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How can I render a protein non-functional to avoid problem during expression?
We're expressing a protein in a model organism for crystallization, however it seems the protein has some toxic effect on the cells.
Is there something we can do to make it non-functional during expression so it won't affect production, in such a way that we can restore function later (ex. after purification) in a simple way?
I know there are other approaches available but I'd like some inputs on this one alone.

That would depend on the specific protein being expressed. You could try secreting the protein or targeting it to inclusions and then refolding.

Can you provide more information? Are you expressing the protein in yeast or bacteria?

@user22542 in yeast, however I'd be interested to hear approaches that can work in different vectors too

I assume the toxicity is limited and not lethal.  Is the protein showing the toxic effect being secreted during production or retained in the cells?

@user22542 It is secreted in the medium

With limited knowledge and information, but intrigued with the question, I can only hazard to ask if it might be possible to alter the pH of the media (or another parameter) enough to render the protein temporarily "non-functional" or at least "less toxic" while maintaining a permissive environment for the growth of the production yeast? Beer becomes a questionable environment yet the yeast don't seem to mind to a point.

@user22542 could be an idea, I guess

You need to add more details or else the question would be considered too broad and most likely put on hold.

Inclusion body (IB) is a technique used to express proteins that are toxic to the host cells. IBs are aggregate of highly similar or the same kind of proteins in the cytoplasm formed as stress reaction, resulting biologically inactive precipitated proteins. Such stress reactions can be induced by high temperatures, pH-shifts or occur due to high feeding rates (1,2). Active proteins can be acquired later via purification and mild solubilization of inactive IBs (1).
The second method is to use special host strains. In terms of E. coli, some strains are specifically mutated and selected to withstand the expression of toxic proteins (3). e.g. C41(DE3) and C43(DE3) are developed to enhance membrane protein production (4).
Another method is to express proteins in the periplasmic space. In E.coli, you can achieve that by fusing your recombinant protein with a proper signal peptide, which targets the recombinant proteins to the periplasm via post-translational Sec-dependent pathway (3).
In addition, I also found this product list that provides several solutions for toxic protein expression, including expression in yeasts. But in that case it is similar to your situation so I am not quite sure why it doesn't work out for you.
Resources
(1) Slouka C, Kopp J, Spadiut O, Herwig C. Perspectives of inclusion bodies for bio-based products: curse or blessing?. Appl Microbiol Biotechnol. 2019;103(3):1143-1153. doi:10.1007/s00253-018-9569-1
(2) Slouka, C., Kopp, J., Hutwimmer, S. et al. Custom made inclusion bodies: impact of classical process parameters and physiological parameters on inclusion body quality attributes. Microb Cell Fact 17, 148 (2018). https://doi.org/10.1186/s12934-018-0997-5
(3) Rosano Germán L., Ceccarelli Eduardo A. Recombinant protein expression in Escherichia coli: advances and challenges. Frontiers in Microbiology 5, 172 (2014). https://www.frontiersin.org/article/10.3389/fmicb.2014.00172
(4) Kwon, SK., Kim, S., Lee, DH. et al. Comparative genomics and experimental evolution of Escherichia coli BL21(DE3) strains reveal the landscape of toxicity escape from membrane protein overproduction. Sci Rep 5, 16076 (2015). https://doi.org/10.1038/srep16076
(5) https://www.neb.com/-/media/nebus/files/brochures/proteinexp_trifold_0912.pdf?rev=3ade8cf2c18b47afb7cc57113df43147&hash=7BEDC3D4DBDAE53A09EC37ADE808C450


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How is mankind important to nature?
Like mosquito eggs are important for fish, what’s our role in balancing the life on earth or its ecosystem.
Please suggest if this question doesn't fit in this community.
I am a mechanical engineer with interest in knowing biology and biochemistry.

Hi and welcome to BIO.SE. Although humans clearly play a major ecological role in the world, the wording/focus of your question (specifically within the context of your use of the word "role") causes your question (and therefore any answers) to be opinion-driven. You can try to to read up on top-down control of ecosystems, given that we are clearly top predators.

The classical division of humans and animals has always been self-centered and artificial. Humans are animals, competing with other organisms under exactly the same rules. Evolution involves trade-offs, strategies, and adaptation. Humans have been set on a path to use their brains to compete, rather than claws. But the concepts are the same. It happens that this is a very effective strategy, such that humans now dominate virtually every ecosystem on Earth, to the point that some are now calling the age we live in as the "Anthropocene". Humans are the apex predator. We now have no natural enemies, however as vectors of disease, mosquitos control our populations more than any other animal.

very useful @KarlKjer
Can we say, human is producer of enough carbon dioxide-- useful for photosynthesis? Though I know, we have been brutal to nature in all the ways.

The carbon dioxide we produce has a benefit to Northern climates, but  is balanced by the detrimental effects of warming in the tropics. Given that plants are also evolved to live in the climates where they exist, and are often tightly linked to their pollinators, the potential decoupling of this relationship with increasing temperatures is not beneficial to plants. Some crops in some places will produce more (as the planet and most life on it suffers)

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Is a wild-type strain more "fit" than its mutant strains?
Question's context
In the context of a presentation on mathematical models for antibiotic-resistance bacteria research, someone mentioned that wild type strain (WT) are expected to be more fit than mutant strains.
Assume that there is one WT introduced to an environment E (no drugs present), and consider the WT mutates, yielding a certain number of fit-enough mutant strains.
Question
Is WT expected to be the ONLY strain to persist in the long run?
How common is this scenario?
What about co-existence?
Examples and references for beginners will be very appreciated.
My context:
Please note that this may be a very naive question, and I may even be using the wrong terminology, given my background on mathematical modeling and a very, very basic knowledge on evolution.
Thinking about dynamical systems, I would have guessed that coexistence would be possible, so I didn't understand how strong was such an assumption.

There is no such thing as a "wild-type" strain.

I will assume the mutation is not under some kind of balancing selection such as negative frequency dependent selection. As fitness is conditional upon the environment, I will assume a constant environment (heterogeneous environment can also lead to balancing selection).

Is WT expected to be the ONLY strain to persist in the long run?

Yes. In fact, even if the mutation was beneficial, as it starts out at low frequency it still has a low probability to actually fix (fixation = reaching a frequency of one).

How common is this scenario?

Mutations happen constantly. For example, every new human baby carry something like 10-100 new mutations that were not present in any parent. Most mutations are neutral or deleterious, only very few are beneficial. New mutations have a low probability to reach fixation even if the mutation is beneficial. The exact probability depends upon the selection coefficient $s$, the dominance coefficient $h$ and the effective population size $N_e$.

What about co-existence?

In absence of balancing selection (or frequent recurrent mutations) and assuming that ressources are limited, then one strain will necessarily end up fixing. Note that this is also true under genetic drift only and does not even require any selection.

Examples and references for beginners will be very appreciated.

Evo101 is a very short, very easy introduction to evolutionary biology. You should probably have a look at it.
Then, for something a bit more advanced, and because your background in mathematical modelling, I recommend having a look at the book Population Genetics: A Concise Guide by Gillespie
For more book recommendations, please have a look at the posts

Books on population or evolutionary genetics?
Text Book Recommendation: Organic Evolution

Perhaps you can add that fitness is conditional.

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What are the max angles of human eyeball rotation?
How much can our eyeballs rotate towards the nose, away from it, towards the top and bottom?

There shall be slight differences due to physiology. Nevertheless, the average vertical ascending angle is 25 degrees and descending angle, 30 degrees.
Within the x-y plane of which we assume to be coplanar with the central line of vision, the maximal angle of rotation is 35 degrees in the left and right directions respectively.

I attempted to construct an image which depicts these angles - simply a Cartesian diagram.
You can find further clarification of details from this link by Nelson & Associates
Finally, it is important to note that although the eye may be capable of these rotations, the eye may not be able focus on all objects in this field acutely, namely, focusing light on the fovea.
Happy muscular experiments.

"Finally, it is important to note that although the eye may be capable of these rotations, the eye may not be able focus on all objects in this field acutely, namely, focusing light on the fovea."  Any ideas wht that happens? Also, how reliable are Nelson & Associates as a scientific source?

@MarkLegault  To answer your first question, I can consider two primary reasons: at the farthest rotation of one of the two eyes respectively, there is no binocular vision. Therefore, the depth-perception is limited in these areas. Moreover, for an object to be acutely focused on by the eye, the reflected light waves must hit a certain area of the retina: the fovea. Full eyeball rotation may allow for increased peripheral vision - around 95 degrees total vision. Regrettably, perhaps due to the difficulty in measuring rotation as opposed to field of vision, data are limited.

These angles roughly correspond to the angle which would achieve the maximum peripheral vision, available from: www.vision-and-eye-health.com/visual-field.html


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What do the column labels in this table mean?
This table shows the effect of sound (song and tones) on female birds. However, I'm not sure what the labels (F1 22, P and η2) mean. I've seen the labels on other tables too.

(from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3508516/)
If anyone could help I'd be very grateful :)
thanks!

F(1,22) is the result of an F-test with degrees of freedom 1 and 22, in this context most likely this is an F-test in the context of ANOVA; for the meaning of those degrees of freedom I would suggest further reading on ANOVA. Specifically, in this table it looks like we have a 2x2 ANOVA: with stimulus songs or tones and treatment E2 or none, and the interaction between them.
P is the P-value associated with that F-test; it is the probability of observing a result as extreme or more extreme than the F-test gave in this circumstance, given the null hypothesis was true (typically the null hypothesis is something like "the groups don't differ"), and assuming all of the assumptions of the statistical test hold true.
η2 is read as "eta-squared" - it is a measure of effect size, meaning it describes the magnitude of an effect controlled for some other characteristics of the measure, typically the variance. Many statisticians prefer presentation of effect sizes rather than p-values. A large value of η2 means that lots of variance in the outcome variable is explained by the parameter of interest.

brilliant answer


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Usage of "lineage" over "species"
Remi.b has suggested here:

The concept of species is poorly defined and is often misleading. The concept of lineage is much more helpful. IMO, the only usefulness of this poorly defined concept that is the "species" is to have a common vocabulary for naming lineages.

