The Sunset Corporation Of America (SCA) Shut Down Its Sunset Book Publishing Company Imprint Last Month

Live Nation and AEG Presents will offer refunds to ticketholders whose events have been canceled due to coronavirus.

Colorado Republican Party Chair Ken Buck, a U.S. representative from Windsor, pressured a local party official to submit incorrect election results to set the primary ballot for a state Senate seat, according to an audio recording of a conference call obtained by The Denver Post.

(United States Supreme Court) - The US Supreme Court held that American Express (Amex) anti-steering provisions, in its agreement with merchants to prohibit merchants who take Amex cards from discouraging customers from using their cards in order for the merchant to avoid paying Amex a fee, do not violate the Sherman Antitrust Act.

The U.S. unemployment rate hit 14.7% in April, the highest rate since the Great Depression, as 20.5 million jobs vanished in the worst monthly loss on record. The figures are stark evidence of the damage the coronavirus has done to a now-shattered economy.

Keke turns Kevin into a scream queen!

Nicki Micheaux learned about how to deal with depression.

Cardi B and Offset perform their songs "Clout" and "Press."

The stars of the 2019 BET Awards jam to "Black Is Love."

The rapper was seen acting bizarre in a series of videos.

Cardi B and Offset perform their songs "Clout" and "Press."

The stars of the 2019 BET Awards jam to "Black Is Love."

Be informed about the power of your vote.

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Upload images and media in the background with WordPress for iOS 9.8

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With Recurring Payments, your supporters become your sustainers, and a reliable income stream frees you to push your creative boundaries.

The government loves its secrets. It loves them so much it does stupid things to, say, "secure the nation..." or "protect the integrity of deliberative processes" or whatever the fuck. We should not trust the government's reasoning when it chooses to redact information from documents it releases to FOIA requesters. These assertions should always be challenged because the government's track record on redactions is objectively awful.

Here's the latest case-in-point: Emma Best -- someone the government feels is a "vexatious" FOIA filer -- just received a completely stupid set of redactions from the Secret Service. Best requested documents mentioning darknet market Hansa, which was shut down (along with Alpha Bay) following an investigation by US and Dutch law enforcement agencies.

The documents returned to Best contained redactions. This is unsurprising given the nature of the investigation. What's surprising is what the Secret Service decided to redact. As Best pointed out on Twitter, the Secret Service decided public press releases by the DOJ were too sensitive to be released to the general public.

Here's one of the redactions [PDF] the Secret Service applied to a press release that can be found unaltered and unedited at the Justice Department's publicly-accessible website:

And here's what the Secret Service excised, under the bullshit theory that a publicly-released press statement is somehow an "inter-agency or intra-agency memorandums or letter which would not be available by law to a party other than an agency in litigation with the agency."

“This is likely one of the most important criminal investigations of the year – taking down the largest dark net marketplace in history,” said Attorney General Jeff Sessions. “Make no mistake, the forces of law and justice face a new challenge from the criminals and transnational criminal organizations who think they can commit their crimes with impunity using the dark net. The dark net is not a place to hide. The Department will continue to find, arrest, prosecute, convict, and incarcerate criminals, drug traffickers and their enablers wherever they are. We will use every tool we have to stop criminals from exploiting vulnerable people and sending so many Americans to an early grave. I believe that because of this operation, the American people are safer – safer from the threat of identity fraud and malware, and safer from deadly drugs.”

Um. Is Jeff Sessions being Yezhoved by the Secret Service? Does the agency consider him to be enough of a persona non grata after his firing by Trump to be excised from the Secret Services' official recollection of this dark web takedown? This insane conspiracy theory I just made up makes as much sense as anything the Secret Service could offer in explanation for this redaction. The redaction removed nothing but the sort of swaggering statement Attorney Generals always make after a huge bust.

Needless to say, Emma Best is challenging the Secret Service's redactions. Pithily.

I am appealing the integrity of the redactions, as you withheld public press releases under b5, which is grossly inappropriate.

Yeah. That's an understatement. The Secret Service has no business redacting publicly-available info. Even if this was a clerical error, it's so bad it's insulting. And that's why you can't trust the government on things like this: when it's not being malicious, it's being stupid.

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.

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.

