Смартфон появился на сайте Google Play Console, благодаря чему стали известны его некоторые характеристики и дизайн.

OK, let’s pick up our discussion where we left off last week, at feasibility.  You did it. You successfully convinced a room full of vice presidents and directors, or maybe even the CEO that they should take your fabulous product idea to the next level.  You’ve got marketing on board, excited to promote it and now it’s time for the work to begin.You are the lead scientist s; (read more)

Source: Suzy - Discipline: BioTech

At least for some kids, yes, being flung from the stress of a super-structured, super-supervised existence is having a calming, life-expanding effect. I discuss this amazing phenom in this Big Think article, including six short essays by kids themselves, and also in this interview with Bored Panda,  the  pop culture site, where I note that […]

The Miami Beach danger zone for mosquitoes carrying Zika virus is expanding. This isn't just about microcephaly in developing fetuses. Since Zika attacks neural progenitor cells it might cause lasting damage in adults too. A case of acute sensory polyneuropathy in an adult caused symptoms that lasted for months. It is suspected that Zika causes inflammation of sensory nerves and possibly an auto-immune response. So Zika is bad. What should we do about it? Wipe out the mosquitoes that carry it. Totally drive them to extinction. These mosquitoes are invasive in the Western Hemisphere. If a mosquito causes major health problems for the human species we should just wipe it out. Wiping out a mosquito species could be done with...

Check out this qz article: The robot that takes your job should pay taxes, says Bill Gates. About 35-40 years ago secretary was the biggest job in most states. Those days are long past. As you can see by advancing the time bar for the USA states map on that page, by 2000 truck driver was the biggest job. So I have a question for Bill Gates: Do you want to tax word processors too? Also, autonomous vehicle technology will surely wipe out most truck driving jobs in the next 20 years. Do you want to tax autonomous truck technology to slow the rate of that transition? Keep in mind that thousands of lives will be saved each year once...

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

We previously established that global deletion of the enhancer of trithorax and polycomb (ETP) gene, Asxl2, prevents weight gain. Because proinflammatory macrophages recruited to adipose tissue are central to the metabolic complications of obesity, we explored the role of ASXL2 in myeloid lineage cells. Unexpectedly, mice without Asxl2 only in myeloid cells (Asxl2ΔLysM) were completely resistant to diet-induced weight gain and metabolically normal despite increased food intake, comparable activity, and equivalent fecal fat. Asxl2ΔLysM mice resisted HFD-induced adipose tissue macrophage infiltration and inflammatory cytokine gene expression. Energy expenditure and brown adipose tissue metabolism in Asxl2ΔLysM mice were protected from the suppressive effects of HFD, a phenomenon associated with relatively increased catecholamines likely due to their suppressed degradation by macrophages. White adipose tissue of HFD-fed Asxl2ΔLysM mice also exhibited none of the pathological remodeling extant in their control counterparts. Suppression of macrophage Asxl2 expression, via nanoparticle-based siRNA delivery, prevented HFD-induced obesity. Thus, ASXL2 controlled the response of macrophages to dietary factors to regulate metabolic homeostasis, suggesting modulation of the cells’ inflammatory phenotype may impact obesity and its complications.

Hearing loss caused by the death of sensory hair cells of the inner ear is an unfortunate side effect for many patients treated with aminoglycoside antibiotics or platinum-containing chemotherapy agents. In animal models, induction of heat shock confers substantial otoprotection against aminoglycoside- and cisplatin-induced hair cell death. In this issue of the JCI, Breglio et al. demonstrate that inner ear tissue released exosomes carrying heat shock protein 70 (HSP70) in response to heat stress. HSP70 acted by a paracrine mechanism that engaged the Toll-like receptor 4 (TLR4) on hair cells to protect them from death. Exosomes and the HSP70/TLR4 pathway could thus provide treatment targets for the protection of hair cells from chemically induced death or from other insults, such as noise.

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.

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.