Definition of lineage from Wikipedia:

An evolutionary lineage is a temporal series of organisms, populations, cells, or genes connected by a continuous line of descent from ancestor to descendent. Lineages are subsets of the evolutionary tree of life

If we're talking about populations, how do we know if two individuals have the same lineage?

Lineages have many levels, it is like using the word groups in some ways, they are stacked inside each other like the worlds biggest branching Russian nesting doll. All vertebrates is a lineage, all birds is another lineage, as is chickens, as is just rhode island reds. Two individuals of any earth life will always share some lineages. Lineage is not the same as clade however since they do not have to be monophyletic and usually refers to a stem line leading to a group, because of how lineage is named, it can be confusing. For instance the gorilla/human lineage could refer to basically all the great apes minus orangutans or it could refer to the sequence organisms leading to their common ancestor, or it could refer to the genetic lines to their common ancestor and back to themselves. And easy way to think of it is the outer boundaries of a lineage is not well defined. What is used to denote the lineage will help with what it is referring too.
You have to look at context. In paleontology because it is assumed you never have a direct ancestor it is used more vaguely almost like a "stem clade", in microbiology however it will be a far more precise term referring to one or more genetic lines.
The concept of species is misleading because people are trying to use our instinctual categorical thinking to describe a continuous series. It is like trying to define a color any category we invent to split the spectrum up will have many problems because it is not something with discrete differences.

So, "lineage" is a synonym of "clade" or "monophyletic group"? I would agree with this definition, however wikipedia (A lineage is a single line of descent or linear chain within the tree, while a clade is a (usually branched) monophyletic group, containing a single ancestor and all its descendants.) and @mgkrebbs (in a comment under my now deleted answer; Lineage refers to a line from one individual to another, whereas a monophyletic group is a tree of descent from one individual to many, and so is not a synonym) disagree.

It can be synonymous with clade, it is not a well defined term. For instance the theropod lineage would basically just be the clade theropoda, but say the tyrannosaur lineage  could mean the tyrannosaur clade or it could include the stem groups leading to tyrannosaurs as well. Context will usually tell you how it is being used. I'll be more clear.


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Do the genes encoded by the nucleus for mitochondrial proteins have introns?
Mitochondria are believed to have transferred much of their genome to the nucleus. I know that mitochondrial protein-coding genes lack introns, but is this true for mitochondrial genes encoded by the nucleus as well?

Nuclear genes for proteins destined for the mitochondrion can have
  introns…

…to the extent that other nuclear genes for that organism have introns.
For certain insects there is a database of such genes entitled MitoDrome, and if you click on D. melanogaster in the side panel on the home page of that site you get to a list of such genes for the eponymous fruit fly. You can inspect each one with the ‘view’ option, and the first few I looked at all had introns. Here is an example for one of the subunits of NADH-ubiquinone oxidoreductase, ND-18:

The subunits of this enzyme complex can be examined in other species, from which one can find that in Homo sapiens these nuclear genes also have introns. A related human gene is NDUFS4. Mutations in this gene have been described, at least one of which results in a genetic desease — Leigh syndrome. One of these mutations involves abberant splicing of the five exons of the gene (Lamont et al. Am J Med Genet Part A 173A:596–600).
The homologous gene in Saccharomyces cerevisiae, NDI1, does not have introns, like most other yeast genes.


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Can one type of bacteria cause several diseases?
If yes.
Does it change its shape in every disease, or does it remain in the same shape and cause several diseases?

If you are describing a taxon of bacterium, then it is definite that a bacterial taxon is capable of this, depending on your definition of disease. A pathogenic bacterium could infect two different host species (Mycobacterium sp. in fish and humans). Additionally, a particular pathogenesis may be determined by the site of the bacterial infection. For example, Staphylococcus aureus is often associated with cutaneous diseases (Staph infection) like dermatitis. It may also induce pneumonia and endocarditis, still retaining the same shape - a coccoid-type - and still cause several diseases.

Yes, one type of bacteria can cause multiple diseases.  For example:
"Rheumatic fever is caused by group A Streptococcus. This bacterium causes strep throat or, in a small percentage of people, scarlet fever. It’s an inflammatory disorder." [https://www.healthline.com/health/rheumatic-fever#causes].
The difference is in how the individual's immune system responds to the infection (and how the infection is treated).  Everyone responds a bit differently to the same infection.

"The difference is in how the individual's immune system responds to the infection (and how the infection is treated). Everyone responds a bit differently to the same infection." Can you support this with a reliable source?

I can give you some good examples:

Valley fever (a fungus disease that affects the lungs) is no more serious than a minor cold to some people, but kills some people.  Although malaria is a multicellular parasite, the fact that people with sickle-cell anemia (which is due to a particular genetic variation) are more resistant than other people shows that a victim's genetics can affect how a disease affects the victim.  Flu often affects certain age groups more severely than other age groups.

And, a classical example is the results of Europeans' introduction of measles to the native Americans: a disease that was a minor discomfort to the Europeans was deadly to the native Americans.

The example of group A Streptococcus causing strep throat sometimes, rheumatic fever sometimes, and scarlet fever sometimes is really perfect: the same bacterium affects different people differently.

Your opinions aren't what I mean by a reliable source, unless you can link to research articles you've written and which have been accepted by peer-reviewed journals. Or if you wrote a chapter on immunology in a textbook, etc.

Do you need research articles, or would you accept, e.g., a statement by the Mayo Clinic? [https://www.mayoclinic.org/diseases-conditions/rheumatic-fever/symptoms-causes/syc-20354588]

Or perhaps The Merck Manual: [https://www.merckmanuals.com/professional/infectious-diseases/gram-positive-cocci/streptococcal-infections].  A good counter-argument would be to assert that scarlet fever, rheumatic fever, strep throat, etc., are all the same disease because they are caused by the same Streptococcus pyogenes bacterium; but per [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1299105/] which points out the vagueness of the definition of "disease", that would just be an opinion. The Merck Manual calls them different diseases.


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Pyura DNA extraction
I'm am struggling with genomic DNA extraction from different samples of Pyura chilensis; the DNA is degraded as can be seen on the gel.
We've always used GeneJET Genomic DNA purification Kit (by ThermoFisher), and it works fine for samples from other species; so the kit isn't the problem.
We've always used tissue samples stored in 95% Ethanol (which are washed with water prior to DNA extraction), but the problem persists irrespective of whether the samples are one day old or a few years old.
The storage method seems to work fine for gDNA extraction from other species.
Then, my guess is that the problem is with Pyura itself. So I have to figure out if either the extraction or the storage isn't appropriate for Pyura. I read that Pyura has a lot of copper in it. We planned to use a new buffer for storing it: salt Saturated DMSO, containing EDTA.
I would like to ask if any of you have ever worked with this organism (and if you have, then how did you manage to extract DNA from it). Do you have any suggestions on any DNA purification protocols?

1st lane is the ladder (1kb) and last 3 lanes with long blurred thing instead of bands are my DNA samples.

With reference to your gel photo, the genomic DNA (in the three Pyura sample lanes) does not look badly degraded.  If the size marker is 1 Kb ladder, then the majority of the DNA is of high molecular size. During extraction it is common for high molecular weight DNA to become "sheared" to some degree (mechanically broken into smaller fragments). This can appear as the faint downward smear. The lanes may be somewhat over loaded as well. You can try to use more gentle extraction technique and see if it helps to your satisfaction. Any of those you mention will work.
Badly degraded genomic DNA would appear as a more intense "smear" near the lower portion of the 1 Kb size standard.

This is from a published work by Segovia et al. 2017:

Mantle tissue (0.2 g) from each individual was used to extract DNA using the DNeasy Blood® & Tissue Kit (QIAGEN®, USA) according to the manufacturer’s instructions. Quantity/purity of DNA was measured in Nanodrop 2,000 (Thermo, USA).

They have done SNP identification from the genome. So I assume that their gDNA would have been of decent quality.


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Sugar metabolism in preserved/cryopreserved livestock semen
I wonder how can semen use di/tri-saccharide (e.g. sucrose, trehalose, raffinose) for spermatozoa metabolism in preservation/cryopreservation of livestock semen, since the semen itself never bring any enzyme to breakdown those sugars and the extender used also don't contain enzyme needed?
Is there any other way to breakdown sugar without enzyme, or is there any component in the extender which can substitute the enzyme function?
Thanks in advance.

The sugars that you mention are primarily used as a "cryoprotectant" and thus to reduce physical damage to the cells while frozen.  The sugars are not used to provide energy to the sperm as the enzymes will not function in the temperatures and conditions of a frozen environment. The addition of sugars is typically used with other types of cells/tissues in their cryopreservation as well.  The abstract in the link below summarized this.
https://onlinelibrary.wiley.com/doi/pdf/10.1111/raq.12195


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Could two women have a child through artificial insemination/genetic engineering?
This is something I just thought of while looking up stuff about matriarchies.
I recall a comic series I heard of once, I think it was called 'Y, the last man'. In that story, all males (besides the main character, and one monkey he keeps as a pet) were wiped out by a plague or something, leaving the world's population entirely female. They of course start focusing on developing cloning technology to avoid the extinction of the human race.
But thinking about it, would it really be necessary for them to develope such a technology? Afterall, females can already incubate offspring, they just can't impregnate each other. But could it possible to extract the DNA from a woman's egg, and put it in another egg?
Note that I know nothing about artificial insemination or genetic engineering, so I don't know if that would work (I've only heard of people putting one animal's entire genome into an egg, not from two individuals). So I'd like a more expert opinion. Could you actually do that? Or the mechanism for mixing the DNA of two individuals more complicated than that?

A related question

I can't make much sense of the post. But from what I can discern, the answer appears to be 'no'.

Related https://biology.stackexchange.com/q/27736/3340

Does this answer your question? Can a human be made with ovum but without sperm?

