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How to Work with Home Stagers Remotely

• Facebook is taking a harder line on misinformation related to coronavirus than it has on other health topics in the past.
• This decision may increase the pressure on the company to act more decisively against other forms of harmful falsehoods that spread on its social networks.
• Facebook is banning events that promote flouting lockdown protests, and is removing the conspiracy theory video "Plandemic."
• But false claims that vaccines are dangerous still proliferate on Facebook — even though they contribute to the deaths of children.

Amid the pandemic, Facebook is taking a harder line on misinformation than it has in the past. That decision may come back to haunt it.

As coronavirus has wreaked havoc across the globe, forcing lockdowns and disrupting economies, false information and hoaxes have spread like wildfire on social media. Miracle cures, intentional disinformation about government policies, and wild claims that Bill Gates orchestrated the entire health crisis abound.

In the past, Facebook has been heavily criticised for failing to take action to stop its platform being used to facilitate the spread of misinformation. To be sure, coronavirus falsehoods are still easily found on Facebook — but the company has taken more decisive action than in previous years:

• For starters, Facebook is now displaying warning messages to people who have shared false information about COVID-19. They're imperfect — Stat reported that they may be too vague in their wording to have a major impact — but it's a step further than Facebook has taken on misinformation in the past.
• The company is also taking down event pages for events that reject mainstream science on coronavirus by calling on people to flout lockdown rules.
• And it is banning "Plandemic," a conspiratorial video about coronavirus that has been going viral on social media and contains numerous falsehoods.

But Facebook's actions to combat COVID-19 misinformation may backfire — in the sense that it has the potential to dramatically increase pressure on the company to take stronger action against other forms of misinformation.

The company has long struggled with how to handle fake news and hoaxes; historically, its approach is not to delete them, but to try to artificially stifle their reach via algorithmic tweaks. Despite this, pseudoscience, anti-government conspiracy theories, and other falsehoods still abound on the social network.

Facebook has now demonstrated that it is willing to take more decisive action on misinformation, when the stakes are high enough. Its critics may subsequently ask why it is so reticent to combat the issue when it causes harm in other areas — particularly around other medical misinformation.

One expected defence for Facebook? That it is focused on taking down content that causes "imminent harm," and while COVID-19 misinformation falls into that category, lots of other sorts of falsehoods don't.

However, using "imminence" as the barometer of acceptability is dubious: Vaccine denialism directly results in the deaths of babies and children. That this harm isn't "imminent" doesn't make it any less dangerous — but, for now, such material is freely posted on Facebook.

Far-right conspiracy theories like Pizzagate, and more recent, Qanon, have also spread on Facebook — stoking baseless fears of shadowy cabals secretly controlling the government. These theories don't intrinsically incite harm, but have been linked to multiple acts of violence, from a Pizzagate believer firing his weapon in a pizza parlour to the Qanon-linked killing of a Gambino crime boss. (Earlier this week, Facebook did take down some popular QAnon pages — but for breaking its rules on fake profiles, rather than disinformation.)

And Facebook is still full of groups rallying against 5G technology, making evidence-free claims about its health effects (and now, sometimes linking it to coronavirus in a messy web). These posts exist on a continuum, with believers at the extreme end attempting to burn down radio towers and assault technicians; Facebook does take down such incitements to violence, but the more general fearmongering that can act as a gateway to more extreme action remains.

This week, Facebook announced the first 20 members of its Oversight Board — a "Supreme Court"-style entity that will review reports from users make rulings as to what objectionable content is and isn't allowed on Facebook and Instagram, with — in theory — the power to overrule the company. It remains to be seen whether its decisions may affect the company's approach for misinformation, and it still needs to appoint the rest of its members and get up and running.

For now, limits remain in place as to what Facebook will countenance in its fight against coronavirus-specific misinformation.

CEO Mark Zuckerberg said the company would immediately take down posts advertising dangerous false cures to COVID-19, like drinking bleach. It is "obviously going to create imminent harm," he said in March. "That is just in a completely different class of content than the back-and-forth accusations a candidate might make in an election."

