text:
Is genetic purging based on random shuffling of the genes of an individual or is it more intentional way of removing deleterious recessive alleles?
Inbreeding depression may be reduced by selection against deleterious alleles, which eliminates, or purges, them from the population. I have two questions:

Is genetic purging based on random shuffling of the genes of an individual or is it more intentional way of removing deleterious recessive alleles?
Do the individuals/couple with deleterious alleles that breed together, pass down the purged genes EACH AND EVERY TIME they produce offspring? Does it happen every time they mate or just some times?

Your terminology is a bit off: especially 'genetic purging' can easily be understood in a very negative way, and I'm not sure you are using inbreeding in the correct way. Otherwise reading up on how genetic inheritance works should help you to answer your question (which is very broad and doesn't really have one general answer).

Check out the Chillingham cattle. They were sectioned off in the 1200s and no new outsiders have been introduced in 300 years.

Is genetic purging based on random shuffling of the genes of an individual or is it more intentional way of removing deleterious recessive alleles?

There is no intention in evolution. Purging refer to the action of selection at removing deleterious alleles. This term is specifically used when a population goes through a demographic change under which purifying selection becomes more efficient (such as an increase in inbreeding coefficient).

Do the individuals/couple with deleterious alleles that breed together, pass down the purged genes EACH AND EVERY TIME they produce offspring? Does it happen every time they mate or just some times?

Purging is a population-level process so your second question does not make much sense
Rephrasing the above a bit differently, purging refers to the reduction in frequency of deleterious alleles in the populations. Individuals will transmit whatever allele they can transmit.


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Can anyone expolain this? Cell culture vials have strange hair-like condensation patterns
What is the hair-like polymer that condenses on the caps of the plastic cell vial? Inside vial are cells in a mixture of FBS and DMSO. The vials were frozen slowly in a special isopropanol-filled container (isopropanol does not touch the vials) to -80 degrees celsius, then put on dry-ice to move to a liquid nitrogen cryogenic freezer. The hair-like crystals appear to be water, but bend toward my finger when nearby, similar to the static attraction.
I suspect the has something to do with DMSO/isopropanol leaking out, and the very low temperatures cause this strange condensation pattern, but I'm not sure.

This question might be better suited for the Chemistry or Physics SE

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What happens if an enzyme stops working in the body?
For example, if the enzymes in the digestive system stop working will the digestion still occur as enzymes are only catalysts for the reactions.
Thank You

It depends on what particular enzyme 'stops' working, and what reaction it catalyzes. For one, the human genome (and that of most organisms) has many genes encoding for enzymes with partially (or fully) redundant functions, and this can mitigate the damage to a particular biochemical pathway in the case that an enzyme within the pathway stops working.
That being said, if the reaction facilitated by the particular enzyme is fundamental for the cell/body physiology, then the embryo/organism would not be viable and thus we would not observe these variants. Thus, whenever a mutation with a 'loss of function' phenotype is observed in an organism, it probably is not essential for its existence (although it might affect a lot the proper functioning).
Enzymes accelerate reactions in various orders of magnitude, and therefore, without them, most of the reactions would not occur fast enough to be useful physiologically. So, yeah, they are 'just' catalysts but quite fine-tuned for physiological needs by millions of years of evolution.

Yes, in general there are multiple enzyme copies that can do basically the same thing; however this doesn’t mean that disease due to a non functional enzyme is impossible: for instance, lactose intolerance is caused at least in part by low or non existent levels of lactase enzyme in the body.

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How do mutations and protein synthesis link to cancer?
How do mutations and protein synthesis link to cancer?
I know that a mutation in DNA can cause the triplet code on the mRNA to change so different amini acids are made and a different order means a different protein is made but how does it link to cancer when cancer is caused by uncontrollable mitosis.
Thank You
This question is at GCSE level so freshman/sophomore level.

Mutation in DNA can be beneficial, harmful, or may have no effect. This is dependent on the gene location where this mutation has occurred.
Various genes linked to cancer are:
Tumor suppressor genes: These genes regulate cell growth by keeping check on cell division, repairing mismatched DNA  and regulating cell death.  Mutation in this type of gene leads to unregulated cell growth and lead to formation of tumor.
Examples:

TP53 is most commonly mutated tumor suppresor gene. More than 50% of
cancers are caused due to mutation in this gene.
Mutation  in BRCA1 or BRCA2 genes is responsible for breast and
ovarian cancers. It  may also increase the risk of pancreatic cancer
and melanoma.

Proto-oncogenes: These genes help cells to grow normally. Mutation in this gene cause its permanent activation and unregulated cell growth takes place and lead to cancer. This abnormal gene is called oncogene.
Examples:

HER2 is responsible for breast and ovarian cancer.
RAS family of genes, responsible for cell communication, cell growth,
and cell death.

DNA repair genes:  These genes play role in repair of DNA, which is mismatched during replication.   Defect in DNA repair gene, leads to synthesis of incorrectly formed DNA and eventually incorrect protein synthesis.

Genes and proteins regulate mitosis.  The most common example of a protein that regulates the cell cycle and prevents cancer is P53.
If you want to learn more, look into cell cycle checkpoints.

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Why is there no solid evidence (histological, fMRI) that the vestibular hair cells of the inner ear contribute to 53% of the respiratory drive?
There are these papers which strongly imply that the inner ear hair cells, and not the medulla, is primarily the driving factor in the CO2 drive reflex
https://www.ncbi.nlm.nih.gov/pubmed/21130842
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3988803/
But every fMRI study done on chemoreceptors has shown only areas of the brain and carotid bodies light up in response to CO2. I could not find any fMRI study papers showing that the inner ears light up in response to CO2 or any histological evidence that the hair cells of the inner ear are chemosensitive and play a larger role in chemosensation than the brain like these studies are trying to imply. It is said the central chemoreceptors in the brain contribute to 85% of the CO2 drive reflex and the peripheral chemoreceptors contribute 15%, which seems to leave little room for the inner ear hair cells to play such a vital and significant part.

I note the two papers from 2011 & 2013 are from an overlapping set of authors, and have hardly any citations outside of later papers involving one or more of these authors.  It looks like very little further research in this area has been reported.


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How much DNA (or genes) do homo-sapiens and ursus arctos (brown bear) share?
How much DNA (or genes) do homo-sapiens and ursus arctos (brown bear) share? There are articles online that indicate that humans share xxx% of DNA with Chimpanzees, bananas, and other assorted organisms, but I can not find how much humans share with brown bears.

These percentage measures do not make a lot of sense. Humans also share a significant number of genes with bacteria. If you want to make comparisons, you should do an extensive analysis of the whole genome. A seemingly minor change in the genome can cause a drastic change in the traits.

timetree.org is a good place to start exploring questions like this. You can put in 'human' and 'brown bear' and it will find a whole bunch of scientific literature about how related the two organisms are, and the best estimate for when they diverged. One of those papers might have a % similarity, but really all the other stuff is the interesting part.

To add to @WYSIWYG's comment, genome-wide DNA similarity is not much studied. The part that would be somewhat interesting (a rigorous full-length nucleotide-for-nucleotide comparison) is computationally and technically extremely difficult if not impossible today, and the methods that have been used in the past to get the numbers you see are both technically difficult and scientifically uninteresting. You might find mitochondrial similarity, or similarity over a few genes, but you are unlikely to find an actual answer to your question, except in general terms.


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What is a proper software to do GWAS analysis of tuberculosiis VCFs and phenotype data?
What is a proper software to do GWAS analysis of tuberculosis VCFs and phenotype data? Need a software which will accept VCF file and phenotype data as an input and produce genome wide association with a report generation.

Have you tried https://omictools.com/gwas-category ?

thx, need 1 or two most relevant can`t experiment with a 100 of them

Analysis of GWAS data generally requires quite a bit of data cleaning, as well as imputation, and the structuring of covariates. These are typically done on unix based clusters with some expertise in bioinformatics and are hardware resource intensive unless the number of subjects is very low.

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Where to download confier (pine) or A. thaliana annotated reference RNA transcriptomes in full .gbk (GeneBank) format?
Where to download confier (pine)  or A. thaliana annotated reference RNA transcriptomes in full .gbk (GeneBank) format?

Annotations are usually provided in GTF format which I personally find more convenient than genbank format. You can download the reference GTFs from NCBI FTP. You can also convert GTF to GB and vice versa. Is there any reason why you would prefer GB over GTF?

You can download the entire set of annotated RefSeq transcripts for a given genome assembly from NCBI Assembly portal.

Go to https://www.ncbi.nlm.nih.gov/assembly and search for Arabidopsis thaliana
Use the 'Download' button to pick 'RNA Genbank format' as the file type and 'RefSeq' as source to download all RefSeq RNAs annotated on this assembly in Genbank format.

Note, however, that the RefSeq transcripts in this file will be the ones that were annotated at the time of the release, June 2018, in this particular case. It is possible that additional RefSeqs have been curated for this species in the mean time, and those will not be a part of this file.


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Is far Infrared heaters in the market truly producing healthy far Infrared and is it practical to install them at home?
I read few blogs and websites about far infrared heaters and all are very possible about this new technology. I bought one of the heaters as a test and find quite impressive also.
However, I am concern about long term health effect. I know, there is no health effect of far infrared but the Heater that is producing infrared, is it truly producing only far infrared?
This business is not regulated so What Type of test (or certificate) the heater has to pass before coming in the market?
I am planning to install this heaters in my whole apartment, anyone has experience to live in a flat/house with far infrared heater? if then can you please share your experience? Is it medically healthy?
Thank you very much.

