#sarcomeric

[castielsbees]

the manacled brainrot is hitting SO hard today and normally i’d be revelling in it but i have so much studying for anatomy to do i can’t be having my brain occupied like this 😭

[bpod-bpod]

Dis-banded

Just like us, fruit flies are stripy beneath the skin. These sarcomeres – repeating bands of stretchy muscle tissue – contain fibres of myosin (highlighted in green) and actin (purple) griping and pulling at each other – as the sarcomeres shorten, the muscle contracts. This is heart muscle from fruit flies (Drosophila), used to investigate common faults in human heart disease. Compared to healthy muscle at the top, the sarcomeres at the bottom are much looser and swollen – in these hearts, researchers used RNA interference to hamper the activity of a protein called filamin, often shown to be altered in heart diseases like hypertrophic cardiomyopathy. Yet altering its activity in a different way – using CRISPR gene editing to change its structure – did not affect the flies as expected. Further studies might aim to solve this mystery, while altering genes and proteins reveals more about what we do, or perhaps don’t, have in common with Drosophila.

Written by John Ankers

Image from work by Flavie Ader and colleagues

Université Paris Cité, Paris, France

Image originally published with a Creative Commons Attribution – NonCommercial – NoDerivs (CC BY-NC-ND 4.0)

Published in Biology Open, September 2022

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[simonh]

Dystrophin Abnormalities in Neuormuscular Disease by National Library of Medicine Via Flickr: Series Title(s): NIH director's Wednesday afternoon lecture series Contributor(s): Kunkel, Louis M. National Institutes of Health (U.S.) Publication: [Bethesda, Md. : National Institutes of Health, 1990] Language(s): English Format: Still image Subject(s): Neuromuscular Diseases, Dystrophin Genre(s): Posters Abstract: Predominantly gray poster with red and white lettering announcing a lecture given Nov. 1990 by Louis M. Kunkel, Ph.D., prof. of genetics at Harvard Medical School. Visual image is an abstraction of the myosin and actin filaments of a sarcomere, depicted with yellow and gray rods. The first iteration shows the rods in a close formation, as in a normal, contracted muscle; they become separated by greater distances in the iterations below. All text near bottom of poster. Extent: 1 photomechanical print (poster) : 72 x 43 cm. Technique: color NLM Unique ID: 101449377 NLM Image ID: A030719 Permanent Link: resource.nlm.nih.gov/101449377

[estefanyailen]

[ooppo]

Hello everyone. Tendons are connected to muscles, which consist of fascial, which consist of muscle fibers, which consist of myofibril. Those myofibril have a sarcoplasmic coating, and are surrounded by T-Tubules which act as pores for the presynaptic site for neurotransmitters coming from motor neurons. Myofibril consists of many sarcomeres, connected together by z-plates. These sarcomeres are made up of thick and thin filaments. The thick filaments are made of myosin, and the thin filaments are made of actin. In muscle contraction, ATP is used to unbind the myosin heads from the actin. It then breaks down ATP into ADP and P. The P leaves the site, causing ADP to have a reaction with the myosin head. The myosin head stands upright and connects with the actin before releasing the ADP. This cycle must repeat many times to have a noticeable muscle contraction.

[charmcoin]

studying muscles is actually super fascinating because like... i'm taking handwritten notes on my ipad and i'm very aware of the movement of my hands the entire time i'm doing this. just continually looking from the online textbook to my hand holding my pencil and back again as my hands move over the screen and adjust the movement of the pencil to write words. and thinking about the hundreds of muscle fibers being activated not just in my hand, but in my wrist and arm as i write, and the thousands of sarcomeres contracting in those hundreds of muscle fibers almost instantaneously to move my hands and write my notes.

when you're studying biological processes it seems like time sort of slows down--the movement of actin against myosin takes a couple seconds, drawn out so it's easier to observe. it's easy to forget that this is happening a million billion times per second all over your body forever

[humancelltournament]

Propaganda!

Smooth muscle is an involuntary non-striated muscle, so-called because it has no sarcomeres and therefore no striations. Smooth muscle is found in the walls of hollow organs, including the stomach, intestines, bladder and uterus.