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

Facioscapulohumeral muscular dystrophy (FSHD) is caused by loss of repression of the DUX4 gene; however, the DUX4 protein is rare and difficult to detect in human muscle biopsies, and pathological mechanisms are obscure. FSHD is also a chronic disease that progresses slowly over decades. We used the sporadic, low-level, muscle-specific expression of DUX4 enabled by the iDUX4pA-HSA mouse to develop a chronic long-term muscle disease model. After 6 months of extremely low sporadic DUX4 expression, dystrophic muscle presented hallmarks of FSHD histopathology, including muscle degeneration, capillary loss, fibrosis, and atrophy. We investigated the transcriptional profile of whole muscle as well as endothelial cells and fibroadiopogenic progenitors (FAPs). Strikingly, differential gene expression profiles of both whole muscle and, to a lesser extent, FAPs, showed significant overlap with transcriptional profiles of MRI-guided human FSHD muscle biopsies. These results demonstrate a pathophysiological similarity between disease in muscles of iDUX4pA-HSA mice and humans with FSHD, solidifying the value of chronic rare DUX4 expression in mice for modeling pathological mechanisms in FSHD and highlighting the importance FAPs in this disease.

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.

Systemic sclerosis (SSc) is an autoimmune fibrotic disease whose pathogenesis is poorly understood and lacks effective therapies. We undertook quantitative analyses of T cell infiltrates in the skin of 35 untreated patients with early diffuse SSc and here show that CD4+ cytotoxic T cells and CD8+ T cells contribute prominently to these infiltrates. We also observed an accumulation of apoptotic cells in SSc tissues, suggesting that recurring cell death may contribute to tissue damage and remodeling in this fibrotic disease. HLA-DR–expressing endothelial cells were frequent targets of apoptosis in SSc, consistent with the prominent vasculopathy seen in patients with this disease. A circulating effector population of cytotoxic CD4+ T cells, which exhibited signatures of enhanced metabolic activity, was clonally expanded in patients with systemic sclerosis. These data suggest that cytotoxic T cells may induce the apoptotic death of endothelial and other cells in systemic sclerosis. Cell loss driven by immune cells may be followed by overly exuberant tissue repair processes that lead to fibrosis and tissue dysfunction.

Hypoxia-inducible factor (HIF) is strikingly upregulated in many types of cancer, and there is great interest in applying inhibitors of HIF as anticancer therapeutics. The most advanced of these are small molecules that target the HIF-2 isoform through binding the PAS-B domain of HIF-2α. These molecules are undergoing clinical trials with promising results in renal and other cancers where HIF-2 is considered to be driving growth. Nevertheless, a central question remains as to whether such inhibitors affect physiological responses to hypoxia at relevant doses. Here, we show that pharmacological HIF-2α inhibition with PT2385, at doses similar to those reported to inhibit tumor growth, rapidly impaired ventilatory responses to hypoxia, abrogating both ventilatory acclimatization and carotid body cell proliferative responses to sustained hypoxia. Mice carrying a HIF-2α PAS-B S305M mutation that disrupts PT2385 binding, but not dimerization with HIF-1β, did not respond to PT2385, indicating that these effects are on-target. Furthermore, the finding of a hypomorphic ventilatory phenotype in untreated HIF-2α S305M mutant mice suggests a function for the HIF-2α PAS-B domain beyond heterodimerization with HIF-1β. Although PT2385 was well tolerated, the findings indicate the need for caution in patients who are dependent on hypoxic ventilatory drive.

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

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

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


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

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

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


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

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

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

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

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Microsoft plans to add trackpad and mouse support to its Word, Excel, and PowerPoint apps for iPad by the fall, according to TechCrunch and The Verge.

iPadOS 13.4 introduced trackpad and mouse support on all iPad models released in the past four to five years. Keyboards with trackpads include Apple's Magic Keyboard and Brydge's Pro+ for the iPad Pro and Logitech's Combo for the 10.2-inch iPad and the 10.5-inch iPad Air.

When using a trackpad, the cursor displays as a circle on the screen, popping up only when you have a finger on the trackpad. The circle then morphs into various other shapes when hovering over app icons, text fields, or other on-screen elements.

This article, "Microsoft to Add Trackpad Support to Word, Excel, and PowerPoint Apps on iPad" first appeared on MacRumors.com

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


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

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

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

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

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

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

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Apple will begin reopening its retail stores in the United States next week, reports CNBC, starting with locations in Idaho, South Carolina, Alabama, and Alaska.


