#electronic transcripts

[rajatjoshiwds]

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[idlingsomewhere]

to me, saying "EDM music" feels like the same thing as saying "chai tea" or "naan bread"

[eyeswaitingfortuesdaynight]

just remembering this absolutely insane dinosaur lawyer we had to deal with today

we sometimes deal with lawyers who are not primarily real estate lawyers, and so don't know anything about real estate because they think it's a cake walk and so also aren't up-to-date with new standards. and this absolute clown of a litigation lawyer was so obstinate about a particular new point that, despite having his mortgage funds at 9 fucking 30 IN THE MORNING, he kept delaying and delaying and delaying to try and strongarm us like this was a case trial and not, you know, a very standard residential real estate transaction, until 5:15 pm, where it would be completely impossible to deliver everything on his end before the deadline at 6 pm, and absolutely fucked over his own clients by not closing today

asshole had to pay my boss' legal fees for this waste of time AND per diem interest on our clients' mortgage and bridge loan in order to secure an extension of the deal to tomorrow. get dunked on, loser

pro tip: never close a sale and purchase of property on the same day because you never know what sort of asshat is working for the other side of the transaction and may completely fuck up everyone's day

[w000ble]

TRANSCRIPT - FROM 31:39

Tim: I found out that atoms don't look anything like every atom I've ever seen drawn looks like. (Bryn: No, that's complete lies) Tim: They're all lies! Bryn: Yep. Tim: Because all of the electrons are basically everywhere in a big cloud of potentialness— (Bryn: Yes, absolutely.) Tim: —and so it wouldn't look anything like every atom I've ever been shown! EXPLAIN!

Bryn: Atoms are drawn like solar systems because... apparently people who draw diagrams of atoms believe children are stupid. Tim: I would have preferred a cloud of— look, here is a globe, the atom is everywhere and nowhere all at the same time— again, if you'd have told me that, and that dude's crazy-ass name, I'd have been much more interested in science! Bryn: (Cracking up) Ben: To be fair though, it would make it much more difficult to count the electrons when you were doing one of those puzzles about like, 'we knock the electron out and what isotope does it become' so you have to count the electrons and work it out. Tim: Just dissolve it into a cloud and go, 'best of luck!' Ben: Yeah exactly, exactly you just flick one out of the cloud and like (PFBBBT) 'Have a guess. :)'

Bryn: This is actually an important point about science— is, y'know we talked about science being a method of understanding truth, or not, as the case may be. Tim: It's an onion of lies! Bryn: —and a lot of science is lies, because what science really is, is a model of the universe; of reality. It's not— you know, it is not necessarily a perfect understanding, and especially when quantum physics was being developed, where we discovered stuff like: an electron is actually a cloud of possibilities, we discovered that the universe is much weirder and harder to understand than we could possibly have imagined before, Tim: So we stopped trying. Ben: (Pffffft) Bryn: Basically, yes. What we have to accept is that our understanding of the universe is what we call a 'model' and the model is only useful as long as it makes predictions. But the model can also be useful, even when it doesn't necessarily reflect reality. And so chemists, to understand chemical reactions, and to understand things like isotopes or chemical bonding between elements— their model of the atom doesn't need to care about the fact that electrons aren't little balls of stuff orbiting around the center of the atom. (Tim: Okay. Alright.) Bryn: Their model allows them to make accurate predictions of the real world based on something that is not technically true, but— We've talked about the scientific method— hypothesis, test conclusion. If their hypothesis is a model that, in certain circumstances, we can say, 'an atom works like this,' and it makes correct conclusions, then it doesn't matter that the real picture is more complicated. And we do this all the time in physics as well. So you've probably both studied— y'know back in school— stuff like the laws of motion, and you probably had to calculate cars moving around, or billiard balls, or things on slopes.