Recently, researchers have been able to produce sperm and ova from germ cells.  It's not been proven yet that the two can produce a viable embryo, but probably the technique will be perfected eventually. [https://www.technologyreview.com/s/608452/a-new-way-to-reproduce/]

Dolly the sheep was made by somatic cell nuclear transfer.  Scientists in China claim to have cloned a monkey in the same way.
https://en.wikipedia.org/wiki/Somatic_cell_nuclear_transfer


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advantages of shivering in cold environments
When we feel cold, our the muscle tries to generate heat by shivering and the brown adipose tissue tries to generate heat by non-shivering methods. The muscle generates heat but also spends energy on movement whereas the adipose tissue produces heat directly. This feels like muscle is not as efficient as BAT in generating heat.
What makes the muscle cause shivering? Isn't it sort of unnecessary movement which wastes energy which could otherwise have been used to directly produce heat?

Firstly, movement by shuddering or shivering, in simplicity, effects the conversion of potential energy into kinetic energy. This is achieved by expending ATP in muscular tissue, causing rapid bursts of contraction.
Brown adipose tissue, although located within most mammals ranging from infants to elderly, is predominantly found in infants differing from white adipocytes insofar as brown adipose tissue has a greater capillary network. Due to the higher surface area to volume ratio of the infant comparative to adults, the rate of heat loss is appreciably greater than a human adult. Thus a more efficient means of thermogenesis is required, namely, when the BAT detects body temperature below the homeostatic norm, the hormone norepinephrine is released, reacting with lipases to form triglyceride. This may subsequently decomposed further, to be converted into heat energy around the body (there are of course various intermediate stages).
Additionally, located primarily in brown adipose tissue is a protein named UCP-1. This allows the cells respectively to undergo 'non-shivering thermogenesis', heat generation without shivering by uncoupling the respiratory cycle in the mitochondria to oxidise more rapidly the substrate. As a consequence, fewer molecules of ATP are produced but heat production is increased.
Therefore, the differences may be rested on 1) the required efficiency of heat generation between infants and adults; 2) the act of shivering per unit of muscle area generates more heat.
You can find further information regarding the UCP-1 uncoupling mechanism in BAT from, https://www.ncbi.nlm.nih.gov/gene?Db=gene&Cmd=ShowDetailView&TermToSearch=7350


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Consistency of consciouness
So I was wondering if consciousness is continous and I found out it might not be the case. But in that case it begs a question, what if in every frame of consciousness my old me dies and new is reborn or rather there is nothing as consciousness but its just a reaction?
What I mean is if I clone a person, the clone would think its the original and we would be unable to determinate it either (if by clone i mean literall copy on the atomic level and with exclusion of any effect of quantum mechanics). If we would annihilate original and put clone into its place noone would be able to tell and to him it would look like everything is continous and nothing happened.
So can it be just illusion in our minds that we are continous sentient beings because we have access to our memory which tells us its like that, same as a clone but as the perception lost focus we die - frame stops to exists?
Can someone clarify this to me or point me to some interesting literature/article on this topic?

This is really not a question biology can answer.  You may find people willing to discuss the definitions of consciousness in a philosophy forum.

I was wondering if there is some sort of scientific view/consensus on this topic. If you suggest that this thing is still rather philosophical question without any viable explanation or evidence then I am OK with it being unanswered but I feel it might be OK to leave it hanging here for times to come when biology will be able to answer it. Anyways thanks for info.

The basic problem is that, so far, there is not a definition of consciousness that provides a way to test by experiment whether a system is conscious or not.  If it can't be tested by experiment, then it belongs to the philosophers (or sometimes to those mathematicians for whom logical consistency is the basic constraint, and to whom physical meaning is irrelevant).

I am not sure it is completely valid to say what you've said in the first sentence. We are not able to determine that something has no consciousness but we are able to state if it does. Well at least that was told to me when I was attending high school (there are some tests to qualify if living organism is indeed conscious). But I understand what you mean. More I think about it, it might be a thing which will be out of our grasp forever.

@S.McGrew "there is not a definition of consciousness that provides a way to test by experiment whether a system is conscious or not" - this is certainly not true. It's true that there isn't agreement but there have certainly been attempts at definitions. I do agree with you, though, that this question as it is framed is not a question for biology.

OK, I need to agree with you: it's certainly possible to make a definition for consciousness that is testable; but there is no consensus that any such definition is useful or correct.

I'm voting to close this question as off-topic because it belongs on psychology.SE.

It is a more psychology than biology I realise that now but I do not think it is completely off and also if in biology manages to get a proof then it is relevant.

You trespass upon a question as old as antiquity: what properties constitute consciousness? The best means to respond to the question concerns a metaphysical answer and an answer in modern biology
We can perhaps divide consciousness into two categories: contiguous thought from past experience and identity and secondly, self-awareness.
The reputed example of the Sorites problem of Theseus' Ship describes how the physical entity of Theseus' ship, during his various battles and broils, loses certain components of his ship: his braces or mast, in example. They are replaced with exact replicates until the time that every component of the ship has been supplanted by a replaced component. Is it the same ship? It is dependent on your definition of identity.
Leibniz's Law of Identity whether in humans, ships or spaghetti monsters, states that objects x and y hold the same identity if and only if they share all the same predicates - qualities or attributes. If this be of functionality, the ship completes the same function and comprises the same components, albeit of different origin - thus, the ship has the same identity. This is important regarding your question whether your 'old [you] dies'. Over time, your cells undergo mitosis and eventually apoptosis. Hence, although your parts are in constant flux, the predicates between your old self and latter self are constant. Ideologically however, there is no set identity!
If you read David Hume's literature, you will observe the notion that one is only the composition of impressions (sensory reception) and thus there exists no identity.
Your question regarding clones is a challenge for biology. Behaviourism is an approach in biology concerning the interpretation of behaviour as a response to a stimulus. Furthermore, humans express complex instinctive behaviours in response to various stimuli. If there exists no 'mental substance' distinct from the body, then it seems plausible to consider human consciousness merely an extension of an advanced instinctive epiphenomenon: self-awareness is a by-product to these advanced behavioural patterns. To support this position, simply recall what factors allow one to discriminate individuals whom one meets, behavioural patterns and appearance.
Finally, one could attempt to assess consciousness in regard to self-awareness by conducting the mirror assessment. If one is capable of identifying himself/herself, then it is indicative of an ability to discern one's personal existence from general matter.
This is by no means a comprehensive answer to this question yet I bid you well in your continued explorations of human consciousness.

Wow thanks, this certainly broadened the way I look at it.


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Mice that have been reconstituted with geneX-transduced cells
I read this article in the following:

... Mice that have been reconstituted with geneX-transduced cells

Now, someone who is not familiar with animal sciences, what does this exactly mean? It is in the context of hematopoietic stem cells. I have two possible interpretations as a result:

An Hematapoetic stem cell with geneX was successfully transplanted into the mouse
The mouse cells (from the embryo) were engineered to contain geneX, and hence the mouse has been reconstituted with geneX transduced cells

Are any of these correct? If I am wrong please let me know!

Your second interpretation is correct.  The mice have been reconstituted from stem cells that were "transduced" (using a viral vector) with a construct containing the appropriate geneX. The link gives comparison of transduction vs. transfection.
https://www.vectalys.com/blog/what-are-the-differences-between-transfection-and-transduction-222


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Can we investigate the cell biology of extinct microorganisms?
I know that there are microfossils, but not if we can we know about the organelles, genetics or macromolecules of the cells that left them behind.

Yes we can, provided that we can extract the dna from these organisms and construct their genomes de novo or with respect to genomes of known organisms. That’s typically little bit difficult because the DNA degraded quickly.

Can you consider adding more details?

What I would like to know is whether we can find out how organelles used to or came to be by analyzing microfossils. During a presentation about the viral eukaryogenesis hypothesis, the absence of "microfossils showing a gradual development of nuclei" was one of the evidences presented. Until that point, I assumed that cells left nothing but "carcasses" upon fossilization and that little else could be known about them.


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What is the difference between a protein and a factor?
In terms of nomenclature/semantics, why are some proteins named proteins, and some named factors?
I've been revising on eukaryotic DNA, and I've come across some proteins that seem to serve roughly the same function, but are named differently. For example,

Replication activator protein
Replication licensing factors
Replication protein A
Replication factor C
Transcriptional factor
Eukaryotic translation initiation factor

TLDR: As far as I know, there's no specific reason some proteins are called "factors"; it's just a matter of what name was chosen.

"Protein" is a specific term meaning a long chain of amino acids. They are typically at least 50 amino acids long.
Conversely, the word "factor" is quite a loose term and is as broad as even being "an element of something". So, essentially anything in biology from a chemical to temperature could be called a factor.
In the context of biochemistry, a factor is a "substance which takes part in a biochemical reaction… …or process". This could include everything from proteins and enzymes (e.g. EGF), to non-protein chemicals such as substrates, co-factors. Even Ca$^{2+}$ (coagulation factor IV) and nitric oxide/arachidonic acid/etc. (EDHF) fall under this umbrella - a single ion is about as far from a protein as it's possible to get! So many proteins are also given the label of "factor". In fact, Protein C has been named both "Protein C" and "blood coagulation factor XIV".
One reason various proteins have been called "factors" is that the word factor used to be used to refer to genes. I'd speculate that another reason may be that certain names and acronyms were already in place. For example, protein C vs. factor C or CREB-binding protein (CBP) vs. core binding factor (CBF).
But as long as the naming of the proteins is standardized, I see no reason why we shouldn't just use acronyms to describe proteins. After all, protein names can be misleading (e.g. Sonic Hedgehog), and there is a large amount of confusion in the literature between names of proteins.

Looks like our answers are nearly identical, even down to the SHH reference - I think this one reference has to come up every time someone talks about protein nomenclature. :)

@BryanKrause I thought the exact same thing! I was slightly worried you'd think I was copying your answer with the SHH point too! I wouldn't have posted if I'd seen yours since you were first and perfectly answered the question but it's quite tricky to delete something that you've just written :)

I think it's pretty obvious with the 4 minute gap and completely different verbiage that no copying was involved. :) Welcome to Bio.SE

To be pedantic, isn't protein reserved for longer amino acid chains? With short chains referred to by the more genetic "polypeptide"?