But in April, President Donald Trump suggested that people might try injecting a "disinfectant" as a cure, which both has the potential to be extremely harmful, and will not cure coronavirus.

Facebook is not taking down video of his comments.

Do you work at Facebook? Contact Business Insider reporter Rob Price via encrypted messaging app Signal (+1 650-636-6268), encrypted email (robaeprice@protonmail.com), standard email (rprice@businessinsider.com), Telegram/Wickr/WeChat (robaeprice), or Twitter DM (@robaeprice). We can keep sources anonymous. Use a non-work device to reach out. PR pitches by standard email only, please.

SEE ALSO: Facebook announced the first 20 members of its oversight board that will decide what controversial content is allowed on Facebook and Instagram

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Protease-activated receptor 2 (PAR-2) is activated by secreted proteases from immune cells or fungi. PAR-2 is normally expressed basolaterally in differentiated nasal ciliated cells. We hypothesized that epithelial remodeling during diseases characterized by cilial loss and squamous metaplasia may alter PAR-2 polarization. Here, using a fluorescent arrestin assay, we confirmed that the common fungal airway pathogen Aspergillus fumigatus activates heterologously-expressed PAR-2. Endogenous PAR-2 activation in submerged airway RPMI 2650 or NCI–H520 squamous cells increased intracellular calcium levels and granulocyte macrophage–colony-stimulating factor, tumor necrosis factor α, and interleukin (IL)-6 secretion. RPMI 2650 cells cultured at an air–liquid interface (ALI) responded to apically or basolaterally applied PAR-2 agonists. However, well-differentiated primary nasal epithelial ALIs responded only to basolateral PAR-2 stimulation, indicated by calcium elevation, increased cilia beat frequency, and increased fluid and cytokine secretion. We exposed primary cells to disease-related modifiers that alter epithelial morphology, including IL-13, cigarette smoke condensate, and retinoic acid deficiency, at concentrations and times that altered epithelial morphology without causing breakdown of the epithelial barrier to model early disease states. These altered primary cultures responded to both apical and basolateral PAR-2 stimulation. Imaging nasal polyps and control middle turbinate explants, we found that nasal polyps, but not turbinates, exhibit apical calcium responses to PAR-2 stimulation. However, isolated ciliated cells from both polyps and turbinates maintained basolateral PAR-2 polarization, suggesting that the calcium responses originated from nonciliated cells. Altered PAR-2 polarization in disease-remodeled epithelia may enhance apical responses and increase sensitivity to inhaled proteases.

JF Oram
Dec 1, 1996; 37:2473-2491
Reviews

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Research

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Research Event

Genetic and genomic research has greatly advanced our understanding of heart disease. Yet, comprehensive, in-depth, quantitative maps of protein expression in hearts of living humans are still lacking. Using samples obtained during valve replacement surgery in patients with mitral valve prolapse (MVP), we set out to define inter-chamber differences, the intersect of proteomic data with genetic or genomic datasets, and the impact of left atrial dilation on the proteome of patients with no history of atrial fibrillation (AF).  We collected biopsies from right atria (RA), left atria (LA) and left ventricle (LV) of seven male patients with mitral valve regurgitation with dilated LA but no history of AF. Biopsy samples were analyzed by high-resolution mass spectrometry (MS), where peptides were pre-fractionated by reverse phase high-pressure liquid chromatography prior to MS measurement on a Q-Exactive-HF Orbitrap instrument. We identified 7,314 proteins based on 130,728 peptides. Results were confirmed in an independent set of biopsies collected from three additional individuals. Comparative analysis against data from post-mortem samples showed enhanced quantitative power and confidence level in samples collected from living hearts. Our analysis, combined with data from genome wide association studies suggested candidate gene associations to MVP, identified higher abundance in ventricle for proteins associated with cardiomyopathies and revealed the dilated LA proteome, demonstrating differential representation of molecules previously associated with AF, in non-AF hearts. This is the largest dataset of cardiac protein expression from human samples collected in vivo. It provides a comprehensive resource that allows insight into molecular fingerprints of MVP and facilitates novel inferences between genomic data and disease mechanisms. We propose that over-representation of proteins in ventricle is consequent not to redundancy but to functional need, and conclude that changes in abundance of proteins known to associate with AF are not sufficient for arrhythmogenesis.

