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How many non-pairing bases can a PCR primer have in directed mutagenesis?
I'm not including a lot of details here, because the problem I'm working with is actually more complex.
Say you have the DNA sequence
5'-...tct gcg gtg gtt ggc att ctg ctg...-3'
Could this sequence base pair with the primer:
3'-aga cgc cac ctt gcc taa gac gac-5'
.. or would the 4 non-bonding bases be too much?
I do realize there exists a better option, which still codes for the desired amino acids:
3'-aga cgc cac cac gcg taa gac gac-5'
Which only has 2 non-bonding bases.

It depends to some extent on experimental parameters. For example, how long can your oligos be? This old publication has a functional site-directed mutagenesis primer with 9 mismatches, but the oligo is significantly longer than the comparator oligos, and it required significantly higher concentrations of $MgCl_2$ (Figure 1). The extra length will buffer the sequence overall against mismatches, as you can imagine, and the higher $MgCl_2$ will lower binding stringency (caveat emptor).
The Addgene blog has the following recommendations for site-directed mutagenesis primers:

As a rule of thumb, 11 bp of complementary sequence on either side of the desired mutation (usually 1-3 mismatched bases) is sufficient for your primers to successfully anneal to the plasmid of interest during the PCR reaction. Ideally, your primers should be free of palindromic and repetitive sequences, but if present, a minor extension can usually ensure that the 3’-base(s) do not form secondary structures. The introduction (or ablation) of a restriction site through mutagenesis vastly facilitates the subsequent process of screening for succesfully mutated clones. Forward and reverse primers are designed to be complementary, but each primer may extend beyond the complementary region as long as an overlap with a minimum 6 bp is maintained. This overlap ensures that the PCR generates a nicked circle rather than a linear product (see figure).

By these parameters, I think that your suggested primer might be ok in theory, but would be more likely to work with additional homology (maybe 2-3bp) upstream and downstream.
It will likely be a finicky reaction as you are pushing beyond the rule-of-thumb limits for mutation size.


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How does oxygen help break down food?
I'm familiar with cellular respiration. Cellular respiration is the set intracellular chemical reactions that utilize oxygen. One example reaction is this:
C6H12O6 + 6O2 -> 6CO2  + 6H20 + heat

Another example reaction is this:
Food + oxygen -> carbon dioxide + water + energy

But there are many chemical reactions in cellular respiration. There are pathways that produce more energy like oxidative phosphorylation. There's glycolysis, the Krebs cycle, and oxidative phosphorylation, and each of these pathways has many chemical reactions.
Why is oxygen so helpful in breaking down food? Why is oxygen so helpful in chemical reactions?
With water, the answer is obvious. Water is a solvent. Water is polar. Water has a polar shape since the two hydrogen atoms are at one side of a tetrahedron and the oxygen's lone valence electrons are at the opposite side of a tetrahedron, which gives water polarity.
What properties of oxygen make oxygen so helpful in cellular respiration? I know that oxygen is an electron acceptor. Are there other properties that make oxygen helpful in cellular respiration?
Is oxidation one of the relevant properties that helps us make energy from food? Is it the oxidation of glucose inside the cytosol at a specific temperature?
When we look at the chemical reaction
C6H12O6 + 6O2 -> 6CO2  + 6H20 + heat

Is that an example of glucose oxidizing inside the cytosol at a warm temperature?
It makes sense that, since fruits and vegetables oxidize at room temperature, small molecules of glucose would oxidize very quickly at warm temperatures inside the cell.
Is oxidation the relevant property of oxygen that helps us get energy from food in cellular respiration?

This is a very basic chemical question and has already attracted three close votes. I suggest you read an elementary biochemical text — but not a biology text. In the past I would have recommended Berg et al. on NCBI Bookshelf, but that has been withdrawn. If you have $100 to spare, the 9th edition would be a sound investment in your education.

Good question. Why oxygen? Why not something else?
Fortunately the answer is well known and a rudimentary one in biochemistry. I offer a great paper on this by Babcock from 1999 in PNAS. I really recommend you read it all, it's relevant, within the scope of your question and well written in my view.
Excerpt with the answer:

Despite its biochemical versatility, however, >95% of the oxygen that
we consume is used in respiration. High-energy electrons derived from
food traverse the mitochondrial electron transport chain in a series
of exergonic redox reactions. These energetically downhill electron
transfers are used to develop the chemisosmotic proton gradient that
ultimately produces ATP. Oxygen is the final electron acceptor in this
respiratory cascade, and its reduction to water is used as a vehicle
by which to clear the mitochondrial chain of low-energy, spent
electrons.

The utilization of dioxygen by life is a very efficient strategy and the movement and control of pathways and mechanisms relating to oxygen is highly conserved and tightly controlled.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

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What chemical to use to recycle microplates used to grow bacteria
We grow bacteria (Escherichia coli) in polypropylene or polystyrene microplates with an optical bottom for some experiments (liquid culture).
I would like to try and recycle those microplates to be able to reuse them.
What chemical could be used? Ethanol, which I expected to kill the bacteria, doesn't work well as it leaves some deposit of bacteria aggregates. I was thinking about a chemical to lyse the bacteria, but I read here that it requires lysozyme to be efficient. I am rather looking for an inexpensive solution.

Would soap and hot water work? I assume you want to avoid scrubbing so as not to scratch the plates and change their optical properties

Are these in liquid culture or in/on solid media?  You could try NaOH and SDS - a la plasmid preparation lysis.

@acvill Thank you for the suggestion, I could try that. Indeed, we would like to avoid altering the optical properties of the optical phase.

@bob1 Yes, experiments are performed in liquid media (I have updated the question accordingly). The NaOH + SDS is a very good suggestion, thank you. I will try that.

Let us know how it goes by self- answering.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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Humans are Apes are Primates. But will they remain so?
Not a biologist here as you will propably be able to tell.
I understand that throughout the tree of life each species at the leaves at the same time also belongs to all the parent categories up the tree. So humans are apes and also are primates. The most frequent use of that fact in everyday discussion is in reply to the question "if humans evolved from apes, why are there still apes?". I also get why that question is silly.
I wonder, however, how biology would treat future evolution.
Assume that 10 million years from now our descendants are still around and have developed some trait that conflicts with the current distinction defining the branching of the taxonomic tree. Let them for instance grow some sort of tail again. Possibly to keep their hands free while still clutching some mobile device (I believe taillessness is one of the characteristics differentiating apes from other primates, if I am wrong about that please just substitute any trait that is).
Also assume that todays' other primates and apes are still around in that future.
Would we still say "homo futurensis are apes", even though they have tails?
Or would future taxonomists rearrange the tree and restate the distinctions? If so would that imply that looking back from that future to today us currently tailless humans would also not be apes after all but on a different branch together with h.futurensis? Is there a time-dimension to the layout of the tree of life? I don't mean corrections as we learn more. But changes due to evolution taking its course. The appearance of a new species forcing a remap.
Or would we just keep the tree and drop the tail-thing from the list of characteristics because there are enough other things that define the commonality? If so we could imagine even further evolution changing those traits too. What then?
Or does the new tail not pose a conflict in the first place because it would be something new. "Tail" being a naive name and the new appendage propably being called something else?
Or is the question plain silly, if so please explain why.
Thank you.

Very simple question that is at the root of systematics/phylogenetics. I think I offer a complete answer: when considering whether a species is considered part of something, it is very crucial to understand (and dependent on) whether the term that uses to group things ("Primates" "apes" "animals", "eukaryotes", etc.) is mono-, para- or polyphyletic. See here.

I'll give you a rudimentary example to explain. Let's say we make a term called 'multi-hearters' and we use it to group animals with more than one heart. This term would be polyphyletic. You'd group squids and roundworms with this approach, though they are not closely related in phylogeny. Whichever way you choose to use the terms ape, primate, simian or human, you have to be clear about what you mean. If "ape" is to be used monophyletically, then any descendants of humans will be apes, by definition. Any descendant of any ape will always be an ape since they are part of "ape" monophyly.

@S Pr: Though that definition runs into the obvious problem that it makes all land vertebrates into fish.  Any descendant of any fish will always be a fish since they are part of "fish" monophyly, no?

@jamesqf Yes, as is currently thought. Under our current system Cyclostomata would be the common ancestor I think. These would be the bony jawless fishes, similar to lamprey now.

Traits that are lost and then redeveloped are called atavisms and can be gained and lost several times in a evolutionary history. I suspect you need to learn about parsimony and why it's not necessarily the true course of evolution.

@bob1: Are you familiar with the logical principle of reductio ad absurdum?  https://en.wikipedia.org/wiki/Reductio_ad_absurdum

@jamesqf - yes I am. But your example isn't RAA in my opinion because land animals are part of the group descended from fishes, though the conclusion may seem absurd becuase most people (myself included) think of fish as scaly, water etc.