Phosphocreatine, also known as creatine phosphate, is a phosphorylated form of creatine that serves as a rapidly mobilizable reserve of high-energy phosphates in skeletal muscle, myocardium and the brain to recycle adenosine triphosphate, the energy currency of the cell.

[youwantedavillain]

Lol She Dmed Me! Let's Analyze It! (Part 6)

Alright let's continue our analysis! The library is open~

If we look at the first one (Dm56) we see her trying to manipulate the situation to make it look like she is virtuous and a martyr when she isn't which is revealed later on in the next few dms (61-67).

I repeatedly point at everything she says. She said before in the previous parts that she wanted attention -- thus the pointing out of "pity points". I again reinstate that I don't believe her due to the many times she has lied to me for her own benefit behind my back in a place that I couldn't reach nor ever know about. I outright state that if she didn't like me pointing out her vile actions then she shouldn't have done them in the first place -- this actively shows that she knows what she did was wrong and extremely disgusting, but it got her rocks off. I then, once again, point out her need for attention by showing her that her confession post got several hits and congratulate her on getting exactly what she wanted, me as her mighty Villain that she must take down at any cost and all the attention. She actively got what she wanted through manipulation and puppet strings. I'm ostracized from her friend group -- they will never believe me, no matter how many screenshots I have, they will not even glance at them or ever hear me out -- and smeared my name so hard that I can no longer even look at it without having those memories come back up. Plus, she now has all the attention she wants.

Upon looking at Dm61 you are probably confused but are also remembering the previous parts. She once again shows that she didn't work on herself as we pointed out previously. She also denied me the ability to try to give everyone a chance to have closure and give me a chance to "redeem myself" despite being the innocent party SEVERAL TIMES. She was uncomfortable because she knew that if I rejoined I wouldn't talk to her anymore and thus she wouldn't have ammunition and people would start realizing that she was full of shit.

Two months later I met Sarcomere after hearing that they had a problem with one of my character designs immensely. Upon meeting up they mentioned that I was nothing like @felicitythekittycat had ever said I was. Well, I told them the truth and they gave me a bombshell of evidence. Upon getting it my mental health took a nose dive off of the nearest cliff and I threatened @felicitythekittycat with a Defamation Lawsuit. She actively admits in this Dm(Dm63) that she wouldn't have stopped if I hadn't done this and acts as though her stopping due to the threat gives her ANY merit or goodwill.

It does not. In fact, it makes her look worse.

It's like a school bully constantly beating up a kid that doesn't fight back up until said kid has enough and gets the heaviest object in the room and starts beating the bully with it. The bully only stops when they realize that their victim has had enough of their shit.

I again ask.... HOW WAS IT MUTUALLY TOXIC? I did nothing. Just exist. She is actively trying to imply that I did something similar when I didn't. The symbolism here is amazing to me because she actually pulled this move previously once before. Not here mind you. Somewhere different. There is a secret player here that I have yet to mention. And that is my stalker: Kronostitan100.

I'd prefer it if I could do another post exclusively about him, but I have no other choice in the matter. Maybe in the future, I'll reiterate my points here in a post exclusive to him.

Kronostitan100 was about two years my junior when we met while I was in High School. We met during a chess game before classes started after lunch. After that game we became friends. I was never interested in him but he pursued me like it was he was a soldier on a mission. Even when I graduated and headed off to college he wouldn't stop the pursuit. He would text me from the moment I woke up to the moment I went to bed. He wouldn't listen to me when I said something made me uncomfortable. He didn't take "No" for an answer. Just claim he did but would still continue the pursuit. Even going as far as making confessions of love extremely often. He would also go as far as getting my friends to dogpile me extremely often by claiming that I told him to kill himself and the like. I'd often find my cellphone with missed phone calls and mountains of text messages all because I made an offhanded comment that he somehow twisted into being negative and about him personally. I remember one, in particular, was me commenting that his laptop was slow, and this somehow got him to run out into a snowstorm crying, only for one of his closest friends to start berating me. Another was when I kept telling him I was in my History Class at a college, and he wouldn't stop texting me, so I turned off my phone so it wouldn't go off only for me to get home and find several missed phone calls and texts telling me I'm the biggest bitch the world has ever seen and the world would be better off without me. One day I hit my limit and decided that something drastic had to happen to get him off of my back. So I faked a suicide attempt. I do regret it and find my current depression to be a bit of well-deserved karma. It took me 8 years to get rid of him (hopefully, I'm still scared he's stalking me). However, @felicitythekittycat was the one to egg me on.