Tim: I was asked to, I can't claim that I ever did— but I was certainly asked to.. Ben: Probably, and at some point I was asked about Boyle's law, and shown a spring, and I was like 'ah, (unintelligible), I dunno.' Bryn: (Cracking up) Sure. In all these examples, we ignore air resistance. Unless you're studying— y'know, and depending on what age you're studying these things, you may or may not ignore friction. But we know these things from our everyday experience exist, and we know that if we wanted to get super accurate results, we'd have to include air resistance and friction, but actually the results that we get by ignoring them are close enough that if we don't need to be 100% accurate, if we're just trying to make a decent prediction, the prediction is good enough most of the time.

Tim: It's spherical chickens again. ((I think this is a reference to the previous Tim & Ben do Science episode)) Bryn: It's spherical chickens in a vacuum, absolutely. And it's an important joke in a way, because what it says is, 'well, reality is complex and messy as we've already established, and science helps us understand it, but if science is making accurate predictions, that's really what's important.' And accurate predictions are essentially specific to a certain field or a certain test. If I say, 'well if I chuck this acid and this alkalide into a cup together, I don't need to know what's going to happen with every single atom inside. What I need to know is what's gonna end up in the cup at the end. Tim: There's potentially a lovely analogy, I think, from cartography where they say 'the only true map is the exact size and shape of the thing you are trying to map.' (Bryn: Absolutely.) Tim: '—but best of luck taking that on a short camper-vanning holiday in the Cotswolds.'

END TRANSCRIPT - AT 35:45

And you're telling me we're supposed to be more engaged, as high school students, with a model by some guy named Bohr than the QUANTUM CAT BOX guy??

[anotherpapercut]

ya boi is officially a licensed substitute teacher in the state of Missouri

[miserye]

Normalize sending slightly bitchy emails to colleges to get them to hurry the fuck up and process the shit you sent to them literally weeks ago

[world-document-services]

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[heartandmusic]

first of all what does this fuck ass grown up job need my transcript for and second of all why am i being charged eight u.s. dollars for the university to email me a pdf

[blueoaknx]

Mitochondrial Dysfunction in Type 2 Diabetes

Introduction

Mitochondria, essential for cellular energy metabolism, play a crucial role in bioenergetics and metabolic homeostasis. Mitochondrial dysfunction has been implicated as a key pathophysiological factor in Type 2 Diabetes Mellitus (T2DM), contributing to insulin resistance, metabolic inflexibility, and beta-cell dysfunction. This review explores the intricate mechanisms underlying mitochondrial impairments in T2DM, including defective oxidative phosphorylation, disrupted mitochondrial dynamics, impaired mitophagy, and excessive reactive oxygen species (ROS) generation, with a focus on potential therapeutic interventions targeting mitochondrial pathways.

Mechanistic Insights into Mitochondrial Dysfunction in T2DM

1. Defective Oxidative Phosphorylation and ATP Synthesis

Mitochondrial oxidative phosphorylation (OXPHOS) occurs through the electron transport chain (ETC), comprising Complexes I-IV and ATP synthase (Complex V). In T2DM, evidence suggests a downregulation of mitochondrial ETC activity, particularly in Complex I (NADH:ubiquinone oxidoreductase) and Complex III (cytochrome bc1 complex), leading to reduced ATP synthesis. This dysfunction is often linked to compromised NADH oxidation and inefficient proton gradient formation, resulting in cellular energy deficits and impaired insulin-stimulated glucose uptake.

2. Elevated Reactive Oxygen Species (ROS) and Oxidative Stress

Mitochondria are a primary source of ROS, predominantly generated at Complex I and Complex III during electron leakage. In T2DM, excess substrate influx due to hyperglycemia leads to mitochondrial overactivation, driving excessive ROS production. Elevated ROS induces oxidative damage to mitochondrial DNA (mtDNA), lipids, and proteins, disrupting mitochondrial integrity and function. Oxidative stress further impairs insulin signaling by activating stress-responsive kinases such as c-Jun N-terminal kinase (JNK) and IκB kinase (IKK), contributing to systemic insulin resistance.

