If you shine light of high enough energy on to a metal, electrons will be emitted from the metal.

More from NotTheMacAnon

In continuum mechanics, stress is a physical quantity that expresses the internal forces that neighbouring particles of a continuous material exert on each other, while strain is the measure of the deformation of the material.

For example, when a solid vertical bar is supporting an overhead weight, each particle in the bar pushes on the particles immediately below it. When a liquid is in a closed container under pressure, each particle gets pushed against by all the surrounding particles.

The container walls and the pressure-inducing surface (such as a piston) push against them in (Newtonian) reaction.

These macroscopic forces are actually the net result of a very large number of intermolecular forces and collisions between the particles in those molecules. Stress is frequently represented by a lowercase Greek letter sigma (σ).

Residual stresses inside a plastic protractor are revealed by the polarized light.

NotTheMacAnon
@NotTheMacAnon1

Transduction is the process by which foreign DNA is introduced into a cell by a virus or viral vector.

Viral vectors are tools commonly used by molecular biologists to deliver genetic material into cells.

Viruses have evolved?

specialized molecular mechanisms

to efficiently

transport their genomes

inside the cells they infect.

Delivery of genes, or other genetic material, by a vector is termed transduction and the infected cells are described as transduced.

A transducer is a device that converts energy from one form to another. Usually a transducer converts a signal in one form of energy to a signal in another.

NotTheMacAnon
@NotTheMacAnon1

2020 marks the start of the quantum dot revolution.

Completely ignoring the fact that "photocatalytic generation of reactive oxygen species (ROS) from quantum dots (QDs) has been widely reported."

Results: It was found that whereas singlet oxygen (1O2) was not produced by photoexcited QDs, superoxide anion(O2− )and hydroxyl radicals(OH) were generated by QDs, especially in the presence of a physiological concentration of electron donating agent including NADH.

Using cell metabolic activity assays and various probes of ROS generation, the formation of ROS in cellular environments was demonstrated.

Conclusion: Illumination of QD-treated cells and bacteria with light did affect viability. The above results, together with those of assays in the presence of various scavengers of specific ROS, indicate that the formation of ROS by QDs mainly proceeded via electron transfer.

NotTheMacAnon
@NotTheMacAnon1

During a normal pregnancy, oxidative stress enhances antioxidant mechanisms that are capable of reacting by way of enzyme activity and non-enzyme free radical deactivators. However, pregnancy is also a state in which this adaptation and balance may be easily disrupted.

There is strong evidence that a chronicin flammatory reaction combined with the presence of a local oxidizing environment may play a vital role in the etiology and development of complications during pregnancy.

In late pregnancy, damage to DNA (especially when it is caused by oxidative stress) is associated with pre-eclampsia(PE), intrauterine growth restriction (IUGR), and the death of mothers in developing countries; it largely determines pregnancy – related susceptibility to diseases

The referential values of ROS and NOS and their minimal and safe concentrations or physiologically beneficial concentrations are yet to be determined.

The measurement of oxidative stress in vivo is perceived as controversial,

as the sen-sitivity and specificity of various oxidative stress markers is unknown.. .

NotTheMacAnon
@NotTheMacAnon1

Did the paedophiles create the virus?

I think so!

Is Joe Biden the paedophiles choice?

Jury’s out.

Scumbags

Lock them all up and f their vaccine.

More from Science

Shrey Srivastava
@BlogShrey

#DDDD $LBPS $LOAC

A thread on the potential near term catalysts behind why I have increased my position in 4d Pharma @4dpharmaplc (LON: #DDDD):

1) NASDAQ listing. This is the most obvious.

The idea behind this is that the huge pool of capital and institutional interest in the NASDAQ will enable a higher per-share valuation for #DDDD than was achievable in the UK.

Comparators to @4dpharmaplc #DDDD (market capitalisation £150m) on the NASDAQ and their market capitalisation:

Seres Therapeutics: $2.33bn = £1.72bn (has had a successful phase 3 C. difficile trial); from my previous research (below) the chance of #DDDD achieving this at least once is at least

While looking at speculative pharmaceutical stocks I am reminded of why I am averse to these risky picks.#DDDD was compelling enough, though, to break this rule. The 10+ treatments under trial, industry-leading IP portfolio, and comparable undervaluation are inescapable.
— Shrey Srivastava (@BlogShrey) December 16, 2020

Kaleido Biosciences: $347m = £256m. 4 products under consideration, compared to #DDDD's potential 16. When you view @4dpharmaplc's 1000+ patents and AI-driven MicroRx platform (not to mention their end-to-end manufacturing capability), 4d's undervaluation is clear.

Matthew Salganik
@msalganik

Announcing the 2021 Summer Institutes in Computational Social Science. #SICSS is for grad students, post-docs & beginning faculty. Free for participants. @chris_bail and I are happy to tell you about all 20 locations. https://t.co/wolhtZIMc5 [thread]

SICSS brings together social scientists & data scientists interested in computational social science for 1-2 week events with intensive study & collaborative research.

Topics covered include automated text analysis, web scraping, non-probability sampling, digital experiments, ethics & much more.

All education materials created for SICSS are available open-source so that people who are unable to participate can still learn. You can also use them in your teaching. Here are materials from previous years:

Because of COVID, all SICSS locations will be online only in 2021.

