mm headphone jack


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


• Touch ID


• T2 security chip


• 720p webcam


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


• Bluetooth 5.0


• Three-microphone array with directional beamforming


• Dolby Atmos surround sound

Advantages of Base 13-Inch MacBook Pro

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


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


• Touch Bar


• Slightly better sounding speakers

Advantages of MacBook Air

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


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


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


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

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

Performance

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

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

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

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


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


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


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


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

Takeaways:

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


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

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

Bottom Line

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

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

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

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

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

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

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As governments restrict gatherings of people, furry conventions are being postponed or canceled. Here's a quick run down of events in April, May, and June and their status as of May 5 17:28 EDT (UTC-4) in response to the COVID-19 pandemic - updates to come.

A new section has been added for past events impacted for historical purposes.

Links go to statements if available, or to their Twitter feed or site. See also: Furry Fandom and the Internet forced back to roots by viral outbreak

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— seeya soon, boring details about today’s comic: made with:

Erowid Exp108047

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

Linda McMahon is running for the US Senate in Connecticut. For twenty (20) years, she ran World Wrestling Entertainment (WWE) with her husband, Vince McMahon. A few years ago, a documentary film examined the WWE's celebration of violence against women. Her campaign doesn't want Connecticut voters to see that film. Watch these excerpts from the film to see why. Continue reading →

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

Thinking of using TurboTax to file your tax returns? Think again. The Minnesota Department of Revenue advises against using Intuit software to file tax returns! It found unacceptable errors in Intuit tax software, including TurboTax, ProSeries, Lacerte, and Intuit online. Continue reading →

Have you ever noticed that the Internal Revenue Service's regulations often are illogical? Does anyone at the IRS think through its regulations? Continue reading →

Are you a taxpreparer who is unsatisfied with the quality of Intuit's ProSeries tax software program? I am not a happy user of ProSeries tax software. Choose your tax software carefully. I will be searching for an alternative tax software vendor for the year 2014. Continue reading →

William Brighenti, who founded the Berlin Property Owners Association, argued that the town can’t afford a new police headquarters, and police should look to clear space in their current building. He thinks one way to accomplish this is to get rid of tactical gear. Continue reading →

A year ago this month the U.S. Department of Justice announced that the banking giant JPMorgan Chase would avoid criminal charges by agreeing to pay $13 billion to settle claims that it had routinely overstated the quality of mortgages it … Continue reading →

Accountants CPA Hartford Connecticut LLC:  This transcript may contain errors. The Willis Report:  And tonight’s stunning accusation against Intuit, the maker of Turbotax, the popular tax preparation software.  Two whistleblowers claim that Intuit knew that criminals used its tax software … Continue reading →

"I think I'm the only candidate who's prepared to take on the billionaire class," Sanders, I-Vt., told ABC's George Stephanopoulos on "This Week." "We need a political revolution in this country involving millions of people who are prepared to stand up and say, enough is enough, and I want to help lead that effort." Continue reading →

The response of Senator Richard Blumenthal to my letter in opposition to the Trans-Pacific Partnership (TPP). Ask yourselves how American labor can compete against Vietnamese workers earning on average $0.56 per hour. Continue reading →

The Senate considered H.R. 1314, the legislative vehicle for trade promotion authority reauthorization.?It would give the president broad fast-track authority when negotiating trade agreements and require Congress to consider treaties without an amendment process. Senator Bernie Sanders speaks out against this bill before the Senate on May 12, 2015. Continue reading →

CNN Brianna Keilar interviews Senator Bernie Sanders on State of the Union May 17 2015. Senator Bernie Sanders says the American people want and deserve a serious debate on the serious issues facing our country today instead of merely the same old, endless 30 second, ad hominem, attack ads. Continue reading →

The Vermont senator and presidential candidate talks to Chris Hayes about his differences with Hillary Clinton and the prospects for his presidential candidacy. Continue reading →

Senator Bernie Sanders does not think that Hillary Clinton can stand up and fight for the middle class. Continue reading →