@JackAidley Thanks for the correction; I've added a note. I was never too fond of the protein vs. peptide distinction, but it's nice to be precise

"As far as I know there is no specific reason…" See my answer for two.

Short Answer
There is no agreed upon naming convention for proteins - there are some rough standards because in language people usually try to convey their ideas in a way others can understand, but that doesn't necessarily mean fixed rules.
Longer Answer
I think it's important to recognize the process for understanding what proteins do is not always straightforward. Most often, a protein's function is first understood by seeing what happens if that protein is absent (and sometimes overexpressed).
The terminology factor implies that a protein is either modulating a process or at least is not by itself sufficient for a process. That is, it is named because when it was omitted, some other measurable process changed. It  maybe implies something that has its main function by binding, rather than catalyzing a chemical reaction, or at least that the actual mechanism of action is not yet known at the time of naming.
You would not expect, for example, an enzyme with a known target to be called a factor: it's most likely to be named according to its target and the type of reaction being catalyzed.
However, it's possible for a name to stick from when there is less complete understanding. Something might be called a factor initially because of how it influences some process, but the actual contribution is only understood later. Just for an example, take Complement factor I. Initially named because it had some role in the complement system, now it's known that it enzymatically cleaves another protein.
Importantly, there isn't any pure terminology here or consistent naming convention: in most cases, it just goes back to however the first person to describe the protein discussed it. Some proteins are named (controversially, I'll add) things like Sonic hedgehog - related to the similarly named Hedgehog signalling pathway which is all named because of one person/group's creative description of a related fruit fly phenotype.
Naming something "protein" just identifies that it's a protein, little more.

Short Answer
All factors are proteins, not all proteins are factors
Background
A factor is typically a small protein that regulates a larger target protein directly by specifically associating with it, or indirectly by affecting its substrate. For example, protein factors play key roles in protein synthesis (Berg et al., 2002) and see Fig. 1.:

An initiation factor binds to the much larger and more complex multi-subunit ribosome during the initiation of translation, a part of protein biosynthesis (fig. 1);
A release factor terminates translation by the ribosome by recognizing the termination codon or stop codon in an mRNA sequence
A transcription factor is a protein that regulates the much more complex and bigger RNA polymerase. Transcription factors control the rate of transcription of genetic information from DNA to messenger RNA, by binding to a specific DNA sequence.

Reference
-Berg et al., Biochemistry, 5th ed. New York: Freeman (2002)
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Fig. 1. Inititation factors are relatively small proteins that interact with the large ribosomal multi-subunit complex. source: Concepts Of Genetics

Only problem I have with this answer is there are lots of proteins that are named "factor" that don't fit into the better-defined categories you mention like initiation/release/transcription factors. Also there are plenty of proteins in those categories that are also certainly not named factor.

@BryanKrause - they are examples, as stated, and not meant to reflect an exhaustive list. It's about the bigger picture. A factor regulates something. Nice answer btw +1. Anyway, naming conventions in Bio are history-related and their systematics murky for sure

Hi, @AliceD, nice answer! I'm not sure about the "all factors are proteins" statement though? While it's clearly true that almost all factors are proteins and that the naming paradigm is pretty nebulous, I think there are still at least a couple (coagulation factor IV, EGHF) which might not be, since they may have been named before their molecular identity was known

@Jam thanks! Factor IV is now simply designated as Calcium. Your other example I don't know what it is, sorry :(

@AliceD Whoops, that was a typo, sorry! https://en.wikipedia.org/wiki/Endothelium-derived_hyperpolarizing_factor My main point about Factor IV was that I think some things are called "factor" before we know whether they're proteins :)

I agree with @Jam, a factor need not be a protein and, AFAIAA that is why many were originally called 'factors' - because it was not known what they were. Since then, of course, the word has been more widely applied.

@JackAidley - I thought that non-protein factors were called co-factors.

@AliceD My understanding is that this is only true where the non-protein is required for the action of the protein.

There are at least two reasons why certain compounds were historically named in the manner ‘function–factor’.

When you have some impure preparation that exerts a biological function but do not know the chemical nature of the component responsible is.

For example an unknown growth factor, could be a protein, but it could also be a steroid etc.

As a deliberate contrast to enzyme to emphasize that the activity is not catalytic. The point here is not the opposition to a different type of protein.

For example, in DNA or RNA synthesis you have the actual enzymes (DNA and RNA polymerases) that work catalytically to form phosphodiester bonds, and then various accessory proteins that are required to bind to specific regions of DNA, but do not catalyse any chemical reaction. In this case the word ‘protein’ does not distinguish the molecule from an enzyme.
In cases where the need to make such distinctions is not evident to a scientist who has established the protein nature of an activity, he may have chosen to designate it protein for greater precision.
Coda
When a field has matured sufficiently there is often an initiative to rationalize nomenclature. This is frequently resisted by the originators of the nomenclature. In this respect Fritz Lipmann is reputed to have said that “changing names is rewriting history”.


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How many ommatidia does a honeybee have?
European honeybees (Apis mellifera) have compound eyes made of tiny facets called ommatidia. The number of ommatidia is usually known in most model insects, but I cannot find reference for the European honeybees, despite bees being highly studied. How many ommatidia does a European honeybee have on average?

4700 - 5400, according to Somanathan et al. (2009). They base their reported values on two other papers.
Reference
- Somanathan et al., J Exp Biol (2009); 212: 2448-53


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What species is this bug that appears in my bathroom?
I'm trying to identify the attached. A few of them appear every day in my bathroom, never more than that, but new ones are there every day. Length is 2-3 mm, and location is the United Kingdom.

Based on my knowledge of species found in Sweden, I think this is a species of Ptinus (Spider beetles), for instance Ptinus sexpunctatus. The general appearance, along with long antenna and long legs fits well. Species in this genus are often also found indoors. Some of the other species in the same genus can also have white/light markings on the elytra, so I'm not absolutely sure about the species. Typical of P. sexpunctatus is that is has six white marking on the wings, but the two hind ones on each wing can sometimes merge into one.

(picture of Ptinus sexpunctatus, from http://www.coleoptera.org.uk/)

(side view, from Wikipedia)


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Identification of protozoa under microscope
I observed maybe Protozoa from standing FRESH water and from slowly flowing FRESH water. I am complete dilettante. Can you tell what these creatures are?
https://www.youtube.com/watch?v=6D5ck3zNJzA&t=474s
Thank you.
Added picture for to be more specific

What level of magnification was employed within the video?

something around 200 I guess

Please put a snapshot of the organism that you want to identify, instead of linking to youtube.

I cut it from the video, it is not very good, but at least it is specific.

At first glance, the organisms may hold the appearance of protozoans like ciliates. However, I am of the belief that these 'totally tubular' micro organisms are in fact diatoms.
The diatoms are a diverse range of eucaryotic microalgae which comprise a large percentage of the phytoplankton group. (Diatomaceous earth is the residual remains of their calcareous walls)
They are likely diatoms because of their apparent hard membrane, and slight brown-green pigment, typical of heterokont diatoms.
I would be unable to specify the organism to family level. However, you may wish to complete your investigation by looking under the order 'Pennales'.
For general information regarding the Diatoms, you may visit https://en.wikipedia.org/wiki/Diatom
Morphology and description available from: https://books.google.co.uk/books?id=xhLJvNa3hw0C&printsec=frontcover&source=gbs_ge_summary_r&cad=0#v=onepage&q&f=false
Good luck

Ok, as noob I need explanation. You mean they are not Protozoan rather algae? And by "they" you mean those which are smaller, but there is plenty of them with "balls" at the end and at beginning and also in the middle of the cell?
(i hope someday make better video with known magnification).

I also asked my former biology teacher and she guessed "Diatomeae". Though I have to google it and translate it.

@weatherman It is likely that your teacher were indeed referring to the Diatom class. 'Diatomea' is deemed a synonym for the Diatom class Bacillariophyceae: https://en.wikipedia.org/wiki/Diatom


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Is there a distinction between the fisherian runaway theory and Fisher's sexy son theory?
In many websites/books they are referred to as part of the same process whereby:

"runaway" describing that the process continues even after traits become maladaptive
the "sexy son theory" explains the mechanism that underlies this.

However many sites (like wikipedia) describe them as two alternative processes.
What am I missing?

The Fisherian runaway is the observed phenomenon of an "arms race" of features and traits in sexual dimorphism, the Sexy sons hypothesis is the theory of why it happens. One is factual/known data and the other is a hypothetical explanation as to why we see that data.

It is necessary to emphasise the role of female directional selection observed in the Fisherian runaway. Koinophilic peahens will select the most ornamental peacocks - it is an arms race of sexual characteristics, even if maladapted to the environment. The Sexy Sons hypothesis is not purely a descriptor of why it arises - it demonstrates that females select males with the probability of ornamental sons capable of widely spreading the mother's genes. The Fisherian runaway could be effected by a non-(Sexy Son) origin.

@epistemonaut- thanks for your response. Please could you give me an example of how runaway selection could arise in the absence of the sexy son mechansim. As I am still unable to understand how this is possible.


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Can you identify this (possibly waterstoring) plant?
My son brought home a sapling, and after 4 years in a pot it is now about 30 cm or a foot high (from the "ground" to the top of the "stem"). It doesn't need a lot of water and can go weeks without being watered, in fact it seems to me as if it is storing water in the thicker upper part of its stem. When I water it "too much", new leaves start to grow. There are tiny "blossoms" along the stem, and every now and then small, dark brown, spherical seeds about 2 mm in diameter pop out from the "blossom" and are thrown across the room as far as a meter (about a yard) or two.
What plant is this?
I believe that it is not native to my European home but some kind of decorative plant imported and sold through a florist or imported privately, but I'm not sure.

