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Can you identify this insect?
I found this insect in my own courtyard in the city of Pamplona, Navarre, Spain; during mid-February. My courtyard is never directly exposed to sunlight and is always cold, poorly lit and humid. It was 15 millimeters (0.6 inches) long when it kept its body still and straight, without counting the antennae which were 3 millimeters long each (0.1 inches). Its abdomen covered 2/3rds of its body length, and it constantly curled up and down. It also had a pair of wings, with the beginning of each partially covered by a shorter, brown, wing-like structure. To the exception of those brown coverings, its entire body was jet black and was slightly shiny.
I kept it in a test tube and put it with a spider that was almost its size. It was undisturbed by the spider and even approached it often.

Update: It dismembered the spider in less than a day.

Could it be a queen ant before it loses its wings? The head and thorax and wings look ant-like, but the abdomen seems strange to me. I'm no ant-ologist.

It is a rove beetle (Coleoptera, family Staphilinidae). These are among the most specious of beetles. You can recognize them because the elytra (forwings) are much shorter than the abdomen.https://en.wikipedia.org/wiki/Rove_beetle


text:
Why some eggs are bile stained?
Why eggs of some helminths( Diphyllobothrium latum, Trichuris trichiura, Ascaris lumbricoides etc)  are stained with bile while eggs of other helminths( Hymenolepis nana, Enterobius vermicularis etc.) are not?

Some sites say that its because, more the lipid content better is the staining with bile of egg, then how eggs of ascaris are bile stained whose outer shell is made of proteins?

source: Stack Exchange

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

sort: votes


text:
Is this a venomous (poisonous) spider?
Today I found a spider in my home that I have never seen before.
I live in Karachi, Pakistan.
I want to know which spider is this and if it is venomous and danger for me or my family ?? Is this spider commonly found in homes. I have seen many home spiders but they were never like that.
The spider is around 2cm long (front legs to back legs span as shown in 1st image)

This looks like either a young or rather hungry Theridiid spider.  I am not particularly experienced with Eurasian spiders, but as far as I know, the only Widows you're likely to come across in Karachi are either the Redback (Latrodectus hasselti) or the relatively non-problematic Brown Widow (Latrodectus geometricus).  This does not appear to be either of these - the front pair of legs is nice and long, but the abdomen is too plain and the bands at the leg joints are not particularly dark brown and contrasting.
Young female Brown Widow from Bug Guide:

Male Widows, both Black and Brown, tend to have small, rather stripy abdomens, and as adults, will have enlarged ball-like structures at the end of the face-mounted pedipalps.
Male Black Widow from Bug Guide:

That just leaves one of the medically unimportant Theridiids as the most likely candidate, and that's where I unfortunately cannot help any further.  Still, the rule of thumb is that unless you identify it as a problem biter, it's not worth worrying about.  The trick is to look at its underside.  If it shows a red hourglass, it's a problem - if not, no worries.
Judging by the photos, I'd go with "no worries", unless you can come up with a clear image of something troublesome.
I include references to support my claims regarding the distribution of Widows in Pakistan:
https://pdfs.semanticscholar.org/f7c7/3ec7c79da6b3b685e4f05649069c4717803e.pdf
http://eprints.iisc.ac.in/15097/1/First_report_of_the_brown_widow_spider%2C.pdf

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


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What are the brain structures directly on top of the brain stem?
I have been trying to learn the anatomy of the brain, and some information on their functions, through an iPad app called 3D Brain.  Whilst going through the different parts, I have noticed that one area doesn’t seem to be mentioned.
If you look at the image below, you get the brain stem (colour highlighted and labelled).

Going from the brain stem upwards, I am then trying to identify the structures in medium grey which sit on top of the midbrain.
I have seen that the bulbous areas left and right are the basal ganglia.

What are the rest of the structures?  I would like to know what all the mid grey structures are in the first image, but I am especially curious to know what I have drawn around below.

Can I ask why I am getting downvoted?

I'm not one of the downvotes, but I think this question comes off as a bit under-researched and poorly motivated, while also being quite broad. Basically this approach to studying the brain doesn't make a lot of sense, and there are lots of sources besides this app to learn basic brain anatomy.