@jamesqf Oops I'm sorry, well spotted. Here's a small amendment to my second comment for OP to understand more clearly: I meant that if "apes" is to be used as a monophyletic designation, then all future descendants from any ape will be apes. One day we may of course designate "ape" as a paraphyletic group. Fish are a great example of a paraphyletic group. What I want to confer/re-state is that it doesn't matter what word you use, you have to understand that the word has to be defined with an explicit category in mind. One must know the categories. That is the crux of the answer IMO :)

Yes, humans will remain members of apes and primates.
The terms "ape" and "primate" are common names representing certain phylogenetic clades. A clade is a group where all members are eachothers' closest relatives compared to members outside the group. Another way to put it is that a clade exists if there is a common ancestor whose descendants include all and only members of that group.
All of today's apes share a common ancestor to the exclusion of all non-apes. The descendants of today's apes will also share that ancestor*, and so will still be within the ape clade. The terms "ape" and "primate" are best thought of as expressions of relationships rather than clusters of traits.
Could humans evolve something very non-ape-like? For argument let's say humans evolved a tail. I suppose colloquially it could become common for people to use the term "ape" to refer only to the tailless apes, but anyone speaking of evolutionary relationships could still use it to refer to all the descendants of today's apes. Then it would just be a matter of clarifying which meaning is intended. Since "ape" is a common name, it might get used more flexibly, but the scientific term for apes, Hominoidea, certainly wouldn't change.
If humans evolved a tail they wouldn't cease to be apes, because "ape" isn't defined as "primates without tails," it really means "all the descendants of [this one ancestor]," which we generally recognize by their lack of tails.
The term "fish" is a similar example. If one calls a shark, a salmon, and a coelacanth all fish, then really humans should be included as well. Otherwise, "fish" stops being a biological term and just means something like "aquatic vertebrates that have gills**."
I'll finally add that it's fairly common for a lost trait to re-evolve, or for a new trait evolved in an ancestor to be missing from some descendants. Often, some additional observation will show that the re-evolved trait is actually different from the lost trait (think, for example of salmon fins vs. whale fins), but not necessarily. This can make it more difficult to accurately reconstruct relationships, but doesn't exclude those organisms from their clade.

*This is ignoring the possibility of hybridization, which is extrememly unlikely for ape/non-ape, but can be common in other groups.
**Mostly


text:
What are the Genes/Enzymes responsible for the supposedly stark between-individual differences in lethargy after eating starches?
Andrew Huberman claims in one if his podcasts episodes that:

[...] because starches cause the release of serotonin in the brain and lend themselves to a state of sleepiness.
Now, I should mention that about about 25% of individuals have genes that encode for enzymes that allow them to eat large amounts of carbohydrate and not suffer from this lethargy.

Timestamped Video: https://youtu.be/aXvDEmo6uS4?t=4333
Sadly he doesn't reference any kind of study or data that this claim is based on.
I am aware that serotonin is involved in digestion and that most serotonin found in the human body is in the gut. Though I do not know what its function is there or if this is even relevant for this question, given that Huberman specifically states

starches cause the release of serotonin in the brain [emphasis mine]

This aligns with my knowledge that Serotonin doesn't cross the blood brain barrier, so the Serotonin released in the gut cannot make its way to the brain somehow. I am also confused how or why Serotonin would cause lethargy, though this still fits with the typically reported side effects of Serotonin Reuptake Inhibtors.
I am also not surprised that this trait varies between individuals, but Huberman's claim is phrased like the difference is not just forming a normal distribution arising from many genes and instead that the distribution seems to be at least bimodal, i.e. "about 25% of people" do not experience this at all.
There are two previous questions on the tiredness after eating,
What is the biological basis for tiredness after eating?
Why do the humans become sleepy after meals?
but neither really discuss anything related to serotonin in the brain, or deal with the factors underlying between-individual differences. One of the answers brings up

Sugary foods lead to the production of insulin. Insulin stimulates cells to take up glucose from blood. It also mobilizes tryptophan to brain. Once in brain, tryptophan triggers formation of serotonin, a hormone involved in controlling mood and slumber.

but this answer only references a blog with no further citations, but is at least some kind of explanation.
My questions is thus:
Is there some well known paper or review underlying this claim that he is implicitly referencing and potentially overly simplifying?
And if this isn't some well known paper, which I can read up on myself, but someone else can answer my more specific questions:
What are the enzymes that influence the "post carb lethargy" in such a strong way and how do they attenuate the serotonin released in the brain?

I don't know about an enzyme that may or may not influence sleepiness after starchy meals, but I do know a fair amount about the physiological effect of somnolence after eating: https://medicalsciences.stackexchange.com/a/1087/169. If there is an enzyme that allows sleepiness after carbohydrate ingestion, I certainly have it. If I can't sleep, a bowl of cereal helps immensely. :)

The video is likely referencing alpha amylase, which is encoded in humans by AMY1A, a gene that is know to have a high level of inter-individual copy number variation. Some scientists have speculated that production of this enzyme in the brain can have an impact on neurotransmitter levels and thus memory in Alzheimer’s Disease (AD)1:

Since we have previously discovered the presence of α-amylase in the brain, we find it tempting to speculate that production of α-amylase is one of these factors. How the very high AMY1A copy number variability (and potentially thereby very high production of brain α-amylase) can be implicated in the lowered AD risk and episodic memory remains to be investigated. But since α-amylase is known to efficiently degrade polysaccharides (such as glycogen) in the periphery, we find it likely that the enzyme has a similar role in the brain. The enzyme might thus be important for the degradation of glycogen in astrocytes and neurons [20, 28], which is known to be crucial for neurotransmitter production and memory formation [21, 29, 30]. The presence of α-amylase in activated astrocytes and neuronal synapses, found in our previous studies [19, 31], supports this idea.

References

Byman E, Nägga K, Gustavsson AM; Netherlands Brain Bank, Andersson-Assarsson J, Hansson O, Sonestedt E, Wennström M. Alpha-amylase 1A copy number variants and the association with memory performance and Alzheimer's dementia. Alzheimers Res Ther. 2020 Nov 21;12(1):158.

My initial reaction was that he must be referring to one of the genes/enzymes that explain the observation that neurotransmitter release by brain neurons may be controlled by carbohydrate (but not protein).  'Carbohydrate consumption--acting via insulin secretion and the "plasma tryptophan ratio"--increases serotonin release; protein intake lacks this effect.' (ref). I have not been able to find the enzyme, but tryptophan hydroxylase must be a likely candidate?

While alpha amylase seems interesting, I am fairly sure that this is not what Professor Huberman was referencing in the podcast. The connection to serotonin specifically seems like a stretch, especially when there are much older results establishing a link to serotonin specifically like @user338907 linked. This would actually be good enough for me to accept as an answer if you want to post it as such, there are enough details in the paper to narrow down the enzymes involved.


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How does NaF protect G proteins from denaturation?
Below is presented Figure 4 from the 1977 paper of Ross and Gilman, which provided evidence for the existence of G proteins:

The protocol (and rationale) is as follows:

Wild-type cell membranes was preincubated at 37˚C for 30min. (This causes loss of adenyl cylase activity, attributed to dissociation from another component — G protein — essential for its activity.)
Gpp(NH)p was then added — with a no-addition control — and the membranes further incubated at 50°C for the times shown. (The higher temperature denatures the second component — G protein —but not the adenyl cyclase. Gpp(NH)p had previously been shown to activate adenyl cyclase and was required to assay activity.)
The extracts were chilled and mixed with adenyl cyclase-depleted membranes to provide the second component. Adenyl cyclase assays were then carried out with Gpp(NH)p or NaF (which was also known to stimulate adenyl cyclase).

When incubation was performed in the absence of Gpp(NH)p, and then stimulated with Gpp(NH)p, much of the G protein denatured quickly during incubation, decreasing AC activity
When incubation was performed in the presence of Gpp(NH)p, and then stimulated with Gpp(NH)p, the G protein showed increased thermal stability, denaturing slower during incubation and decreasing AC activity to a smaller extent
When incubation was performed without Gpp(NH)p, and stimulated with fluoride, the G proteins showed similar activity to the sample stabilised with Gpp(NH)p, despite no Gpp being present during incubation.

How is the presence of fluoride ion seemingly able to reverse the denaturation of the G protein? How does it allow a level of activity similar to the Gpp(NH)p-stabilised G protein, despite the fact that the G protein was not stabilised during incubation?

Welcome to SE Biology. I have edited the first part of your question, correcting the order of authors, modulating the statement of its significance, and describing the experiment and its rationale. I think your bulleted interpretation is incorrect, but I have retained it in order to present an alternative in my answer.

Could you tell me why you think my bulleted interpretation is incorrect?

I am composing an answer — be patient. I am having to read and re-read the original paper and this is taking time.

The question is whether the authors are really using open circles for two conditions — membranes incubated with and without Gpp(NH)p but assayed in the presence of NaF. It beggars belief. But the text suggests that this is so, contrasting half-lives of 8min and 2min for NaF and Gpp(NH)p with unpreincubated membranes. Not sure you are going to get an answer now. I was attracted by the mechanism of stabilization at the protein level, which is actuall through aluminium fluoride.


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Slightly different sequences returned by BLASTP
Probably this is very trivial but I am self-learning bioinformatics and I don't know who to ask for this kind of stuff. Also, apparently it is really hard to find information on general topics like this.
I am learning how to use BLAST. I tried to use the sequence of the COVID-19 delta variant spike protein. I used BLASTP and I obtain as results a lot of proteins (all classified as surface glycoprotein [Severe acute respiratory syndrome coronavirus 2]) that vary just for a single aminoacid. The majority of these changes is I to V or viceversa.
What does it mean? Are these all variants of the protein? Are these all sequences with mistakes? And why does it entail only the interchange between I and V?

It would help to know the blastp database you use (e.g. just default with the "run blast" button?), what the output is, what the position is, etc. Briefly, we would expect those to all be real variants, it is comforting that they are replicated in different isolates.

Note: by default blastp web interface or the command-line program may only return some number of the most similar sequences ("Max target sequences" under "Algorithm Parameters" on the web interface). You may want to look into adjusting this parameter if you want more, less similar seqs.

For the moment I just tried to get the best 50 candidates. I don't really care, it's just to try it out. I just changed the expected value to be less than 0.05. The other parameters are left to default. So from what you are saying I assume those are all genuine variants of the protein, is it correct?