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Inflammation contributes to ventricular remodeling after myocardial ischemia, but its role in nonischemic heart failure is poorly understood. Local tissue inflammation is difficult to assess serially during pathogenesis. Although ¹⁸F-FDG accumulates in inflammatory leukocytes and thus may identify inflammation in the myocardial microenvironment, it remains unclear whether this imaging technique can isolate diffuse leukocytes in pressure-overload heart failure. We aimed to evaluate whether inflammation with ¹⁸F-FDG can be serially imaged in the early stages of pressure-overload–induced heart failure and to compare the time course with functional impairment assessed by cardiac MRI. Methods: C57Bl6/N mice underwent transverse aortic constriction (TAC) (n = 22), sham surgery (n = 12), or coronary ligation as an inflammation-positive control (n = 5). MRI assessed ventricular geometry and contractile function at 2 and 8 d after TAC. Immunostaining identified the extent of inflammatory leukocyte infiltration early in pressure overload. ¹⁸F-FDG PET scans were acquired at 3 and 7 d after TAC, under ketamine-xylazine anesthesia to suppress cardiomyocyte glucose uptake. Results: Pressure overload evoked rapid left ventricular dilation compared with sham (end-systolic volume, day 2: 40.6 ± 10.2 μL vs. 23.8 ± 1.7 μL, P < 0.001). Contractile function was similarly impaired (ejection fraction, day 2: 40.9% ± 9.7% vs. 59.2% ± 4.4%, P < 0.001). The severity of contractile impairment was proportional to histology-defined myocardial macrophage density on day 8 (r = –0.669, P = 0.010). PET imaging identified significantly higher left ventricular ¹⁸F-FDG accumulation in TAC mice than in sham mice on day 3 (10.5 ± 4.1 percentage injected dose [%ID]/g vs. 3.8 ± 0.9 %ID/g, P < 0.001) and on day 7 (7.8 ± 3.7 %ID/g vs. 3.0 ± 0.8 %ID/g, P = 0.006), though the efficiency of cardiomyocyte suppression was variable among TAC mice. The ¹⁸F-FDG signal correlated with ejection fraction (r = –0.75, P = 0.01) and ventricular volume (r = 0.75, P < 0.01). Western immunoblotting demonstrated a 60% elevation of myocardial glucose transporter 4 expression in the left ventricle at 8 d after TAC, indicating altered glucose metabolism. Conclusion: TAC induces rapid changes in left ventricular geometry and contractile function, with a parallel modest infiltration of inflammatory macrophages. Metabolic remodeling overshadows inflammatory leukocyte signal using ¹⁸F-FDG PET imaging. More selective inflammatory tracers are requisite to identify the diffuse local inflammation in pressure overload.

Research Event

This awards ceremony, honoring the 2011 recipients of the E Pluribus Unum Prizes — a national awards program for exceptional immigrant integration initiatives — featured panel discussions with the awardees and federal officials and remarks by White House Director of Intergovernmental Affairs Cecilia Muñoz and Assistant Secretary of Education Brenda Dann-Messier.

This awards ceremony, honoring the 2011 recipients of the E Pluribus Unum Prizes -- a national awards program for exceptional immigrant integration initiatives -- featured panel discussions with the awardees and federal officials and remarks by White House Director of Intergovernmental Affairs Cecilia Muñoz and Assistant Secretary of Education Brenda Dann-Messier.

This awards ceremony honored the 2013 winners of the E Pluribus Unum Prizes, which provides $50,000 prizes to exceptional U.S. immigrant integration initiatives. The awardees took part in a panel discussion with White House and state officials, followed by remarks from Congressman Luis Gutierrez and U.S. Senator Amy Klobuchar.

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OBJECTIVE

To determine the effects of dapagliflozin in patients with heart failure (HF) and type 2 diabetes mellitus (T2DM) on left ventricular (LV) remodeling using cardiac MRI.

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