Eric Feigl-Ding
@DrEricDing

JUST ONE PERSON—UK 🇬🇧 scientists think one immunocompromised person who cleared virus slowly & only partially wiped out an infection, leaving behind genetically-hardier viruses that rebound & learn how to survive better. That’s likely how #B117 started. 🧵 https://t.co/bMMjM8Hiuz

2) The leading hypothesis is that the new variant evolved within just one person, chronically infected with the virus for so long it was able to evolve into a new, more infectious form.

same thing happened in Boston in another immunocompromised person that was sick for 155 days.

3) What happened in Boston with one 45 year old man who was highly infectious for 155 days straight before he died... is exactly what scientists think happened in Kent, England that gave rise to #B117.

Immunocompromised 45 year old suffered from #COVID19 for 155 days before he died. The virus was changing very quickly inside the man's body\u2014it acquired a big cluster of >20 mutations\u2014resembled the same ones seen in #B117 & #B1351. (NPR audio Part 1 of 2)\U0001f9f5https://t.co/7kWiBZ1xGk pic.twitter.com/ZJ7AExB78Y
— Eric Feigl-Ding (@DrEricDing) February 8, 2021

4) Doctors were shocked to find virus has evolved many different forms inside of this one immunocompromised man. 20 new mutations in one virus, akin to the #B117. This is possibly how #B1351 in South Africa 🇿🇦 and #P1 in Brazil 🇧🇷 also evolved.

2) NPR report audio part 2 of 2:

Dr. Li couldn't believe what they found. "I was shocked," he says. "When I saw the virus sequences, I knew that we were dealing with something completely different and potentially very important." pic.twitter.com/HT3Yt6djFd
— Eric Feigl-Ding (@DrEricDing) February 8, 2021

5) “On its own, the appearance of a new variant in genomic databases doesn’t tell us much. “That’s just one genome amongst thousands every week. It wouldn’t necessarily stick out,” says Oliver Pybus, a professor of evolution and infectious disease at Oxford.

Dr. Angela Rasmussen
@angie_rasmussen

Hard agree. And if this is useful, let me share something that often gets omitted (not by @kakape).

Variants always emerge, & are not good or bad, but expected. The challenge is figuring out which variants are bad, and that can't be done with sequence alone.

Feels like the next thing we're going to need is a ranking system for how concerning "variants of concern\u201d actually are.
A lot of constellations of mutations are concerning, but people are lumping together variants with vastly different levels of evidence that we need to worry.
— Kai Kupferschmidt (@kakape) January 15, 2021

You can't just look at a sequence and say, "Aha! A mutation in spike. This must be more transmissible or can evade antibody neutralization." Sure, we can use computational models to try and predict the functional consequence of a given mutation, but models are often wrong.

The virus acquires mutations randomly every time it replicates. Many mutations don't change the virus at all. Others may change it in a way that have no consequences for human transmission or disease. But you can't tell just looking at sequence alone.

In order to determine the functional impact of a mutation, you need to actually do experiments. You can look at some effects in cell culture, but to address questions relating to transmission or disease, you have to use animal models.

The reason people were concerned initially about B.1.1.7 is because of epidemiological evidence showing that it rapidly became dominant in one area. More rapidly that could be explained unless it had some kind of advantage that allowed it to outcompete other circulating variants.

Yardley Yeadon
@MichaelYeadon3

https://t.co/xvP6tVlIaE
Quite a surprise. Ferguson isn’t qualified to comment on such things. He lacks understanding of basic biological concepts, partly explaining why his predictions are often so extreme.

That said, I’ll take him as an ally. It’s clear we’re already at herd immunity. How can I be sure? London had a huge peak of excess deaths in spring. The timing of peak deaths showed clearly that the pandemic was self-limiting. Recall much debate about whether the interval...

...between lockdown & peak deaths was long enough for lockdown to have been the cause of reducing deaths? The answer was “no”. But it was close & I can understand people thinking “well, it’s close, so perhaps it was lockdown that did it?”, thereby establishing a foundational...

...myth favoured by those who genuinely believe lockdown saves lives (it clearly doesn’t).
I’ll get to London & here immunity. But those wavering about the evidence about lockdown in spring really will benefit from cogitating on this graph.

In blue are the 30 trusts with the earliest date of peak deaths in spring. In red, the 30 with the latest peak deaths. For me, this is proof that national lockdown, which began Mar 23, played no role whatsoever in turning the pandemic. You’ll see some areas had peak daily...

🌸KANTHIMATHI-Mother of Sri Ramanuja. Kanthimathi was the sister of sri periya thirumalai nambi .
🌸SRI YAMUNACHARYA-Acharya of Sri Ramanuja.Also known as Alavandar.
🌸THIRUKOKOSHTIYUR NAMBI-Also known as Ghosti Purna.He instructed the Rahasya Traya to Sri Ramanujar.

He lived in thirukoshtiyur.
🌸THIRUKKACHI NAMBI-Kanchi purna was born in puvirunthavalli near kanchipuram and met the young ramanuja at an important time.He did the service of Lord Varadha.

🌸THIRUVARANGA PERUMAL ARAIYAR-Important acharya lived in srirangam and rendered the service of playing music for lord Sriranganatha.

🌸PERIYA THIRUMALAI NAMBI-He was the maternal uncle of Sri Ramanuja.He taught sri ramanuja about the epic of sri ramayana and other ithihaas and puranas.Served sri venkateswara at tirumala.

$k\u0101rthik \u0b95\u0bbe\u0bb0\u0bcd\u0ba4\u0bcd\u0ba4\u0bbf\u0b95\u0bcd \u0915\u093e\u0930\u094d\u0924\u093f\u0915 \U0001f1ee\U0001f1f3\U0001f1ee\U0001f1f3\U0001f1ee\U0001f1f3 | Sanatani$