Unless you have some reason to expect systematic error, that is my expectation. Viral protein sequences vary significantly, that is normal. Unfortunately in this case!

However what really leaves me wondering is that (at least in the top 50 candidates) we can only see interchange of I and V. Any idea why it might be the case?

Probably because there are so many publicly available sequences now that you will highly sample closely related sequences!! What blast is doing is just saying "give me the 50 most similar sequences to the one that i put in", and it's doing its job, it just turns out that we have so many covid genomes now that the top 50 most similar are indeed very similar!

The answer is that I and V are similar in their biochemical properties. By the way I see some V-I substitutions as well as the I-V in query vs subject and also some others (e.g. B-D, L-M). These are all real and natural variations in the sequence.
If you look at the table here, you will see that Valine and Isoleucine are both hydrophobic and similar in structure. If you delve deeper into the numbers, you will see further that they have similar charges, similar sizes, and are aliphatic. This means that they are likely to conserve protein structure in the folded form. Valine is less energy expensive in synthesis for the cell, so perhaps this plays into it a bit, but as this is a virus that is hijacking the cell processes I have no real idea if the energetic cost comes into it.
BLAST, as mentioned in the comments, returns a certain number (usually 50) of the most similar sequences to the query. You can adjust the number and specificity limits during your setting of the search parameters.  If you do something like blast the spike reference sequence from Wuhan-Hu-1 (YP_009724390.1) against your sequence (put yours in query, and the Wuhan-Hu-1 one in the subject or vice-versa), you will see a number of substitutions, indels etc, none of which are I-V. From this you can deduce that your findings of I-V and V-I are simply a matter of sampling based on the most similar sequences.
I don't know the algorithm for BLAST (or anything else for that matter), but it may well take similarity of biochemical properties into account when searching for most similar sequences. Given that there are millions of submitted sequences for the spike of SARS-CoV-2, there are likely to be many thousands of highly similar sequences in the database.


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What are these bugs eating my lumber?
Duplicate of this question.
I found bugs in wood that I've had air drying for the last few years. What are they?
I had a tree cut down a few years ago and some of the wood milled in to slabs. However, I've found a few pieces that appear to have bugs living in it. They seem to be some kind of larva.
The larva seem to be approximately 2cm long and maybe 1-2mm across. There have also been larger tunnels from what I assume is the adult insect that are more like 3-4 mm across. I haven't found any adult insects to get pictures of though.
Tunnels are usually packed with sawdust, but sometimes the bigger tunnels are packed with what looks more like leaves.
The picture below is of a piece of oak, but I've seen similar tunnels in some maple also.
Current searching online leads me to the Emerald Ash Borer (but it seems to only eat Ash trees?) or termites (but the larvae size doesn't seem to quite match).
I'd like to identify the insects so I can evaluate whether I can use the wood.
This is in Eastern Missouri (USA).

Welcome to Biology.SE. Please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site. In particular, please note that crossposting, is considered rude — instead differentiate the questions so that they are not duplicates and are appropriate for the two sites. Also note that organism ids need more information: 1) one or more clear closeup photos (from multiple angles if possible); 2) the location (e.g. country and region); and 3) an estimate of the size.

tyersome, Thank you for the welcome. I've added the location. Unfortunately, only the one photo is immediately available. If I manage to obtain others, I will add them.
The answers on the previous question directed me here. While the fundamental question (help identify the bug) remains the same, the question is not an exact duplicate. It has been tailored for this site. If further tailoring is needed, I look forward to your proposed edits.

These are larvae of some species of wood-boring beetle. It is quite possible you've had multiple species eating your various species of wood.

Many species of boring insects have white, segments, worm-like larvae.

I do not know for certain what species you have, but size, phenology (e.g., timing of metamorphosis/emergence), type of wood infected, and time of infection (dead wood vs dying wood) all are helpful in narrowing down to a specific species. I recommend placing some wood with a borer in a terrarium with a screen on top and waiting to see what the adult looks like when it emerges -- and recording when it emerges.
One possibility, I suppose, is the red oak borer (Enaphalodes rufulus), though only infected specimens look like yours (though, it does appear you've only shown us the caudal side of the insect -- any head shots??).
I couldn't find evidence from a short search as to whether the invasive goldspotted oak borer (Agrilus auroguttatus) has been found in Missouri or not yet, but I will provide an image demonstrating a similar larvae morphology of this species:

 Credit: Mike I. Jones ; Source: UCANR -- L>R: 4th instar, 4th instar in hairpin configuration, 4th instar constricted form, pupa, adult
If you could update with more info (e.g., specific species of tree) and additional photos (especially of larvae head and any emerged adults), ID to specific species would be easier.
According to forestpests.org:

Larval tunnels cause lumber cut from infested logs to be downgraded, reducing log value by up to 40% compared to top quality wood.


text:
There are some species that grow throughout their lives -- is there evidence that even in adulthood their brains increase in size?
One species I have read about is carp whose growth is limited only by food supply and space. One can actually, because their skin is almost transparent, see their brains and it sure does look like larger carp indeed have proportionately large brains. If this is so, are their behavioral consequences and do such carp recover from brain injury?

Please note that I've focused on the question in your title. It is best to have only one question per post since that makes it easier for other users to find material. It also helps you get more complete answers. Please post your follow-up questions  separately.

Your question falls into an area of study known as allometry.
It is generally believed that brain size must increase as body size increases1,2. This relationship has been demonstrated  in fish 3,4, including carp. This phenomenon is also seen in other (non-mammalian) vertebrates including the Nile Crocodile (Crocodylus niloticus)5.
This continued growth is correlated with the ability to regenerate after brain injury2.
References:

Jerison, H. (2012). Evolution of the brain and intelligence. Elsevier.

Kaslin, J., Ganz, J., & Brand, M. (2008). Proliferation, neurogenesis and regeneration in the non-mammalian vertebrate brain. Philosophical Transactions of the Royal Society B: Biological Sciences, 363(1489), 101-122.

Bauchot, R., Diagne, M., & Ribet, J. M. (1979). Post-hatching growth and allometry of the teleost brain. Journal fur Hirnforschung, 20(1), 29-34.

Brandstätter, R., & Kotrschal, K. (1990). Brain growth patterns in four European cyprinid fish species (Cyprinidae, Teleostei): roach (Rutilus rutilus), bream (Abramis brama), common carp (Cyprinus carpio) and sabre carp (Pelecus cultratus). Brain, behavior and evolution, 35(4), 195-211.

Ngwenya, A., Patzke, N., Spocter, M. A., Kruger, J. L., Dell, L. A., Chawana, R., ... & Manger, P. R. (2013). The continuously growing central nervous system of the Nile crocodile (Crocodylus niloticus). The Anatomical Record, 296(10), 1489-1500.


text:
What is this spider with blue striped head?

I found this spider on the balcony of a Brisbane, Australia quarantine hotel. About 1.5cm. Anyone know what it is?

Colourful find, it's not among the common listed types, or the common poisonous ones. Best to be careful and not handle until identified. Please take our [tour] and refer to the [help] for guidance.  Also, take a read of our species ID guidelines and see what you can add that might help.

+1 for excellent photo

Related: https://biology.stackexchange.com/questions/79038/what-is-the-name-of-this-red-and-blue-striped-spider-brazil-rio-de-janeir

I knew Australia was taking COVID seriously, but to quarantine the spiders too is quite impressive.

@BruceWayne Perhaps the spider isn't quarantined; perhaps it's a guard to prevent the "guests" from escaping ;)

I was simply writing this as a comment, but it became too long/detailed. I wanted to supplement @timeskull's answer with a bit more nuance.
I agree that this looks like a female Cosmophasis micarioides
A more similar looking specimen to the OP's photo:

 Credit: Tony Bailey , Source: findaspider.org
You can read more about the species here, including that its "extremely variable." Importantly, the mature male is much darker with blue and black lines, while the female is much brighter with reds/yellows. Sub-adult males actually look like a cross between the two:

The female can feature combinations of orange, black, red or blue-green, usually with metallic bands across the cephalothorax. The males look like females until they become sub adult, when they look like a cross between the female and the adult male...You can recognise C. micarioides males by their black face lines

@timeskull's answer looks different from the OP's specimen because the specimens in that photo are likely sub-adult males or juveniles vs. females. -- they're actually identified as juveniles here
According to Whyte & Anderson (2017)1, the species is widespread and common in tropical Australia south to Brisbane.

1. Whyte, Robert; Anderson, Greg (2017). A Field Guide to Spiders of Australia. Clayton South Vic. 3169: CSIRO publishing. p. 236. ISBN 9780643107076

"Toxicity: May cause local inflammation". - "The jumping spiders are not toxic except for the Mopsus mormon."

Looks like we have another "What color is the dress?" meme candidate - the blue in the original image is likely due to the reflected light appearing that color from certain angles...

@DarrelHoffman right you are. The name micarioides actually refers to the "micaceus" (mica-like) body scales that reflect different colors when viewed from different angles.

It's a female Cosmophasis micarioides.
It's obviously a salticid, so I looked through the thumbnails of jumping spiders at arachne.org.au until I saw the green and orange head bands. Fortunately they used the female spider for the thumbnail as the male looks quite different and I wouldn't have checked if it was pictured.

Description and more images on the species page:
http://www.arachne.org.au/01_cms/details.asp?ID=2583

Good find. Colorful like a jumping spider, but the eyes weren't clear in the OP's photo.