She even told him that she thought he deserved what he got.

Sounds familiar, doesn't it?

Also, those "traces of me on the internet" she found.... was likely just me posting a final picture to deviantart of my oc killing herself: Social Suicide (Vent Art -- TW: S-icide) by Tailsgothicangel on DeviantArt

What a wonderful trace showing that I'm TOTALLY okay. TOTALLY...

What? I'm TOTALLY FINE!

Next... they claim that they thought about what I said before I initially blocked her... but that's bullshit because they claimed it was "mutually toxic" only a paragraph earlier, and in the beginning of this whole conversation they claimed they didn't know they should've reached out earlier. Also "rumors" is a pretty light word for "Ruining someone's social life and mental health so badly that they become suicidally depressed and were accused of committing the same crimes that traumatized them as a child.". Someone call a doctor; I think she shot herself in the foot with a shotgun here.

How-fucking-dare, you claim that jealousy wasn't a motive. Why were you scared that I was gonna ruin you? Because you were spreading lies? Because I had friends? With my "success" which I don't have, I was gonna specifically hurt you for what again? How is this not jealousy and paranoia? You were bitter because your friends were supporting my projects like they do with yours? I don't get how this is supposed to be "mutually toxic". Sounds more like a lie that you are trying to use to cover your ass as you fall into the fucking lava pit you dug yourself into. I can't grill this whore more than I did in Part 2 over this part of her paragraph.

So.... "I don't care about the damage I did but I know it hurt you, I looked just enough to know that you suffered because I did it all deliberately because it made me wet UwU". That is what that statement says to me.

"I don't want to portray you as the Villain" tell that to what you said in your previous paragraphs and that "Mutually Toxic" claim. Also, you claim to want to confess to your previous fuck-ups... yet here you are lying your ass off to try to take the heat off of you. You also claim to want to help me... but it looks to me like you are just trying to help yourself.

You were jealous of the attention I got from your friends and were thus threatened by it.

You were also envious of my skills.

Boo.

Fucking.

Hoo.

Cry some more.

[fmarkets]

Operating expenses on the rise for Edgewise Therapeutics Inc in Q1 2024 $EWTX #Major Pharmaceutical Preparations #Nasdaq

EWTX recorded first quarter of 2024 operating loss of $-34.753 millionThe recent announcement from Edgewise Therapeutics regarding the initiation of the Phase 2 CIRRUS-HCM trial for their oral medication EDG-7500 suggests potential positive implications for the company going forward. With EDG-7500 being a selective cardiac sarcomere modulator, it aims to address specific issues related to impaired cardiac relaxation and slower early contraction velocity seen in patients with Obstructive Hypertrophic Cardiomyopathy (HCM)

[bpod-bpod]

Disc Error

Studying life is often a matter of peeling back layers, revealing its workings piece by piece like a watchmaker with a pair of pliers. And when human tissues reveal something surprising, researchers often turn to simpler, similar organisms like fruit flies to fill in the gaps. Following their discovery of 'branches' between human sarcomeres – the short stretchy units that make up muscle fibres – a team of muscle biologists turns to the fly for answers. Yet they find altering the proteins involved also creates defects elsewhere in the muscle. Here they use 3D electron microscopy and artificial colours to highlight 'holes' in parts of the fly’s fibres called z-discs that the sarcomeres usually pull against to create tension. Revealing the delicate balances at play in muscle biology, the scientists are now looking for new ways to explore the role of branching in generating muscular forces.