It is an Euphorbia leuconeura (Madagascar Jewel), which is native to Madagaskar. The leaves and the thick (waterstoring) stem with a narrow base is very typical.
The plant is cool in the sense that it easily produces seeds (also as potted) which it can shoot away from the plant. I've had it myself and you can sometimes hear seeds hitting the window or floor. Even if it is easy to grow and to reproduce it is actually considered threatened in its native habitat (IUCN Red-listed as Vulnerable) due to habitat loss
The flowers are very small and found directly on the stem, see below:

(picture from Wikipedia)

Thank you! It seems to be called a "spitting palmtree" in my mother tongue :-)

In Swedish, the translated name is sort of splash-a-way


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Anatomy of joints of human hand
Q) A girl slipped and is falling. She puts out her arms to prevent falling. Which joints are most affected by her fall?

Fibrous and Synovial joints.
Cartilagenous and Synovial joints.
Fibrous and Cartilaginous joints.

The answer is 1.
Attempt:
Since it is the arms that will be affected, Synovial joints will be affected. But I don't remember there being any fibrous or cartilaginous in hands.
Are there any fibrous or cartilaginous joints in hand?

What does "cartilaginous joints" mean? That seems really imprecise.

The intermediate radio-ulnar joint is fibrous in arms.

[Source: Slideshare.net]
You can see the the interosseus membrane between radius and ulna which is composed of white collagen fibres.
Furthermore, there is a cartilaginous joint between epiphysis and diaphysis of humerus which is made up of hyaline cartilage. But it is lost during development and is absent in adults.

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Insertion of an additional base at start codon make the protein still functional?
So the question is if:
a deletion of a codon for the amino acid lysine (AAG) is more or less likely to cause nonfunctionality of the protein than:

Insertion of an additional base (C) within the start codon for this protein
Mutation of the stop codon (TAG) to an arginine codon (CGC)

My attempt at an answer:

Not more likely. Since the insertion of the “C” base is done at the very start, the reading frame could be shifted and the sequence would remain the same after the first base. Since the most common start codon is “ATG”, the “C” would not affect it and the “reading” of the sequence would start after the “C” and at “ATG”
More severe as the stop codon is what signals that the translation of the sequence has ended, so if the stop codon got modified then the sequence would continue into the untranslated region. More peptides would be added to the sequence which would only stop when the next stop codon is reached. If the next stop codon is relatively close and the length if similar to a normal protein then it would still be functioning. But most cases it would continue for a considerable length and cause it to be non-functional

I think the question is fairly confusingly worded, so good job on your attempt based on that.

If a C is inserted within the start codon, I presume that is referring to making a sequence that was originally ATGXXX and making it either ACTGXXX or ATCGXXX. Either insertion means the start codon will be missing completely. This is going to either cause no protein to be made whatsoever, or for the beginning of the protein to be severely truncated or completely frameshifted if there is another open reading frame created downstream. This is going to be magnitudes more serious than a deletion of 3 bases corresponding to a lysine.
I think your answer here is fine - lots can happen with a missing stop codon. If there happens to be another stop codon in the same reading frame shortly downstream, then the effect could be not that severe, but if not it could result in a substantial additional peptide chain added to the end of the protein, which could cause all sorts of issues with folding, and the mRNA may not even be functional and be degraded.

Again, this question isn't worded in the best way, but I think the general principle it is trying to convey is that whole missing codons do a lot less damage to the structure of a protein than mutations that affect the reading frame or the stop/start codons, because they affect only a single amino acid. Of course, it could turn out that that amino acid is crucial to the structure of the protein, but the question is about what is most "likely."

I would interpret "within the start codon" as meaning changing ATG to ACTG or ATCG or ATGC.  All of which are going to destroy the start codon, which is likely to ruin the protein.
Whereas adding extra amino acids at the end might not affect the protein function of the rest of the protein.  Protein functions tend to be based on domains, and adding more amino acids to the end might not disturb the structure, and therefore function, of the domains that belong to the protein.

There can be nonstop decay if there is no downstream stop codon.


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Human ancestor reproduction after chromosome fusion
I read somewhere that human chromosome 2 is the result of 2 primate chromosomes fusing together somewhere along our evolutionary journey. This is why we have 23 chromosomes while other primates have 24. My question is this: for the first ancestor whose chromosomes fused to have 23 chromosomes instead of 24, how did he reproduce? Don't offspring receive half of their genetic makeup from each parent, so if one parent has 23 chromosomes and the other has 24, how would that work? I know that there have been animals with different chromosome counts being bred together, but the offspring typically have issues and are sterile, so even if the difference in chromosome count was not a problem, wouldn't the offspring between an organism with 23 chromosomes and one with 24 be infertile, thus leading to the end of animals with 23 chromosomes? Would there have to be two organisms of different genders experiencing the same chromosome fusion at the same time in order to avoid this problem? I'm just a bit confused as to how this would work exactly.

Related: Polymorphism in number of chromosomes?

Strangely enough we actually do have an answer for that.
There are a several examples of individuals who are born with two chromosomes fused together in all their cells.
We even have a few examples where these fused chromosome is in a diploid state, ie all instances of that chromosome are fused in the individual. Such individuals come from families in small isolated villages that are very inbred.
Chromosome number does not prevent fertility but it does reduce it in heterozygous state as it is now harder to get correct chromosome distribution during meiosis and thus fewer functional gametes are made. However in terms of function, as all genes are present in a somatic cell in the correct number, function is usually normal and the individual is alive.
If the population is inbred, it is possible to get an egg and a sperm that carry the same fused chromosome to meet. In which case you get a diploid individual with fused chromosomes. Fertility is now restored. And in an inbred population, a homozygote individual for the fused chromosome can meet another similar individual, and have offspring who are fully fertile.
AS you can imagine, over time there is a selection pressure for the population to separate. The homozygous state (be it fused or unfused chromosome) is more fertile that the heterozygous state.
So to put it short, chromosome fusion does not kill a cell. All gene are still present. However in the heterozygous state, where both fused and unfused chromosomes are present, fertility is dramatically reduced BUT is none zero. Fertility is restored in a homozygous state when an individual is diploid for either fused or unfused chromosomes. In small isolated populations, inbreeding allows for the emergence of diploid individuals which can reproduce with each other
http://genetics.thetech.org/original_news/news124

My question is this: for the first ancestor whose chromosomes fused to
  have 23 chromosomes instead of 24, how did he reproduce?

He or she reproduced the same way people today with balanced Robertsonian translactions reproduce.  During meiosis I, the separated chromosomes line up with the fused one, so the resultant cell gets either the replicated fused chromosome, or the replicated separate chromosomes.  Then meiosis proceeds as usual, with half the gametes having the fused chromosome, and half having the two separate chromsomes.  The fused chromosome has just about all the information the two separate ones have, so the gametes with the fused chromosome can go one to make a organism with all the required genetic information.


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Why is the Mongolian Horse superior in stamina?
I've heard a lot about the Mongolian Horse over the years, especially that it has more stamina than the Arabian Horse. It's a little smaller/lighter than an Arabian.

Apparently the Mongol Horse can outlast an Arabian, despite having a lower top speed, due to stamina. NOTE: I could not find a good source for this, especially when talking about medieval times. It's very hard to find a true apples-to-apples comparison, because of things like a heavy Knight vs a lightly-armored Mongol, and back then Arabian horses were a little different anyway.
The Mongolian Horse can subsist on grass alone, whereas the Arabian Horse needs a lot of oats if its gonna do heavy hauling or riding.
The Mongolian Horse doesn't need horseshoes, since for some reason the hoof doesn't wear down much over its lifetime.

Source 1, Source 2
I would like to know, what biological differences can explain this? Do they have a different kind of muscle? Is their heart or lungs significantly different? Bones?
And the granddaddy point: What percentage difference exists between the DNA of a Mongolian Horse versus an Arabian Horse? For reference, the difference between a human and a chimp is about 1.2% .

This question appears a bit broad. You should consider narrowing it down.


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Why is there a carbon atom without a greek letter in protein residues?
For protein residues I know that $C\alpha$ denotes the first carbon atom attached to a functional group. Each subsequent carbon is given a corresponding greek letter ($\beta, \gamma, \delta$) except for one. For example, each residue in a PDB file has a list of atoms that looks something like this:

ATOM     32  N  AARG
ATOM     33  CA AARG
ATOM     34  C  AARG
ATOM     35  O  AARG
ATOM     36  CB AARG
ATOM     37  CG AARG
ATOM     38  CD AARG

(A,B,G,D are stand-ins for the greek letters). Why is there just a plain C in this list? What is significant about that carbon?

In your context, the "plain-C" labelled carbon is the carbon atom in the carbonyl ($\ce{C=O}$) group.
In organic chemistry, the alpha carbon is the carbon immediately adjacent to a functional group. In general, the greek letters in alphabetical order denote the distance in increasing order from a functional group.  The $\ce{C_\alpha}$ in the case of amino acids is alpha carbon with respect to both the amine and carbonyl.

The edit seems to have spoiled your answer. I imagine you can easily edit it to fit the new question that does not mention the phantom C'.

@David Done....


text:
Identify plant stem parts

What are the names of the parts A, B, C and D?
This is not homework. I am not a biology specialist. Looked through books for than 30 min. Most of them are schematic diagrams, not photos. Furthermore, the vascular bundle is normally shaped like a cone but this one is crescent shaped.

Hi hagawaga. I think this is something like your homework. Please, before you post something try to read the terms of posting (homework usually is closed, because this web site is not right for it). Anyway this task can be done in 30 minutes by yourself.

You said that is not homework, but this is typical question for bio homework. If is not you school duty just tell me for what did you need these think?

I reckon that picture as cauloma. Because it has a trichoms on epidermis. A_ corical parenchyma B_Phloem C_ xylem D_pitch. I hope it will help you.