Far infrared is also known as thermal radiation. It is less harmful to the human body than red light and blue light. If you are under a cloudy sky and it is hot, say 30 degrees, that is how harmful thermal radiation is to the body.
The hight you climb up the electromagnetic spectrum, from radio waves to thermal waves to light waves to UV Xrays and Gamma rays, the more they can interfere with atoms and molecules, because they can disrupt bonds, ionize, and so forth.
So IR can only heat the body and can't ionize or disrupt the body.
Far infrared is the heat you feel when you are far away from a fire and the heat travels towards you without air transport. Near infrared is the heat you feel closer to the radiator, and that which causes convection nearest to the heat source, it gets absorbed faster by the air.
Insulation is most important for heating, as more than 50 percent of heating is lost through the ceiling. modern buildings in the west have high roof insulation standards.
oil heaters tend to absorb near infrared and reflect it back as far infrared better.
I think that the smaller and hotter the source, the nearer thermal wavs it produces, and the larger and less hot surfaces can make more far infrared.
It sounds like a lot of marketing terms.
Oil heaters are traditionally very efficient. I had one which i bought a bit rusty for 15 euros and it has lasted 5 years. the only issue with oil heaters is that they can eventually leak when very worn or less strongly welded.
microwaves are less HF than thermal, and they have not been associated with any health risks either even from phones used all day beside the ear.
You can think of far infrared as the warmth that is reflected from a hot wall heated by the sun. It is one of the least dangerous forms of radiation.
you may consider investing in a HPS lamp of 600 or 1000w because it produces 90 percent heat from that, and also vast amounts of light which are good for mental biology and good for growing tomatos and strawberries in the middle of winter. because they go in a ventilated area under a table in the house, the also radiate well. of all kinds of radiators, i prefer by far sitting under a hot lamp with a summer hat tending plants in the middle of winter, it's definitely hot. A 600W lamp can produce about 200 tomatos, 100 strawberries and 20 peppers and some melons/beans etc, in the winter months.

Thanks for your wonderful reply. I am not using far infrared heater outside though. I will use inside in my house to get heat in this coming winter. more or less 16 hours i will get heat from these heaters. I am a small child. My main concern is on her health. These heaters are cheap and feels comfortable. just i am concert about longer term effect. In UK I haven't seen any far infrared heating system. I wonder why?

hot tea is also full of radiation. so how is an IR heater made... some electricity passes through some flat metal zigzags of a larger surface area than a normal heat and the heat is therefore lower on a larger surface. that's all it is. you generate far infrared inside your own body, about 50W of it. it is radiation because you emit heat. it's safe, probably better than a cheaper heater, both are safer for your child than pesticides on fruit, factory foods and excessive cleanliness, none of which are healthy, 100 degrees radiators are as healthy as standing beside a hot pan of water.

Thank you very much. I am using FI heater now and feel really comfortable at home and cheaper heating.


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Plants and Specialised Cells
Would the number of specialised cells in a leaf decrease if the plant was located in a shadier area? I thought it would decrease as there would be no need to store as much food in the plant and that the plants usually take nutrients from the surrounding environment. However, I don't know if this is correct; it would be nice if someone could provide a better/correct deduction or explanation defining the difference in the number of specialised cells in the leaf in shadier areas.


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What is this passage trying to say about Darwin's difficulty in explaining variation?
This passage, from the book "How humans evolved" by Robert Boyd, says that one of the problems Darwin had at the time was that he struggled to convincingly explain how variation could be maintained; this was needed to theorize that evolution is the result of cumulative adaptations over many generations. According to the book, there are four problems, one of them being that selection removes variation:

For example, suppose the environment changes so that individuals (finches) with
  small beaks are less likely to die than those with large beaks. The
  average beak size in the population will not decrease because there
  are no small-beaked individuals. Natural selection destroys the variation needed to create adaptations.

I understand the idea, but don't really understand what the example is trying to illustrate. The example seems to be saying if small beak finches survive better, then there would be no small-beaked finches...?
The second difficulty Darwin had was in explaining how animals "might evolve beyond it's range of variation (?)"

Selection can cull away some characters from a population, but how can
  it lead to new types not present in the original population?

The bit above I understood; however, I struggle to see the point of the example that was given for it:

How could elephants, moles, bats and whales all descend from an
  ancient shewlike insectivore unless there were a mechanism for
  creating new variants not present at the beginning?

Please help rephrase or explain again what these two difficulties actually are, or help make sense of the two examples that the book gave.

Sort of related Q: Did darwin ever reach the conclusion that selection will remove variation?

Remember this is all before the rediscovery of Mendel and the understanding of things like recessive traits and inheritance of discrete rather than blended traits. The problem is that, given an environment in which large beaks are beneficial, over geological time selection will tend to eliminate the small beaks. Then, if the geological environment changes such that small beaks are favored, there are no small-beaked individuals to benefit from the change: they would have been eliminated gradually during the long time when long beaks were preferred. The paradox or difficulty Darwin had was explaining how populations could maintain sufficient variability for selection to act to generate new traits.
This issue is similar to the first: the process of natural selection is all about what happens to existing populations. It explains what happens when you have variation existing in a trait. Natural selection by itself does not explain how mutations could occur to produce those new traits.

Darwin was concerned about both of these issues because at the time he saw them as serious threats to his theory (and specifically, like most good scientists, he worried that these things could mean that he was wrong). It seemed like a weakness of exactly the type he saw in prior works on transmutation of species that he was trying to work beyond. It took a few decades and a lot of scientific progress including the rediscovery of Mendel and the Modern synthesis for these problems to be truly worked out. As for Darwin, the best he could come up with was his somewhat-Lamarckian pangenesis idea, which he defended strongly.

You explained point 1 and Darwin's concern in your 3rd paragraph well; I now understand what the book was trying to say. As for the second point, I had to re-read your explanation once or twice, but eventually understood what you're trying to explain. Overall you're answers are good explanations, as I now understand what's being conveyed.


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Classification and differences between homologous, homoplastic, analogous, derived and ancestral traits?
My question is contextualised for basic phylogeny knowledge. Here is my understanding: similar or identical traits between any two species, at the basic level, can be either homologous, meaning the trait is developed from a common ancestor, or homoplastic, meaning that the trait was independently developed.
Homologous traits can be either ancestral or derived, and derived traits are a subset of ancestral traits as derived traits need to be from the most recent common ancestor.
Homoplastic traits can be analogous, meaning they developed independently without any common ancestor or commmon initial trait, or can be traits that arose due to convergence, where species with the same (distance/close) ancestor independently developed the traits.
Please evaluate whether my understanding is correct.

This vocabulary is common in textbook but not in the peer-reviewed literature
First please note that while those terms are often used in intro class to evolutionary biology, they are actually rarely used in the peer-reviewed literature.
No trait value is fundamentally derived / ancestral
Note also that any given set of shared trait could be called ancestral or derived depending on the size of the tree that you consider. A trait is therefore not fundamentally ancestral / derived, it depends upon what other trait value you compare it to. Per consequence, it would easier to have a tree under our eyes to discuss these terms.
Note that there is one exception to that. Traits that are shared with LUCA are fundamentally ancestral!
Two states in different lineages can be fundamentally homologous / homoplastic
In general, when we are interest in a given trait, we display a tree so that all homologous trait states appear ancestral. While it is true that homoplastic trait state are necessarily derived when shown, homologous trait state can be shown as derived from a yet more ancestral trait state.
Analogy vs homoplasy
Many think of an analogy as a synonym of homoplasy. However, have a look at @GerardoFurtado's answer for the subtle difference between the two.


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Does pre-operational exercise affect recovery from surgery? Statistical Analysis
https://www.medicaljournals.se/jrm/content/html/10.2340/16501977-2210
I understand the difference between statistical significance and effect size, but I am having trouble interpreting the data on Table III in the article linked above. I am evaluating the WOMAC scores. My first question is can effect size confidence intervals cross zero and still be valid? My second question is about the negative and positive values of the Hedges'g. The first study scores the WOMAC in a way where the higher the score, the better the outcome. The second two studies score the WOMAC in a way where the lower the score, the better the outcome. Does this mean that in the first study a positive Hedges'g indicate larger effect for the treatment group and a negative Hedges' g for the other two studies indicate larger effect for the treatment group?

I think is a question for another section of the community, the statistical one: Cross Validated

Welcome to Biology.SE. I'm voting to close this question as off-topic because it belongs to stats.SE (or at worst Health.SE but definitely not Biology.SE). +1 to @vkehayas answer though.

Also, please always narrow your posts down to a single question.

Regarding your first question, the effect size is not invalid if the confidence interval (CI) crosses 0. The effect size is a point estimate. When the CI -a range estimate of the coverage probability- includes 0, the probability that the range of the effect size can include 0 cannot be rejected at the $1-\alpha$ level of confidence.
Regarding your second question, from the definition of Hedge's g:
$$g = \frac{\bar{x_1} - \bar{x_2}}{sd_{pooled}}$$
we can see that if $\bar{x_2}$ is larger than $\bar{x_1}$ then $g$ will be negative. So, the sign only determines which of the estimates is larger and that will depend on which estimate is considered as the reference.


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What is the most primitive organism that can die of aging?
I know that simple organisms containing of just few cells have no mechanism of dying because of aging. I guess, they typically die due to being out of food or due to becoming someone else's food.
Leaving aside the numerous theories of what can be the origin of such phenomenon as aging, I'm asking a simple question: what is the most primitive organism known so far which has the feature of aging and (as a consequence) dying, even if the environment is perfect?

I feel it's essentially a dupe of question mentioned by Remi, as OP could easily call bacteria simplest organisms.

The adjective primitive is undefined, at least when comparing extant species. We have all gone through almost 4 billions years of evolution.
I would suspect you would consider a bacteria quite primitive though, so note that bacteria appears to age (see Do bacteria die of old age?).


