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#force

2 posts2 participants0 posts today
Continued thread
Public
Nonilex

#Trump’s WH budget office has sought to understand the potential cost to maintain #Greenland if it were acquired…. They are also attempting to estimate what #revenue the #US #Treasury could gain from Greenland’s #NaturalResources.

…Trump has said repeatedly that the US will “get” Greenland.

“100%,” he told NBC News on Sat. Asked whether it would involve #force, he said that there is a “good possibility that we could do it without #military force” but that “I don’t take anything off the table.”

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Antoine

Je viens de traverser Paris Montparnasse - gare de Lyon en 25 min en courant avec ma valise de 40 kg. On aurait dit un film avec Virginie Effira.
L’accueil embarquement s’est fait sous les encouragements des contrôleurs et la porte s’est littéralement refermée sur moi 😌
J’espère qu’ils prendront Hugo Becker ou Louis Garrel pour jouer mon rôle.
#Force a ma voisine de wagon qui m’a entendu faire un remake d’accouchement pendant les 30 min pour m’en remettre.

Replied in thread
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doboprobodyne

@RussCheshire

I'm usually a bit wary of boosting news articles where I'd like to know more of the story before forming an opinion. For this story though, I think it worthy of a boost regardless. Sadly I can't expect to ask anyone for the minutes of the meeting because, well, it got raided by the police. I'd dearly love to know if any of the police thought "Gee, we're going to break into a quaker meeting house and arrest people... are we modestly sure this is a proportional use of force?".

I hate to reduce things to pithy memes, and we have some superb civilian police officers in the UK who do a very difficult job, but I can't help but think of the Mitchell & Webb "Hans... Are we the baddies?" sketch.

I'm told it takes a very special person to flourish in the met police, and I assume policing a capital has nuances that are less relevant elsewhere. I'm disappointed that their surveillance apparatus was not felt capable of monitoring them adequately, and that it was felt force was necessitated.

"Are we the baddies?": m.youtube.com/watch?v=ToKcmnrE

YouTubeMitchell and Webb: "Are we the baddies?"By CrystalRoseCreations
#ethics#law#lawfare
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Rxiv mechanobio

📰 "Ca (2+) increases cardiac muscle viscoelasticity independent of active force development"
doi.org/doi:10.1101/2025.02.26
pubmed.ncbi.nlm.nih.gov/400604
#Mechanical #Myosin #Force

bioRxiv · Ca2+ increases cardiac muscle viscoelasticity independent of active force developmentIn addition to activation of muscle contraction by Ca2+, recent studies suggest that Ca2+ also affects muscle passive mechanical properties. The goal of this study was to determine if Ca2+ regulates the stiffness of cardiac muscle, independent of active contraction. The mechanical response to stretch for mouse demembranated cardiac trabeculae was probed at different Ca2+ levels after eliminating active contraction using a combination of two myosin ATPase inhibitors: para -nitroblebbistatin (PNB, 50 μM), plus mavacampten (Mava, 50 μM). Myocardial force level was assessed during large stretches (≍ 20% initial muscle length) with a range of stretch velocities. For relaxed muscle, in response to stretch, muscle force rose to a peak and then decayed toward a lower steady-state level, consistent with the viscoelastic nature of cardiac muscle. Peak force was higher with faster stretch velocity, but the steady-state force was independent of stretch velocity, consistent with the presence of both apparent viscous and elastic components of the stretch response. In the presence of the inhibitors PNB plus Mava, when Ca2+ level was increased, active contraction was completely prevented. However, the viscoelastic force response to stretch was markedly increased by high Ca2+ and was > 6-fold higher than at low Ca2+ level. The relationship of viscous force to Ca2+ level had a similar form to the relationship of active force to Ca2+ (measured in the absence of inhibitors), suggesting a common regulatory mechanism is involved. As expected, Ca2+-activated contraction was inhibited by lowering the temperature from 21°C to 10°C. In contrast, the Ca2+-activated viscous property was not inhibited at lower temperature, further suggesting that active contraction and the viscous property involve distinct mechanisms. This study demonstrates that in addition to triggering activation of contraction, Ca2+ also increases the apparent viscous property of cardiac muscle. New and Noteworthy Ca2+ is well-known to trigger activation of muscle contraction. This study demonstrates a new mechanical role for Ca2+ in cardiac muscle involving a >6-fold increase in the apparent muscle viscoelasticity. Activation of a viscous element by Ca2+ might influence the mechanical properties of activated cardiac muscle. ### Competing Interest Statement The authors have declared no competing interest.
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ScienceCommunicator

The Sun ☀️, for the Scientifically Literate, is the nearest Star to planet Earth. And an endless source of energy. Or rather, at least on a timeline of billions of years.

