The Internet is full of cats—and in this case, malware-delivering fake cat websites used for very targeted search engine optimization.

Ji Eun Kim
Dec 20, 2020; 0:RA120.002159v1-mcp.RA120.002159
Research

Alison B. Ross
Nov 30, 2020; 0:R120.002190v1-mcp.R120.002190
Review

Autophagy plays critical roles in the maintenance of endothelial cells in response to cellular stress caused by blood flow. There is growing evidence that both cell adhesion and cell detachment can modulate autophagy, but the mechanisms responsible for this regulation remain unclear. Immunoglobulin and proline-rich receptor-1 (IGPR-1) is a cell adhesion molecule that regulates angiogenesis and endothelial barrier function. In this study, using various biochemical and cellular assays, we demonstrate that IGPR-1 is activated by autophagy-inducing stimuli, such as amino acid starvation, nutrient deprivation, rapamycin, and lipopolysaccharide. Manipulating the IκB kinase β activity coupled with in vivo and in vitro kinase assays demonstrated that IκB kinase β is a key serine/threonine kinase activated by autophagy stimuli and that it catalyzes phosphorylation of IGPR-1 at Ser220. The subsequent activation of IGPR-1, in turn, stimulates phosphorylation of AMP-activated protein kinase, which leads to phosphorylation of the major pro-autophagy proteins ULK1 and Beclin-1 (BECN1), increased LC3-II levels, and accumulation of LC3 punctum. Thus, our data demonstrate that IGPR-1 is activated by autophagy-inducing stimuli and in response regulates autophagy, connecting cell adhesion to autophagy. These findings may have important significance for autophagy-driven pathologies such cardiovascular diseases and cancer and suggest that IGPR-1 may serve as a promising therapeutic target.

The subcellular localization of Arf family proteins is generally thought to be determined by their corresponding guanine nucleotide exchange factors. By promoting GTP binding, guanine nucleotide exchange factors induce conformational changes of Arf proteins exposing their N-terminal amphipathic helices, which then insert into the membranes to stabilize the membrane association process. Here, we found that the N-terminal amphipathic motifs of the Golgi-localized Arf family protein, Arfrp1, and the endosome- and plasma membrane–localized Arf family protein, Arl14, play critical roles in spatial determination. Exchanging the amphipathic helix motifs between these two Arf proteins causes the switch of their localizations. Moreover, the amphipathic helices of Arfrp1 and Arl14 are sufficient for cytosolic proteins to be localized into a specific cellular compartment. The spatial determination mediated by the Arfrp1 helix requires its binding partner Sys1. In addition, the residues that are required for the acetylation of the Arfrp1 helix and the myristoylation of the Arl14 helix are important for the specific subcellular localization. Interestingly, Arfrp1 and Arl14 are recruited to their specific cellular compartments independent of GTP binding. Our results demonstrate that the amphipathic motifs of Arfrp1 and Arl14 are sufficient for determining specific subcellular localizations in a GTP-independent manner, suggesting that the membrane association and activation of some Arf proteins are uncoupled.

In Alzheimer's disease (AD), tau, a microtubule-associated protein (MAP), becomes hyperphosphorylated, aggregates, and accumulates in the somato-dendritic compartment of neurons. In parallel to its intracellular accumulation in AD, tau is also released in the extracellular space, as revealed by its increased presence in cerebrospinal fluid (CSF). Consistent with this, recent studies, including ours, have reported that neurons secrete tau, and several therapeutic strategies aim to prevent the intracellular tau accumulation. Previously, we reported that late endosomes were implicated in tau secretion. Here, we explore the possibility of preventing intracellular tau accumulation by increasing tau secretion. Using neuronal models, we investigated whether overexpression of the vesicle-associated membrane protein 8 (VAMP8), an R-SNARE found on late endosomes, could increase tau secretion. The overexpression of VAMP8 significantly increased tau secretion, decreasing its intracellular levels in the neuroblastoma (N2a) cell line. Increased tau secretion by VAMP8 was also observed in murine hippocampal slices. The intracellular reduction of tau by VAMP8 overexpression correlated to a decrease of acetylated tubulin induced by tau overexpression in N2a cells. VAMP8 staining was preferentially found on late endosomes in N2a cells. Using total internal reflection fluorescence (TIRF) microscopy, the fusion of VAMP8-positive vesicles with the plasma membrane was correlated to the depletion of tau in the cytoplasm. Finally, overexpression of VAMP8 reduced the intracellular accumulation of tau mutants linked to frontotemporal dementia with parkinsonism and α-synuclein by increasing their secretion. Collectively, the present data indicate that VAMP8 could be used to increase tau and α-synuclein clearance to prevent their intracellular accumulation.