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Is it possible to become pregnant indirectly?
Is it possible to become pregnant indirectly? For instance, if there is some wet semen left behind inside tight clothing, jeans for example, and a woman tries them on for a couple of minutes? What is sperm's motility after it's deposited on cloth in room temperature? Can sperm still swim inside from outside if it's near the vaginal opening in the cloth? What are the chances of pregnancy if the woman is/is not wearing any underwear?

Good question but poorly narrated. Refine your question by reducing questions to just single one. It's sounding pretty curious but snappy question. Once refined, it will be very good question

yes this is possible, as long as the sperm make it onto the mucus membrane of the vagina. the LIKELYHOOD depends on the fabric and how much semen is in the fabric, if it's still clotted or not, and environmental factors.

Sorry, I forgot to add that I meant liquefied semen on the cloth so that it appears as a wet spot, the kind of semen smudge you get when it has seeped through thin clothing (underwear) before being deposited on that outer layer (jeans).

if youre being that specific, it probably happened to you. take a pregnancy test. if positive, there is sadly not much you can do except murder the unborn child. his body your choice


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Lungs permeability
My question is:
$O_2$ and $CO_2$ pass to (in & out) the bloodstream due to difference in partial pressure and its permeability to those gases (I suppose that's why no $N_2$ passes). So, to what other molecules do lungs are permeable and what molecules can and can't pass to the bloodstream from the lungs?
Thank you.

VTC as too broad. All manner of things pass into the blood through the lungs. Anesthetic gasses like halotane, aerosolized drugs (vaping TC), CO, and too many others to list.

Nitrogen do indeed pass to the bloodstream from the lungs. That is what divers experience when breathing compressed air. It causes decompression sickness and nitrogen narcosis.

For the N2, we do not absorbe a lot of that, do we? I mean, where can I find the proportions of absorption (most of air is N2 but we don't absorb that proportion of N2 from air although N2 partial pressure is higher than O2). Do we absorbe all gases that go through lungs? Must say I'm really noob in these themes, so thank you for your answers.

When the blood is in equilibrium with the ambient atmosphere, the net transport of N2 to and from the blood is equal to zero. However, this dosen´t mean that no nitrogen crosses the blood-lung membrane, only that the amount entering equals  the amount leaving.

SOME ANSWERS HERE https://www.google.com/search?sxsrf=ACYBGNSAggw7-B8xkNYtd6-y2i70YFwopQ%3A1571218905884&ei=2eWmXa6_NZLRxgPz2oWYDw&q=MOLECULES+THAT+CAN+BE+ABSORBED+BY+LUNGS&oq=MOLECULES+THAT+CAN+BE+ABSORBED+BY+LUNGS&gs_l=psy-ab.3..33i22i29i30l2.11408.16251..16381...0.4..0.116.3507.32j7......0....1..gws-wiz.......0i71j35i39j0i273j0j0i67j0i10i67j0i20i263j0i22i30j0i13i30.GEIFqmfe_Vk&ved=0ahUKEwjuj__FvqDlAhWSqHEKHXNtAfMQ4dUDCAs&uact=5

Thank you all for the answers, it's now clearer to me.


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Spatial sequence of autumn leave colouring: top to bottom
Leave colours on trees seem to vary on the same tree from top to bottom. Leaves higher up are already further ahead in the shedding process. What's the reason for this tempero-spatial gradient?


text:
Why Differential equation is not a good way to model chemical reaction networks
I'm a computer scientist and mostly code and have worked with Boolean models of cell level molecule transfer. Now i'm reading about the Biological pathways and modelling chemical reaction networks / Actions / Post translation modification and have no idea about differential equations.
What are the  pro's and con's of modelling these situations as differential equation Vs Boolean Vs Rule based approach.

Can you please clarify what you mean by these situations? The expression chemical reaction network is extremely broad and one cannot answer your question is such general terms. Also, it is unclear to me why you would consider by default that differential equations are "not good" to model "chemical reaction networks". The most famous equation in the field of molecular biology is Michaelis-Menten kinetic which result form a series of non-linear ordinary differential equations. I am voting to close as too broad.


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How did ancient human deal with biting insects like mosquitos?
How did early humans, once hairless, but before clothes and ointments.
I understand that hairlessness was an advantage against parasites but it it seems like a disadvantage antagonistic for mosquitos and such.


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Meaning of acceptor/donor splicing sites?
What is the meaning of acceptor and donor in acceptor site and donor site expressions in the context of RNA splicing. Note that I know the biological meaning of these concepts. I am just intrigued by the terms acceptor and donor.
I just cannot seem to find the reason why one is called acceptor and other donor. What exactly is being accepted and donated? In addition, it would be nice to have a reference to the original work that used this terminology.


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What is the definition of Mitotic Index?
Sometimes I find Mitotic Index defined as (i) the number of dividing cells over the number of non-dividing cells, other times as the (ii) the number of dividing cells over the total number of cells...
When reading a paper, which definition is more likely to be correct?

According to cancer.gov, it's the ratio of number of dividing cells to the number of cells not undergoing mitosis. This is equivalent to the number of dividing cells over the total number of cells.
Note that most papers, such as this one, report the mitotic index as a value from 0-100 (I.E. a percentage)

I might be missing something... but is it not the total number of cells = dividing (undergoing mitosis) + non-dividing cells (not undergoing mitosis)?

Yes, that's correct. A 1:1 ratio of dividing cells to non dividing cells would result in a mitotic index of 1/(1+1) = 50%.

The answer is slightly misleading, as "dividing cells" can refer to cells being in cell cycle (as opposed to G0 / senescent state), whereas the mitotic index refers to cells "undergoing division" (cancer.gov), which refers to cells where the material is currently being divided to two different daughter cells - which corresponds to the "mitosis" cell cycle phase of dividing cells.


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What kind of spider has colonised my timber framework?
I'm in the south east UK. I have a site I'm doing intermittent timber work on, that's been left idle for much of the summer. When I came back it has huge webs strung from walls to beams and across the open spaces, everywhere, with the spiders in this picture sitting in them.
At a a guess they are about 30 - 40mm across (maybe 25 when 'sitting' with legs curled at rest close to body?). They sit in the middle of the webs, not hidden at the edges. The webs are quite strong and look like they are durable, as webs go.
Any ideas?

You've encountered a very common spider, found all over holarctic.
Common names: European garden spider, diadem spider or cross spider
Scientific name: Araneus diadematus
link to wiki:
https://en.wikipedia.org/wiki/Araneus_diadematus
They can bite, but are hard to provoke.
If bitten it will feel similar to a wasp sting.
So nothing to worry about, unless you are allergic.
picture from underneath:

source: http://c8.alamy.com/comp/H45CTY/spinning-network-garden-spider-araneus-diadematus-bottom-side-animal-H45CTY.jpg
picture from above:

source: enter link description here


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Does aneuploidy include the loss of chromosome arms?
I'm wondering if the definition of aneuploidy includes loss of a chromosome arm (telosomy) or arms (ditelosomy).
I'm aware that aneuploidy normally depends on the number of discrete chromosomes (so a chromosome without an arm would be treated as one chromosome), but in the genetics course I'm taking, telosomy and ditelosomy were listed in 'types of aneuploidy'. Was this just for convenience, or does the definition include them?

To my knowledge aneuploidy regards to chromosome numerical change, not to losses within chromosomes.
Take a look at this paragraph from An Introduction to Genetic Analysis. 7th edition (Griffiths AJF, Miller JH, Suzuki DT, et al. New York: W. H. Freeman; 2000.)

Aneuploidy is the second major category of chromosome mutations in
  which chromosome number is abnormal. An aneuploid is an individual
  organism whose chromosome number differs from the wild type by part of
  a chromosome set. Generally, the aneuploid chromosome set differs from
  wild type by only one or a small number of chromosomes. Aneuploids can
  have a chromosome number either greater or smaller than that of the
  wild type. Aneuploid nomenclature is based on the number of copies of
  the specific chromosome in the aneuploid state. For example, the
  aneuploid condition 2n − 1 is called monosomic (meaning “one
  chromosome”) because only one copy of some specific chromosome is
  present instead of the usual two found in its diploid progenitor. The
  aneuploid 2n + 1 is called trisomic,2n − 2 is nullisomic, and n + 1 is
  disomic.

This term (aneuploidy) was coined by Gunnar Täckholm in 1922, and if you want to check the original description you can just look for his original paper:
Täckholm, G. Zytologische Studien über die Gattung Rosa. Acta Hort. Berg. 7, 97–381 (in German) (1922).


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What forms the base of the coral reef ecosystem?
Corals are small animals that form a symbiotic relationship with algae. The algae produce sugars for the corals and are in turn provided with needed nutrients and protection from predators.
That's all great, but it doesn't explain where the amazing diversity of fish, mollusks, crustaceans, everything else comes from. As far as I can tell, the whole point of the coral's success is that their hard skeleton protects them from all but the most specialized predators.
So if the corals don't directly add (much) energy input to the coral reef ecosystem, what is it that makes the reefs so productive and diverse? Or, put another way, what makes a coral reef environment more productive than simple phytoplankton floating in the open ocean?

One role of corals is to provide structure that offers protection from predation to many prey species as well as larvae and hatchlings. Reefs also provide relief from strong currents which, again, afford protection. Many other critters such as sponges, tunicates and other sessile animals use the reef as a substrate for attachment.
Don't be fooled by the apparent inedibility of coral, many fish eat it, notably Parrotfish. To give an idea of the extent of this activity, the bleached white beaches in Palau are carbonate "sand", not silica. They are the product of millenia of Parrotfish activity on the coral. (I don't have a link, this knowledge is courtesy of the Oceanic Society guide on our snorkeling trip.) In addition to Palau, I've snorkeled Indonesia, Honduras, Hawaii and elsewhere. In every venue, multitudes of many species of Parrotfish were to be seen aggressively chomping away at coral.
Also, the reef is also a substrate for many algae which serve as a food for other varietiesw of fish. Many of the coral inhabiting algae wouldn't be recognized as such looking like bubbles, fans and other oddities unlike common kelp.
Other species also feed on coral including welks, fireworms, nudibranchs and some starfish. Here's a link:http://infolific.com/pets/coral-reef-life/eating-the-coral-reef/

So I was aware of the parrotfish, and I get that the shelter is a plus. But do you have other examples of fish that eat the coral? How do you get from coral to the incredible diversity of sea lillies, nudibranchs, and all the other various non-coral eating organisms? What is the food source?