You're looking at many structures in this area.
The region directly above the midbrain is the diencephalon (meaning "across + brain"). From inferior to superior it's composed of the hypothalamus, thalamus, and structures that developed from a developmental region referred to as the epithalamus that include the pineal gland, habenular trigone, and choroid plexus. Between the hemispheres of the thalamus/hypothalmus lies the third ventricle (which may be "bridged" by a structure called the interthalamic adhesion).
Of each of these structures, only the thalamus and hypothalamus are truly visible from your images -- with the hypothalamus articulating with the midbrain and the thalamus emerging superior and slightly lateral to he hypothalamus. The following structures are also visible in your image:
The most inferior structure you see is the pituitary gland, while the "X" shaped structure superior to it is the optic chiasm with cut optic nerves anteriorly and optic tracts continuing posteriorly out of view.
It's not entirely clear, but I believe the two protruding structures posterior to the pituitary are the paired oculomotor nerves.
Finally, the two long ribbon-like structures that extend anteriorly are the olfactory tracts of cranial nerve I that terminate anteriorly in optic bulbs.


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Can the heart generate its own rhythm independent to the SAN?
My textbook and a revision guide, which I believe is a reinterpretation of the textbook, state that:

The SAN initiates waves of excitation that usually override the myogenic action of the cardiac muscle.
  From the textbook

The revision guide is more direct in its interpretation of the textbook:

The heart muscle is myogenic, which means that it can generates its own rhythm. However, this rhythm is overriden by the sinoatrial node (SAN).

I wonder whether the textbook was interpreted incorrectly, or if in fact the heart can contract independent to the SAN?

Your textbook and review guide are correct, but the missing details may be a little confusing. Yes, the heart has the property of automaticity, meaning action potentials fire on their own at a certain rate, without input from the nervous system. Yes, the SA node typically controls the overall rhythm of the heart because it overrides the rhythm of the rest of the heart.  However, not all cardiac muscle cells have automaticity. Cells in the SA node, the AV node, and to a certain extent, the conducting system all exhibit a physiologic automaticity, that is, they have ion channels that carry what is called a pacemaker current (or sometimes "funny current"), that slowly depolarizes their membranes after each action potential. When this slow depolarization reaches the threshold voltage, another action potential fires. The SA node drives the rate of the heart because an action potential reaches these other automaticity centers, or latent pacemakers, before they would fire on their own. Normal, non-conducting atrial and ventricular myocytes do not exhibit a pacemaker current (except in certain pathological situations), so do not contract independently. So, while the heart muscle is, as your textbook describes it, "myogenic", normal cardiac myocytes (in an intact organ) are not.
This becomes important in cases where the SA node is unable to generate an action potential, is suppressed (is generating an action potential at a slower rate), or other cells with a pacemaker current have increased their rate of firing. In these cases, you can experience an escape beat (a single action potential from a latent pacemaker propagates through the conducting system to cause a heart beat), or an escape rhythm (a series of escape beats).
These are general textbook level principles. You can refer to the wikipedia entry linked above. They are discussed, perhaps more authoritatively, in Lilly's pathophysiology of heart disease. Chapter 1, under electrophysiology, discusses the general principles of automaticity, pacemakers, and latent pacemakers. Chapter 11, under native and latent pacemakers, alterations in sinus node automaticity, and escape rhythms, goes into more detail about the circumstances in which latent pacemakers drive the heart.


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If bacteria with recombinant DNA molecules do not survive in gene cloning, how they can be grown into a colony after being isolated?
This is as far as my understanding of gene cloning goes. Let's say that the plasimd (vector) in the bacteria contains an ampicillin resistence gene. Through restriction enzymes, the ampicillin resistance gene is cut through and foreign DNA is inserted. This creates a recombinant DNA molecule.
Once many bacteria are introduced to a medium that contains ampicillin, only ones that have no recombinant DNA and functional ampicillin resistance genes will survive and those with the recombinant DNA won't. Through the addition of some chemicals, the surviving bacteria will turn blue and those with the recombinant DNA will turn white. Thus, bacteria with recombinant DNA can be taken and grown in their own culture, the recombinant DNA can be isolated, and research goes on.
However, if all the bacteria with recombinant DNA have been killed because they have no functional ampicillin resistance genes, how can they be 'grown' in their own colony? They're all already dead, aren't they?

This topic has been covered in previous questions, e.g. https://biology.stackexchange.com/questions/69141/selection-of-recombinant-host-by-color-selection-method.