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How many genes of an individual are homozygous?
We have 20000 to 25000 protein-coding genes. Considering an individual, how many of his\her protein-coding genes are homozygous? I am looking for an estimation of gene homozygosity ratio in human individuals and\or other organisms and appreciate any help (preferably with the support of an academic paper).

Do you mean the number of homozygous genotypes? A single gene contains many different genotypes, some which are homozygous and some heterzogygous.

@user438383 I mean how many of genes of a person are homozygous and how many are heterozygous? I think you meant that a person has many genes, some are homozygous and some are heterozygous.

No, I meant what I said. Unless you are using a different definition of 'gene', then to my knowledge, a single gene contains many different genotypes, which may be either heterogyous or homozgous.

I do think this could be caused by 'gene' having multiple, related definition. How are you defining it?

A single gene across a population may contain many genotypes, but an individual can't have more than 2 genotypes for a single gene (barring trisomies or other gene duplications)

I think it's going to vary quite a lot...someone with one parent who is pure Chinese, and the other parent is pure Swedish is probably going to have more heterozygosity than someone who can trace their ancestry on both sides to, say, Limerick.

Recall that a gene generally consists of DNA sequences, which may yield numerous alleles, each of which is a variant at a discrete positions within the DNA sequence of the gene. For example, there are numerous known variants of the beta-globin gene, some of which cause inherited anemias such as sickle-cell anemia. A variant at coding position 40 causes beta-thalassemia, and a variant at coding position 6 causes sickle-cell disease.
It is possible (though unlikely) for a person to be heterozygous for each of these variants independently (when the variants are so closely linked, i.e. the same gene, this might be called "compound heterozygosity").
The terminology is admittedly confusing, and there is a tendency to be sloppy with language particularly in medical genetics and population genetics talking about "genes" being heterozygous, or "gene frequencies" meaning allele frequencies. This is very old terminology from before when we knew what genes were made out of (DNA).
But when we talk about heterozygosity in the sense that you mean ("how many [x] are heterozygous?"), we can only answer this where [x] = positions, not when [x] = genes.
In terms of positions of the human genome, estimates differ among populations but I believe that something like 0.5%-1% of variable positions are heterozygous (see e.g. Figure 1 of this paper, note scaling of axis). Of course, the number of variable positions in the genome is relatively small (0.6%). So you might expect that on the order of 0.001% to 0.01% of positions in the human genome are heterozygous in any given person, depending on their population of origin.
I was unfortunately not able to immediately find a study that directly estimated this number, though I'm sure it exists somewhere.


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Why can sodium oligomannate (GV-971) improve cognition in people with Alzheimer's Disease?
There is a Phase 3 placebo-controlled clinical trial to evaluate the efficacy of sodium oligomannate (GV-971) in the treatment of mild to moderate Alzheimer's disease (AD).
A Study of Sodium Oligomannate (GV-971) in Participants With Mild to Moderate Alzheimer's Disease (GREEN MEMORY)
Why can sodium oligomannate (GV-971) improve cognition in people with Alzheimer's disease? What is the mechanism of this drug in AD?

Are you asking us to judge the outcome of a trial in advance? Could you [edit] to tell us what the actual question is, add relevant detail, at the moment it's not clear how the trial you've linked might relate to the mechanism of action (if there is one).

I am just curious about the mechanism of this drug.

From Wikipedia, albeit not the best source for this sort of thing:

The mechanism by which sodium oligomannate may function is unclear and several possibilities have been proposed,[6] including amyloid beta disaggregation,[7] mediation of inflammatory responses to amyloid plaques,[8] protein binding inside neurons,[9] and alteration of intestinal bacteria.[10]

The page also mentions:

It was conditionally approved in China by the National Medical Products Administration in 2019 for mild to moderate AD to improve cognitive function.[1] However, the clinical data supporting its potential benefits have been received skeptically elsewhere[2][3][4] and are considered insufficient for approval in other countries.

Importantly, it's not necessary to know a drug's mechanism to get it approved, only to show that it is safe and effective. The mechanism for antidepressants, for example, is still not known, for any of them, we just know that they work better than a placebo. We also know what receptors in the brain they affect and the local mechanisms there, but without a better scientific understanding of depression it's not currently possible to understand which combination of those molecular effects give the behavioral effects.
Similarly, Alzheimer's disease is not understood mechanistically, so it's very plausible to develop drugs for it without knowing the mechanism. For this drug, it seems like both the mechanism and efficacy are not known to the standards expected by regulators in the US and EU for approval.
The proposed list of mechanisms mentioned on the Wikipedia page sound a bit to me like a collection of all the different theories of mechanisms for Alzheimers' disease itself, which is still poorly understood.


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Number of "mutations" in Omicron variant
Currently in the media they say that the Omicron variant has more than 30 "mutations", ie changes in spikes. I find this confusing, because the way I understand a single change in the virus can alter more than one spike in one go. I assume there is some randomness to mutations. So one mutation (new copy) can change 2 spikes, another can change 0 or 5.
Is it misleading?

Welcome to Biology StackExchange! I don't think I understand what you mean with "a single change in the virus can alter more than one spike in one go". All of the spike proteins that build a virus particle are (more or less) identical, because they are a product of the same gene – there is only one gene for S protein in the SARS-CoV-2 genome. Therefore, if there is a mutation in the S gene, all the spike proteins produced will carry this same change.

I think the OP does not understand what spike means in the context of a coronavirus. Spike is the name of one of the important proteins of the virus and it is around 1200 amino acids long. Three copies of this protein form the characteristic surface structures of the virus well known from cartoon drawings.

Mutations are generally random, yes, but the "30 mutations" referred to are not random among omicron-variant virions, but rather 30 differences between the omicron variant and the reference genome they are comparing to from early in the pandemic. Most omicron virions will have the same 30 "mutations" as all the others, because that's why that group was given a name. These are not new mutations in every virion, they are mutations that happened earlier in the lineage that were passed down to all the descendants of that lineage. They are only "mutations" in comparison to the reference genome. If it helps, substitute the word "differences" for "mutations": Omicron has 30 differences in the genome coding for the spike protein compared to the reference strain of SARS-CoV-2.
For a single virion, the cell it infects is going to produce all spike proteins that are the same, because they are built from the same genetic template. You wouldn't typically have multiple spikes of different types in the same virus particle (theoretically possible with errors, etc, of course).
Since the pandemic started, an incomprehensible number of different mutations have occurred in SARS-CoV-2 virions replicating in human hosts. However, most of these mutations are not consequential because they did not spread in the population. For ones that do spread, you can track their origin in a sort of "family tree". See for example on NextStrain:
https://nextstrain.org/groups/neherlab/ncov/21K.Omicron

Bryan Krause has the answer, but I wanted to add a note about the connotation of the word mutation and what it actually means.
The word mutation just means genetic change that a cell (or virus) doesn't fix by the time it replicates itself. That's it. There are a few different ways to skin this cat, but the situation you're imagining is if the virion (viral genes) copied itself multiple times, called polyploidy. The thing is that mRNA viruses don't really have the ability to do that, because they can't self replicate, and so the required mechanism is off limits until they infect someone. When you say that a mutation could double the number of spike proteins, it makes me think that you assume that more genes = more proteins. While this is sometimes the case, what determines how many proteins (called protein products) come from genes is their level of expression and regulation.
So, what determines how many spike proteins a virus makes depends on how well the virus can convince the host to make more spike proteins, which might come from a mutation in a gene, but having multiple genes is not always the source of multiple copies of a protein. If we want more protein, we need more mRNA, which means we need more expression of a gene. You might say, well more copies of the viral mRNA would produce more proteins right? Yes, true, but again in a situation like that, you're really describing a higher viral load (just more of the same virus) than an instance where an entire viral genome has spontaneously doubled itself.
Some people interpret mutations, because of entertainment, as the source of genetic change responsible for dramatic differences that are cartoonish and comical. Think of the cyclopes from Futurama, for example. But no, mutations are often no so exaggerate in their appearance. Most mutations, in fact, are unhelpful and depending on how often mutations are produced in a species, are typically selected against quickly. This is an indication of two things:

The 30 or so mutations you report are the source of differences in traits that give the virus an advantage. Yes a mutation in a Hox gene for example could result in drastically different results. But more often, mutations that are helpful come in more subtle and less dramatic forms.

A variant of the virus is identified based on its genetics. Each variant of the virus is classified by its genome. So yes, the Omicron variant might produce a slightly different antigenic site than the Delta variant. We're not changing the number of spike proteins, we're changing the identity of the virus.

As it’s currently written, your answer is unclear. Please [edit] to add additional details that will help others understand how this addresses the question asked. You can find more information on how to write good answers in the help center.


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How much MPa of pressure can human cells survive?
Is there any research on this topic with concrete numbers? I found some papers of high pressure tests on microbes, but not on human/mammal cells. What I want to find is true "crush depth" for a human (assuming full liquid breathing and CO2 scrubbing from veins).
One in one Youtube video author claimed that 1000 m (10 MPa/100 Bar) is maximum depth human can reach, because at such pressure human cells will fail. Membranes will get so stiff, that it will fail to exchange oxygen/nutrients/energy, so, effectively, neurons will die at such depth. Author didn't provide any sources whatsoever for such claims, though. He just provided Blobfish (Psychrolutes marcidus) example. It has jelly-like, very soft cell membranes that at 1.6 km depth are as rigid as our own membranes at sea level, but when brought to sea level pressure loose structural integrity.
Yet, I highly doubt this claim, considering that Sperm Whales casually dive to 2 km depth and Cuvier's beaked whale dives 3 km. They do not turn into jelly like Blobfish at the surface, yet still manage to remain at such huge pressure as 30 MPa for hours. Of-course, they don't live permanently at such depths, but human diver is not required to live there too - just survive and go back without major trauma.
So if a Sperm whale can do it, can't we too? Or can we? At what pressure our cells will fail?