@kingledion. I've added to my post. Sorry, I was a tad rushed before having forgotten about coral as an algae substrate.


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Evidences supporting that coronavirus (SARS-CoV-2) came from bats
I was trying to find evidence that the coronavirus (SARS-CoV-2) came from bats. So far I know that coronavirus shared 96.2% overall genome sequence identity with a bat coronavirus RaTG13 from horseshoe bats who identified as natural hosts for SARS-related coronaviruses which were the direct progenitors for the origin of SARS-CoV and also comparing the receptor-binding domain (RBD) of 2019-nCoV to SARS-CoV, the structure of the RBD allowed for the use of ACE2 (angiotensin-converting enzyme 2) as an entry receptor. I wanted to know that apart from these two pieces of evidence are there any major evidence that also suggests that indeed SARS-CoV-2 came from bats.

I think the current consensus is that SARS-CoV-2 didn't originate in bats, but rather passed through them from another species before jumping to humans. I don't believe that other species has been identified yet, but I may be wrong - this is from news reports.

@MattDMo Isn't the hypothesis the reverse? I mean the virus existed in bats, then was passed to another species, then to humans?


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How does energy conversion happen (chemical to mechanical?) in moving body muscles?
From my understanding, the brain sends electrical pulses through neurons to different part of the body to initiate a movement. My question is, how is the movement realized? For example, in a train, steam engine is used to convert heat energy to mechanical energy to move the engine. Similarly, in the body, I understand the energy is stored in chemical form. How is this converted to the mechanical motion of a body part?

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I do not work in Biology and I'm long out of school,so it is not a homework question. When I searched the above, I didn't get any insight into how the conversions work.Perhaps I didn't use the proper terms involved. My doubts were clarified with Joce's answer.

Questions don't have to be homework assigned for a class to be considered homework on this site — if you wish to understand how this site works please consult the links I provided in my original comment.  If you are interested in brushing up on the basics of biology (or any other subject — they helped me relearn calculus) I recommend Khan Academy.

The conversion from chemical to mechanical energy is in general done by molecular motors which perform a power-stroke, using the hydrolysis of adenosine triphosphate (ATP) or more rarely of GTP to power a change of their conformation while bound to cytoskeletal elements.
Molecular motors include myosins, which is the molecular family powering muscles in interaction with actin filaments but also other cells e.g. for their motility or for morphogenesis. animation  of muscle contraction
There are also kinesins and dyneins, not used for muscle function, but which perform e.g. transport of "cargo" organelles along microtubules.
An alternative way to produce mechanical energy is via ion pumps, as is the case in flagellar rotors.

@Joce, your answer is exactly what I was looking for. I mentioned brain and neurons only to clarify that I had an idea about how those are involved, but that was not what I wanted to be answered. I thought it would be pretty clear. Sorry for the misunderstanding.


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How do homologous pairs find each other
If I'm not mistaken the only time homologous pairs of chromosomes need to find each other is during gamete formation in preparation for crossover recombination.
How do they find each other?

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I found this review from 1999.  From the abstract:

It is concluded that DNA-DNA interactions cannot bridge the distances between homologous chromosomes in the nucleus, and it is suggested that protein chains are formed between homologous segments. These attach to homologous chains emanating from homologous sequences in other chromosomes, and the chains move along each other until the homologous DNA sequences meet.

For more recent publications, you can search the citing articles here.


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What are reciprocal inhibitory synapses?
Quoting Kandel's Principles of Neural Science, 2013,

Amacrine cells generally receive excitatory signals from bipolar cells at glutamatergic synapses. Some amacrine cells feed back directly to the presynaptic bipolar cell at a reciprocal inhibitory synapse. Some amacrine cells are electrically coupled to others of the same
  type, forming an electrical network much like that of the horizontal cells.

(Page 593)
I tried searching for what a reciprocal inhibitory synapse is but could not find any relevant information.

It might be better understood if written with a comma as:

reciprocal, inhibitory synapse

though the rules for this comma usage in English might discourage this because writing "inhibitory reciprocal synapse" doesn't sound quite right. I would say the author wrote it correctly even though it is not perfectly clear.
In this context, they are separate adjectives describing the synapse: inhibitory, because it suppresses firing, and reciprocal because Cell A gives input to Cell B, and Cell B also gives input to Cell A (where Cell A is the amacrine cell and Cell B is the bipolar cell).
The word reciprocal in this context is the adjective definition of the word reciprocal:

given, felt, or done in return.

Note that it isn't the synapse itself that is reciprocal or in both directions, but that the cells have a reciprocal relationship.


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What causes the preliminary changes in resting membrane potential in neurons?
Background: The neuron's membrane resting potential is maintained at a certain voltage. The neuron has a lipid bilayer with certain protein channels which allow the movement of ions in both directions (in and out). Some of these protein channels are gated by:
1) mechanical changes (stretching, pressure, etc)
2) voltage changes- regulated by electrical signals (transport of Na+, K+ through protein channels)
3) Ligands (neurotransmitters, etc)
(Guyton and Hall, Textbook of Medical Physiology, 2016)
Question: If action potentials are brought about by voltage-gated channels which are activated by the change in voltage, what brings about this change in voltage which activates voltage-gated channels?
It sounds a bit convoluted. Here's a quote from Wikipedia's Membrane Potential page:

Because voltage-gated ion channels are controlled by the membrane potential, while the membrane potential itself is influenced by these same ion channels, feedback loops that allow for complex temporal dynamics arise, including oscillations and regenerative events such as action potentials.

Hopefully this quote will help to communicate my confusion.

You have already listed two possibilities:

1) mechanical changes (stretching, pressure, etc)

and

3) Ligands (neurotransmitters, etc)

In the central nervous system, ligands and in particular neurotransmitters are going to be the overwhelming cause of most initial depolarization. Ligand-gated ion channels are the simplest mechanism: some examples include AMPA receptors, GABA-A receptors, and nicotinic acetylcholine receptors, but it is also possible to change the membrane potential via second messenger systems that open or close other channels.
In the periphery and in sensory organs, sensory-evoked potentials can be caused by mechanical gating, as you mention, as well as by specialized channels that respond to particular stimuli, for example the TRP family which includes channels sensitive to temperature (for example TRPV1, which responds to heat and also responds to capsaicin, the chemical that makes chili peppers 'hot') and to certain chemicals in food (resulting in taste).
The other category you missed is that some cells generate a spontaneous depolarization because they contain channels that are activated around the resting potential (and/or potassium channels that close, which also depolarizes the membrane). This is crucial for the cardiac pacemaker but can also be found in the central nervous system in some cell types.


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What is the direction of the processing of light by the (human) retina and how does it happen?
Quoting Textbook of Medical Physiology by Guyton and Hall, 2016, page 647,

...the functional components of the retina, which are arranged in layers from the outside to the inside as follows:
(1) pigmented layer, (2) layer of rods and cones projecting to the pigment, (3) outer nuclear layer containing the cell bodies of
   the rods and cones, (4) outer plexiform layer, (5) inner nuclear layer, (6) inner plexiform layer, (7) ganglionic layer, (8) layer of optic nerve fibers, and (9) inner limiting membrane.
After light passes through the lens system of the eye and then through the vitreous humor, it enters the retina from the inside of the eye (see Figure 51-1); that is, it passes first through the ganglion cells and then through the plexiform and nuclear layers before it finally reaches the layer of rods and cones located all the way on the outer edge of the retina. This distance is a thickness of several hundred micrometers; visual acuity is decreased by this passage through such nonhomogeneous tissue. However, in the central foveal region of the retina, as discussed subsequently, the inside layers are pulled aside to decrease this loss of acuity.

I have attached Figure 51-1 for people who would like to see it.
My questions are: How does light travel to the inner parts of the retina first even when there are so many impeding layers preceding it? Why does it not stimulate the photoreceptors first? What is the pathway of the light after it travels to the the innermost retinal layer? Are the photoreceptors the first to be stimulated by the light?

As can be understood, I am quite confused, so if the framing of any question is reflective of erroneous understanding, kindly let me know. All help appreciated.