You are mixing up too many things: 1) the ampicilin gene is normally not cut out to make recombinant DNA. Instead 2) cutting/pasting into a vector is usually performed at a multiple cloning site (MCS) independently of the ressitance gene. 3) The blue/white screening uses a beta-lactamase gene and is also unrelated to ampicilin.

@Nicolai yep I realized how off it was and answered my own question. I would've deleted the question because of how confusing it was but wasn't able to because it already had an answer.

The question confuses too many things. The process being described, Lac Z Blue-White Screening, doesn't involve cutting the ampicillin gene, nor do the bacteria with the recombinant DNA or without the recombinant DNA die in the process of the experiment.
The plasmid contains a Lac Z gene involved in creating enzymes that break down galactose. In a test tube, the vector plasmids take up the gene of interest and the recombinant DNA is produced. The recombinant DNA is then added to the medium of bacteria, but only some of the bacteria will be transformed and take up the plasmid vector. In these bacteria, restriction enzymes will 'cut open' a space for insertion in the Lac Z gene, and DNA ligase will seal it up. The insertion of the gene in a bacterium disrupts the Lac Z gene and make it unable to produce the required enzymes to break down galactose. Then, the bacteria are applied to a Petri dish that contains growth media with a derivative of galactose, X-gal in it. When X-gal is broken down by the bacteria able to create the necessary enzymes from their functional Lac Z genes, the bacterial colony will turn blue. So, when you add these bacteria into the Petri dish, only the bacteria without the recombinant DNA will break down X-gal and turn blue, whereas bacteria with the recombinant DNA will not be able to break it down and remain white. This allows the researcher to distinguish between the bacteria with and without the recombinant DNA, and allow them to isolate for the ones with it.

I answered my own question because I learned in the time since I asked it just how off it was.

Your description of how blue/white staining works is (essentially) correct, however the generation of recombinant DNA does not happen in bacteria. Recombinant plasmids are generated by researchers in vitro (meaning in a test tube) using restriction enzymes (and more like DNA ligase). Note that in most cases even a plasmid that did not receive the gene of interest would still be recombinant, since the even the base plasmid used is usually not found in that form in the bacteria used.

@Nicolai I've updated the answer given your remarks. Do you think it's good now?

I’ll elaborate on this answer in the future but, in the meantime, blue/white screening is used to differentiate between bacteria that were transformed with the vector and gene of interest and bacteria that were transformed with an empty vector. An empty vector still confers antibiotic resistance and thus allows the bacteria to grow, but it does not contain the gene of interest and is therefore useless to the researcher.


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GEN file format, SNPs and alleles
I have a few questions I can't seem to get a straight answer to, regarding the .gen file format and also biology in general.
The .gen file format specifies SNPs for individuals.
Since each SNP has associated allele A and allele B, I assume that the file only contains Causative SNPs, and not Linked SNPs, since the former reside in the gene, and the later don't. Since each SNP in the file has an associated gene (actually genotype, some combination of allele A and B). Correct?
SNP indicate a single position in genome, so why can allele be identified with a sequence larger then one? Or does it indicate just a starting point, where each allele can be of different length, which can be greater than 1?
Allele should be a particular variant of a specific gene, but in other places I saw the definition "Alleles are alternative forms of a particular sequence.". The later seems more logical, if looking at the .gen file, but it's contradictory to the first statement. So, what's the correct definition?
EDIT:
After further research I came up with findings, demonstrated in an example row for .gen file:
--- rs200405949 10023   CCAA    C   0.249   0.745   0.007   0.005   0.84    0.155 ...