How do you propose the research be conducted? On paid volunteers? Prisoners? Illegal immigrants? What difference does knowing this make, practically (or scientifically)? If people need to go deeper, they get into mini subs that can withstand great pressures now. Nobody dies finding the answer. (This kind of extreems of endurance research was done, oh, 70-80 years ago...)

Well, with modern technology there is no need to even go into the ocean. And this is very cheap experiment for somebody with required tech. Just get some human liver or neuron cells, put them into pressure chamber and start increasing pressure while monitoring their status. As simple as that. It is really weird that nobody don this yet, as it is very important to know our theoretical limits so that we can improve our exoskeletons (yes I call body exoskeleton, because the human is neuron connections and currents within them, and body is just an external structure that supports this system).

Seems like nobody in the World can provide any information on this topic. I will assume, for now, hard limit of 3 km depth, judging from deep diving whales. I don't know why they don't dive deeper, maybe there is no food there, but maybe they actually reached hard limit of what surface mammal can achieve in terms of cell membrane pressure.

@anongoodnurse at the very least, tests on mice might give pretty accurate results for surface optimised organism's crush depth.

Why kill a mouse for such useless information?


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If male songbirds fail to learn songs from older males, which makes them less attractive to females, will that species eventually die out?
I recently read that a species of critically endangered song bird (Regent honeyeater) may go extinct if there aren't any older males around for younger males to learn their song. From this article.
But will this species eventually die out because males cannot attract a mate or can scientist use play back recordings (of song) to teach these young males how to sing?

Clearly they can go extinct: "Researchers say a decline in singing culture could drive the species to extinction." There are very few of the birds left; it might be difficult to figure out where to put the speakers to target the sparse males. (That's why the young males aren't hearing the older males' songs: too far apart.) Did you google "can scientists teach male regent honeyeater to sing correctly?" If you didn't, could you please try that, and tell us if you had any luck finding anything helpful? Why or why not? Thanks!

The article you reference is behind a paywall, but I believe I've found the study they're referencing anyhow. You can find it here for free.
To directly answer your question: no one can really answer that right now. That's not to undermine your question. Any population can go extinct when put in certain conditions.
The authors of the paper call for more controlled research,

Experiments in captivity that replicate a range of demographic
scenarios could help improve our understanding of the process of
cultural song erosion and its impacts on fitness and population growth
[42].

I know that's rather unsatisfying, but it's straight from the horse's mouth. That's science for you. But I'll try to entertain you for a bit, because what would a good answer be without a bit of supposition? As I'm sure you've read, it isn't that the birds aren't singing, it's that they're not singing the right song. The authors note

Regent honeyeaters exhibit strong conspecific attraction, once roaming in flocks of hundreds [23]. However, at least four of the interspecific singers were more than 100 km from the nearest known male at the time they were detected.

Which means when they sing the right song, they do a darn good job of recognizing each other. But unfortunately, these guys are too far apart, and as their population density decreases, they're more likely to learn songs from interspecifics (other species). The authors also measured the ability for birds in captivity to learn their own song and they suspect it could cause problems upon release. A scientist teaching a bird to sing might not be a solution either. Sure, we could just stick a speaker out in the woods and let it go all day, but it's kind of like putting a bandage on a sinking ship.
The real issue here is conservation of these guys' habitats, which involves a variety of processes beyond a boombox in the woods. There are tons of questions we still need answers to. For example, if a population decrease results in young birds learning the wrong songs, what causes the population to decrease in the first place? It's a sort of chicken or the egg question. Or, what if we just take the birds and combine their populations? Well, that might be more harm than good. What causes these birds to learn the songs of other species? Are they too smart for their own good? How heritable are the genes that encode these important songs? So on and so forth, you understand.
For more about conservation, and what can be done, check out an example of the Florida panther and what's been done to protect them. Of course, every group is unique in their needs, but just to get an idea of what it takes to conserve a species.

Great literature review from @BrownBag of the original paper. A notable addition to whether the speakers will be effective in teaching the young males the "correct" song brings in the topic of acoustic propagation.
Even if the speakers are placed in the areas with the most young males /and/ are "singing" the correct song, it does not mean all of the song's important features will projecting equally throughout the environment where the young males would be positioned. Consider these three examples:

If air temperature is higher to the East than to the West

There is denser foliage to the North vs the South

There is a highway in the NE corner of the habitat.

All the frequencies of the "correct" song will still not propagation equally under these conditions.
Overall: lower frequencies propagate further than higher frequencies, so a young male further from the speaker may only receive the low frequencies of the song and therefore still learn a low-frequency-only "wrong" version of it.
In terms of the specific examples 1-3 above:
1A) Sound waves travel faster in cooler temperatures, so young males towards the West will have a better chance of hearing the song at further distances to the speakers.
2A) Denser foliage reduces propagation distance by absorbing and scattering sound waves, so young males listening through the leaves (literally) towards the North may learn a diluted version of the "correct" song.
3A) Highway noise masks low frequencies more than high frequencies, so young males positioned closer to the highway (in the NE corner of the habitat) may learn a high-frequency-only "wrong" version of the song.
All these environmental limitations to propagation can shape song over time. They are also not predictable from day to day, so the ideal placement of a speaker could change from day to day.
In terms of time scales of evolution, it is likely that the Regent honeyeater has been able to adapt to temperature and foliage differences over millennia (since they are not extinct yet). But the human-driven effects of masking have occurred on a faster time scale (over decades, not millennia). Therefore, the Regent honeyeater may or may not be able to adapt its song fast enough under the faster anthropogenic pressure and could go extinct as a result.


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How does sea plants undergoes photosynthesis?
Since most of them do not have the chloroplast.
And if they undergo how do they perform it ( thus the light stage)

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Who says they don't have chloroplasts?


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Why did scientists state that the Omicron COVID-19 variant was a reason to get a booster?
I was watching Vox’s video, Big questions about the Covid booster shot, answered, which references the New York Times article Omicron Prompts Swift Reconsideration of Boosters Among Scientists.
In these sources, it is mentioned that the scientific community used to be mostly against giving a COVID booster shot to the less vulnerable. With the emergence of the Omicron variant, the same scientists who were opposed to booster shots had changed their minds.
However, no complete explanation was given for this in these sources, and my further research led to nothing concrete.
As per my understanding, vaccinations provide protection both by increasing antibodies in the blood (which provides protection for about 2 weeks), or by increasing B cells which would be able to identify the spike protein of the virus and help create antibodies (which provides more long-term protection).
With the SARS-CoV-2 Omicron variant, my understanding is that there were several mutations in the spike protein, which means that B cells may not recognize it or the antibodies might not bind to its receptors. If this is the concern, then how was the Omicron variant a reason for extra doses of the preexisting vaccines?

I think it's important to recognize that scientists "against giving a booster shot to the less vulnerable" had that position for public health reasons of reserving the available doses for those who had not yet received any vaccine.

Just because Omicron has come out, it doesn't mean the others have died down.  They are still about.  Some vaccines may not be effective against omicron but they may be effective against all the others before or even after omicron.  Note that vaccines are not the magic bullet that some govts and newspapers sell it to be - you can still get infected after having the vaccine.  There is no magic bullet.

This came out today (BBC): "Two doses of a Covid vaccine are not enough to stop you catching the Omicron variant, UK scientists have warned. Early analysis of UK Omicron and Delta cases showed the vaccines were less effective at stopping the new variant. However, a third booster dose significantly increased protection to around 75%."

@BryanKrause The scientists against giving the booster shot to the less vulnerable are motivated by the risks to individuals.  "One big reason for the panel’s skepticism: the risk of myocarditis and pericarditis … particularly in men aged 18 to 25. Those  patients, several panelists said, are also at the lowest risk of Covid." https://www.statnews.com/2021/10/14/fda-advisory-panel-meeting-moderna-covid-vaccine-booster/

(note: I'm simplifying things a bit here by only talking about antibodies; I don't mean to downplay other aspects of the immune response, just to keep it focused for a lay audience)
Natural antibody responses by the immune system are polyclonal - there isn't just one antibody to meet one antigen, but numerous different antibodies that may each recognize a slightly different part of the antigen.
Antibody binding (or ligand binding more generally) is also not "all-or-none". We usually describe ligand binding in biology by "affinity". When a receptor has a lower affinity for some ligand, you need higher concentrations of the ligand to saturate the same fraction of receptors (or vice-versa).
You can expect that antibodies raised against a coronavirus spike protein may have lower affinity for spike proteins altered by mutations in a viral lineage. It's also reasonable to expect that the more changes (mutations) there are, the more the affinity will change and the more antibody clones will be affected.
It's still unlikely that every different antibody in a polyclonal response will stop binding completely, but the reduced affinity is likely to equate to a reduced immunity. It's not easy to quantify this at the level of the whole organism, but it's normal to do in vitro binding experiments where you mix a mutated viral protein with some antibodies raised to a previous version. The extent of binding is a good qualitative approximation for how well immune responses will transfer.
Probably the best approach would be to give boosters with a spike closer to the new dominant variant at any point. However, that requires testing and manufacturing and simply isn't going to happen in time to be useful. In the meantime, the best alternative is to be prepared against the next-closest thing. As an approximation, you might say that if binding affinities are reduced by 50%, then if you can double your antibody response you've got about the same immunity.
Previous experience with the delta variant showed that antibodies raised in response to vaccination with the original spike protein still bound, even if they didn't bind as strongly. It seems like vaccinated people had good protection against delta even if it wasn't as good as their protection against the original strains. We can expect the same trend for the new variant, though we'll need further data to understand quantitatively where that protection level is at.