Short answer
Photoreceptors are the only cells in the retina that directly detect light; they can detect light through the other layers because those layers are so thin and effectively transparent: light passes right through to the photoreceptors.
Longer answer
The retina is fairly thin, and the bipolar/RGC layers don't contain much pigment. Have you ever looked at a thin slice of tissue under a microscope? You can do this and focus to different layers because single layers of cells are fairly translucent (remember they contain a lot of water): most light passes right through them. Some cells, such as red blood cells or photosynthetic plant cells, are harder to see through, but that's only because they are full of pigments.
The reason the photoreceptors respond to light in a way that can be detected biologically is that they contain special photosensitive pigments. In rods, this pigment is called rhodopsin and it is composed of a protein and a molecule of retinal. Most other cells in the retina don't have any such photoreceptors (there is a special class of retinal ganglion cells that is an exception, see for example here - these cells have a pigment melanopsin and contribute to light detection for circadian rhythms rather than vision).
Other cells in the retina respond to light only because they are sensitive to neurotransmitters released by photoreceptor cells and other retinal cells.
As far as why this is the arrangement, with photoreceptors in the back, it's really just a fluke of evolution and evidence that evolution and not design is the best explanation for diversity in biology. Eyes have evolved more than once in animals, however, and cephalopods like squid do not have their retinas arranged this way; in squid the photoreceptors are the most superficial layer.
Because the retina is so thin, this arrangement doesn't provide a large enough disadvantage to be selected against given the complexity in changing the organization. One exception to the thinness, however, is in the blind spot. The blind spot exists because all of the axons from the retinal ganglion cells have to exit the retina someplace. They exit in a big bundle, and there can't be any photoreceptors where that bundle is, so there is a spot where you cannot see. However, the position of the spot is not in the center of your vision, and that part of the visual field is usually covered by the other eye

The Müller cells act as light guides that differentiate among wavelengths of light and make sure that both rods and cones receive their optimum wavelengths without much loss. Since Müller cells span the whole thickness of the retina from the retinal ganglion cells (RGCs) to the the beginning of the photoreceptors, they act as optical fibres allowing the light to pass unhindered through the rest of the retina to the photoreceptors.
Refer to this publication for more details - Labin, A. M., Safuri, S. K., Ribak, E. N., & Perlman, I. (2014). Müller cells separate between wavelengths to improve day vision with minimal effect upon night vision. Nature communications, 5(1), 1-9.

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Number of Bacteria
I am creating a mathematical model for the growth of Synechocystis. sp PCC 6803 and Methanosarcina barkeri Fusaro in photobioreactors and anaerobic membrane bioreactors respectively. I have a couple of questions regarding this:

When you buy these strains, or bacteria in general, from a supplier, how many bacteria will you receive? (I need this for the initial number of bacteria)
How do you find/calculate the half-saturation constant? (Used in Monod's equation)
How do you find/calculate the growth limiting substrate? (Used in Monod's equation)

Any help would be appreciated!

What are your thoughts on questions 2 and 3? We can't really help you if you haven't even tried to answer these questions by yourself...

When you buy these strains, or bacteria in general, from a supplier, how many bacteria will you receive? (I need this for the initial number of bacteria)

You don't know how many cells you'll get. Depending on the strain and on how it was preserved (frozen, freeze-dried, liquid culture), the percentage of viable cells in the sample you get can vary a lot. Anyway, it is not like this that you will find the initial number of bacteria for your model. Before inoculating your bioreactors, pre-cultures have to be prepared. You won't be directly using the supplier's sample as inoculum.
As for how to determine the cell count in your pre-culture, it really depends on what kind of equipment you have access to. If you have access to a flow cytometer, then you can get the cell count directly. Otherwise, you can use more "traditional" microbiological techniques (Optical density, Petri dishes, Dry weight ...).
You might even consider using another variable than cell number for your growth model. It is often the optical density or the dry wheight that is modelled, rather than the number of cells.


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What is the function of spongin in sea sponges?
Sea sponges (Porifera) use different types of skeletons to support their structures. Some skeletons are built from minerals, some are built from proteins like spongin, and some use both.
My question is about spongin. What is the benefit of having a skeleton made exclusively of spongin? (What advantages does it have compared to other types of skeletons?)

Although I didn't get pin point answer, it may be for following reasons.Spongin is a collagen protein.Collagen proteins are usually found in places where elasticity/flexibility is required but not compromising with strength.These collagens provide rigidity (strength) but also some sort of flexibility. You know these poriferans live under high pressure of water (rigidity is essential) and also flexible enough to allow water (some wavy motion to body) in between for getting some food and dissipating wastes.

Sponges are more brittle and don't adopt the same shapes without spongin, which has mechanical and other advantages. https://books.google.fr/books?id=iUI_AAAAQBAJ&pg=PA109&lpg=PA109&dq=Spongin+brittle&source=bl&ots=rhoVDq_IpD&sig=ACfU3U2pDZT364-K2SOVtIo37kT4ByrnZA&hl=en&sa=X&ved=2ahUKEwiovMLjgNrjAhUE5uAKHealBqcQ6AEwAXoECGMQAQ#v=onepage&q=Spongin%20brittle&f=false

If you have ever used a natural bath sponge, you know that the structure of a sponge's spongin skeleton is great for absorbing water and squeezing that water back out.  The sponge's skeleton contains millions of tiny holes, all connected in a massive network of internal tunnels, through which the sponge takes in food and eliminates waste.  It feeds by use of cells that wave tiny cilia to push water into the sponge.  Nutrients are absorbed by the animal and spent water and waste are expelled by the help of similar cells, spinning their flagella to force the water out of the sponge.  A third class of cells, comprising a basic immune system, move around the organism engulfing microbes potentially dangerous to the animal.
This unique system is facilitated by the structure of the spongin skeleton.  The skeleton needs to be strong enough to retain this complicated microstructure, while also having enough give and flexibility that its network of delicate tunnels don't buckle under the force of water pressure, deep currents, or fish and other matter bumping against it.  Notice that, when you squeeze the water out of a sponge, it snaps back into place, the tunnels still open for business.  Given that these tunnels are how the sponge eats, this is very important.  To build a complex tunnel system with millions of tiny little tubes running through it out of something hard and brittle would make it very easy for tunnels to collapse, cracks to form, and other damage to be sustained.  Some sponges, as you mention, have hard, brittle "spicules" in addition to the spongin, but these sponges tend to live in deeper regions and need extra strength to deal with the pressure.


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What if we blend hydras to form a soup. will they still regenerate to form new individuals?
Hydras can regenerate if cut into pieces. But if we take a pound of alive hydras in a blender/grinder and blend/grind them to form a jelly like liquid made of hydras where we have finely blended them, then will this soup turn into millions of hydras or they will die and rot

depends some on if you're doing damage on a cellular level, which you probably are.

Based on this article, the answer is probably no. Quote (emphasis mine):

Small tissue pieces were excised from wild-type polyps of Hydra magnipapillata, allowed to regenerate, and the size-dependent characteristics of head regeneration were examined. The excised tissue piece was initially a square flat sheet. This piece gradually rounded up and, within 24 hr after excision, turned into a "spherical shell" which had a continuous ectodermal layer outside, a continuous endodermal layer inside, and an empty cavity at the center.
The smallest spherical shell that could be produced had a diameter of 0.2 mm and contained 270-300 epithelial cells. A tissue piece too small to form a spherical shell always disintegrated, presumably due to lack of an osmotic harrier between the tissue and the environment.

In short: any piece of hydra tissue with a diameter less than 0.2mm or that contains less than 270-300 whole epithelial (skin) cells is incapable of surviving and regenerating. It is highly unlikely that any hydras would survive being blended because the pieces would probably be too small or too damaged to be viable. Of course, if you had a chopping machine that cut hydras into large enough pieces without causing any significant cell damage, you could probably manage to create a large number of hydras in a very short time span. (I'm not sure why you would want to, though.)


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Which species has the highest proportion of homosexual individuals?
Are there more homosexual individuals in ducks, humans, or some other species?

100% of male flour beetles are bisexual.

Homosexual behavior have been observed more than 1500 species (according to Museum of Natural History of the University of Oslo). A full comparison between all known species is far beyond the scope of this site, but below I discuss three species of interest. Also, the details of what counts as an homosexual behavior, and also whether you compute incidence or prevalence makes the whole discussion semantically complicated.

According to Simon Levay and Aldo Polani, in domesticated sheep, 10% of the rams (males) prefer mating with other rams than with ewes (females).
About 25% of black swans are homosexuals (Braithwaite, 1981).
In lions, 8% of the mounting is in between two males (Bagemihl 2000)

In humans, around 3%-5% of the surveyed people claim being homosexual or bi-sexual (see wiki > demographics of sexual orientation#Modern_survey_results).

Any evidence (link) for the claim of the 1500? Otherwise nice answer!

@RHA Reference added. I would not call it an evidence as it is not a peer reviewed paper though. Thank you

Good enough (and +1), I just knew you hadn't made that number up yourself.


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What did the evolution of multicellular animals look like?
What did the evolution of multicellular animals look like?
Aspects of this question include:
(1) Are there any living organisms that might be helpful in visualizing "transitional forms" between unicellular organisms and multicellular animals? E.g. I have heard of slime molds as one example. Would love to hear of as many good examples as you can come up with. Not looking for strict hereditary relationships here, and I am fine with plausible but unproven theories. E.g., mudskippers might help a person visualize the evolution of amphibians, even if they aren't in fact closely related to amphibian ancestors.
(2) Do we think that the first animals evolved into sponges, or cnidarians/ctenophoroans, or something else? Did sponges and cnidarians/ctenophoroans evolve multicellularity separately? As this is probably a big topic, feel free to just post a link or two.
(3) For any examples that you can think of for #1, would love to hear of any good citations of articles or books for me to read, but keep in mind that I am not a scientist and not looking for anything extremely technical.

Welcome to Biology.SE. I am afraid your question is way too broad to be answered here. A SE post must always be restricted to a single, clearly defined question that can ideally be answered without having to write a whole book!

http://www.bbc.com/earth/story/20150112-did-snowball-earth-make-animals

Evolutionary biologists have frequently cited volvocine green algae, which include both unicellular and multicellular members, as a useful model system (your point #1), e.g. see this article

Thanks, that article looks like what I needed, and contains a few details I hadn't thought about -- e.g., the development of more than one cell type within an organism that has unicellular living relatives.

Choanoflagelates are single-celled eukaryotes that are almost identical to the flagellated cell type in sponges, and are thought to be the sister taxon of Metazoa (Multicellular animals) http://www.ucmp.berkeley.edu/protista/choanos.html

Thank you! I had heard that choanoflagellates were likely related to sponge ancestors, and it intrigues me that free-living unicellular organisms might go from using their flagella to swim around, to using their flagella to draw a current of nutrient-rich water through the body of a sponge. Truth be told, I am a fiction writer and was hoping for more details of this sort to inspire me to write a story about the evolution of multicellular animals, even if the story is not documentably accurate in all its details. I was hoping for more examples, but thanks, this is a good one.

