TRB’s Airport Cooperative Research Program (ACRP) Research Report 16: Guidebook for Managing Small Airports. Second Edition is designed to help airport practitioners, owners, operators, managers, and policymakers of small airports, who may have varying degrees of experience and backgrounds, to fulfill their responsibilities in such areas as financial management, oversight of contracts and leases, safety and security, noise impacts, community relations, compliance with federal and state obligations, facil...

Staff from smaller airports typically lack specialized expertise in the negotiation and development of airport property or the resources to hire consultants. The TRB Airport Cooperative Research Program's ACRP Research Report 213: Estimating Market Value and Establishing Market Rent at Small Airports provides airport management, policymakers, and staff a resource for developing and leasing airport land and improvements, methodologies for determining market value and appropriate rents, and best practices ...

University of California Pavement Research and National Center for Sustainable Transport have postponed the International Symposium on Pavement Life Cycle Assessment from June 3-6, 2020 to January 13-15, 2021 in Sacramento, CA. TRB is pleased to cosponsor this event. The symposium will focus on the implementation of Life Cycle Assessment (LCA) for pavements. The workshop address the implementation of LCA in pavement operations at the network and project levels.

EPA announced the availability of the Guidelines for Human Exposure Assessment (hereafter "Guidelines"). The Guidelines present the current policies and practices of exposure assessors across the Agency and supersede the 1992 Guidelines for Exposure Assessment Edition.

A new breed of smart telescopes is set to take users past these hurdles, and get them out under the night sky. We recently had a chance to put Vaonis’ Stellina ‘smart telescope’ through its paces, and we’re intrigued at the glimpse it provides at the future of observational astronomy.

The post Our Review of Stellina: a ‘Smart Telescope’ for 21st Century Astronomy appeared first on Universe Today.

Accelerated bridge construction (ABC) utilizes rigorous planning, new technologies, and improved methods to expedite construction. Prefabricated columns and their connections to adjoining bridge members (cap beams, footings, pile caps, and pile shafts) are the most critical components of ABC in moderate- and high-seismic regions. The TRB National Cooperative Highway Research Program's NCHRP Research Report 935: Proposed AASHTO Seismic Specifications for ABC Column Connections develops AASHTO specificatio...

Přes čtyři roky uzavřený případ nabral nečekaný spád. Tehdy měl přijít o život fotbalista Hiannick Kamba při autonehodě v rodném Kongu. Německý bulvární deník Bild však v pondělí zveřejnil informace dokazující opak. Bývalého hráče FC Schalke 04 údajně našli v Německu živého a zdravého. Falešnou smrt má patrně na svědomí exmanželka, která se tímto způsobem dostala k penězům z pojistky.

Bojíte se, že letos nebudete zatlačovat slzu u zlatavých nekonečných obzorů? Ale budete. A mnozí alergici na řepku slzy zatlačují už teď. Rajčata stojí sice 170kč za kilo, květák je už také kaviárem českých domácností, ale heslo "řídit stát jako zemědělství" nám zajistilo širé moře zlaté barvy. Sice se z řepky nenajíme (teda až na ty, co z pěstování rýžují zlaté dotace), ale že jsou to panorámata, co? 

Most nuclear data measurements are performed at accelerators large enough to occupy a geologic formation a kilometer wide. But a portable device that can reveal the composition of materials quickly on-site would greatly benefit cases such as in archaeology and nuclear arms treaty verification. Research published this week in AIP Advances used computational simulations to show that with the right geometric adjustments, it is possible to perform accurate neutron resonance transmission analysis in a device just 5 meters long.

I lost my beloved cat Gemma, seven months ago and when I think about her, I can smile a little. I can now think of the happy times and not that dreadful

A few weeks ago, the US telecom industry began pushing a bullshit narrative through its usual allies. In short, the claim revolves around the argument that the only reason the US internet still works during a pandemic was because the Trump FCC ignored the public, ignored most objective experts, and gutted itself at the behest of telecom industry lobbyists. The argument first popped up over at AEI, then the Trump FCC, then the pages of the Wall Street Journal, and has since been seen in numerous op-eds nationwide. I'd wager that's not a coincidence, and I'd also wager we'll be seeing a lot more of them.

All of the pieces try to argue that the only reason the US internet works during a pandemic is because the FCC gutted its authority over telecom as part of its "restoring internet freedom" net neutrality repeal. This repeal, the story goes, drove significant investment in US broadband networks (not remotely true), resulting in telecom Utopia (also not true). The argument also posits that in Europe, where regulators have generally taken a more active role in policing things like industry consolidation and telecom monopolies, the internet all but fell apart (guess what: not true).