AMP-activated protein kinase (AMPK) is a key regulator of energy metabolism that phosphorylates a wide range of proteins to maintain cellular homeostasis. AMPK consists of three subunits: α, β, and γ. AMPKα and β are encoded by two genes, the γ subunit by three genes, all of which are expressed in a tissue-specific manner. It is not fully understood, whether individual isoforms have different functions. Using RNA-Seq technology, we provide evidence that the loss of AMPKβ1 and AMPKβ2 lead to different gene expression profiles in human induced pluripotent stem cells (hiPSCs), indicating isoform-specific function. The knockout of AMPKβ2 was associated with a higher number of differentially regulated genes than the deletion of AMPKβ1, suggesting that AMPKβ2 has a more comprehensive impact on the transcriptome. Bioinformatics analysis identified cell differentiation as one biological function being specifically associated with AMPKβ2. Correspondingly, the two isoforms differentially affected lineage decision toward a cardiac cell fate. Although the lack of PRKAB1 impacted differentiation into cardiomyocytes only at late stages of cardiac maturation, the availability of PRKAB2 was indispensable for mesoderm specification as shown by gene expression analysis and histochemical staining for cardiac lineage markers such as cTnT, GATA4, and NKX2.5. Ultimately, the lack of AMPKβ1 impairs, whereas deficiency of AMPKβ2 abrogates differentiation into cardiomyocytes. Finally, we demonstrate that AMPK affects cellular physiology by engaging in the regulation of hiPSC transcription in an isoform-specific manner, providing the basis for further investigations elucidating the role of dedicated AMPK subunits in the modulation of gene expression.

Acute lung injury (ALI), is a rapidly progressing heterogenous pulmonary disorder that possesses a high risk of mortality. Accumulating evidence has implicated the activation of the p65 subunit of NF-κB [NF-κB(p65)] activation in the pathological process of ALI. microRNAs (miRNAs), a group of small RNA molecules, have emerged as major governors due to their post-transcriptional regulation of gene expression in a wide array of pathological processes, including ALI. The dysregulation of miRNAs and NF-κB activation has been implicated in human diseases. In the current study, we set out to decipher the convergence of miR-99b and p65 NF-κB activation in ALI pathology. We measured the release of pro-inflammatory cytokines (IL-1β, IL-6, and TNFα) in bronchoalveolar lavage fluid using ELISA. MH-S cells were cultured and their viability were detected with cell counting kit 8 (CCK8) assays. The results showed that miR-99b was up-regulated, while PRDM1 was down-regulated in a lipopolysaccharide (LPS)-induced murine model of ALI. Mechanistic investigations showed that NF-κB(p65) was enriched at the miR-99b promoter region, and further promoted its transcriptional activity. Furthermore, miR-99b targeted PRDM1 by binding to its 3'UTR, causing its down-regulation. This in-creased lung injury, as evidenced by increased wet/dry ratio of mouse lung, myeloperoxidase activity and pro-inflammatory cytokine secretion, and enhanced infiltration of inflammatory cells in lung tissues. Together, our findings indicate that NF-κB(p65) promotion of miR-99b can aggravate ALI in mice by down-regulating the expression of PRDM1.