One thing you could think about it how evolutionarily difficult (and thus rare) multicellularity is, because evolution favors selfishness. For a colony of individual cells, each independently reproducing, to become a multicellular organism, then some of those cells must give up their own reproduction to support others. This is "against the rules".Choanoflagellates do congregate, but remain reproductively independent.


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Why does the upper respiratory tract not fill with water when diving?
When we swim, I know we close the some of the vestibular folds in the larynx part of the throat to hold our breath (and to avoid water from getting into the lower respiratory tract, I suppose).
I wondered, what avoids water from running into the upper respiratory tract (such as the nasal cavity and pharynx), when we e.g. dive to the bottom of a swimming pool and lie on our back on the bottom of the pool?
I've tried googling for an hour (during which I learned most of the above anatomical words), but I have not been able to find any bodily mechanic that prevents water from entering the nasal cavity... How does the body avoid this, since there is clearly two holes in our nose, which could lead to water filling our whole upper respiratory tract, if they are not closed?
Thanks!


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What is the difference between Warburg effect and Crabtree effect in metabolism?
In addition to answering my question, please suggest a good review article that provides comparison of the above effects. Which pathways affect central carbon metabolism to produce these effects? Also, how many unique metabolic effects are known for metabolism in general? Is there a good article which covers such unique aspects of metabolism?

Your question is quite broad (multiple questions and overall broad nature). Can you please narrow it down a bit so that it is answerable in a few paragraphs at most?

Welcome to Bio.SE! What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!


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Why is thymidine incorporation (DPM) normalized to per mg protein content while testing for cell proliferation?
Sorry for this naive question. After performing the thymidine incorporation assay to test proliferation, many papers report normalization of disintegrations per minute (DPM) to per mg protein content? What does this normalization or ratio of DPM to cellular protein content exactly signify?
Thanks in advance.

I'm not sure that there is a strongly disciplined reason for the mg protein content as the normalization, but there is obviously a need for some normalization for different amounts of tissue- if you use 10X as much tissue, you should expect DPM to be 10X as high!
For example, in this somewhat old paper, They normalize not to protein content but to wet tissue mass or to intestinal crypt count (as they are looking at incorporation in intestinal crypts). So the normalization that you observe is not universal (or more likely, is a more recent innovation). They observe that the cruder measure of wet mass provides a poor normalization:

Instead there was a positive intercept of dpm/mg tissue which represented about
25-30% of the maximal tritium content of the intestine. (abstract)

That is a good reason to use a more precise normalization! They find that the more precise normalization of dpm/crypt works better, presumably because the crypt is the incorporating tissue.
I would suspect that the dpm/mg protein is simply a more precise method for normalization.
A yet more precise method would be the one used in this 1987 paper, in which thymidine incorporation is estimated as dpm / microgram DNA- here, you are actually directly comparing to the mass of the DNA, which is where thymidine is incorporated. That is a more obvious normalization than protein content.
However, for crude tissue extracts I suspect that it is more straightforward to estimate protein content than DNA content. So protein content is used as a "good enough" normalization.


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What is the length of tunnels puffins dig in the Farne Islands?
I was watching this video and the host said that the puffins dig over 80km of tunnels in the Farne Islands. Is that true? I couldn't find a source to confirm that number.

If that's the current number of tunnels at any one time, it can be right, it depends if they dig a new nest every year.
Farne islands has mostly horned puffins with rainbow beaks as opposed to tufted puffins which have an different beak, the former makes nest around 1 meter and the latter up to 2.75 meters,
Puffins lay one egg per year, there are 30-50,000 pairs of them on Farne islands, that's about 40km of new tunnels every year.
Every five years the trust carries out a larger audit, the last being in 2013, when puffin numbers on the islands were strong, at just under 40,000 pairs.
That was an increase on the 2008 figure when a stormy summer hit numbers hard from a high of more than 50,000 down to 36,000 breeding pairs.


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All neuromodulators (dopamine, serotonin, acetylcholine, histamine, and norepinephrine) act only on metabotropic receptors?
All neuromodulators like dopamine, serotonin, acetylcholine, histamine, and norepinephrine act only on metabotropic receptors?

What research have you done to answer this on your own? The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked, what you do know about the topic, and where exactly you still have questions. Unresearched questions may be subject to down-voting and closure.

I have already search about this and I found that the receptors for neuromodulators are typically metabotropic receptors, what I want to know is if this is always the case, or there are cases where neuromodulators like dopamine act directly on ionotropic receptors. Any help will be appreciated

No, they don't act only on metabotropic receptors - please look into each of them if you can't find the information with broad search terms.

Also, do you consider neuropeptides such as endorphins, enkephalins, etc. (opiod peptides), oxytocin, and Substance P as neuromodulators? What about GABA? Are you just wondering about internally-synthesized molecules, or do you include pharmaceuticals and "natural products" like SSRIs, psilocybin, phencyclidine (PCP), opiates (natural and synthetic), etc.? This question can get too broad very quickly...

Not all neuromodulators act only on metabotropic receptors. However, you are correct to observe that this is a general rule of thumb.
Of the substances you have listed:

Acetylcholine is not primarily a neuromodulator, but rather a "normal" neurotransmitter. As such it acts on both ionotropic and metabotropic receptors.
Serotonin - the one exception among the neuromodulators you have listed - acts on numerous classes of metabotropic receptors, but also on the 5-HT3 receptor, which is ionotropic.
All other neuromodulators you have listed act on metabotropic receptors only.

This tendency of neuromodulation to be metabotropically mediated is possibly a consequence of the nature of the neuronal function itself. Neuromodulatory systems do not per se relay information, but change how other information relays work. As such there is no need for the most rapid, temporal, coding (best achieved via the more rapid ionotropic signal transduction), and a slower coding may even be more efficient.


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It there any experimental approach to determine the electronic structure of a given aminoacid inside a protein?
It there any experimental method to determine the electronic structure of a given amino acid inside a protein?

I mean the electronic configuration of all orbitals in a given amino acid, but something like you describe: "Within the active site of an enzyme, is a tyrosine -OH protonated or not," could help

The two most often used methods used to determine protein structures are X-Ray crystallography and NMR (nuclear magnetic resonance spectroscopy). Both of these allow some deductions of electron configuration, but don't actually measure it directly (and as far as I know there is no method available that can do that, but physicists might know more about that).
X-Ray crystallography essentially detects the electron density of a protein crystal. Usually this density is 'only' used to calculate the structure of the protein, but using good controls and smart math might allow one to also detect charges or specific electron configurations (I haven't checked if anyone ever tried something like this). One general caveat of protein crystallography is that the protein structure/configuration in a crystal may not actually correspond 100% to the state of the protein in its normal environment.
NMR measures the chemical shifts and coupling (quantum) spin of atom nuclei (usually H, N & sometimes C), which is more or less directly depend on its electronic micro-environment. Since structural biology usually doesn't care about things like orbitals, protein NMR data is then used to determine the distance of specific nuclei, which allows derivation of a protein structure.
Since NMR data directly measures atomic properties of single nuclei, I think it is probably the closest to what you are looking for, but asking actual NMR experts will be necessary to figure out whether determining specific orbital configurations could be possible (and even then it would likely be a multi-year interdisciplinary research project).
Another approach, that was mentioned in the comments on the question, would be determining charges on specific amino acids, which could be done using biochemical or spectroscopy assays, if one is only looking at one (or a few) specific amino acids in a protein. These assays need to specifically designed for your protein and amino acid of interest - I can't give specific sources here, but reading up on how people (started to) figure out the chemical mechanisms of enzymes might give you some insights on possible experiments.


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What species is this little white bird?

This bird was found in my backyard in the north east of Italy. It's about 5cm long and can fly as high as 1.5m (so far).

It's probably a white zebra finch:

Such as... do you need instructions for an ophtalmologist.


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Can different bacteria strains of same species have different genomic sizes?
Can two different strains of a single species have different genomic sizes? I am not asking about plasmid. Can they have different sizes of actual chromosome?

Yes, and one could argue that the differences between two strains of the same species are entirely due to their collections of genes (and therefore different genome sizes).
Take the plant pathogen Pseudomonas syringae, for example. There are many different strains, categorized by the plant hosts they cause disease on. This host range is determined by different collections of virulence genes in their genomes. So although they are the same species, they can be remarkably different in their genomes. See this (open access) paper by Baltrus, et al for more information.
A point to remember... "species" is a manmade concept, and there can be different definitions. Some species can have less than 90% similarity at the genome level!

This answer seems decent, but I'm curious what example you have for that last sentence.

I guess there are two ways to look at it... at the genome level, or homology of orthologous proteins. To keep with the example above, we found that several P. syringae strains have less than 80% similarity of orthologs.
The same figure shows that there are on average 26 SNPs per KB, which is only 2.6% differences at the genome level, but that also is across only the genome portions that are actually comparable, and the overall differences at the nucleotide level are much higher.


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Is it correct to classify technolgy as a kingdom?
I recently read some article about a possible 7th kingdom of classification . They considered technology as a kingdom and named it Technium. Actually I was not sure whether it could be called a kingdom as of course we do not consider machines to be living. Thus my doubt was whether there is any biological significance to this claim or is it simply a term that represent technology? https://www.google.co.in/url?sa=t&source=web&rct=j&url=https://www.edge.org/conversation/kevin_kelly-the-technium-and-the-7th-kingdom-of-life&ved=0ahUKEwi1i7vgyd7XAhVCpI8KHfiTCagQFggkMAA&usg=AOvVaw0vYZQy60vYGU0WkN0cBrBi

Kevin Kelly writes some interesting books, but I don't think this is a very useful idea from him. Of course, you can classify entities (frogs, busses, rocks) in all sorts of ways but biological classification into kingdoms surely only works for biological entities. Since technology is not biological, it doesn't make sense to classify it within a biological hierarchy. I might as well classify rocks as another kingdom - Rockium.