We're getting the first, non-peer reviewed yet, reports and it doesn't look good: https://www.medrxiv.org/content/10.1101/2021.12.07.21267432v2.full.pdf. I need to go through it a bit more carefully, but they are claiming that two jabs of BionTech gives 0% protection from omicron. Apparently, the best results are a combination of vaccine and infection. This is only about omicron and only about several months past the first vaccine, it shouldn't be taken as an indication of the efficacy of recent vaccination.

@terdon 0% protection against what? Infection / transmission / symptomatic cases / hospitalisation / death / all of the above?

@Tim none of the above. This is an in vitro study using blood serum extracted from people with different combinations of vaccine doses. The serum should contain antibodies against the virus, which should be able to neutralize the virus when put in a solution with it. The paper claims that serum from individuals with only 2 vaccination doses (no booster) had no effect on Omicron (but did on Delta). Exactly what such an in vitro study means for the effects in vivo is unclear, but it isn't encouraging. The good news is that sera from people who had had a booster shot did better.

@terdon Interesting. I would have thought a spike that mutated past antibodies completely would also not bind to the same receptor. But I guess that's too much to hope for.

"...not "all-or-none". (...) When a receptor has a lower affinity for some ligand, you need higher concentrations..." - Would like to know about role of concentration in respect of antibodies compared to t-cells and their receptors.

to the above: https://twitter.com/CiesekSandra tells - 8th of dec. 21 - antibody neutralization by 3 doses Biontec 25 percent effectivity after 100 days compared to roughly 90 percent with Delta.

Some Clarification:

Scientist were not opposed to a third dose, they were opposed to the rich country getting a third dose before we vaccinated the rest of the world. The WHO is right to call a temporary halt to COVID vaccine boosters
With Covid immunity either from vaccination or infection weaken with timeIsraeli Study Shows How COVID-19 Immunity Wanes over Time. Thus, a booster shot help your immunity.Immunogenicity and safety of a third dose of CoronaVac

What changed the mind of expert? Even if Omicron is not more dangerous than delta. (dangerous here: For 1000 persons, How many needs hospitalization, ICU, will got sequels and long covid or will die?)
Omicron is "at least time 2" more contagious. In terms of spreading capability, it is a monster. It is estimated that case double each 3 days (All number you are seeing right now will evolve as we get more data).
EDIT: This number is changing as new data emerge, cdc only state that omicron is more transmissible: cdc. The number I gave 2 times more transmissible and doubling every 3 days are from non peer reviewed source, take them with a grain of salt. Other sources are more dramatic, to have the real number science need a bit more time and more data.
Omicron seems to be able to reinfect people infected previously.
All together, those two points are scary. We expect to have a lot of covid case in a shorter time span. Followed by hospitalization with all the negative attached to it. To a degree we have never seen. Yes you heard it right, we expect it to be bad...  Hospital saturation, economic going slow.
In this context, a booster shot may impose itself as a way to preserve life and avoid hospital saturation. Early data show a weak protection to infection from previous infection or vaccination (but everything help in this regard)Omicron likely to weaken COVID vaccine protection. But we still hope that the third shoot preserve from dangerous form of the disease.
Summary :
The Goal of a third shot is to avoid a saturation of the health care system, a lot of people still seem to minimize this eventuality, but it is terrible. It is what cause government to impose shutdown and lockdown.

(Update Dec 15: See update in my 2nd answer below, describing new study based on actual patient data, published in just the last few days, relevant to the current question.)
This answer is a supplement to the answer of @Bryan Krause. It responds to a comment by original questioner @hb20007, who pointed out that
"My question was about the seeming logical contradiction where the concern with the Omicron variant is that it might have too many mutations in the spike protein to be recognizable by existing immune cells, but the proposed solution is extra doses of the same old vaccines."
This comment makes a reasonable point: there might indeed be a 'logical contradiction' if it were true that a booster only provides more of the very same immune response that the previous dose(s) evoked.
But in fact, vaccine doses of identical content not only can generally produce different immune responses in different people: it's also the case that successive doses of the same vaccine can also produce different immune responses in one and the same vaccinated person.  This is fundamentally due to the presence, as part of the normal mechanism of immune response, of a stage that involves random mutations, even hypermutation (followed by selection) of the somatic genes encoding antibody proteins.
When a booster vaccine is given, it not only boosts the quantity of the immune response, it also causes a process called antibody affinity maturation. (See also a recent review in 'Frontiers in Immunology'.) The mutations involved in this process can increase the diversity of the immune response. This mutation round is built-in to the system, so this is 'good' mutation (when it goes to plan*) -- and it is followed by selection of those mutation products that have affinity for the antigen.
As a result, the enhanced immune response after a booster vaccine is not just a 'carbon copy' of the earlier immune response.  As long as the antigen underlying the vaccine retains some relevant cross-reactivity with a variant antigen of concern, there is the possibility of increasing the response against the variant antigen by the booster.
At the same time, it does seem obviously more desirable that the vaccine against a variant antigen should be tailored as closely as possible to any new antigenic identity of concern. The chances of relevant protection are so much the better, as the resemblance between the vaccine antigen and the variant antigen is closer. So far, the experts who have made recent statements, about the value of boosters using the original coronavirus vaccines types, do not seem to be denying (as far as I read them) that a variant vaccine tailored to the mutated variant antigen would be desirable, but they are emphasising the point that the potential utility of the current vaccines is still there in spite of the mutations.
Perhaps a variant coronavirus vaccine will be produced along lines parallel to the annual flu vaccines, where an existing manufacturing and formulation method is repeated for the variant except for the identity of the antigen(s) included. Because of the commonality these are subjected to (abbreviated) testing and regulatory examination.  There may be more happening in the reserach pipelines for the coronavirus than we are currently getting news of -- but we are not there yet, and the only vaccines around appear to be those targeted on a spike protein with sequence close to that of the original SARS-Cov-2.

*(Somatic hypermutation does occasionally suffer genetic accidents, see for example  (https://pubmed.ncbi.nlm.nih.gov/30874354/). But it remains a vital stage in the normal immune response.)

"...there is the possibility of increasing the response against the variant antigen..." Could you please add some reference? That's because there was no specifity "at all" before? Possibility in a literal sense?

@Peter Bernhard  -- I didn't say or suggest there was 'no specificity at all before'. Also, according to my understanding, the reports of reduced effect of the immune response arising from the current vaccines against the new variant are just that, reduced effect, they do not say that there is no binding effect at all. The references I've given about the hypermutation and affinity maturation already appear to provide what you asked.

@hb20007 -- thank you!

No pun intended (globally) drawing your attention to your source "Frontiers...", citing: "Indeed, the periphery may offer more suitable sites for optimization because these regions are typically more flexible and tolerant to mutations than central sites." The more affinity maturation the more cross-reactivity (which is more)? Thanks!

Pathogens (and unfortunately sometimes unrelated things) have antigenic sites. These antigenic sites are responsible for acting as antigens by which an antibody can respond to, or perhaps a larger immune response can initiate. Viruses and pathogens are constantly evolving to try to better hide from their hosts' immune systems, called the Red Queen hypothesis.
One reason why the Omicron variant may be more transmissible than the current Delta variant is because of difference in these antigenic sites. If an immune cell can't recognize a pathogen, the pathogen can sneak by undetected and may later initiate infection. In essence, subtle differences in new variants are what give those variants a potential advantage over each other. This variation is a source of evolution, and you can't forget that viruses are evolving too, just like every other species on Earth. Often, viruses are phylogenetically monitored for their level of divergence to try to plan ahead and determine which viruses are going to be the most troublesome next year.
So, what needs to be investigated now? Well, much research is being done trying to figure out how much conserved information there is between variants, called homology, as well as other factors like hospitalization, virulence, and so on. Depending on how alike Omicron is to Delta will depend on how well our vaccines are against it. If our vaccines have a chance at doing something, then being immunized right now is absolutely crucial in preventing the evolution of future variants and later strains that may be more pathogenic. While it may seem like a time to rest on our laurels, the Omicron variant gives rise to new genetic variation that may result in future evolution and extend this pandemic long beyond what we have the patience for. It is our responsibility to beat out that evolution before it can occur.
But, then again, the immune system is a complicated mess of unintuitive situations, and I would encourage you to read into all of the science a little further.
Here are some resources:
A little bit about the immune system.
About how viruses must balance transmission and virulence (lethality).
How evolution helps us understand viruses.

Be careful: The transmission rate has nothing to do with the immune system. This is a "simple" stick and fit to the receptor which is needed for cell entry. That this is the same as we are vaccinating against has reasons.

I'm not talking about the lock and key model, I'm discussing the evolution of a virus. Viruses with high transmission are weakly selected against in virulence, they can kill people because they spread easily. Viruses with low transmission can't get away with this, and so virulence is selected against. Variants with differences in antigenic sites can become more transmissible. Why? Because the immune system is naïve to them.

This answer has a lot of great information but I feel like it does not completely answer my question. My question was about the seeming logical contradiction where the concern with the Omicron variant is that it might have too many mutations in the spike protein to be recognizable by existing immune cells, but the proposed solution is extra doses of the same old vaccines.