--- - chromosome number, which is missing because it can be inferred from the filename, belonging to each chromosome
rs200405949 - ID of the SNP - a single nucleotide which can vary between samples/people; there are usually only two possible variations, but in rare cases there is a third or even fourth - which are ignored in .gen?
10023 - allele pair (base pair) coordinate/position inside the said chromosome. Either both major and minor allele are made of a single nucleotide (in which case the SNP coordinate/position inside the said chromosome might coincide with this position), or one of the alleles will have more than one nucleotide and the other allele will be the same as the first nucleotide of the former allele - because we need only one distinct sequence, and all other combinations of same nucleotide length are automatically the other allele?
CCAA - (usually?) major allele - the most common allele (specifically in this context, a single nucleotide or a sequence of nucleotides) for a given SNP (or near it, i.e. somehow connected to it) IN the cohort in question, i.e. the cohort being all the samples/people in the experiment/.gen file (hence, the number of samples equals the number of triplet columns after the 5-th column onwards). It occurs in more than 50% of the times COMPARED to minor allele. Compared to minor allele, they both start with C - shouldn't they differ at this SNP position by definition? Also, more than one nucleotide is specified here - why? SNP always has one nucleotide...
C - (usually?) minor allele - the second most frequent allele (specifically in this context, a single nucleotide). The SNP site can be bi-allelic (mostly picked/studied), in which case the major and minor alleles are the only possible alleles, but some sites are tri- or quad-allelic - in which case we don't have the info for the third (and fourth) allele variants, but we know they are even less common then the major and minor alleles?
0.249  0.745   0.007
0.005   0.84    0.155
... - each subsequent triplet of values then indicate likelihoods of homozygote CCAA/CCAA, heterozygote CCAA/C, and homozygote C/C genotypes (allele pairs) at this SNP, respectively, for one sample/person (each allele is present on one of the two copies of the said chromosome, either maternal or paternal). If one of the three values has a value 1 and the other two have 0, I guess this actual SNP was (somehow) tested for, hence we can be 100% sure which allele pair it is, and if not, then the probabilities were somehow deduced (e.g. from other, somehow related SNPs perhaps). What if they add up to less than one? Or even what if all of the three values are 0?
Are my conclusions correct? And what about the open question?

Based on https://www.sciencedaily.com/terms/allele.htm, each gene can be represented by a set of alleles, and alleles are just alternative forms of a particular single-nucleotide sequence; and since they can posses 2 different forms for the given genome (resulting in a 3 distinctive combinations), they are called SNPs. Besides alleles, there are also other in-between single-nucleotides in the gene, but these are the same for the whole population of a given (e.g. human) genome. True?

The definition of allele depends on the context.
If you look at the DNA of a single person you have usually two copies of each autosomal chromosomes. Each copy is called an allele. If you know look at the sequence at a specific position, you can say one of the two bases are located at one allele and the other base on the other allele.
Beside this there is a definition of allele if you take a look at a many persons or a whole population. Here you call an allele "as alternative forms of a particular sequence".

But how is SNP, which indicates a single nucleotide, associated with a major and minor allele, since either one can be of length greater than on? Does it mean that starting from the specific SNP position, it can either be the start of the major or the minor allele?

From what I could find the .gen file format for SNPs was developed for the IMPUTE2 program and is generally meant to be a flexible file format for SNP data. The description of the file format is supposed to documented here (multiple pages pointing to that link), sadly that link is broken / the site is removed.
However, I found some other descriptions of the format:

In the GEN format each SNP is represented as a set of three
  probabilities which correspond to the allele pairs AA,AB,BB.

from here

The genfile contains predictor values, one row per predictor.
  --gen-skip indicates how many header rows (typically 0 or 1);
  --gen-headers indicates how many header columns (typically 0 to 5).
  --gen-probs should be 0, 1, 2, 3 or 4:
   0 - haplotypes - predictor values should be "0 0", "0 1", "1 0" or "1 1"
   1 - dosages - predictors provide the (expected) number of A alleles
   2 - two probs - providing probability of being AA or AB
   3 - three probs - providing probabilities of being AA, AB or BB
   4 - four probs - providing probabilties of being AA, AB, BB or NA, where A and B are the A1 and A2 alleles

from here
Like finswimmer already wrote in his answer, it is very important to be clear about what is considered an allele in the context of SNPs. For the .gen file format this is the identity of the base at a given (SNP) position and since humans have a diploid genome, the allele of a specific individual can be one of three versions (usually called AA, AB & BB).
Regarding your specific points:

Since each SNP has associated allele A and allele B, I assume that the file only contains Causative SNPs, and not Linked SNPs, since the former reside in the gene, and the later don't. Since each SNP in the file has an associated gene (actually genotype, some combination of allele A and B). Correct?

The alleles in the .gen file refer to the respective SNPs not genes.
There is no reason to assume that an given .gen file only contains certain SNPs; if it does this is not due to the data format.
The SNPs in a .gen file do not generally have to be linked to a gene.

I've added example, can you comment on it and answer the remaining of my questions?