3. Mitochondrial Biogenesis and Transcriptional Dysregulation

Mitochondrial biogenesis is regulated by the transcriptional coactivator Peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC-1α), which modulates downstream transcription factors such as Nuclear Respiratory Factors (NRF-1/NRF-2) and Mitochondrial Transcription Factor A (TFAM). In T2DM, PGC-1α expression is downregulated, impairing mitochondrial biogenesis and reducing mitochondrial density, leading to decreased oxidative capacity in metabolically active tissues like skeletal muscle and liver.

4. Disrupted Mitochondrial Dynamics and Mitophagy

Mitochondrial quality control is maintained through dynamic fission and fusion processes. Fission, mediated by Dynamin-related protein 1 (Drp1), is necessary for mitochondrial fragmentation and mitophagy, while fusion, regulated by Mitofusin 1/2 (Mfn1/2) and Optic Atrophy 1 (OPA1), maintains mitochondrial integrity. In T2DM, an imbalance favoring excessive fission leads to mitochondrial fragmentation, impairing energy metabolism and exacerbating insulin resistance. Moreover, defective mitophagy, regulated by PTEN-induced kinase 1 (PINK1) and Parkin, results in the accumulation of dysfunctional mitochondria, further aggravating metabolic dysfunction.

Implications of Mitochondrial Dysfunction in T2DM Pathophysiology

1. Skeletal Muscle Insulin Resistance

Skeletal muscle accounts for ~80% of postprandial glucose uptake, relying on mitochondrial ATP production for insulin-mediated glucose transport. Impaired mitochondrial function in muscle cells reduces oxidative phosphorylation efficiency, promoting a shift towards glycolysis and lipid accumulation, ultimately leading to insulin resistance.

2. Pancreatic Beta-Cell Dysfunction

Mitochondrial ATP production is essential for insulin secretion in pancreatic beta cells. ATP-sensitive potassium channels (K_ATP) regulate glucose-stimulated insulin secretion (GSIS), with ATP/ADP ratios dictating channel closure and depolarization-induced insulin exocytosis. In T2DM, mitochondrial dysfunction leads to inadequate ATP generation, impairing GSIS and reducing insulin secretion capacity. Additionally, oxidative stress-induced beta-cell apoptosis contributes to progressive loss of beta-cell mass.

3. Hepatic Mitochondrial Dysfunction and Lipid Dysregulation

Mitochondrial dysfunction in hepatocytes contributes to hepatic insulin resistance and non-alcoholic fatty liver disease (NAFLD). Impaired fatty acid oxidation due to dysfunctional mitochondria leads to lipid accumulation, exacerbating hepatic insulin resistance and systemic metabolic dysregulation.

Therapeutic Strategies Targeting Mitochondrial Dysfunction

1. Exercise-Induced Mitochondrial Adaptation

Physical activity upregulates PGC-1α expression, enhancing mitochondrial biogenesis and oxidative metabolism. High-intensity interval training (HIIT) and endurance exercise improve mitochondrial efficiency and reduce oxidative stress, mitigating insulin resistance in T2DM patients.

2. Pharmacological Modulation of Mitochondrial Function

Metformin: Enhances mitochondrial complex I activity, reducing hepatic gluconeogenesis and oxidative stress.

Thiazolidinediones (TZDs): Activate PPAR-γ, promoting mitochondrial biogenesis and improving insulin sensitivity.

Mitochondria-targeted Antioxidants: Agents like MitoQ, SkQ1, and SS-31 reduce mitochondrial ROS, preventing oxidative damage and preserving mitochondrial function.

3. Nutritional and Metabolic Interventions

Ketogenic and Low-Carb Diets: Enhance mitochondrial fatty acid oxidation, reducing lipid accumulation and improving metabolic flexibility.

Intermittent Fasting: Induces mitochondrial biogenesis and autophagy, improving metabolic homeostasis.

Nutraceuticals: Coenzyme Q10, resveratrol, and nicotinamide riboside (NR) enhance mitochondrial function and energy metabolism.

4. Emerging Gene and Cellular Therapies

Gene Therapy: Targeted upregulation of PGC-1α and TFAM to restore mitochondrial function.

Mitochondrial Transplantation: Direct transfer of healthy mitochondria to replace dysfunctional ones, an emerging frontier in metabolic disease management.