Hey that's fair. Allow me to clarify. Boosters for everyone were previously recommended against so that people who were at high risk had access to them, because their immune responses are typically weak and the level of immunity they achieve isn't as great as say a young person. But now, we have a new variant to worry about, and there's a reasonable chance that, because of evolutionary homology, our vaccines may do something about it. To prevent this variant from spreading and creating another worse variant, it's important to immunize ourselves as best as possible.

@BrownBag: Can you add the information to the answer, please? Comments may be deleted at any time. (But without "Edit:", "Update:", or similar - the answer should appear as if it was written right now.)

@Chris - please would you clarify your comment that "transmission rate has nothing to do with the immune system"? Literally that statement would include claim that transmission rate is the same in a population of non-immunised susceptibles as in a heavily immunised population -- clearly not so.

@terry-s Sure. Omikron is not more transmissable because of the changes, but because it can infect the cells more efficiently and probably because it causes a higher viral load (which is not completely clear at this point to my knowledge). Immune evasion helps the infection but has no effect (or only a minor) on the transmissability.

@Chris You don't think those 'changes' that result in greater infection, or better immune evasion then subsequent infection, have an effect on the susceptible population? As a consequence, this notion implies that the effective reproduction number is not somehow directly proportional to the rate of transmission. I perhaps see what you're saying, that transmission and infection are not the same. But there are implications of increased infection, whatever the mechanism, however the cause, that affect the dynamics of transmission.

This is a second/supplementary answer, bringing newly-published data relevant to the question
"Why are scientists saying that the Omicron COVID-19 variant is a reason to get a booster?" and in particular, why "the proposed solution is extra doses of the same old vaccines" (when initial courses of those original vaccines have shown clear signs of relative ineffectiveness against this new variant).
My earlier answer (Dec 11) tried to describe the part of the normal immune system that enables a booster vaccine dose to generate a diversified immune response, through the intervention of the random-mutation part of the system.
While this describes an in-principle mechanism for booster effectiveness against Omicron in the current scenario, descriptions of mechanism inevitably leave aside an important point : 'how effective' can such booster vaccine doses be?
To answer that, as the old saying goes, "the proof of the pudding is in the eating".  But with the Omicron variant so new, the main scientific results until the last few days had to be based on laboratory-bench testing of blood-serum/antibody samples.
Naturally of great interest is actual clinical data, and within the last week, the original laboratory data have been supplemented by publication of a (preprint) report of a UK-based case-control study surveying actual patients.
Again, since the Omicron variant is still so new, and the Omicron-caused diseases still so recent and perhaps in early stages, the new study is "unable to determine protection against severe forms of disease, due to the small number of Omicron cases so far, and the natural lag between infection and more severe outcomes".  Nevertheless, the new results do show that the indications from the laboratory antibody studies are being confirmed in the early clinical experiences of covid-19 due to Omicron, i.e. the results are showing that booster dosing with the Pfizer-Biontech vaccine gives a marked improvement in protection against the Omicron-caused disease seen so far compared with the effects of either of the previous 2-dose vaccine programs alone.
The report is still too recent to have been refereed, but can be read at "Effectiveness of COVID-19 vaccines against the Omicron (B.1.1.529) variant of concern". The authors come from hospitals and research institutions in London, Oxford and Cambridge plus the national health-security agency. The data analysis was enabled by the UK National Immunisation Management System with details of covid vaccinees.
The authors' introduction cites previous "preliminary neutralisation data" (that is, laboratory studies of antibody inactivation of virus) against the Omicron variant.

"The South African and German studies, as well as unpublished data
from the UK, indicate a 20- to 40-fold reduction in neutralising
activity in sera from 2-dose [Pfizer/Biontech] vaccine recipients
compared to early pandemic viruses, and at least a 10-fold reduction
compared to the Delta variant." Thus the "effectiveness [of available
vaccines] against symptomatic disease with the Omicron variant is
significantly lower than with the Delta variant."

Among those who had received 2 doses of [Pfizer/Biontech], vaccine
effectiveness [against Omicron] was 88.0% ... 2-9 weeks after dose 2,
dropping to 48.5% ... at 10-14 weeks post dose 2 and dropping further
to between 34 and 37% from 15 weeks post dose 2.
Vaccine effectiveness increased to 75.5% ... after the booster among
those who had received [Pfizer/Biontech] as the primary course."

"Among those who had received 2 doses of [Oxford/AstraZeneca], there
was no protective effect of vaccination against symptomatic disease
with Omicron from 15 weeks after the second dose.
Among those who received [Oxford/AstraZeneca] as the primary course,
from 2 weeks after a [Pfizer/Biontech] booster dose, vaccine
effectiveness [against Omicron] increased to 71.4% ... .

"All of the Omicron estimates are subject to significant uncertainty with wide confidence intervals", because of the low number of patients with identified Omicron-caused disease (just under 600 patients between 27 November when Omicron patients began to be identifiable and 9 December when the data were obtained, although Delta patients and test-negative controls in the data came from a larger time-interval and numbered over 56,000 and over 130,000 respectively.
Thus the new study concludes that

"a booster dose of [Pfizer/Biontech] following either
[Oxford/AstraZeneca] or [Pfizer/Biontech] as a primary course" brings
"moderate to high vaccine effectiveness against mild infection [due to
Omicron] of 70-75% ... in the early period after [the booster dose]."

By contrast, for patients without booster doses,

"Our findings indicate that 2 doses of vaccination with
[Pfizer/Biontech,] or [Oxford/AstraZeneca] are insufficient to give
adequate levels of protection against infection and mild disease with
the Omicron variant, although we cannot comment on protection against
severe disease."

"Booster doses of [Pfizer/Biontech] provide a significant increase in
protection against mild disease and are likely to offer even greater
levels of protection against severe disease. As such our findings
support maximising coverage with third doses of vaccine in highly
vaccinated populations such as the UK. Further follow-up will be
needed to assess the duration of protection of booster vaccination."

So the boosted patients in the study experienced very much better protection against Omicron than patients who had only received two doses, whether of Oxford/AstraZeneca or Pfizer/Biontech.
In the US, in reaction to recent results, "Dr. Anthony S. Fauci said Wednesday [Dec 15] ... that “at this point, there is no need for a very specific booster” designed especially to fight Omicron." New York Times.


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Why does Meiosis produce 4 daughter cells instead of 2? Won't splitting the initial diploid cell into two haploid cells be easier?
At first, I thought it was because of crossing-over, but when I thought more about it, that didn't seem reasonable. Why don't cells just do meiosis like this? (I know that we don't understand all the why's and how's in biology yet, but if anybody has an explanation for this I would appreciate it)

Diploid cell has 46 unique chromosomes - 23 homologous pairs
Cell crosses over the homologous pairs WITHOUT duplicating them first
Metaphase and Anaphase produce two haploid daughter cells, each with a unique combination of genes within a chromosome - 23 total

Instead, this is what they do (or at least, how I understand them to do)

Diploid cell has 46 unique chromosomes - 23 homologous pairs
Cell duplicates all chromosomes - 92 in total - 46 unique chromosomes - 23 homologous pairs
Cell crosses over the homologous pairs
Metaphase and Anaphase produce two haploid daughter cells, each with 46 chromosomes - but only 23 are unique - the others are duplicates of that 23 (with the exception of the variance caused by the crossing over - what I mean is, all 46 were all initially from the same parent instead of the 23/23 found in a diploid cell)
The two daughter cells undergo Meiosis II in order to produce four total daughter cells -  Each has 23 chromosomes - All 23 are unique

So why does the cell take this more difficult path in order to achieve the same thing? Am I missing something out here? I would really appreciate some help. Thanks!

here is what I think why cells evolved to do meiosis like as it is now and not like you mentioned.
First I will try to tell you briefly (not in detail) how crossovers are made and how they ensure the segregation of chromosomes.
During meiosis the  cells are programmed to make DNA double strand breaks (DSBs). These DSBs are repaired by a pathway called Homologous Recombination (HR), where the breaks can be repaired into cross overs (CO) or non cross overs (NCO) using a template DNA (which could be DNA from sister chromosome or from homologous chromosome). For the homologous chromosomes to properly segregate during Meiosis I, at-least there should be 1 CO per homolog pair.
But in most studied organisms (including humans, mice), the number of DSBs largely outnumbers the CO number. For instance in mice there are 20 homolog chromosome pairs, so they need 20 COs for proper homologous chromosome segregation; but to produce 20 COs the cells are making 200-300 DSBs. And the remaining are repaired as NCO with homologous chromosome or as both CO and NCO with sister chromosomes.
So coming back to your possibility, if the cell was trying to do CO without DNA replication (without sister chromosome), it is risking its genome for less options for repair. More molecularly, sister chromosome is the ideal template to properly repair a DSB than homologous chromosome!

Your answer could be improved with additional supporting information. Please [edit] to add further details, such as citations or documentation, so that others can confirm that your answer is correct. You can find more information on how to write good answers in the help center.


text:
How much do the COVID vaccines decrease the spread of SARS-CoV-2?
The vaccines targeted at COVID-19 are measured against their ability to reduce the occurrence of the disease, COVID-19 (The Vaccine Efficiency or VE).  It does not measure its effect on the underlying virus' ability to spread.  From what I understand, this is the standard approach used for measuring the effectiveness of vaccines.  So called "sterilizing" vaccines, which prevent infection of others, are relatively rare.
From what I have read, it is generally accepted that the COVID-19 vaccines do indeed decrease the rate of transmission of SARS-CoV-2 (if I am understanding properly, this reproductive rate is typically given the label $R_T$, distinguishing it from $R_0$ which is the reproductive rate excluding any proactive behaviors we undertake).  However, I have not found any estimates as to how much it decreases transmission, which is an important number to estimate when projecting the long term behaviors of SARS-CoV-2 in society.
Are there any estimates to the effect the COVID-19 vaccines have on the reproductive rate of SARS-CoV-2 backed by studies?

https://www.nature.com/articles/d41586-021-02054-z cites some Israeli studies stating that vaccinated, infected people are 78% less likely to transmit to members of their household than unvaccinated, infected people ...