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Does sex-chromosomes exist in all the cells in a human body?
Each cell of a human body contains 46 chromosomes. So every cell must contain a pair of sex-chromosome. Is it true? Then a cell of a male and a cell of a female are always different and never be the same?

Like the other answer already said: yes, all cells in the human body contain all 2x 23 chromosomes (with the exception of cells that loose all nuclear DNA during maturation, like red blood cells, or cell produces by meiosis, which contain only a single set of 1x 23 chromosomes).
However, the more interesting part of your question remains to be answered:

Then a cell of a male and a cell of a female are always different and never be the same?

Technically it is true, that cells from a male and female can never be the same, however that difference is vanishingly small.
Genetically the difference is that female cells have two X chromosomes and male cells have one X and one Y. However:

in all female cells one of the two X chromosomes is permanently silenced (turned off), so essentially they also have only one (active) X chromosome.
the male exclusive Y chromosome is tiny. Size wise it is ~1% of the human genome, but it only has ~200 genes (of which only a portion is protein coding), which is even below 1% of all human genes (there are ~25.000 protein coding genes, around twice that much in total). Many of these genes are also only used/active in male exclusive organs.

These two points taken together mean that the majority of male and female cells do actually have the same active genes - and are therefore "the same" (there are of course many many other factors in biology, including individual differences, that require putting this into quotes).

+1 for recognizing that red blood cells are not the only cells that extrude their nucleus on maturation

All cells except mature rbcs contain genetic material. So every cell must contain 46 chromosome containing sex chromosome as well

Please provide a citation or link in reference to support for your answer. Thanks.

Yes, all cells except mature RBC have all the 23 pairs(22 autosomes + XX/XY) but due to different regulation mechanisms and deactivation due to heterochromatin, only the part of DNA actually useful to that particular cell type (like the gene for insulin in beta cells of pancreas) is used by it.
For Example: In the testis in the Leydig cells, only the androgen producing genes and other related genes are kept active.
https://en.wikipedia.org/wiki/Heterochromatin#Function
https://en.wikipedia.org/wiki/Regulation_of_gene_expression

Please provide a citation or link in reference to support for your answer. Thanks.


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Do primates have genetic predisposition to dominance hierarchies
I’m looking for some evidence to prove (or disprove) that primates are genetically predisposed to dominance hierarchies. I would appreciate any pointers/references to scientific literature.
PS:
The reason I am interested in this is as follows: primates (unlike many other less sophisticated animals) have a very little number of instincts. And yet certain types of behavior (for instance strong dominance hierarchies) seem to be a common case for some species; baboons, for example. And yet there are known cases of baboons (Sapolsky’s example) of a radical shift in social behavior towards less agressive and less dominance-based. This nevertheless looks rather as an exception and if so, raises the question if there indeed is a genetic predisposition to a certain behavior type.

This is one of those questions, where depending on how a person interprets the terms you use, one may give one answer or another. Hence it is difficult to answer.
You say that primates have very little number of instincts. And I react by: huh? Why would you say that? Then I realize it may depend on what you mean by instinct.
To the question on genetic predisposition. My reaction is: of course. Were you thinking of any other explanation? Which? But then I realize that it might depend on exactly what you mean by genetic predisposition.

And what kind of evidence might satisfy you? I very much doubt that know which primate alleles that affect dominance behavior. At least I doubt we know sufficiently much that it may be difficult to answer.

Eff, as an example: primates cannot swim (although as we know, humans can master it) while dogs, horses and plenty of other species have it encoded in them. So is a large number of other instincts. It regulates much less of primates behavior compared to other species. In terms of “what other explanation” could there be? Environment, as opposed to genetics. This also dictates the test criteria: genetically predisposed means validated across a broad array of environemntal conditions.

When something is 'genetic' and when something is 'environmental' is a difficult philosophical question. Do birds make nests because of the environment (availability of twigs etc) or because of their genes? What I would dare to say is that if the baboons had totally different genetics, then their behavior would most likely also be different. And for certain genomes, they most likely wouldn't engage in dominance behavior.

Also, just because something only happens in certain environments, that doesn't mean it wasn't genetic. You can easily imagine two species A and B, and two environments M and N. Species A might engage in dominance behavior in environment M, but not N. Species B does not engage in dominance behavior in either environment. This difference could be due to genetic differences, and yet the behavioral difference only manifests in environment M.