Apple plans to limit the number of customers in the store at a time, and temperature checks will be performed at the door. Apple also has a number of other measures in place to keep customers and employees safe, as we outlined this morning.

"We're excited to begin reopening stores in the US next week, starting with some stores in Idaho, South Carolina, Alabama and Alaska. Our team is constantly monitoring local heath data and government guidance, and as soon as we can safely open our stores, we will."

"Our new social distance protocol allows for a limited number of visitors in the store at one time so there may be a delay for walk-in customers. We recommend, where possible, customers buy online for contactless delivery or in-store pick up."

Reopened Apple Stores will operate on reduced hours and will primarily focus on repairs, with Apple encouraging customers to purchase online where possible.

Most stores are not listing hours at this time with the exception of Apple Boise Towne Square, which reopens Monday at 11:00 a.m.

During last week's earnings call, Apple CEO Tim Cook said that Apple planned to start reopening some stores in the United States in May. Store reopenings are done on a city by city, county by county basis, with Apple taking into account local data and guidelines.

Apple has already reopened stores in South Korea, Austria, and Australia, with plans to also reopen stores in Germany next week.
This article, "Apple to Start Reopening U.S. Stores Next Week" first appeared on MacRumors.com

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

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

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New experience reports published by Erowid on May 01 2020

New experience reports published by Erowid on May 02 2020

New experience reports published by Erowid on May 04 2020

New experience reports published by Erowid on May 05 2020

New experience reports published by Erowid on May 06 2020

New experience reports published by Erowid on May 08 2020

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 →

I am still holding on a call to the Internal Revenue Service, even though I called (800) 829-0115 two hours ago. This telephone number is the one often included in notices from the Internal Revenue Service for overdue business taxes. … Continue reading →

Senator Max Baucus, Chairman of the U.S. Senate Committee on Finance, releases a staff discussion draft on international business tax reform. Continue reading →

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

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

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

Online criminals have been systematically targeting TurboTax, filing fraudulent tax returns of individuals, and diverting their tax refunds to prepaid debit, cards, stealing their personal information, and using and impairing their credit ratings. Continue reading →

TurboTax’s Anti-Fraud Efforts Under Scrutiny Two former security employees at Intuit — the makers of the popular tax preparation software and service TurboTax – allege that the company has made millions of dollars knowingly processing state and federal tax refunds filed … 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 →

Democratic presidential candidate Bernie Sanders (I-VT) on Tuesday unveiled a plan to address income inequality by taxing Wall Street speculation and using the money to eliminate college tuition. Continue reading →

Presidential candidate Bernie Sanders says he wants to offer tuition free at public colleges and universities, paid for with a new tax on Wall Street. Ed Schultz and Sanders discuss the senator’s proposal. Continue reading →

Eyewitness News has learned that the Berlin High School football recruiting scandal may have cost Berlin taxpayers tens of thousands of dollars. Continue reading →

Bill Curry:  “In some ways, you would be [surprised that the polls in Connecticut are busy today]. Last week, on the Democratic side, every story said that it’s all over for Bernie; it’s so difficult to put this nomination together. … Continue reading →

There's got to be a reason for the Democrats to suppose to exist. And the reason the Democrats are supposed to exist is to be an opposition party to the Republicans. If you're in bed with the same people, taking money from the same people, you're no longer an opposition party. There's no reason for you to exist. And guess what? Don't be surprised that people don't vote for you. Continue reading →

Donald Trump sold out his supporters and the 99% by selecting Wall Streeters and war mongers for his top cabinet positions. Continue reading →

NEWS 8 IS YOUR LOCAL ELECTION HEADQUARTERS…. AND TONIGHT…VOODOO ECONOMICS! CHIEF POLITICAL CORRESPONDENT MARK DAVIS TELLING US HOW REPEALING THE STATE INCOME TAX IS THE LATEST HEATED TOPIC BETWEEN THE CANIDATES FOR GOVERNOR.   DEMOCRAT NED LAMONT IS OPENING A … Continue reading →