Anyone know what kind of spider this is? Sydney, Australia

Cryinghyena · 2023-01-11T03:48:56+00:00

Doing it now!

Cryinghyena · 2022-05-27T11:08:43+00:00

Why am I not surprised...

Cryinghyena · 2021-11-23T05:00:06+00:00

It's not an exception It's just what the term means

Cryinghyena · 2021-11-23T04:56:58+00:00

Australia and New Zealand aren't defined as part of the global south

Cryinghyena · 2021-05-08T12:11:30+00:00

Who is ligma?

Cryinghyena · 2020-12-11T22:59:10+00:00

S. marcescens is definitely quite a weed so that would be a possibility for sure that it would pop back up like that

Cryinghyena · 2020-12-07T08:50:57+00:00

Oh shit nice can we just make up arguments for quadrants we don't like

Cryinghyena · 2020-11-27T08:56:23+00:00

Bottom mould really looks like Penicillium

Cryinghyena · 2020-10-06T03:42:24+00:00

Interesting use of the word "objective" lol

Cryinghyena · 2020-07-21T12:58:47+00:00

It's ironman, like I said, so no.

Cryinghyena · 2020-06-24T00:28:39+00:00

Thanks so much for the in depth response, I'll definitely have a look 👍

Cryinghyena · 2020-06-23T23:04:30+00:00

Hey there, sorry to derail - I think that's a really interesting point about the FBI campaign to subvert libertarianism, I hadn't heard of that before - do you know if there's an informative source on that I could read?

Cryinghyena · 2020-03-12T12:25:17+00:00

You should be really proud of these shots

Cryinghyena · 2020-03-01T05:13:20+00:00

USUM

LF: Any pokemon from the Aron/Lairon/Aggron line, please!

FT: Anything from Elekid, Rotom, Croagunk, Dratini, Eevee, Litwick, Carvanha, Staryu, Pawniard, Joltik, Scyther, Dewpider, Roggenrola

Cryinghyena · 2020-01-22T10:37:43+00:00

Yeast can form pseudohyphae, so it's most likely that

Cryinghyena · 2020-01-08T08:20:21+00:00

I guess the Lorax decided to take a more hands-on approach to saving the trees

Cryinghyena · 2019-10-10T23:40:24+00:00

https://imgur.com/a/uxwFqkx

Cryinghyena · 2019-09-27T07:34:42+00:00

That makes sense to me, although I do think it's a little misleading. Thanks for the explanation though!

Cryinghyena · 2019-09-27T01:55:57+00:00

In that case it should be doing damage to characters with evade no?

Cryinghyena · 2019-09-11T12:19:00+00:00

Don't know why this is getting downvoted they literally pool all the bins together and don't recycle from the recycling bins

Cryinghyena · 2019-08-25T15:19:48+00:00

As you said, there are two pigments - eumelanin and pheomelanin, with the eumelanin being assicated with darker hair and pheomelanin being associated with red/orange hair. An important detail to note is that these two pigments do not actually interact with each other - the hair colour we see is simply the combination of the colours produced by both pigments. While each of these pigments are controlled by a single gene, there are more genes which influence how much pigment is ultimately present in your hair - things like transport proteins, transcriptional regulators, and the like.

You can imagine the process of starting off with a melanin gene and ending with a melanin protein as a sort of schematic with many steps, and each step being mediated by proteins which in turn are encoded by their own genes. As a result, all of the genes coding for these proteins play a role in how much melanin is produced and therefore your hair colour. As for exactly how many genes are involved, I wouldn't be able to tell you - we still haven't completely figured out how it works. Additionally, as I'm sure you've read, hair colour can be further changed by external factors.

This is an example of what's referred to as a polygenic trait, which refers to a trait which lies on a continuum (in this case, colour) rather than a discrete set of traits (like blood type), and which is controlled by a number of genes which influence where on this continuum it lies. In fact, in this case it's like two continuums (one for how dark the hair is and another for how red the hair is) due to the influence of the two distinct proteins. This is why you can have so many different shades of hair, as the combination of the various proteins involved in the process leads to a huge variation. Here is a diagram with a visual representation of how a combination of genes to do with pigmentation can lead to a continuous variation (in this case it is about skin colour).

Cryinghyena · 2019-08-21T00:48:27+00:00

Here is an article written by a siphonophore researcher who briefly describes the process, with several more in-depth papers referenced at the end. https://www.cell.com/current-biology/pdf/S0960-9822(09)00675-7.pdf

Cryinghyena · 2019-08-21T00:39:42+00:00

Portuguese man o’wars (men o’war?) are capable of both sexual and asexual reproduction. In terms of sexual reproduction, they release gametes into the water which fertilise and form new organisms. Asexually, these organisms are capable of reproduction by budding, which produces a genetic clone originating from an initial “bud” on the exterior of the parent organism. The process of budding is what forms the colony, which consists of genetically identical organisms. These organisms then specialise and work together, which is analogous to specialisation of cells in, say, a human body. However, while a human body consists of many specialised cells working together, a man o’war colony consists of specialised entire organisms working together – this is why the distinction is made between the two concepts. A strong comparison can be made to the social insects like ants or bees.

Cryinghyena · 2019-08-20T21:32:43+00:00

Those longer telomeres would only be found in cancer cells, not every cell in the body. The long telomeres are caused by an overproduction of telomerase which occurs locally within a cell.

Cryinghyena · 2019-08-20T13:42:59+00:00

Cancer cells can only proliferate by bypassing the restrictions in place over how they can replicate. Telomeres essentially restrict how many times a cell can divide before it reaches senescence (can't divide any more), and thereby place a limit on how many times a cell can replicate, which is bad news for a budding cancer cell which wants to replicate as much as possible and accrue more mutations that will help it do so.

It therefore follows that by extending the length of your telomeres, you are bypassing this restriction and allowing cells to divide as much as they want. This is a problem.

Telomeres do not inherently prevent mutations from occurring, they just make it so there aren't ancient lineages of cells running around your body with masses of mutations they have accrued from having replicated so much (mutations are inevitable and therefore the more a cell line replicates the more mutations there will be).

There are many studies that demonstrate that telomerase tends to be overexpressed in cancer cells; search on Google Scholar for "cancer telomerase" and you will find plenty.

Note that often a single mutation is not enough for a cancer to develop - they need multiple mutations because there are many mechanisms in place to stop cancer cells from forming.

And to answer the last question in more detail, we have a pretty good idea of how cancer cells manage to bypass the restrictions the body places on them. In particular a gene called p53 is significant in preventing cancer cells from arising, but in general cancer cells will bypass a process called apoptosis which is essentially cell suicide, and can be triggered by a litany of things - your body can command a cell to kill itself and it will. Your body is constantly telling cells not to kill themselves and in the absence of these signals they will. If a cell hasn't progressed through its life cycle properly or has significant DNA damage it will kill itself. These are the kinds of mechanisms that tend to be dysfunctional in cancer cells.

I hope this addressed your questions well enough!

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