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eosinophil question
Which of the following statement(s) is/are incorrect?
A. All cells of the immune system originate in the Bone Marrow
B. Lymphoid progenitor cells originate from a pluripotent stem cell
C. B cells develop in the thymus
D. Eosinophils are highly phagocytic
E. Both (b) and (d)
F. Both (c) and (d)
I suspect the answer is E, but I'm not entirely sure how phagocytic eosinophils are (I think it's pretty low b/c they mainly degranulate)
Reasoning:
A-correct because all immune cells originate from hematopoietic stem cells (HSC) from the bone marrow (BM).
B-wrong bc the HSC only gives rise to blood cells and is not pluripotent
C-Correct, B cells are differentiated in the BM, but mature in the thymus.
D-Wrong??, My lecture notes say that eosinophils are granulocytes (their main function), but google says they also phagocytose, so my conclusion is that they are NOT highly phagocytic.
->>> answer = E?

Did you google any of this? If so, what did you find out? (Showing your research - not just what you suspect - is pretty much required in questions here, or it will be closed as a homework question.)


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How does an animal having toes create more friction than not?
I was looking at the morphology of different animals when I found that apparently part of the reason vertebrate mammals have toes is that they grip the ground. But, why is that better than having a solid foot with no toes if friction increases with the surface area in contact with the ground?

I would say that the premise that "the surface area of contact with the ground increases in case of solid foot" is incorrect.
In practice, the ground is very far from being even and flat, and the animals need to navigate themselves throughout different terrains that include very uneven ground, stones, growing & lying plants, etc. In that case, having toes, in general, offer an advantage of gripping to the ground (and increasing contact area in multiple directions) in a large set of terrains. Then, different animals will develop their toes in different shape/form tailored to the dominating usage (including, but not limited to gripping the ground).

I guess that would make sense. It seems like ostriches have flatter toes and seemingly not coincidentally, they run on flatter land, but so do lions and giraffes. But assuming that pattern, it would seem to suggest flat/solid feet are then more optimal for flat land, like how webbed feet are optimal for water, which, has a relatively constant density in an environment.


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How do we sweat immediately after drinking water on a hot day?
On hot summer days, when I drink water to quench my thirst, my body immediately responds by sweating in 5 to 10 seconds or maybe less. How does our body detect the presence of water in the stomach so fast. Does our body detect the sudden decrease in temperature of the stomach or is it by some other mechanism. Why do we sweat after drinking water in the first place. Is it to remove the excess water or to cool the body down on a hot day?

interesting biology experiment: lemon balm is one of the most comment garden herbs, that looks a bit like mint, and that grows in most gardens and wild. If you drink it in a tea, it causes immediate sweating. check wiki if you want. I tried some on a hot day and i was immediately cooled by profusive sweating. cool. https://www.anniesremedy.com/diaphoreticsudorific-property-39.php

Me too, same situation.  Happy to see i am not alone

Not everyone sweats in seconds after drinking water in summer.
Also, sweating in seconds after drinking water is not likely due to water being absorbed (Nutrition Reviews, 2015):

Ingested fluids are not immediately available for assimilation into
  the body. They are initially stored in the stomach, and there is
  little net absorption of water or solute across the gastric mucosa.

There are a lot of receptors, including stretch receptors and various chemoreceptors, in the stomach, so your stomach will likely recognize water as water and signal the brain via the nervous system, probably via the visceral afferent fibers.
One of two things may then happen:

Your brain can perceive a sudden appearance of water in your stomach as stress and react with sweating, like when you are embarrassed or excited.
When dehydrated, you sweat less to prevent further dehydration; when your brain recognizes there is new water in your stomach, it can now allow the signals coming from warm skin to trigger sympathetic nerves to release some sweat to cool you down.

Thanks for the answer. Do you have any idea why this is more likely in summer? And not everyone? Why me? It's cool to know that we have chemoreceptors in the stomach. Is there any other   normal day-to-day situation when we can be aware of the chemoreceptors in the stomach?

If it's only in summer, it's more likely related to thermoregulation, as I suggested in my second hypothesis (in winter it may not be warm enough to sweat). Why not everyone? Because there can be great personal differences in how someone reacts to "stress" (water suddenly appearing in your stomach). It may be partially psychological. It's like when people are embarrassed or scared, but not everyone responds by sweating. Other examples or receptors: The stomach can detect the amount of calories in the food and releases only a certain amount of calories in a certain time into the intestine...

...Stomach can detect toxins from spoiled food and signals the vomiting center in the brain, which induces vomiting. Most gastrointestinal receptors are associated with nutrients and satiety, though.

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text:
What is this weird spider?
Today while we're cleaning our storage room I saw this strange looking spider and I'm not even sure if this is a spider, it has two claws folding inward to its mouth and two long weird limbs, it is about 2 inch long and rarely move on its place. Is it poisonous or dangerous to us? What should I do with it?

Could you give a size estimate for one of the features, and tell us what continent you live on?

It is about 2 - 2 1/2 inches, it is hiding in our storage room which is so dark and full of mosquitoes here in Leyte, Philippines.

It looks like a species from the Arachnid order Amblypygi (Tail-less whip scorpions), which are closely related to Thelyphonida (Whip Scorpions). As part of Arachnids, both of these taxa are related to spiders and scorpions, but belong to a separate order.
Even if they look scary, they are harmless to humans, even if they can sometimes bite.
According to this checklist/site only three species are listed from the Philippines, so if you want to determine it more closely, it might be useful to start from this list. The list includes: Sarax brachydactylus, Phrynus grayi and Charon grayi.
Here is an example picture (from wikipedia):

Charon grayi (giant whip-spider) from biotagua.org:


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Is starch a better coagulant than cellulose?
In an experiment, I used plantain peels (with a very high starch content and very little cellulose) and grapefruit peels (with a very high cellulose content and no starch) as coagulants (ensuring that I used equal masses of each peel) to improve the turbidity of water contaminated with wood chips and kaolin. Although the grapefruit was able to remove turbidity, I found that the plantain worked better. By the way, the same amount of cellulose was present (50%) in the grapefruit peels as starch present (50%) in the plantain peels. However, I can't work out why a coagulant concentrated with starch is more effective at lowering the turbidity of water compared to a coagulant concentrated with cellulose? Essentially, I don't know why starch helps more than cellulose with coagulation. Help would be much appreciated :)
If you use this link, you will find the method I used under "Preparation of Bio-flocculant" to turn the peels into coagulants: akademiabaru.com/doc/progeeV1_P47_56.pdf. To summarize, I dried them in an oven and turned them into very fine powder.
Search this up and you'll find previous experiments using polysaccharides (i.e. starch and cellulose) for coagulation: Chapter 2 Mechanistic Insight into the Coagulation Efficiency of Polysaccharide-based Coagulants

Did you use equal mass of each peel? If you didn't account for differences in content it could be that the plantain peels contained more starch per kg than the grapfruit peels contained cellulose per kg. Were the peels just tossed in or macerated, how were they pre-treated? Starch from the plantain peels may dissociate into the water faster than the grapefruit peels, for example.

Yes, I used equal mass of each peel. If you use this link, you will find the method I used under "Preparation of Bio-flocculant": http://www.akademiabaru.com/doc/progeeV1_P47_56.pdf. To summarize, I dried them in an oven and turned them into very fine powder. The same amount of cellulose was present (50%) in the grapefruit peels as starch present (50%) in the plantain peels.

@Julie please [edit] the question to add all necessary details instead of answering in comment. Also, please add a link to the reference that you cite.

Sorry long work day, what's your sample size? Does n=1?

What do you mean by sample size? I repeated the experiment three times, adding the same mass (4g) of each peel into the solution.

Please do not expect people to do the web search to find out the details. All the necessary details should be contained in your question.


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How is it known that Homo sapiens and Homo neanderthalensis interbred?
Many recent articles maintain that a small percentages of Neanderthal genes (up to 2%) are found in modern non-African people. (I believe that currently there is insufficient genetic material from older hominids, such as H. erectus, to decode a genome).
My question is: how is it known the “Neanderthal genes” found in modern humans got there by way of interbreeding? What distinguishes those genes from genes that both species inherited from a common ancestor? After all, Neanderthals and H. Sapiens are over 99% genetically identical. How is it determined that gene A is found in both because it was from H. erectus, from which both evolved; but gene B was not already present in H. sapiens, so it must have arisen through interbreeding?

Good question +1. About the claim Neanderthals and H. Sapiens are over 99% genetically identical (and the similar claim about the chimpanzee and human comparison), you should read the post “Same” DNA vs genes

@Remi.b Read that question. It left me very confused. I kind of understand it, but not fully

You will not have found a value of 40% in any reputable source, and it implies that you have not properly researched your question to mention it without citation. I have edited your question using 2% as the upper limit, consistent with reputable studies, such as the one I cite in my answer.

@David As far as the 40% goes, I'm mostly reading layperson articles because either I don't have access to the scientific ones, or they're just way above my pay scale. I'll look for the one that had that number later, but I think it was not saying that 40% of our genome is Neanderthal, but that 40% of the Neanderthal genome can be found in various modern humans. So I mis-stated that. I'll leave your edit. I just wanted to indicate that I spent days worth of reading online trying to figure this out.

OK. The three papers I cite are all available in free-to-view format, although in some cases it is as manuscript versions.

@David Thank you for those links. Reading the Green paper right now. Just as an aside, I think part of the problem with academic papers is that they often have such generic titles (i.e. “A Draft Sequence of the Neandertal Genome”) that search engines do not find them, or if they do show up in the search queue it doesn’t look to the user (i.e. me) like they will be useful. Academic writers should put a bit of thought into how their titles look in a search queue. If someone is researching a topic they often only see the title to determine if it is relevant.

Given your question, it makes sense to recommend David Reich's recently published book Who We Are and How We Got Here. Reich has been one of the principal people working on genetics of archaic peoples. In his book he goes into further detail on the methods used to detect interbreeding.