Nicholas D. LeBlond
Dec 1, 2020; 61:1697-1706
Research Articles

Natalie Bruiners
Dec 1, 2020; 61:1617-1628
Research Articles

In SAS Customer Intelligence Studio, you might notice that you cannot clear warnings for decision campaign nodes by selecting either the Clear Warnings  option or the Clear All Warnin

In SAS Retail Space Management, it should be possible to click on any location object, then Show Properties, and change the location fill color. This can be done on the gray-filled objects. However, w

Titles and footnotes do not span the entire width of the page when you use the COLUMNS= option with a value that is greater than 1 with the TAGSETS.RTF_SAMPLE tagset. When a value that is greater than 1 is specified for th

This manuscript has been withdrawn by the Author.

The dysregulation of myeloid-derived cell metabolism can drive atherosclerosis. AMP-activated protein kinase (AMPK) controls various aspects of macrophage dynamics and lipid homeostasis, which are important during atherogenesis. Using LysM-Cre to drive the deletion of both the α1 and α2 catalytic subunits (MacKO), we aimed to clarify the role of myeloid-specific AMPK signaling in male and female mice made acutely atherosclerotic by injection of AAV vector encoding a gain-of-function mutant PCSK9 (PCSK9-AAV) and WD feeding. After 6 weeks of WD feeding, mice received a daily injection of either the AMPK activator A-769662 or a vehicle control for an additional 6 weeks. Following this (12 weeks total), we assessed myeloid cell populations and differences between genotype or sex were not observed. Similarly, aortic sinus plaque size, lipid staining, and necrotic area did not differ in male and female MacKO mice compared with their littermate floxed controls. Moreover, therapeutic intervention with A-769662 showed no treatment effect. There were also no observable differences in the amount of circulating total cholesterol or triglyceride, and only minor differences in the levels of inflammatory cytokines between groups. Finally, CD68+ area and markers of autophagy showed no effect of either lacking AMPK signaling or AMPK activation. Our data suggest that while defined roles for each catalytic AMPK subunit have been identified, complete deletion of myeloid AMPK signaling does not significantly impact atherosclerosis. Additionally, these findings suggest that intervention with the first-generation AMPK activator A-769662 is not able to stem the progression of atherosclerosis.

The rise of drug-resistant tuberculosis poses a major risk to public health. Statins, which inhibit both cholesterol biosynthesis and protein prenylation branches of the mevalonate pathway, increase anti-tubercular antibiotic efficacy in animal models. However, the underlying molecular mechanisms are unknown. In this study, we used an in vitro macrophage infection model to investigate simvastatin’s anti-tubercular activity by systematically inhibiting each branch of the mevalonate pathway and evaluating the effects of the branch-specific inhibitors on mycobacterial growth. The anti-tubercular activity of simvastatin used at clinically relevant doses specifically targeted the cholesterol biosynthetic branch rather than the prenylation branches of the mevalonate pathway. Using Western blot analysis and AMP/ATP measurements, we found that simvastatin treatment blocked activation of mechanistic target of rapamycin complex 1 (mTORC1), activated AMP-activated protein kinase (AMPK) through increased intracellular AMP:ATP ratios, and favored nuclear translocation of transcription factor EB (TFEB). These mechanisms all induce autophagy, which is anti-mycobacterial. The biological effects of simvastatin on the AMPK-mTORC1-TFEB-autophagy axis were reversed by adding exogenous cholesterol to the cells. Our data demonstrate that the anti-tubercular activity of simvastatin requires inhibiting cholesterol biosynthesis, reveal novel links between cholesterol homeostasis, the AMPK-mTORC1-TFEB axis, and Mycobacterium tuberculosis infection control, and uncover new anti-tubercular therapy targets.

The organic anion transporters (OATs) and organic anion–transporting polypeptides (OATPs) belong to the solute carrier (SLC) transporter superfamily and play important roles in handling various endogenous and exogenous compounds of anionic charge. The OATs and OATPs are often implicated in drug therapy by impacting the pharmacokinetics of clinically important drugs and, thereby, drug exposure in the target organs or cells. Various mechanisms (e.g. genetic, environmental, and disease-related factors, drug-drug interactions, and food-drug interactions) can lead to variations in the expression and activity of the anion drug-transporting proteins of OATs and OATPs, possibly impacting the therapeutic outcomes. Previous investigations mainly focused on the regulation at the transcriptional level and drug-drug interactions as competing substrates or inhibitors. Recently, evidence has accumulated that cellular trafficking, post-translational modification, and degradation mechanisms serve as another important layer for the mechanisms underlying the variations in the OATs and OATPs. This review will provide a brief overview of the major OATs and OATPs implicated in drug therapy and summarize recent progress in our understanding of the post-translational modifications, in particular ubiquitination and degradation pathways of the individual OATs and OATPs implicated in drug therapy.