The Sun ☀️, for the Scientifically illiterate, that bright \ shiny yellow circle in the sky.

The Sun ☀️, is an endless source of "wow!" factor for me.

"a red giant," esa.int/Science_Exploration/Sp

FYI, It's ignorant to teach "the end" first!

#science #education #chemistry
#physics #AtomicPhysics #Gravity #force #NuclearFussion

www.esa.intThe SunThe Sun is our nearest star. Nuclear reactions deep within create energy in the form of the light and heat that we need to survive. To generate this energy, the Sun consumes four million tonnes of hydrogen fuel every second, and has done so since it was born, around 4.6 billion years ago.
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Rxiv mechanobio

📰 "Actin crosslinking is required for force sensing at tricellular junctions"
biorxiv.org/content/10.1101/20 #Mechanical #Force #Actin #Cell

bioRxiv · Actin crosslinking is required for force sensing at tricellular junctionsMechanical forces are essential for tissue morphogenesis, but risk causing ruptures that could compromise tissue function. In epithelial tissues, adherens junctions withstand the forces that drive morphogenesis by recruiting proteins that stabilize cell adhesion and reinforce connections to the actin cytoskeleton under tension. However, how junctional actin networks respond to forces in vivo is not well understood. Here we show that the actin crosslinker Fimbrin is recruited to tricellular junctions under tension and plays a central role in amplifying actomyosin contractility and stabilizing cell adhesion. Loss of Fimbrin results in a failure to reorganize actin under tension and an inability to enhance myosin-II activity and recruit junction-stabilizing proteins in response to force, disrupting cell adhesion. Conversely, increasing Fimbrin activity constitutively activates force-response pathways, aberrantly stabilizing adhesion. These results demonstrate that Fimbrin-mediated actin crosslinking is an essential step in modulating actomyosin dynamics and reinforcing cell adhesion under tension during epithelial remodeling. ### Competing Interest Statement The authors have declared no competing interest.
Public
Rxiv mechanobio

📰 "Control of the force-bearing properties of microtubule-associated proteins via stalk/linker regions: insights from the NDC80 complex"
biorxiv.org/content/10.1101/20 #Microtubule #Mechanical #Force

bioRxiv · Control of the force-bearing properties of microtubule-associated proteins via stalk/linker regions: insights from the NDC80 complexMany microtubule-associated proteins (MAPs) function under mechanical loads. Among them, motor proteins and passive couplers link microtubules with other cytoskeletal filaments, membranous structures and diverse scaffolds to enable cell shape changes, locomotion and other important processes. A key kinetochore complex, NDC80, transmits forces from microtubule disassembly to chromosome motion during cell division. Recently, this complex has been shown to detach from microtubules more easily when pulled toward the minus-end of the microtubule than when pulled in the plus-end direction. Here, we used coarse-grained molecular dynamics and Brownian dynamics simulations to explain the asymmetric effect of the directional load on the unbinding of the NDC80 complex from microtubules and then generalized our findings to other MAPs. We found that the lever arm created by the stiff stalk of NDC80 tilted toward the plus-end of the microtubule is critical for asymmetric unbinding of this complex, similar to that of dynein. In contrast, EB-proteins, the microtubule crosslinker PRC1, and kinesins are predicted to lack pronounced unbinding asymmetry, either due to their almost perpendicular anchorage to the microtubule wall or due to the high flexibility of their linker regions proximal to the microtubule-binding domains. Thus, our study highlights some of the design principles of MAPs, explaining how their distal parts can impart, modulate or eliminate the dependence of unbinding on the direction of external loads. This information deepens our understanding of the load-bearing properties and functions of diverse MAPs and may guide the design of synthetic protein systems with predefined mechanical characteristics. ### Competing Interest Statement The authors have declared no competing interest.
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