Although this question makes some false assumptions, it is fundamentally interesting as the methodology used is neither simple or easy to understand. It is not my area, but I have found it especially interesting to read the long 2010 Science paper by Green et al.. One really needs to read it for oneself (it is free view), but it is not a trivial undertaking.
False assumptions / misconceptions in the question
The main misconception in the question are:

That it is necessary to know anything about the genome of H. erectus to make these conclusions. The methods used do not require this. (Although comparison with chimpanzee is sometimes used to give an indication of whether a genetic change occured in humans or Neanderthals.)
That the similarities and differences under discussion relate to differences in complete genes — “but gene B was not already present in H. sapiens…”. They do not, which makes the analysis more complex to follow.

Towards an explanation
Let me start by addressing the question “What distinguishes those genes (purported to have been acquired by H. sapiens from Neanderthals) from genes that both species inherited from a common ancestor?”. The answer relates to the absence of such genes from modern humans of African origin, and the fact that we know the general evolutionary relationship between neanderthals and modern humans (African and non-African) from a wealth of non-sequence paleontological evidence. This is shown in the diagram below, modified from a recent and recommended review by Nielsen et al. in Nature (2017).

Clearly any gene present in the common ancestor to humans and Neanderthals should be present in both African and European populations, unless it had been lost from the African population.
So if the analysis is not done by detecting gain/loss of individual genes, how is it done? Certainly not by overall percentage sequence similarity, because of the high overall similarity and the population variation. It is done by studying SNPs — single nucleotide polymorphisms — in particular genes.
For example, consider a gene that has only a single haplotype in Neanderthals, and originally had a single but different haplotype in humans. (This might determine something like eye colour, although this is not an actual example.)  If the other haplotype were acquired by humans as a result of interbreeding, then the modern human population would contain both alleles. When you compared the relationship of the SNPs for this gene between different humans and between humans and Neanderthals you would find different results from those for a gene the variant of which had not been acquired by interbreeding. The acquired gene in humans would be more related to that in Neanderthals than non-acquired genes, but less related to that  in other humans (because of its more recent appearance in the population and time for homogenization, I believe).
The African/non-African aspect is explained in the Science paper cited in my introduction, but there is a good visual diagram in a 2014 Nature paper by Sankararaman et al., the manuscript of which can be viewed freely in PMC through the US HHS.

(1) Sites where a panel of sub-Saharan Africans carries the ancestral allele and where the sequenced Neanderthal and the test haplotype (marked non-African) carry the derived allele are likely to be derived from Neanderthal gene flow; (2) Haplotype divergence patterns. Genomic segments where the divergence of the test haplotype to the sequenced Neanderthal is low while the divergence to a panel of sub-Saharan Africans is high are likely to be introgressed.
These papers contain a wide range of controls, including comparisons of different non-African population groups, and detailed discussion of alternative possibilities.
A final point of interest is that Sankararaman et al. examined some of the genes in which these SNPS suggest Neanderthal origin. They write:

“…genes involved in keratin filament formation and some other
  biological pathways are significantly enriched in Neanderthal
  ancestry in European populations, east-Asian populations, or both
  …. Thus,
  Neanderthal alleles that affect skin and hair may have helped modern
  humans to adapt to non-African environments.”

Coda
It would be scientifically dishonest not to mention some oddities. One is that the Green et al. paper suggested that gene flow had been uni-directional: from Neanderthals to humans, which is apparently unusual in interbreeding. However a more recent study (Kuhlwilm et al., 2016) shows some human gene flow into Eastern Neanderthals, although not into European Neanderthals. (Thanks to @iayork for pointing this out.). The other is that modern Asians appear to have more Neanderthal DNA than modern Europeans. (This is discussed in the paper already mentioned by Green et al.)

+1 This makes much sense now. I'm confused about relate to differences in complete genes. Are you talking about the fact that the genes are there, but different alleles of those genes? Because that I understand. I maybe should have said "alleles" in my question. Or are you referring to something different?

I mean the same genes are there, but there are alleles in Neanderthals that are were not present in the  human population before mixing. I had been thinking I could clarify my answer and will do so now.

One is that gene flow appears to have been uni-directional: from Neanderthals to humans. Ancient gene flow from early modern humans into Eastern Neanderthals

@iayork — Thanks for pointing that out. I have ammended my answer accordingly. Do raise any other points you feel I have not addressed correctly or clearly enough. I find the question interesting, but it is not my area of expertise.


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Can Meiosis 2 be called as mitosis?
I know Meoisis involves a reductional division and an equational division.Say if I am asked a question to find the no. of divisions an egg mother cell undergoes in a Polygonum type division to form the 7 celled 8 nucleate stage, would the Meoisis2 be counted as a mitosis?
Then would it be said to have undergone 1 reduction division and 2 equational division(1Meoisis +2Mitosis).
Or is it just 1Meoisis +1Mitosis ?

Meiosis 2 can not be called mitosis.
You correctly recognized there are similarities between Meiosis 2 and mitosis. In other contexts, however, there are further differences. For instance Mitosis usually does not recombine genetic material (https://en.wikipedia.org/wiki/Meiosis), and the molecules that regulate Meiosis 2 and Mitosis are different. Calling "Meiosis 2" "mitosis" could lead to miscommunication.

But  there aint any recombination in meoisis 2.And are the enzymes mediating Meoisis 2 different from Mitosis even if both are equational divisions?

In mitosis (usually) no crossovers have to be resolved - which contrasts meiosis 2; The results of mitosis and meiosis 2 are also different in terms of chromosome copy number; mitosis entry is regulated by the cell-cycle machinery whereas meiosis 2 is not. The resulting cells have distinct biological functions too - for instance in meiosis 2 the resulting cells will be gametes


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What is the biological/evolutionary advantage to baldness?
Male pattern baldness is a common genetic trait. With a distinctive pattern/ density gradent (as apposed to general old age thinning as the body ages)
Hair has an advantage of protection from the sun/weather. So to lose it in a distinctive pattern (and lose that advantage) appears to have a reason*; and as it is a genetic trait, it seems like it would have been something that was selected for (or it would be more likely to be selected out).
So why is it better to develop pattern baldness as someone gets older?
So what might be the biological/evolutionary advantage to developing baldness?
Traits get selected for good and bad reasons(in retrospect), however I am interested in the reason why this particular trait has been selected.
* Lets assume that there is a specific cause (causes) and it is not just a leftover evolutionary artifact.

The related question: Why do some bad traits evolve, and good ones don't? provides some interesting background, but doesn't specifically address the What causes in this question.

You need to show some evidence in support of your premise that a trait "looks" selected.

@swbarnes2 I never said "looks" , but I have taken what you on board said and have rewritten to better layout my premise, with evidence for it.

@david Can you please remove the duplicate. As per the 3rd paragraph in this meta post https://biology.meta.stackexchange.com/questions/3116/questions-asking-for-evolutionary-reasons This question is about "specific hypothesis" In other words this is not a 'Why does evolution...' question; but a 'What caused this evolution...' question.

"Appears to have a reason" is not any different from "appears selected". Not every trait you find distinctive has been specifically evolutionary selected for.

@swbarnes2 The question is: there appears to be a reason What is the reason. If you think that the answer is "There is no reason" then put that as a answer and it can be voted on along with other answers of: "The reason is XYZ",  "The answer is ABC"

If I pour our some M&Ms from a bag, and I assert that there are a disproportionate number of red ones in the bowl what is the reason?

@swbarnes2 Either "Common cause" or "Special cause". Respectively:  Luck (Good or bad depending  on your taste in M&Ms) or something (I don't know what, but there is a reason) which is causing the M&M production line to add more Reds than other wise would be expected. "I wonder what the reason is?" How would you work out which of those two options is the actual cause?

I'd be interested if anyone can come up with a plausible evolutionary advantage to male pattern baldness; reduced susceptibility to head lice and lice bourne diseases was the best I could do, but I don't see how it would be selected for when the trait mostly emerges after most of the natural and sexual selection and reproductive successes have already taken place. Mmm, I would also be interested to see a plausible reason why it has to have an evolutionary advantage and cannot be something tolerated.

You aren't understanding.  You can't give a meaningful answer to a question if the premises are unfounded.  You can't meaningful answer "Why is the sky green and purple stripe" if it isn't actually that color.

@swbarnes2 Would it make a difference if the question was changes to: ... appears to have a reason (assuming that there is one, and it is not just a ransom evolutionary artifact)...

@swbarnes2 What makes you think that the premise is unfounded? (unproven, sure; but unfounded !?!)

@KenFabian I (the OP) have one, but I wanted to give others time to put up other conjectures before mine (so I don't taint their responses)

Baldness would appear to be a trait on display. That being said, hair loss can be selected against the opposite condition (full head of hair), or selected by way of precise pattern deemed attractive. So, male pattern baldness evolution for mate selection purposes is probably a factor in play. But, either way, hair loss appears to have both its advantages and disadvantages as far as both fitness and mate selection is concerned.
Similarly, in terms of fitness, the advantage/disadvantage you state is the immediate positive advantage of hair as a protectant.  The immediate advantages of hair diminish as one grows older, making age apparent. Old age is disadvantageous in itself (older can mean less fit). Hence, the immediate advantage for a protection against the elements decreases and becomes less relevant to survival as one grows older. Please see the references below.
https://en.wikipedia.org/wiki/Mate_choice
https://en.wikipedia.org/wiki/Evolution_of_ageing

"Questions like this are in the domain of mate selection (or choice) in biology" - citation needed. It is not at all clear that the answer to OP's question has anything to do with mate selection, unless you can cite evidence that it is.


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Plants anti-aging process
Every cell has its division limit. But plants cell looks like don't have it (like Sequoia sempervivens D.). I searched a little for it but what I have found didn't help to answer my question. I found a paper http://epsce.com/wp-content/uploads/2016/02/EMBRYONIC-PLANT-EXTRACTS-EXTEND-THE-HAYFLICK-LIMIT.pdf, which states that plants cell have something call EPE. Which seems to me like super telomerase ( Just kidding don't take it seriously).
My question is: How do plants slow their aging process? Have they different limits for cell division? Are phytohormones related to this phenomena?