High-speed analysis of large (prote)omics sample sets at the rate of thousands or millions of samples per day on a single platform has been a challenge since the beginning of proteomics. For many years, ESI-based MS methods have dominated proteomics because of their high sensitivity and great depth in analyzing complex proteomes. However, despite improvements in speed, ESI-based MS methods are fundamentally limited by their sample introduction, which excludes off-line sample preparation/fractionation because of the time required to switch between individual samples/sample fractions, and therefore being dependent on the speed of on-line sample preparation methods such as liquid chromatography. Laser-based ionization methods have the advantage of moving from one sample to the next without these limitations, being mainly restricted by the speed of modern sample stages, i.e. 10 ms or less between samples. This speed matches the data acquisition speed of modern high-performing mass spectrometers whereas the pulse repetition rate of the lasers (>1 kHz) provides a sufficient number of desorption/ionization events for successful ion signal detection from each sample at the above speed of the sample stages. Other advantages of laser-based ionization methods include the generally higher tolerance to sample additives and contamination compared with ESI MS, and the contact-less and pulsed nature of the laser used for desorption, reducing the risk of cross-contamination. Furthermore, new developments in MALDI have expanded its analytical capabilities, now being able to fully exploit high-performing hybrid mass analyzers and their strengths in sensitivity and MS/MS analysis by generating an ESI-like stable yield of multiply charged analyte ions. Thus, these new developments and the intrinsically high speed of laser-based methods now provide a good basis for tackling extreme sample analysis speed in the omics.

In all cells, proteins are continuously synthesized and degraded in order to maintain protein homeostasis and modify gene expression levels in response to stimuli. Collectively, the processes of protein synthesis and degradation are referred to as protein turnover. At steady state, protein turnover is constant to maintain protein homeostasis, but in dynamic responses, proteins change their rates of synthesis and degradation in order to adjust their proteomes to internal or external stimuli. Thus, probing the kinetics and dynamics of protein turnover lends insight into how cells regulate essential processes such as growth, differentiation, and stress response. Here we outline historical and current approaches to measuring the kinetics of protein turnover on a proteome-wide scale in both steady-state and dynamic systems, with an emphasis on metabolic tracing using stable-isotope-labeled amino acids. We highlight important considerations for designing proteome turnover experiments, key biological findings regarding the conserved principles of proteome turnover regulation, and future perspectives for both technological and biological investigation.

Urinary proteomics studies have primarily focused on identifying markers of chronic kidney disease (CKD) progression. Here, we aimed to determine urinary markers of CKD renal parenchymal injury through proteomics analysis in animal kidney tissues and cells and in the urine of patients with CKD. Label-free quantitative proteomics analysis based on liquid chromatography-tandem mass spectrometry was performed on urine samples obtained from 6 normal controls and 9, 11, and 10 patients with CKD stages 1, 3, and 5, respectively, and on kidney tissue samples from a rat CKD model by 5/6 nephrectomy. Tandem mass tag-based quantitative proteomics analysis was performed for primary cultured glomerular endothelial cells (GECs) and proximal tubular epithelial cells (PTECs) before and after inducing 24-h hypoxia injury. Upon hierarchical clustering, out of 858 differentially expressed proteins (DEPs) in the urine of CKD patients, the levels of 416 decreased and 403 increased sequentially according to the disease stage, respectively. Among 2965 DEPs across 5/6 nephrectomized and sham-operated rat kidney tissues, 86 DEPs showed same expression patterns in the urine and kidney tissue. After cross-validation with two external animal proteome datasets, 38 DEPs were organized; only 10 DEPs, including serotransferrin, gelsolin, poly ADP-ribose polymerase 1, neuroblast differentiation-associated protein AHNAK, microtubule-associated protein 4, galectin-1, protein S, thymosin beta-4, myristoylated alanine-rich C-kinase substrate, and vimentin were finalized by screening human GECs and PTECs data. Among these ten potential candidates for universal CKD marker, validation analyses for protein S and galectin-1 were conducted. Galectin-1 was observed to have a significant inverse correlation with renal function as well as higher expression in glomerulus with chronic injury than protein S. This constitutes the first multi-sample proteomics study for identifying key renal-expressed proteins associated with CKD progression. The discovered proteins represent potential markers of chronic renal cell and tissue damage and candidate contributors to CKD pathophysiology.