Conclusion

Mitochondrial dysfunction is a central determinant in the pathogenesis of T2DM, affecting insulin signaling, glucose metabolism, and lipid homeostasis. Targeting mitochondrial pathways through exercise, pharmacological agents, dietary modifications, and emerging gene therapies offers promising avenues for improving metabolic health in T2DM. 

[muhdanas]

International Diploma in Healthcare Documentation: A Pathway to a Successful Healthcare Career

[scoringeffects]

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[absentlyabbie]

seriously, though. i work in higher education, and part of my job is students sending me transcripts. you'd think the ones who have the least idea how to actually do that would be the older ones, and while sure, they definitely struggle with it, i see it most with the younger students. the teens to early 20s crowd.

very, astonishingly often, they don't know how to work with .pdf documents. i get garbage phone screenshots, sometimes inserted into an excel or word file for who knows what reason, but most often it's just a raw .jpg or other image file.

they definitely either don't know how to use a scanner, don't have access to one, or don't even know where they might go for that (staples and other office supply stores sometimes still have these services, but public libraries always have your back, kids.) so when they have a paper transcript and need to send me a copy electronically, it's just terrible photos at bad angles full of thumbs and text-obscuring shadows.

mind bogglingly frequently, i get cell phone photos of computer screens. they don't know how to take a screenshot on a computer. they don't know the function of the Print Screen button on the keyboard. they don't know how to right click a web page, hit "print", and choose "save as PDF" to produce a full and unbroken capture of the entirety of a webpage.

sometimes they'll just copy the text of a transcript and paste it right into the message of an email. that's if they figure out the difference between the body text portion of the email and the subject line, because quite frankly they often don't.

these are people who in most cases have done at least some college work already, but they have absolutely no clue how to utilize the attachment function in an email, and for some reason they don't consider they could google very quickly for instructions or even videos.

i am not taking a shit on gen z/gen alpha here, i'm really not.

what i am is aghast that they've been so massively failed on so many levels. the education system assumed they were "native" to technology and needed to be taught nothing. their parents assumed the same, or assumed the schools would teach them, or don't know how themselves and are too intimidated to figure it out and teach their kids these skills at home.

they spend hours a day on instagram and tiktok and youtube and etc, so they surely know (this is ridiculous to assume!!!) how to draft a formal email and format the text and what part goes where and what all those damn little symbols means, right? SURELY they're already familiar with every file type under the sun and know how to make use of whatever's salient in a pinch, right???

THEY MUST CERTAINLY know, innately, as one knows how to inhale, how to type in business formatting and formal communication style, how to present themselves in a way that gets them taken seriously by formal institutions, how to appear and be competent in basic/standard digital skills. SURELY. Of course. RIGHT!!!!

it's MADDENING, it's insane, and it's frustrating from the receiving end, but even more frustrating knowing they're stumbling blind out there in the digital spaces of grown-up matters, being dismissed, being considered less intelligent, being talked down to, because every adult and system responsible for them just

ASSUMED they should "just know" or "just figure out" these important things no one ever bothered to teach them, or half the time even introduce the concepts of before asking them to do it, on the spot, with high educational or professional stakes.

kids shouldn't have to supplement their own education like this and get sneered and scoffed at if they don't.

[todays-xkcd]

After initial tests created a series of large holes in the wall of the lab, the higher-power Scanning Tunneling Tennis Ball Microscope project was quickly shut down.

Tennis Balls [Explained]

Transcript Under the Cut

[Cueball fires eight tennis ball at decreasing heights using a tennis ball machine, making four "thunk" noises. Megan is standing behind him.]

[Ten noises come from the right side of the panel.] Bonk Bonk Bonk Bonk Bonk OW! Bonk OW! Bonk Bonk

[Megan has her hand to her chin.] Megan: Ok, there's definitely a person over there. Let's do one more pass to try to measure their height.

[Caption below the panel:] Electrons are small and hard to work with, so some scientists have developed a scanning tennis ball microscope instead.

[thetransia]

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[worldwidetranscript1]

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[world-document-services]

Symbiosis International University, Pune

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