I am not so big plant fan. So sorry if is just basic questions for you guys.

Can anybody even tried to answer this. I am really curious about aging process in plants. Any articles about it might help too.

Sequoias are perhaps not the best example.  Consider clonal organisms like the quaking aspen (Populus tremuloides), one grove of which is estimated to be about 80,000 years old (and some suggest much older): https://en.wikipedia.org/wiki/Pando_(tree)

Wow didnt know about it. And now the question about aging is much more interesting!!

Check this paper, it is a great starting point! https://www.sciencedirect.com/science/article/pii/S1568163713000615?via%3Dihub


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Which kind of electrical brain activity is associated with consciousness and why?
According to this article The ethical brain
At the end of the week 5 into the 6 (42-43 days) the first electrical brain activity occurs in a pre-born developing human.
And according to the same article

This activity, however, is not coherent activity of the kind that
  underlies human consciousness, or even the coherent activity seen in a
  shrimp's nervous system

My question is, which kind of electrical brain activity is associated with consciouness and why?

Gamma band oscillations (GBO) (Wikipedia) (NCBI)  are 30-90 Hz electrical waves generated by the brain and are thought to possibly be associated with cognition and consciousness (Panagiotaropoulos, 2012). Some evidence for this putative relationship can be seen with experiments such as pre-pulse inhibition (PPI), which can describe how our sensations are interpreted by the brain. Also, PPI may be aberrant in Schizophrenic patients (who have altered cognition). Changes to PPI are associated with aberrant GBO, which could imply an association between GBO and an individual's interpretation of stimuli, their cognition and by extension consciousness.
But of course, the counter-argument is that the intrinsic activity of the brain isn't changed, merely how the brain processes stimuli. However, all forms of measuring cognition that I've studied involve investigating responses to external stimuli, so as far as I know, this is a universal problem. Furthermore, there's a lot we still don't know about consciousness and no model or measurement is perfect. This article gives quite a nice overview on neural correlates of consciousness.

Can you cite some sources on "experiments as pre-pulse inhibition"? For me it should be clear that we dont know a lot of things about consciousness since human features such as intelligence and learning can be partially reproduced in computers, but as far as I know anything about consciouness can be reproduced.

@Pablo I've tried to expand my answer - I've only studied this in relation to changes to cognition in Schizophrenia but I know some people who research changes to attention via EEG and fMRI studies, so I'll ask them and try to add to my answer.


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Unknown aquatic larvae
These critters have taken up residence in standing water in a small terrarium. It is home to several frogs and lizards. If they will coexist peacefully, I have no objection. If they will harm plants or critters I'll have to evict them.

Related: Bug Identification: Tiny Bugs in Fairport NY, What are these tiny, swarming, jumping bugs?, Help identifying tiny jumping bug, Can Anyone Identify This Insect?, Taxonomy: Categorising Collembola, What kind of small insect is this?

Those are collembolans. The common name is "springtail". Several groups of collembola are semi-aquatic. They are not larvae, but adults. There is a nice paper on aquatic collembolans here: https://link.springer.com/chapter/10.1007/978-1-4020-8259-7_36

Not harmful at all.


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What do firebugs do when they "connect" by their rear?
See this image for example.
What are they doing? What is the name of this process?

They mate!
These matings can be very long

When copulating, firebugs (Pyrrhocoris apterus) form tandems for prolonged periods. Half of the copulations of marked individuals in the field lasted longer than 12 h, and some lasted up to 7 days. (Schöfl and Taborsky (2002))

The likely reason for such a long mating is for males to guard the female to prevent future matings and therefore to prevent sperm competition

males prolong copulations as a form of ejaculate-guarding under high competition with other males. (Schöfl and Taborsky (2002))


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How to estimate MOI for a complex cell type
I am currently confused about the estimation of multiplicity of infection (MOI), here is an example in a scientific article
in figure 3b, they tested the virus, and get estimated MOI based on this:

To estimate the MOI, we isolated a total of 45 individual neurons from three animals injected with MAPseq virus into the right LC and sequenced the barcodes within each neuron. On average, infected LC neurons contained 1.2 ± 0.1 barcodes each, implying MOI of 0.43 (Figure 3B).

I am confused which equation they used for estimating?
Thanks in advance!


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Difference between Sphyraena obtusata and Sphyraena novaehollandiae
"Striped barracuda" is the common name for both Sphyraena obtusata and the Sphyraena novaehollandiae.
Here's links to both fish species from fishesofausralia.net: S. novaehollandiae and S. obtusata
Are they the same fish just found in different parts of Australia, or are they completely different species? If they are different species, what is the difference between them?

I think you may have looked at these species too quickly.
They are in fact different species.
Sphyraena obtusata is referred to as the obtuse barracuda, the striped barracuda, or various other names that your linked website (fishesofausralia.net) provides:

Dingo Fish, Obtuse Barracuda, Pike, Sennit, Short-finned Seapike, Short-finned Sea-pike, Short-jawed Sea-pike, Striped Sea Pike, Yellowstripe Barracuda, Yellowtail, Yellowtail Barracuda, Yellowtail Sennit

Sphyraena novaehollandiae, on the other hand, is referred to as the Australian barracuda, arrow barracuda, Australian sea pike, sea pike, snook, or shortfin barracuda.

Even your linked post doesn't provide "striped barracuda" as a common name for this species.

Differentiating the two species:
Your fishesofausralia.net links demonstrate these fish are found on different sides of Australia (S novaehollandiae in the south and S. obtusata in the North of Australia.
The Wikipedia articles for these fish (linked previously in my answer) indicate that S. obtusata only reaches maximum lengths of 55cm, while S novaehollandiae can reach sizes exceeding 1 meter.
Both sources also list a number of additional color and morphological variations you can use to differentiate the two species.

@AshleyS if this adequately answers your question, please consider accepting the answer. Thanks :)


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How to obtain normalised ECG given ECG readings across lead 1, 2, and 3?
I saw this youtube video on ECG readings and cardiac dipole vector locus of the heart across the three leads. Posting screenshots from it:

My question is how to obtain the graph (2nd image) from the 3 graphs in the first image? Should I simply add them or is there something more to it?

link: https://www.youtube.com/watch?v=H8jVRhQkRjg


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What species of spider is this?
I'm trying to find out what kind of spider is this little fellow:

It really seems to like our garage and is the bane of my girlfriend (as evidenced by all the screaming when on two occasions one got into our home somehow). I was never able to spot this kind outdoors, which is rather odd (there are plenty of Araneus diadematus spiders in the area which are fairly easy to spot).
It's hard to tell on the photo, but these spiders seem rather big (at least as far as spiders in Poland I was able to spot go)... somewhere around 5cm at least (legs included)? They really do make for rather large, black spots against an otherwise white garage wall.
I'd really like to find what kind of species this is so that I can, hopefully, convince my GF that it's harmless to humans. Unless it isn't, in which case I'll start getting scared of walking into our garage. ;)
PS. We live in Poland, Poznań.

This is a giant house spider, Eratigena atrica complex group. It could be one of the species of E.atrica, E.duellica, E.saevus. It is too dark for E.agrestis.
Eratigena is a genus spun-off from Tegenaria. But the other suggested answers of T.domestica is a spider that remains in the Tegenaria genus. This spider in the question does not exhibit the leg-bending (annulations) that are present in T.domestica.
The abdominal pattern is the classic 'herringbone' pattern that places this in Eratigena, while Tegenaria abdominal patterns are a different sort of a spotty pattern.
The habitat of giant house spiders overlaps fairly consistently with T.domestica - human-made structures, indoors, garages, etc.
Giant house spiders are typically larger than E.agrestis and T.domestica, particularly in their leg spans.

I think this is just
Tegenaria domestica. I am from Czech republic and this is really big and kinde everywhere. Specialy in garages.

Just a minor note - it would be helpful if the link wasn't for the mobile version of Wikipedia and was for an English article...

I am sorry for that but I thought when you are from Poland u would prefer something a bit closer to your language.

Well, no offence, but those are still different languages. ;) Plus, this is StackExchange, which is English-based, AFAIK.

This is a giant house spider, not Tegenaria

I'm not a European spider pro, so although I think it looks rather like a Tegenaria, I can't be positive it isn't something else that I'm unfamiliar with.
However, I can state confidently that it is not any of the problem biters known on Earth.  In Europe, you're going to be careful around any of the Black Widow group (Latrodectus spp.) and perhaps be cautious if you should come across a Mediterranean Recluse (Loxosceles rufescens) - but this isn't either of those possibilities.  Widows are small, globular cobweb spiders with relatively short, arched legs, and Recluses are very plain spiders with a dark central 'fiddle' mark on the 'head'.
By elimination, if it isn't any of the known problem biters, it's harmless.
However, what you can do to get a better identification, is to submit your photo to Ed Nieuwenhuys at his website which deals with European spiders.


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What happens to lipoprotein lipase after a sugar only diet?
Insulin increases the activity of lipoprotein lipase thay allows cells to take in lipids from chylomicrons in the blood.
If a person takes a sugar only meal like drinking coke, insulin is released. Will this insulin activate the lipoprotein lipase despite the lack of chylomicron synthesis due to lack of fat in the diet?
Could activation of the enzyme without adequate substrate be of any harm?

From the name "lipoprotein lipase" I guess that it acts not only on chylomicrons (which are proteins, by the way, not so much different from the  "regular" Lipoproteins) but on VHDL as well, which, like chylomicrons, transport triglycerides to the "arterial wall" to unload. Now, if there is no fat in food, just sugar from coke, the liver will take up sugar then and convert it to triglycerides, of which very few is stored in liver - any surplus is said to be packed into VLDL to be delivered to arterial wall. From there to adipose tisssue - and not to muscle? Maybe that's the basis...

Highly intersting I find this question: as it is the "starvation" situation that might be basic in nature, thus for understanding. There wouldn't be much cholesterol contained in coke (smile!), what would liver synthesize cholesterol from to go with tryglycerides surely made from sugar, to go with, in the VLDL, off liver?