In eukaryotic DNA replication, DNA polymerase ε (Polε) is responsible for leading strand synthesis, whereas DNA polymerases α and δ synthesize the lagging strand. The human Polε (hPolε) holoenzyme is comprised of the catalytic p261 subunit and the noncatalytic p59, p17, and p12 small subunits. So far, the contribution of the noncatalytic subunits to hPolε function is not well understood. Using pre-steady-state kinetic methods, we established a minimal kinetic mechanism for DNA polymerization and editing catalyzed by the hPolε holoenzyme. Compared with the 140-kDa N-terminal catalytic fragment of p261 (p261N), which we kinetically characterized in our earlier studies, the presence of the p261 C-terminal domain (p261C) and the three small subunits increased the DNA binding affinity and the base substitution fidelity. Although the small subunits enhanced correct nucleotide incorporation efficiency, there was a wide range of rate constants when incorporating a correct nucleotide over a single-base mismatch. Surprisingly, the 3'→5' exonuclease activity of the hPolε holoenzyme was significantly slower than that of p261N when editing both matched and mismatched DNA substrates. This suggests that the presence of p261C and the three small subunits regulates the 3'→5' exonuclease activity of the hPolε holoenzyme. Together, the 3'→5' exonuclease activity and the variable mismatch extension activity modulate the overall fidelity of the hPolε holoenzyme by up to 3 orders of magnitude. Thus, the presence of p261C and the three noncatalytic subunits optimizes the dual enzymatic activities of the catalytic p261 subunit and makes the hPolε holoenzyme an efficient and faithful replicative DNA polymerase.

Phillies manager Gabe Kapler has a little advice for the players who could be impacted most if the team signs Bryce Harper or Manny Machado.

The countdown to pitchers and catchers reporting is down to single digits for all 30 MLB clubs, but as exciting as it is to see the return of Major League stars, it's also a time to dream about the next wave of baseball talent.

Spring Training is officially here for the Angels, with pitchers and catchers reporting to Tempe Diablo Stadium on Tuesday. And there's a new face at manager, with Brad Ausmus replacing longtime skipper Mike Scioscia this offseason.

I’m often asked if I miss working in the House of Commons. Of course I do; it’s one of the most amazing places in the world and remains the cockpit of our nation.There are obviously days I miss it more than others, usually around the big national moments. Whatever your view of Kim Leadbeater’s private member’s bill—the Terminally Ill Adults (End of Life) Bill—its second reading this month will be one of those big moments.Kim is a friend of mine, and we spoke before she decided to put her bill forward after it topped the private members’ ballot at the start of the new parliament. My advice was to proceed with great care, to remember that this will take over your career in many ways, and to read the report produced earlier this year by the Health and Social Care Committee, which I chaired, on the subject of assisted dying/assisted...

Q&A: Maria Kolesnikova The World Today rescobales.drupal 29 September 2021

The jailed Belarusian opposition activist says: ‘It’s worth it’

Earlier this month, the Belarusian opposition activists, Maria Kolesnikova and Maxim Znak, were sentenced to long prison terms on charges of conspiring to seize power and crimes against national security. Both Kolesnikova, a prominent musician, and Znak, a lawyer, are supporters of Sviatlana Tsikhanouskaya, who ran against President Alexander Lukashenka in last year’s election and is now in exile in Lithuania. European Union countries have called for all political detainees, including Kolesnikova, to be released, but so far these calls have fallen on deaf ears. Alistair Burnett interviewed Maria Kolesnikova.