Usually, like in this op-ed, there's ample insistence that the US broadband sector is largely wonderful while the EU has gone to hell:

"Unlike here, European networks are more heavily regulated. This has led to less investment and worse performance for consumers for years. American consumers are being generally well served by the private sector."

Anybody who has spent five minutes talking to Comcast customer support -- or tried to get scandal-plagued ISP like Frontier Communications to upgrade rotten DSL lines -- knows this is bullshit. Still, we penned a lengthy post exploring just how full of shit this argument is, and how there's absolutely zero supporting evidence for the claims. The entire house of cards is built on fluff and nonsense, and it's just ethically grotesque to use a disaster to help justify regulatory capture and market failure.

While it's true that the US internet, in general, has held up relatively well during a pandemic, the same can't be said of the so called "last mile," or the link from your ISP's network to your home. Yes, the core internet and most primary transit routes, designed to handle massive capacity spikes during events like the Superbowl, has handled the load relatively well. The problem, as Sascha Meinrath correctly notes here, is sluggish speeds on consumer and business lines that, for many, haven't been upgraded in years:

"Right now, an international consortium of network scientists is collecting 750,000 U.S. broadband speed tests from internet service provider (ISP) customers each day, and we’ve been tracking a stunning loss of connectivity speeds to people’s homes. According to most ISPs, the core network is handling the extra load. But our data show that the last-mile network infrastructure appears to be falling down on the job."

Again, your 5 Mbps DSL line might be ok during normal times, but it's not going to serve you well during a pandemic when your entire family is streaming 4K videos, gaming, and Zooming. And your DSL line isn't upgraded because there's (1) very little competition forcing your ISP to do so, and (2) the US government is filled to the brim with sycophants who prioritize campaign contributions and ISP revenues over the health of the market and consumer welfare. And while there's a contingency of industry-linked folks who try very hard to pretend otherwise, this is a policy failure that's directly tied to mindless deregulation, a lack of competition, and, more importantly, corruption. In short, the complete opposite of the industry's latest talking point.

For years we've been noting how US telcos have refused to repair or upgrade aging DSL lines because it's not profitable enough, quickly enough for Wall Street's liking. Facing no competition and no regulatory oversight, there's zero incentive for a giant US broadband provider to try very hard. Similarly, because our lawmakers and regulators are largely of the captured, revolving door variety, they rubber stamp shitty mergers, turn a blind eye to very obvious industry problems, routinely throwing billions in taxpayer money at monopolies in exchange for fiber networks that are usually only partially deployed -- if they're deployed at all.

Meanwhile, US telcos that have all but given up on upgrading aging DSL lines have helped cement an even bigger Comcast monopoly across vast swaths of America. It's a problem that the telecom sector, Trump FCC, and various industry apologists will ignore to almost comical effect. Also ignored is the fact that this results in US broadband subscribers paying some of the highest prices for broadband in the developed world:

"Numerous studies, including those conducted by the FCC itself, show that broadband pricing is the second-largest barrier to broadband adoption (availability is the first). It’s obvious that if people are being charged a lot for a service, they’re less likely to purchase it. And independent researchers have already documented that poor areas often pay more than rich communities for connectivity. Redlining of minority and rural areas appears to be widespread, and we need accurate pricing data from the FCC to meaningfully address these disparities."

Try to find any instance where Ajit Pai, or anybody in this chorus of telecom monopoly apologists, actually admits that the US broadband market isn't competitive and, as a result, is hugely expensive for businesses and consumers alike. You simply won't find it. What you will find are a lot of excuses and straw men arguments like this latest one, designed to distract the press, public, and policymakers from very obvious market failure. Market failure that was a major problem in normal times, and exponentially more so during a pandemic where broadband is an essential lifeline.

Zero-click remote-code exec hole found by Googler, updates emitted

Samsung has patched a serious security hole in its smartphones that can be exploited by maliciously crafted text messages to hijack devices.…

Opposition spokesman on tourism, Dr Wykeham McNeill, is calling for an investigation into allegations that some employers of tourism workers have not been turning over income tax deductions to government.  The situation has resulted in...

Благодаря чипу Kirin 710F смартфон получил предустановленные чипы Google.

This flow chart, created by University of Virginia Psychology Professors Jim Coan and Daniel Willingham, is just plain terrific. “Could a child do this alone?” asks the chart. Then let ’em! “Could a child do this with some instruction?” Then let ’em. Etc. etc. Check it out — print it out! — by clicking here. […]

---------------------------------------------------[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?