I'm voting to close this question as off-topic because it has nothing to do with biology in the terms of this list.

The classification of organisms on Earth is a highly regulated science. It may be interesting to talk about non-living things as a "Kingdom", just to provoke discussion. But under the rules set out by the International codes of zoological/botanical Nomenclature, all higher classifications are the descendants of a common ancestor. Only living things are classified under this code. So, no, technology is not a kingdom. And the term "Kingdom" has undergone so many changes under the rules of cladistic nomenclature, that it is not nearly as relevant as it was when I was a kid (with only 3 kingdoms), since most of the familiar kingdoms are not monophyletic. https://en.wikipedia.org/wiki/Kingdom_(biology)


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What counts as a 'breach of the skin' for infections(like rabies) that spread via wounds?
I've been looking at several sources on how the virus spreads and they all mention that the skin has to be broken, but does it mean broken to the naked eye?
A minor scratch where the skin appears unbroken and there was no bleeding could still have microscopic breaks of the skin, therefore it seems risky to rely on the naked eye.

It seems some skin pathogens can't even infect visible skin breaches like abrasions (https://www.ncbi.nlm.nih.gov/pubmed/24722416). Better to be safe than sorry though when it comes to protecting skin from potentially lethal infections.

I believe that your books refer to 'broken' not necessarily meaning broken to the naked eye, but as in any broken epidermis.
The outer layer of your skin that protects you against infection is the epidermis. It's a water-tight layer mostly composed of keratinocytes joined together by adherens junctions. Logically, even if you can't see a breach in your skin (epidermis), there may still be one. While the chance of getting an infection from a non-visible break is less than the chance of infection from a visible scratch, it's still possible.

Source, please?


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Does Antioxidant prevent oxidation that creates free radical?
I have already known that antioxidant can neutralize oxidant/free-radical, but i want to know if antioxidant can also prevent the oxidation or not. I want to know to how it works if antioxidant can prevent it.
By the way, my point in asking this question is actually to answer my final question: Does vitamin C (antioxidant) inhibit the oxidation in ripening fruits?
thank you!

Welcome to Biology S.E From my knowledge free radicals in human body are produced as a unwanted consequence of oxidations-hydroxylations-coupled oxidation reductions etc.involving cytochromes, EC1 enzymes.If anti oxidants were to prevent them forming directly from source reactions then they would have to be inhibitors of such enzyme systems....

So, antioxidant cannot prevent the making of free radical, it cannot prevent the oxidation? okey then... thank you !

...the second half of youre question is interesting.But ripening of fruit is usually caused by ethylene in plucked fruits mainly...but for an info I can tell u that most of the ascorbate in cut & uncovered citruses is lost because of its conversion to dehydro ascorbate...Good luck with the question

OKEEEEEEYYY...! Thanks for helping, i guess i can answer that question now :)


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Identify this tuber like object found on beach
Can anyone identify this tuber-like object I found on a beach in South Wales, UK? It's about 25 cm long and looks like a deflated football. Pretty spongy, saturated with water. I was hoping it was ambergris, but that seems unlikely.

Mabye it is a carcass or sea sponge or a rooton object. i am only nine!!!

Hi @EthanXiao. Welcome to Bio. We are a scientific stack and request answers to be backed up by scientific sources. Our target are people with a level of education matching that of a bachelor's or master's, and folks above that. Say 18+ years. Perhaps wait a few years before answering any other questions :)

It is spongy because it is a sponge, specifically a sea sponge. There are quite a large number of them native to the waters around england. I would guess Craniella cranium based on shape and location but I am by no means an expert on sponges.
Here  a cross section of a cleaned sponge

and sediment laden potato sponges after a hurricane.

you can see more images of collecting these here, http://www.vims.edu/newsandevents/topstories/archives/2011/irene_blobs.php
Here is a whole website dedicated to english sea sponges, http://www.aphotomarine.com/sponge_suberites_ficus_sea_orange_sulphur.html


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Biological terminology: "codes for" vs. "codes a"
Maybe this is answered already before, but I cannot find it:
Most authors say/write "a gene codes for a protein", some use "a gene codes a protein". The latter seems to me the grammatically correct use of the verb "code".
What's the reason for saying "code for"? Is it because of RNA processing (e.g. splicing)? What about the coding of single amino acid: "AAA codes Lysin" or "AAA codes for Lysin"?
I would also like to know some history of the use of these (and may be other) terminologies.
Tia Udo

In the second usage ("a gene codes a protein"), it's likely the authors meant to write, "a gene encodes a protein". That would then be grammatically correct and correct phrasing.

I'm voting to close this question as off-topic because it is not about biology.

I'm voting to close this question as off-topic because it belongs on SE English Language & Usage (especially the history part), but the poster would need to do some research first.

@DevonRyan "encode" is just the term I've found on Jennifer Doudna's talk.This question may be closed...

This is an English usage question more than one of biology.  The verb code has two main meanings(1):

(transitive) to put into the symbols of a code
(intransitive) to be a code symbol

The first, which being transitive takes an object, is used for the act (as by a person) of translating a plain message into a corresponding encoded form. This is not the meaning used in "AAG codes for lysine".
The second form does not take an object.  It is not being done to something, but rather is just a state of being.  This form is almost always followed by a prepositional phrase "for noun", as in "INS codes for insulin".
Hence it is not correct English to say things like "INS codes insulin", as the use of "insulin" as an object implies the first meaning, as if one were saying "INS takes an insulin molecule and puts it into an encoded form" (whatever that would mean).
The reader would likely try to interpret "INS codes insulin" with the intended meaning, but the incorrect usage makes it seem equivalent to something like "INS is a DNA sequence insulin."  Leaving out the preposition for may be shorter, but it gives a bumpier ride.
(1): Merriam-Webster.  For more variants see Wiktionary, esp. encode.

Thanks for the quick answer! I agree with the intransitive form "be a code for", e.g. "Gene G is a code for Protein P". I've put that question on (https://english.stackexchange.com/questions/416263/general-examples-of-to-code-for) to get examples of non-genetics usage of "code for". btw: I'm just watching a video of Jennifer Doudna, which is an expert in the field of genetics, and she uses "Gene G encodes Protein P" which look very fine to mee (https://www.youtube.com/watch?v=SuAxDVBt7kQ?t=254)

I couldn't edit the last comment since it was older than 5 mins:
... I've read Merriam-Webster's and Wiktionary's articles and agree with the intransitive form "be a code for", e.g. "Gene G is a code for Protein P".
I've put that question on (https://english.stackexchange.com/questions/416263/general-examples-of-to-code-for) to get examples of non-genetics usages of "code for".
btw: I'm just watching a video of Jennifer Doudna, which is an expert in the field of genetics, and she uses "Gene G encodes Protein P" which looks very fine to me (https://www.youtube.com/watch?v=SuAxDVBt7kQ?t=254)


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What vitimins are there?
What vitimins are there and why and what are they?
they do appear in apples and other fruit but just how many are there

Vitamins are compounds that the body needs to function. They are similar to minerals but differ in the fact that Vitamins are organic and minerals aren't. There are 6 vitamins (A,B,C,D,E,K) but many are suffixed with a number, like B12 or D3. They can be found in fruits and vegetables, as well from meat or other sources.
In total, there are 13 different amount of vitamins that humans need in some amount to function:
A, B1, B2, B3, B5, B6, B7, B9, B12, C, D, E, K

thanks jacob. i need this for a project or writing informal language one

You do not appear to have read the guided tour and I imagine also not how to write a good answer. Your answer provides no evidence in its support. This is essential for anyone to judge whether or not it is correct. In fact, the statement "There are 6 vitamins...but many are suffixed with a number" is nonsense. For example Vit B1 (thiamine) and Vit B12 (cobalamin)  are completely different chemically and functionally.


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Why do cats' claws retract?
Humans have nails, horses have hooves - but they are always exposed. Why are cats' claws retractable rather than always exposed? Is it related to "Why are there nail growth differences  between humans and other mammals?"?

Just a speculation, but cats' claws are a lot sharper than the other examples you gave, and are more likely to get caught on things(particularly when a cat is stalking prey), dulled by the environment, or cause self-injury. The purposes and uses of hooves, in particular, are quite different. When would it ever be beneficial for a horse to retract its hooves?

Retraction of claws is a feature of the cat family, Felidae along with some civets that helps them keep those sharp by preventing unwanted wear.These claws are important for the members of cat family, including domestic cats that hunt preys by grasp attack rather than bite.
However cheetah among the big cats that usually hunt through bite-attack, has evolved to have semi-retractable claws that help it generate traction.
In pet cats it has offered another advantage:
Retraction keeps them from getting tangled in fabrics.
Sources:

Wikipedia
Russell AP, Bryant HN. 2001. Claw retraction and protraction in Carnivora: the cheetah (Acinonyx jubatus)
as an atypical felid. J Zool ,Lond 254:67-76.

A footage of cat hunting.

from my understanding the reason cats claws are retractable due to the tendons in the cats paw http://kids.britannica.com/comptons/art-53056/All-cats-except-the-cheetah-have-retractable-claws


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Using distilled water on sterile swab for collecting microbes on solid surfaces
I was wondering if it is acceptable to use distilled water on a sterile swab for the collection of microbes on a solid surface. - in this case, Salmonella and Shigella.