What is your response to the verdict and the 11-year sentence handed down to you?

My conscience is clear. We didn’t break the law. We followed the law at all the stages of the electoral campaign.

After the verdict, we applauded when the judges left the courtroom. They fulfilled their despicable role in this historical process – now this decision is on their conscience.

It is impossible to take the court and the verdict in any way seriously. This is not a verdict on Maxim and me but on the authorities themselves, on the system itself.

It is evidence not only of a legal default, but of a system-wide default. I feel sorry for those who did not understand what happened and did not learn history’s lessons.

Your trial was held behind closed doors and you were charged with conspiring to seize power and crimes against national security. What can you tell us about the prosecution’s case against you?

If there had been any evidence against us, the trial would have been open.

The very existence of accusations like this denies people the potential to participate in election campaigning and in political activity generally. It also prohibits public criticism of the authorities.

Such a judgment and verdict is a Pandora’s box with far-reaching negative consequences.

After the crackdown over last year’s protests and now your sentencing, what is the state of the opposition within Belarus?

I am in prison, so it is hard for me to judge objectively people’s attempts to fight for their freedom and basic human rights. According to what I see on TV, as well as the mood of those few people I have had a chance to talk to, I can say that the authorities are scared by the people’s activism.

They understand that though they can put down protests, they can’t change people’s mindsets. I see the fear in their eyes. I also believe that even those outside of Belarus can do a lot, and it’s important to continue opposition activity both inside and outside the country.

Sviatlana Tsikhanouskaya has been visiting European countries and the United States to maintain their support. Has international pressure, including from human rights groups, had any effect on the Lukashenka government?

I will use this opportunity to say hi to Sviatlana: ‘You are amazing. Keep it up.’

I’m sure Lukashenka is scared. He turned from a person who meets presidents to talk about Ukraine into an outcast no one wants to shake hands with.

It is traumatic for him, but the fear will pass. He will get used to it.

That is why it’s important to think about the next step, to understand what American and European partners are ready to offer Lukashenka in return for him to change course. If they aren’t ready to offer him anything – it’s important to know how long they are ready to maintain the pressure.

It concerns Russia as well. Maybe they simply don’t understand that Lukashenka and his government are in a bad way.

To what extent do you believe the futures of the Lukashenka and Russian President Vladimir Putin are now intertwined?

Lukashenka is a famous manipulator. Almost 30 years in power has made his self-preservation instincts automatic. It’s a tactical choice. There’s nothing behind it besides the willingness to stay in power till he dies.

But a trapped person is a dangerous and unreliable partner. It won’t remain like this for a long time. His partners will sooner or later face unpleasant surprises.

What can the international community do?

Hundreds of political prisoners, thousands in exile, tens of thousands arrested, fined, subjected to violence, and the media and businesses are being destroyed. The authorities are at war with their own people and leading the country into an abyss.

The support of the international community is very important for Belarusians. We need to look for an opportunity to start a dialogue, both within the country and with international partners.

Why did last year’s protests last as long as they did? Was it the relative youth of the protesters; the use of social media; the prominence of women; and did COVID restrictions play any part?

For me, the protests aren’t the main thing. The transformation of Belarusian society is the most important thing.

Most Belarusians decided what they want to see in their county: Belarus as a free, democratic, sovereign country. And the current authorities aren’t able to provide that.

Regarding new technology, of course, it gives more opportunities for people to organize, however, social media users are still the minority in Belarus. Everything happened on a deeper level after being built up over time through people’s real-life experience.

Throughout the campaign, I have been surprised by the fact that most of the activists are middle-aged people from different professions. There were plenty of women who expressed their objection first.

Through the situation with COVID, we gained a new experience of solidarity and mutual assistance, so when the government turned against the people, we realized then how many we were.

Looking back now at the protests, would you do anything differently and have you learned lessons for the future?

We definitely have more appreciation for what we already have. We appreciate our amazing journalists, our civil society, and private businesses. And, of course, our upcoming victory.

What could we have done differently? We could have been more consistent in terms of our willingness to resolve the crisis quickly and painlessly for the country. We were calling for dialogue in August, and then we had this unfortunate period of ultimatums that damaged both sides.