Written by John Ankers

Video from work by Peter T. Ajayi and Prasanna Katti, and colleagues

Muscle Energetics Laboratory, NHLBI, NIH, Bethesda, MD, USA

Video originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in Nature Communications, May 2022

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[leedsomics]

Single nucleus transcriptomics supports a role for CCNA2-induced human adult cardiomyocyte cytokinesis

Cyclin A2 (CCNA2) is a master regulatory gene of the cell cycle that is normally silenced in postnatal mammalian cardiomyocytes. We have previously demonstrated that it can induce significant cardiac repair in both small and large animals when delivered to the heart via a viral vector. To date, whether CCNA2 gene delivery can induce cytokinesis in isolated cardiomyocytes from adult human hearts has not been investigated. Therefore, we designed a human gene therapy vector featuring a replication-deficient, E1/E3-deleted human adenovirus 5 encoding human CCNA2 driven by the cardiac Troponin T promoter to enable expression of CCNA2 in freshly isolated human cardiomyocytes. Utilizing time-lapse microscopic live imaging of cultured adult human cardiomyocytes isolated from a 21-year-old male, 41-year-old female, and 55-year-old male, we now report that human adult cardiomyocytes can be induced to undergo complete cytokinesis in response to CCNA2 gene delivery with preservation of sarcomere integrity in the resultant daughter cells. To elucidate the mechanistic underpinnings of CCNA2-dependent gene regulation in governing cardiomyocyte cytokinesis, we conducted single nucleus transcriptomics (SnRNA-seq, 10X Genomics) analysis in hearts isolated from adult transgenic mice that constitutively express CCNA2 in cardiomyocytes (CCNA2-Tg) and non-transgenic mice (NTg). Remarkably, we identified a subpopulation of cardiomyocytes enriched with cytokinesis, proliferative, and reprogramming genes in hearts obtained from CCNA2-Tg mice as compared to hearts obtained from NTg mice. We also performed bulk RNA sequencing of human adult and fetal hearts, and we identified key reprogramming genes that are targets for CCNA2-induced cytokinesis. These results provide a compelling pathway forward for the clinical development of cardiac regenerative therapy based on strategic manipulation of the cardiomyocyte cell cycle. http://dlvr.it/T3Xhr9

[fruit-worm-papers]

Segregated localization of two calponin-related proteins within sarcomeric thin filaments in Caenorhabditis elegans striated muscle

http://dlvr.it/Sx0fQj

[afactaday]

#aFactADay2023

#769: the other process which causes muscle contractions is called the cross-bridge cycle. all along the myosin filaments are tiny protrusions called "cross-bridges" each with two little heads that point at the actin filaments. let's start with a nerve impulse: this comes straight from the brain and the fibres release calcium 2+ ions (charged particles and therefore quite reactive) into the cytoplasm. the calcium goes through a complex dance with "tropomyosin" which basically has the effect of removing a barrier from the actin. this reveals a bunch of active sites on the actin which can bond to the myosin heads. the heads each still have a residue ADP*, phosphate ion* and potential energy from the previous cycle, but in bonding to the actin they drop the phosphate. they then use said energy to perform a "power stroke", which exerts a force of about 2 piconewtons on the actin filament, pushing it backwards (or the myosin forwards). this results in the shortening of the sarcomere, which is the contraction we wanted with our initial nerve impulse. but all is not finished: during the power stroke, the ADP is dropped, leaving the head naked and attached to the actin. it remains this way until an ATP* comes along and attaches itself to the head, which detaches from the actin. the head moves back forwards to its original position but in doing so hydrolyses* the ATP. this fills it with energy (ready for the next power stroke) and allows it to reattach to a new active site on the actin filament, thus restarting the cycle. this cycle occurs many times in a single contraction, all insanely quickly and on such a small scale but in so many different places all at once to result in precise and powerful macromovements of your body.

if you're still confused (it took me a literal whole week to get it) then i'll try to simplify it:

a thick wall with arms sticking out is next to a thin wall.

the arms grab and pull on the thin wall backwards, which makes the room smaller.

the arms are now in an awkward backwards position but need energy from magical batteries to move back forwards.

they get this energy and let go of the wall to move forwards. the cycle repeats and the room becomes increasingly smaller.

*ATP, adenosine triphosphate, is basically the "battery" of a cell. it is a base group (adenosine) with three phosphate ions attached. these ionic molecules can be "hydrolysed" (broken down - think of it like snapping off and releasing energy in the process) which powers the functions of a cell. obviously the snapping means you end up with ADP, adenosine diphosphate and a phosphate ion.

how does the energy get into the batter in the first place, i hear you ask? well, the mitochondria are the powerhouse of the cell :P

[ugsource]

The Scientific Research of Muscle Hypertrophy

Raising muscular tissue mass is an important goal for numerous professional athletes, particularly those associated with stamina sporting activities like football as well as powerlifting. It is likewise the primary objective of UGSOURCE bodybuilders.