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Is bacterial resistance caused by underdosing?

The phenomenon of antimicrobial resistance caused by overuse of antibiotics was predicted as early as 1945 by Alexander Fleming who said "The time may come when penicillin can be bought by anyone in the shops. Then there is the danger that the ignorant man may easily under-dose himself and by exposing his microbes to nonlethal quantities of the drug make them resistant."

Source: https://en.wikipedia.org/wiki/Antimicrobial_resistance#History
Obviously quotes from the history section are hardly authoritative, but I just wanted to check that although his prediction was correct, the mechanism that caused it was misunderstood at that time? My own understanding would be that resistance is about random bacteria being resistant and those bacteria thriving because all other bacteria were killed.

In a 2017 analysis in The BMJ, Martin Llewelyn and colleagues addressed the question of whether it is good to advise people prescribed antibiotics to "finish the course".1 I've copied their key takeaways below, but I encourage you to read the full article as they present a convincing argument that overtreatment is more dangerous than undertreatment in regards to the emergence of resistant organisms.

Patients are put at unnecessary risk from antibiotic resistance when treatment is given for longer than necessary, not when it is stopped early
For common bacterial infections no evidence exists that stopping antibiotic treatment early increases a patient’s risk of resistant infection
Antibiotics are a precious and finite natural resource which should be conserved by tailoring treatment duration for individual patients
Clinical trials are required to determine the most effective strategies for optimising duration of antibiotic treatment

References

Llewelyn MJ, Fitzpatrick JM, Darwin E, SarahTonkin-Crine, Gorton C, Paul J, Peto TEA, Yardley L, Hopkins S, Walker AS. The antibiotic course has had its day. BMJ. 2017 Jul 26;358:j3418.

You have to either subscribe (157 dollars per year) or  buy  the  individual  article (£30 / $37 / €33 (excludes VAT)) to read it in full. Regarding 'finishing the course'. Can we trust our doctors to prescribe a course that is commensurate with the illness the antibiotic is designed to treat? If so we should finish the course. If not, how do we decide when to stop? When we feel better? I recently had an abscess on my gums (ew). By day 3 (of a 7 day course) the pain had disappeared. Would it have been a good idea to stop then?

@Naj -- Here's a PDF hosted elsewhere. My answer addresses the question of antibiotic use in regards to antibiotic resistance, not in regards to disease treatment. Always take your medication as it is prescribed.

Hi, thanks, read the PDF. Of course, I acknowledge that your answer is about antibiotic resistance. However, the linked article does say the following (addressing my concerns about how you know when you're actually cured, as opposed to just 'feeling better') : "Outside hospital, where repeated testing may not be feasible, patients might be best advised to stop treatment when they feel better, in direct contradiction of WHO
advice." and "Research is needed to determine the most appropriate simple alternative messages, such as stop when you feel better."


text:
What do cats see when they look at 2D, still images?
My cat doesn't like other cats. She doesn't really like anyone that isn't part of our family. So when she sees other cats she will aggressively try and chase them out of her area. She will also do the same to dogs, if she thinks she can take them on (she is a medium-large cat). She used to occasionally go after her own image in a mirror, until she basically gets bored or realizes that the 'other cat' is behind a barrier she can't cross. Nowadays, she appears to have either given up, or realized on some level it is her (I know cats don't have mirror recognition).
However, when presented with the image of a cat, like one on the side of a food bag that is the same size as her, she completely ignores it. I would get it if she dismissed it once she realized it wasn't moving, doesn't smell like a cat, and therefore is not alive (aka, not a threat), but she doesn't even acknowledge it. And the image on the bag isn't of a cat in a field or obscured at all. It's Hill's Science cat food, which is basically a white bag with a forward facing, unobstructed cat on it the same size as an actual cat.
Her completely ignoring it makes me wonder how well she can actually see it. Can she see the details at all, or is it just a dark blur on a white background? I've seen videos of cats playing games on tablets and other 2D surfaces, but those games again feature moving objects on the screen. Given that cats generally have excellent vision for hunting, how well can they see 2D, static images? And if she can see it, do cats really have the cognitive ability to dismiss an image so quickly?

Does she respond to images of cats on a tv screen?

Yes! And to bugs; etc. But again, those are moving. I'm more curious about static images.

Clearly, if she reacts to TV images, the issue isn't 2D vs. 3D, or not only that.  Maybe she's learned that cats that never move and never change perspective even as you move around them are not threats.  OTOH, there has been cross-cultural perception research suggesting that humans have to learn to interpret photos as images of the world.  That conclusion was controversial, iirc, and I don't know where the science stands at present.  If that conclusion about humans was correct, interpreting static photos as reality ought to be even more difficult for cats, one would think.

Maybe, but I just started on this food because of a medical issue she had. She's never seen this image of a cat before, which is why it surprised me!
I focused on 2D, static images because she can react to sculptures. Often she goes and checks them out, a bit aggressive at first until she smells them and realizes that they are made of stone or similar. She just had no reaction to the 2D images, which I found interesting.

So, oddly enough, I found a decent answer in a Business Insider article, How cats see the world compared to humans by Dina Spector. She consulted with a few animal ophthalmologists, and it seems that cats' eyes and brains are more focused on detecting motion, and cannot see a wide range of color. Therefore, it is likely that my little fur-ball cannot even discern that the image on the food bag is a cat at all.
That being said, I did find this interesting article about cats responding to illusory motions, like rotating snakes. However, the sample size for this study was shockingly small.  I may try and show these images to my own cat and see what she makes of it...

Refs
Bååth, R., Seno, T., & Kitaoka, A. (2014). Cats and illusory motion. Psychology, 5(9), 1131-1134.

some additional information https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.1970.sp009270

Have you watched this video?

Thank you, @RodrigodeAzevedo for bringing that into my life.


text:
Why does vasodilation increase blood flow in the capillaries, but decrease it in the chest during inspiration?
From Guyton and Hall Textbook of Medical Physiology:

Every time a person inspires, the pressure in the thoracic cavity becomes more negative than usual, causing the blood vessels in the chest to expand. This reduces the quantity of blood returning to the left side of the heart and thereby momentarily decreases the cardiac output and arterial pressure.

Why does vasodilation increase blood flow in the capillaries, but decrease it here?
As I understand it, vasodilation results in decreased resistance. According to Ohm's law, decreased resistance should increase blood flow.

The passage isn't talking about a magical diameter increase in a physics problem. If negative outside pressure causes blood vessels to increase in diameter, something has to fill the vacated space inside: blood.
That means that some of the blood that would be flowing through the vessels into the heart is instead filling the extra space in the vessels themselves.
You could most directly model this in terms of analogy to electricity by thinking about the vessel walls as a capacitor, and it takes some time to charge that capacitor when the outside pressure is released. If you measure flow at the input, you'll see a higher flow because a good portion is charging the capacitor/filling the vessels, but if you measure flow at the output you'll find a reduction.
I'm not strongly familiar with the effect described in Guyton and Hall but I'm guessing that the "momentarily" word in there is doing a lot of work, as this effect is going to be brief relative to the respiratory cycle.

...if you measure flow at the output you'll find a reduction. This doesn't seem to happen in the capillaries (any capillaries, not necessarily in the chest) during vasodilation. Why?

@athlonusm It would momentarily if arterioles suddenly expanded. Once they are expanded and "full", though, there's nowhere to go but through. I don't know that it's possible for arterioles to expand via vasodilation as rapidly as you get in the chest from inspiration, though.


text:
What kind of spider is this from New Zealand?
This is biggest one I have caught so far:

They would occasionally walk into my house and wait for the night to go out and about.

The features are fairly generic. It is probably a house spider, genus Badumna

Please let it go free. It shares this living space with you!!

Spiders are much more likely to be highly beneficial to you than to be harmful. Please consider leaving them alone, or if you can't, catch and release.

With the limited info and only a side image (top/bottom photos more helpful for ID), it's hard to pinpoint a specific species. To complicate matters, Manaaki Whenua Landcare research suggests:

Over 90% of New Zealand spiders are endemic, the rest are natural introductions through windborne or human activities. The species we frequently see around are houses and gardens are usually introduced species. Most of the endemic species are restricted to native habitats, from forest to alpine regions

One possible group are the sheetweb spiders (family Stiphidiidae).
According to Wikipedia, most species are speckled brown with long legs with a body length < 2.5 cm and leg-span < 15 cm. This family of spiders is nocturnal, and they can be found in gardens or (ales) even enter homes.
Here's an example specimen from this family:

 Source: Manaaki Whenua Landcare research
According to Arachne.org.au, the Stiphidion genus is the most commonly seen group from this family.

Their image of a female Stiphidion, also closely resembles yours:

 Credit: Dr Greg Anderson, Source: Arachne.org.au


text:
Cortisol in sharks
Is there an established method for measuring stress hormone levels, like cortisal, in sharks? If so, is it known what levels of such hormones create significant detrimental effects like decreased immunity?

This is not simply an answer site, but instead a site that promotes self-learning with some expert help. Consequently, questions that show little or no prior research effort are off-topic on this site — have you tried searching for "stress hormone levels sharks"? Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Please take the [tour] and consult the [help] starting with [ask] for details.

https://pubmed.ncbi.nlm.nih.gov/17977765/