The situation is different now, and everything is more complicated. The moment has gone, and I don’t think that negotiation or national dialogue in the form we expected a year ago is possible anymore.

We had to make very hard choices many times, but the most important thing is that we never deviated from our principles and values - the fairness of the law, kindness, respect and love. I believe it is the only right way.

How can you now achieve your goal of removing President Lukashenka from power?

To be a politician in Belarus nowadays means to be in prison. In this way, I can contribute to the common endeavor. It’s not our objective, though.

Our objective is a country free of current and future forms of authoritarianism.

How to free the country? On the one hand, we all have to maintain our effort, cohesion and solidarity. We should try not to lose that. On the other hand, we should focus on limiting the political space for the government. We should show that the system will have to deal with us, the Belarusians.

Thirdly, we have to think about the future of Belarus. We have to dream about it, believe in it and stay active. Everything is up to us.

You were a musician before becoming active in politics. Has music shaped your approach to political activism and have you had the chance to continue playing in detention?

The artistic path shapes the personality. Of course, teamwork, looking for unusual solutions, and the ability to stay concentrated and work for a long time in critical situations, as well as performing in public, is what I’ve been learning my whole life as a musician.

Management of contemporary art projects and partnerships with businesses, like with Viktar Babaryka, the former presidential candidate, for example, gave me even more experience.

I miss music a lot, but in Belarusian prisons, even books aren’t really allowed. I don’t have an opportunity to play.

Do you have any regrets about your decision to become involved in opposition politics?

I consider my decision to participate in the campaign the most important and responsible one of my life. I knew it would be hard, but the future of the nation is at stake. So it’s worth it. My love for Belarus and Belarusian people didn’t allow me to stay aloof.

Oct. 24, 2024 — The San Diego Supercomputer Center (SDSC), part of the School of Computing, Information and Data Sciences at UC San Diego, has been leading the Open Storage Network (OSN) program for years, and along […]

The post SDSC Leads Expansion of Open Storage Network to More Campus Computing Sites appeared first on HPCwire.

Air Force Special Operations aims to test the MC-130J Hercules transport aircraft's amphibious capability in 2022, the commander said Monday.

Bahraini leaders committed Thursday to partnering with a new U.S. Navy task force to ramp up new unmanned system efforts.

It will cost $55.7 million to repair Tropicana Field, home to the MLB Tampa Bay Rays, in time for the 2026 home opener, St. Petersburg., Fla., city officials said Tuesday.

A former Jeopardy! winner led a new study that probes how linked memory systems may give trivia buffs an edge in their game

Nov. 1, 2024 — NCC France & NCC Slovakia announce a free online training on Numerical Computing With Rust on CPU. The training is spread over three days, from November […]

The post NCC France & NCC Slovakia Announce Numerical Computing With Rust on CPUs Training appeared first on HPCwire.

India is eying a return to the moon in 2028, aiming to collect 6.6 pounds of lunar samples from an area thought to be rich in water and ice near the lunar south pole, the Indian Space Research Organization has announced.

The two motivational keys to becoming a champion.

Exploring the history and evolution of vampire lore, author Eric Nuzum traces the origins of these spooky stories, from misunderstandings of death to the sparkly pop culture icons we know today. Beyond the fangs and garlic, he digs into the deeper, everyday fears that vampires reflect.

Several states this year sought to replace their funding formulas, a monumental fiscal and political feat, but only a handful of legislatures have been able to get proposals to their governors' desks.

This Quality Counts 2019 Highlights Report captures all the data you need to assess your state's performance on key educational outcomes.

Instead of creating change through compliance and extrinsic motivators, the new era of education and education policy will require ecosystems of policy, regulation, investment, and operating structure that enable, rather than dictate. Under New Hampshire's PACE accountability system districts and sc

The study found that youth in rural New Hampshire have poor perceptions of job opportunities in the area, and are more likely to be depressed or abuse substances than other rural youth.

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Best known in education circles for its performance assessment, New Hampshire is a hotbed of innovation around personalized learning, writes Adriana Martinez of the Innovation Lab Network.