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

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

Approximately half of the world’s population is infected with the stomach pathogen Helicobacter pylori. Infection with H. pylori is the main risk factor for distal gastric cancer. Bacterial virulence factors, such as the oncoprotein CagA, augment cancer risk. Yet despite high infection rates, only a fraction of H. pylori–infected individuals develop gastric cancer. This raises the question of defining the specific host and bacterial factors responsible for gastric tumorigenesis. To investigate the tumorigenic determinants, we analyzed gastric tissues from human subjects and animals infected with H. pylori bacteria harboring different CagA status. For laboratory studies, well-defined H. pylori strain B128 and its cancerogenic derivative strain 7.13, as well as various bacterial isogenic mutants were employed. We found that H. pylori compromises key tumor suppressor mechanisms: the host stress and apoptotic responses. Our studies showed that CagA induces phosphorylation of XIAP E3 ubiquitin ligase, which enhances ubiquitination and proteasomal degradation of the host proapoptotic factor Siva1. This process is mediated by the PI3K/Akt pathway. Inhibition of Siva1 by H. pylori increases survival of human cells with damaged DNA. It occurs in a strain-specific manner and is associated with the ability to induce gastric tumor.

Lamin A is a component of the inner nuclear membrane that, together with epigenetic factors, organizes the genome in higher order structures required for transcriptional control. Mutations in the lamin A/C gene cause several diseases belonging to the class of laminopathies, including muscular dystrophies. Nevertheless, molecular mechanisms involved in the pathogenesis of lamin A–dependent dystrophies are still largely unknown. The polycomb group (PcG) of proteins are epigenetic repressors and lamin A interactors, primarily involved in the maintenance of cell identity. Using a murine model of Emery-Dreifuss muscular dystrophy (EDMD), we show here that lamin A loss deregulated PcG positioning in muscle satellite stem cells, leading to derepression of non–muscle-specific genes and p16INK4a, a senescence driver encoded in the Cdkn2a locus. This aberrant transcriptional program caused impairment in self-renewal, loss of cell identity, and premature exhaustion of the quiescent satellite cell pool. Genetic ablation of the Cdkn2a locus restored muscle stem cell properties in lamin A/C–null dystrophic mice. Our findings establish a direct link between lamin A and PcG epigenetic silencing and indicate that lamin A–dependent muscular dystrophy can be ascribed to intrinsic epigenetic dysfunctions of muscle stem cells.

As of today, my current job is now the longest one I’ve ever held.

Sen. Bernie Sanders (I-Vt.) warns not to underestimate him in the 2016 Democratic race for the White House. Sanders, who is formally launching his campaign Tuesday, said he has a strong message. Continue reading →

The Vermont Senator and Presidential candidate talks Hillary Clinton, the 2016 race, and an essay he wrote in the 70's about sex. Continue reading →

The AFP’s media raid warrant gets slapped down by the High Court.  Plus, Trump and the media’s latest bout, Boris Johnson gets released from “prison”, the Daily Mail find a bogus Barnsey, and an angry shop keeper flips the bird.

White marble, dark chocolate, one light source. Problem?

Not at all. Because pretty much everything you can actually see across the top of that box is not really the "correct" tonality of the chocolate. It's all specular highlights.

Controlling the density of specular highlights is what compresses the subject's wide tonal range and unifies everything into one smooth exposure.
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Many years ago, I attended a talk by Cynthia Good, publisher of Penguin Canada. When asked what was the first thing she looks for in a book submission, she said, “A way to get the author on TV.” I’ve now got over 400 TV appearances to my credit, and an equal number of radio interviews […]

We'll be at the Small Press Expo in Bethesda Maryland!

This is our first time at SPX! If you're there, feel free to stop by and see us in the Artist Alley – we'll be at table W49!

See you there! <3 -Hamlet

U.S. Unemployment Reaches 14.7 Percent – Chart from Great Depression Shows Risks Ahead

By Pam Martens and Russ Martens: May 8, 2020 ~   The data is out this morning and it’s not pretty. Nonfarm payrolls collapsed by 20.5 million jobs in April and the unemployment rate rose to 14.7 percent. The United States is now seeing the worst unemployment rates since the Great Depression. We prepared the above chart from data available at the Federal Reserve Economic Data (FRED) archives at the Federal Reserve Bank of St. Louis. Following the stock market crash of October 29, 1929, it was not until August 1931 that the unemployment rate reached 15.01 percent. We’re now at 14.7 percent unemployment from a rate of 3.5 percent just two months ago in February. Consider using the chart above to figure out just how much cash on hand you need to maintain.

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ICMR teams up with Bharat Biotech to develop COVID-19 vaccine  The Financial ExpressView Full coverage on Google News

The growls from the caged hyena reverberate through the room as Mohamed Sheikh Yakub slumps silently in a chair nearby, hoping the animal will frighten away the evil spirits he says have troubled him since his divorce.