Muscular tissue hypertrophy is brought on by a boost in the dimension of muscle cells. This increase happens as a result of resistance training, which entails modern overload.

Cellular Hydration

Muscular tissue mass is a key purpose of numerous professional athletes, especially those associated with strength sports like Football, rugby and also powerlifting. It is likewise gone after by bodybuilders, that look for to raise both the size as well as toughness of their muscles with anabolic supplementation as well as training protocols.

A vital consider muscle hypertrophy is an increase in cell volume. This increase is driven by a combination of elements, including anabolic protein synthesis as well as the expansion of non-contractile cell components (e.g. sarcoplasmic reticulum and t-tubules).

A second consider muscle mass hypertrophy is a rise of the number of sarcomeres within an offered myofibril. This can be achieved by either adding sarcomeres in collection to existing fibers or by creating completely new myofibrils through myofibrillogenesis.

Mechanical Tension

Many innovative toughness trains comprehend that mechanical stress is a key component in muscle mass development. However, they commonly concentrate entirely on the extraction of muscular hypertrophy with the use of high-load resistance training.

This is because it's usually believed that just heavy loads generate the required mechanical stress to make muscular tissues expand. While this might be true for the total muscle mass, it is not necessarily real for private muscle fibers.

For instance, if you perform a collection of bicep curls with 80% of your 1RM for a number of sets, you will certainly experience similar mechanical tension to doing a deadlift with a light tons. The difference is that the force-velocity partnership on your specific arms fibers will certainly be various, but your overall muscle contraction will certainly be the same.

The trick to optimizing growth is not simply boosting the quantity of mechanical stress, yet also switching over up your workout regular and including brand-new activity patterns. This will certainly guarantee your body needs to re-adapt as well as react to the new stimulations, setting off hypertrophy.

Metabolic Stress and anxiety

For body builders, professional wrestlers and also your favorite concealed (or caped) superheroes, loading on the muscular tissue mass is the large reward for their dedication to physical training. Muscle growth happens when muscle mass protein synthesis is higher than failure, resulting in a general positive internet equilibrium of muscle mass tissue.

When we perform exercises calling for considerable mechanical anxiety such as eccentric contractions and high-intensity interval training, we create metabolic stress that develops metabolites like lactate, hydrogen ion as well as not natural phosphate in muscle. This build-up is thought to raise neural drive, as well as in turn, even more motor systems are hired to finish the exercise.

One more concept is that this metabolic stress and anxiety stimulates development via a variety of anabolic signaling paths including hypoxia, hormone launch, mobile swelling and the manufacturing of reactive oxygen species. Nonetheless, placing evidence suggests that muscular tissue damages is not a key stimulus for hypertrophy. Thus, it's finest to prevent concentrating on muscle damages when training for hypertrophy and rather prioritize the various other devices gone over above.

Apoptosis

Muscular tissue development takes place when muscular tissue protein synthesis exceeds healthy protein break down. This produces a positive web equilibrium of healthy protein that promotes lean mass development. On the other hand, when the web healthy protein balance is negative, muscular tissue degeneration happens.

A vital factor in identifying muscle hypertrophy is the capacity of satellite cells to proliferate as well as fuse with existing myofibers, creating new myotubes (187 ). Normally quiescent, satellite cells become activated by mechanical anxiety, such as resistance exercise. When activated, they release anabolic endocrine signals as well as development elements that advertise the combination of satellite cells right into myotubes.

It is not yet clear whether the decrease in myonuclear domain dimension that is seen throughout atrophy induced by detraining, hind arm or leg suspension, as well as microgravity is triggered by apoptosis of muscle mass centers or one more device. Nevertheless, the recent finding that DIAP1 suppression decreases atrophy in skeletal muscular tissues recommends that apoptosis plays a role in muscular tissue degeneration.

[ameerunsblog]

General Anatomy Muscles Notes And Important Questions With Answers

[vasanthasworld]

General Anatomy Muscles Notes And Important Questions With Answers