Arterial cardiovascular events are the leading cause of death in patients with JAK2V617F myeloproliferative neoplasms (MPNs). However, their mechanisms are poorly understood. The high prevalence of myocardial infarction without significant coronary stenosis or atherosclerosis in patients with MPNs suggests that vascular function is altered. The consequences of JAK2V617F mutation on vascular reactivity are unknown. We observe here increased responses to vasoconstrictors in arteries from Jak2V617F mice resulting from a disturbed endothelial NO pathway and increased endothelial oxidative stress. This response was reproduced in WT mice by circulating microvesicles isolated from patients carrying JAK2V617F and by erythrocyte-derived microvesicles from transgenic mice. Microvesicles of other cellular origins had no effect. This effect was observed ex vivo on isolated aortas, but also in vivo on femoral arteries. Proteomic analysis of microvesicles derived from JAK2V617F erythrocytes identified increased expression of myeloperoxidase as the likely mechanism accounting for their effect. Myeloperoxidase inhibition in microvesicles derived from JAK2V617F erythrocytes suppressed their effect on oxidative stress. Antioxidants such as simvastatin and N-acetyl cysteine improved arterial dysfunction in Jak2V617F mice. In conclusion, JAK2V617F MPNs are characterized by exacerbated vasoconstrictor responses resulting from increased endothelial oxidative stress caused by circulating erythrocyte-derived microvesicles. Simvastatin appears to be a promising therapeutic strategy in this setting.

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 The anti–programmed cell death 1 (anti–PD-1) antibody pembrolizumab is clinically active against non–small cell lung cancer (NSCLC). In addition to T cells, human natural killer (NK) cells, reported to have the potential to prolong the survival of patients with advanced NSCLC, also express PD-1. This study aimed to investigate the safety and efficacy of pembrolizumab plus allogeneic NK cells in patients with previously treated advanced NSCLC.METHODS In total, 109 enrolled patients with a programmed death ligand 1 (PD-L1) tumor proportion score (TPS) of 1% or higher were randomly allocated to group A (n = 55 patients given pembrolizumab plus NK cells) or group B (n = 54 patients given pembrolizumab alone). The patients received i.v. pembrolizumab (10 mg/kg) once every 3 weeks and continued treatment until the occurrence of tumor progression or unacceptable toxicity. The patients in group A continuously received 2 cycles of NK cell therapy as 1 course of treatment.RESULTS In our study, patients in group A had longer survival than did patients in group B (median overall survival [OS]: 15.5 months vs. 13.3 months; median progression-free survival [PFS]: 6.5 months vs. 4.3 months; P < 0.05). In group A patients with a TPS of 50% or higher, the median OS and PFS was significantly longer. Moreover, the patients in group A treated with multiple courses of NK cell infusion had better OS (18.5 months) than did those who received a single course of NK cell infusion (13.5 months).CONCLUSIONS Pembrolizumab plus NK cell therapy yielded improved survival benefits in patients with previously treated PD-L1+ advanced NSCLC.TRIAL REGISTRATION ClinicalTrials.gov NCT02843204.FUNDING This work was supported by grants from the National Natural Science Foundation of China (NSFC) – Guangdong Joint Foundation of China (no. U1601225); the NSFC (no. 81671965); the Guangdong Provincial Key Laboratory Construction Project of China (no. 2017B030314034); and the Key Scientific and Technological Program of Guangzhou City (no. 201607020016).

The prevalence of nonalcoholic fatty liver disease (NAFLD) is increasing worldwide. Although gene-environment interactions have been implicated in the etiology of several disorders, the impact of paternal and/or maternal metabolic syndrome on the clinical phenotypes of offspring and the underlying genetic and epigenetic contributors of NAFLD have not been fully explored. To this end, we used the liver-specific insulin receptor knockout (LIRKO) mouse, a unique nondietary model manifesting 3 hallmarks that confer high risk for the development of NAFLD: hyperglycemia, insulin resistance, and dyslipidemia. We report that parental metabolic syndrome epigenetically reprograms members of the TGF-β family, including neuronal regeneration–related protein (NREP) and growth differentiation factor 15 (GDF15). NREP and GDF15 modulate the expression of several genes involved in the regulation of hepatic lipid metabolism. In particular, NREP downregulation increases the protein abundance of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) and ATP-citrate lyase (ACLY) in a TGF-β receptor/PI3K/protein kinase B–dependent manner, to regulate hepatic acetyl-CoA and cholesterol synthesis. Reduced hepatic expression of NREP in patients with NAFLD and substantial correlations between low serum NREP levels and the presence of steatosis and nonalcoholic steatohepatitis highlight the clinical translational relevance of our findings in the context of recent preclinical trials implicating ACLY in NAFLD progression.

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.