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Shell-less Chick development - Incorporation of Calcium carbonate instead of Calcium lactate pentahydrate powder?
I'm a college undergrad biology student and currently studying developmental biology as part of my curriculum.
I've read a research journal titled, A Novel Shell-less culture system for chick embryo using a plastic film as culture vessels. by Yutakah Tahara and Katsuya Obara, and happened to be interested with this method but stumbled with a question that kept bugging me out of pure curiosity. While reading their journal I encountered a statement
"...250-300mg calcium lactate pentahydrate powder (Showa Chemical Co., Tokyo, Japan) was added to the culture vessels." and they also added distilled water.
The proponents seem to use Calcium lactate pentahydrate as a substitute for the chick's source of calcium. In dev bio class, I've learned that the chick embryo has two main sources of calcium - the yolk and the egg shell. The egg shell contains 94% Calcium carbonate (literally a major source of calcium). I've read that the Chorioallantoic membrane (CAM) is responsible for the mobilization or transport of calcium from egg shell to the chick's circulation -https://www.ncbi.nlm.nih.gov/pubmed/2955074 - and here is where my question starts:
I understand that the proponents used Calcium lactate pentahydrate powder because its soluble in water - making it easier for the chick to incorporate the dissolved  Calcium lactate. I also understand that Calcium carbonate is insoluble in water BUT If CAM is responsible for the mobilization of calcium from egg shell to the chick's circulation to form the skeletal structure of the bird, what difference does it make if I use sterilized powdered egg shells as the chick's 2nd major source of Calcium carbonate?
Thank you for taking the time to read and trying to answer my question! It means a lot

I don't know if it helps, but calcium carbonate is not insoluble in water. It doesn't dissolve very well, but insoluble is something different.


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How do you culture Cutibacterium acnes?
I've been thinking of culturing Cutibacterium acnes (old name is Propionibacterium acnes) for a thesis topic of mine on the comparison of the efficacy of local antibacterial topical skin care products but I have no idea how to culture it. I haven't encountered any definite instructions on the process in culturing it aside from it being an aerotolerant anaerobe and requring an anaerobic incubator.


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Are mediterranean sharks shyer than ocean sharks?
I have been diving in the mediterranean for some time and have never seen a shark, heard of anyone seeing one or seen shark diving advertised. And still there are all kinds of sharks in the mediterranean. Why are they so hard to spot?
For comparison: There are a lot of accounts of people seeing sharks in for example the Maldives and other places.
Something like this would be unthinkable in the Mediterranean:
https://www.youtube.com/watch?v=Yg-dUPVzWiM

It’s not just the Mediterranean, but depending upon many factors, such as the species, typography, depth, current, and availability of food, your chance of encountering a shark in the wild changes, though generally through scuba or skin diving it is still rare.

@Sudachi sure, but I am talking about any sharks at all, not a specific species. I have never seen one in the Mediterranean, although they are out there. Sharks should be active somewhat near shore and in somewhat shallow water right? I have dived to 40m but have seen 0 sharks.

It really boils down to the species and the conditions. You are only able to cover a limited area and shallow depth and limited amount of time as a diver. Many species of shark are likely to know you are there before you know they are there and sharks can be shy and avoid divers. However certain shark spots can be popular feeding grounds, sleeping grounds, or mating areas. While I think there is a lot more historical pressure from fishing sharks in the Mediterranean, I don’t think there is anything innate about the sea there that makes all shark species there shy. I have heard of shark spots in Lebanon: http://www.nisd-online.com/article-101506-talesanddivesinlebanon.htm, though I do know the Red Sea offers a lot more in terms of shark encounters. There simply is a lot that goes into a shark encounter and we do not know nearly as much as we would like on their behavior. I’ve been on many dives in different parts of the world to see hammerheads in the wild and it can be a shot in the dark. It takes many years of local knowledge of the species’s behavior and conditions (season, tides, current, temperature, time of day, moon phases, undersea typography, etc). They are out there, but my best advice is to speak to fisherman and local divers, and also get creative in how you approach them (think about boat sounds, consider beach entries only, go in small groups, try early morning, try different seasons, etc.) Many scientists doing research on certain species in a locale find talking to fisherman to be a huge source of knowledge too.


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How can I determine the mRNA sequence from a given template DNA strand?
Can I determine the sequence of nucleotides of the mRNA strand transcribed from a template DNA strand that goes from (5' to 3')?
I know that RNA-Polymerase enzyme cannot work but on the (3' to 5') direction of the template DNA strand. So, for instance, if the question was to:
Determine sequence of nucleotides in the transcribed mRNA from the DNA strand
5'...A-T-T-C-G-T-T-A-C....3'
Which direction should I start with?

If that is the template strand, and you know RNAP travels along the template from 3' -> 5', you are able to determine the answer.

And remember that the direction has to be complementary to the template strand. Or, identical to the coding strand.

@canadianer  The problem is that when I got a bit confused and referred to an answer to the question, the answer was to use the complementary strand to this as a template and transcribe the mRNA strand so I just got more confused not sure if this was the right thing to do..

Is the sequence you wrote the template or coding strand?

@canadianer the question was exactly to determine the sequence of nucleotides in the transcribed mRNA from this strand of DNA molecule, doesn't that mean that this is the sequence of the template strand?

I'm assuming you are working with a small sequence, but for larger sequences, or if you want to double check your answer, you can use tools like this one: http://www.attotron.com/cybertory/analysis/trans.htm


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What is the biological function of nose, underarm, and pubic hair?
What is the biological function of nose hair? In general, can we consider underarm hair and pubic hair to be vestigial structures?

It’s weird that sometimes, that the question lacking basic research or any effort to answer the question at all, rise to top Despite the site’s policies.

@Chemist This is very old (~5 yrs) question. Standards change over time.

From this article I quote

Hair in the nose is one of the body's first lines of defense against
  harmful environmental pathogens such as germs, fungus, and spores.
Another purpose for nose hair is to provide additional humidity to the
  inhaled air. As the air passes through the nasal passages, the mucus
  and hair provide heat and moisture. Humidity is an important factor
  for the rest of the respiratory system, such as the larynx and lungs.
Hair in the form of tiny cilia also draw solid particles towards the
  interface between the nose and throat. Harmful debris is generally
  directed towards the back of the throat and esophagus for swallowing,
  while the filtered air continues towards the larynx and lungs.

If you look on an evolutionary perspective, the arm pit hair follicles as well as pubic hair have a type of sweat gland associated with them, called an apocrine gland, that begins to function at puberty and is widely associated with scent-communication via chemicals known as pheromones (reference).
Some other functions that are associated with pubic hair are:

Keeping the genitals warm.
Drawing attention to the genitalia.
It also decreases friction during intercourse (reference).

The nose hair is definitely not vestigial. As long as the armpit hair (between the body and arm in certain heavyset individuals) and pubic hair serve to reduce friction and male sweat serves to increase female hormones, I wouldn't call them vestigial (reference).

Keeping genital may not appropriate reason,as in male it’s located outside to keep it cool, it could be to reduce friction between genitals and limbs while walking etc

I meant keeping genital warm is the first line


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Does cortical nephron has just thin ascending loop of Henle?

Guyton and Hall , South Asian edition states that, in Table 76-1 that ascending limb of loop of Henle has thin segment only. But, none diagram in book or internet explain this.
Can any one explain this difference in text and diagram please?

Note: AK Jain Textbook of physiology 6th edition. states on Table 55.1

The descending limb of loop of henle contains a thin segment whereas ascending limb contains a thick segment.

This does explain diagram a bit.
This makes Guyton contradictory.
Edit: From comments, no where the table states part of loh in medulla.

https://goo.gl/Yiz7f5 ascending limb is 'thick' not thin only. See the diagram.

@JM97 So, is the given information on table wrong?

There is also no link on wikipedia or anyother site for cortical nephron ,I could find.

@Anubhav Goel no! that is not what it implies.for the cortical nephron only the thin limb is present in the medulla but both thick and thin limbs are present in the medulla for the juxta medullary nephron so it provides for functional diffrrences between the nephrons.REFER TO THE DIAGRAM ON PAGE 463.(Fig-76-5)

@CATHARANTHUS It is no where written in table part in medulla.

@Anubhav https://ntp.niehs.nih.gov/nnl/urinary/kidney/index.htm see the figure 3.

Most probably the wording is wrong.

@JM97 Ok, you can add that whole as an answer, if you wish or have time?  Thanks for help.

@Anubhav Goel JM97 is correct...besides its a table to help you memorise not understand concepts...thats why i precisely mentioned the diagram in your edited question.

@CATHARANTHUS A table memorising wrong things actually.. Well,  thanks for your efforts.


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What animal/insect is this?
I saw this animal (probably insect) in my house in the Netherlands:

I have searched on the internet but was not able to find what this is, I first thought it was a kind of dragonfly, however there are only two wings which is not usual for a dragonfly. Any suggestions what this is?

I agree with the determination, though the picture is not this clear... Green lacewings have a good appetite for aphids and other plant parasites. I suggest you could try to rear and breed it, if you have several plants within your flat. Both larva and adults exert a regular and continuous control on phytoparasites, particularly Hemiptera...

It is an insect of family Chrysopidae under the order Neuroptera (net-winged insects).
The insects of this family are commonly called Green lacewings.
Neuropterans have large lateral compound eyes, four wings and a generalised pattern of veins.

(Source: Wikipedia)
Identifying morphological features:

Soft-bodied insects with copper-colored eyes, long thread-like antennae, and lacy wings.
Most species are green, but some are brown, especially overwintering adults of certain species

( Reference: Bugguide )
A similar family of lacewing, Hemerobiidae also exists which are brown, have rounded smaller wings and found throughout the world.
Here's a link to wikipedia showing the phylogeny of the Neuroptera as explored using mitochondrial DNA sequences: link .