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Why is xylem a tissue and not an organ?
My textbook "CGP AS-Level Biology Exam Board: Edexcel Complete Revision & Practice" says xylem is a tissue.
Then I read from this website that "[Xylem's] major components include xylem parenchyma, xylem fibers, tracheids, and xylem vessels." Therefore, from my understanding, xylem is made up of multiple tissues including xylem parenchyma tissues, xylem vessel tissues and etc to carry out the functions of transporting water and nutrients in plants? Therefore that would make xylem an organ instead of a tissue?

In plants, there are three types of tissue: meristematic, simple, and complex.
Meristematic (embryonic and totipotent)
Simple (composed of only one type of cell), such as

parenchyma
collenchyma
sclerenchyma

Complex (composed of more than one type of cell), such as

dermal (protective covering)
vascular (conducting tissue)
xylem (conducts water and dissolved minerals)
phloem (conducts water and dissolved organics)
ground (bulk of the body; primarily parenchyma, collenchyma &
sclerenchyma)

With this information in mind, let's take a look at what the source you provided says that makes up Xylem tissue.

"[Xylem's] major components include xylem parenchyma, xylem fibers, tracheids, and xylem vessels

Here are the roles of said cells in Xylem:

Xylem parenchyma are cells specific to storage and short distance transport.
Sclerenchyma Cells (xylem fibers) are specific to support and protection.
Vessel Members (which are conducting cells) are specific to water, mineral transport, and support mostly in advanced angiosperms.
Tracheids (which are also conducting cells) are specific to water, mineral transport, and support mostly in gymnosperms and lower angiosperms.

I hope this information helped you understand why Xylem is not an organ, but rather a complex tissue of plant.
References:
http://facweb.furman.edu/~lthompson/bgy34/plantanatomy/plant_cells.htm
http://www.bio.miami.edu/dana/226/226F09_5.html

Thank you very much for the detailed answer. May I then ask what is the fine line that distinguishes complex tissue and organ? (i.e. at what point can we say something is an organ and not a complex tissue?)

Ok, so just disregard the accessory word 'complex' for a moment and think about just tissue. A tissue is the combination of cells. Xylem is made up of a collective of specialized cells in order to perform its tasks. An organ is made up of a collective of tissues. The reason xylem is a complex tissue is because different cells make it up, whereas in a simple tissue is made up of the same cells. Hope this helped!

Thanks again. But I'm still not sure at what point can we say something is an organ and not a tissue. In the case of xylem, your argument is that it is a tissue since it is made up of different cells to perform its tasks. But can't I also say, xylem is made up of different tissues to perform its task e.g. xylem parenchyma tissue, sclerenchyma tissue, vessel members tissue and tracheids tissue - since tissue is simply a combination of cells. Thereby, making xylem an organ?


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Identifying statistically significant gene rich and gene poor regions
I am just wondering If there any adapted way of Identifying significant gene rich and gene poor regions in each chromosome for a given genome say mm10?

What research effort of your own have you put into answering this question? We ask that all posters here do some of their own research, report what they've performed and what they found out, and then specify a question that  focuses on something specific about a topic that they still don't understand. Please update with some of your own research effort findings and sharpen your question some. Thanks!

Interesting question. I don't myself know how to do this but a literature search returns some older papers on how this was achieved for pig and chicken genomes over a decade ago. The best way to do this today is to look through annotated genomes (like the mouse mm10) and use a gene density metric. You can achieve this with R code, writing your own code, trying to use some of the rich features provided in-browser at the UCSC genome browser (for mice, otherwise start here), or perhaps try to search literature for gene density stuff. I defer to others for more specialized answers.
PS. Since you're also interested in determining statistical significance, you probably will need to apply this over a sliding window across chromosome lengths, and this kind of question has been answered often elsewhere on SE (example). Sorry I can't be of more help; good luck!

Thank you for your comment. I found that coverageBed from bedtools  has some useful output for identifying gene densities.


text:
How is the right amount of nucleotides synthesised during homologous recombination?
I'm reading about homologous recombination in the context of double-strand break repair. It seems like the trick is that around the break, homologous recombination uses a template duplex to generate some overlap between the broken parts so that the strands can just be complementarily repaired. However, when reading from the template, unbroken duplex, it seems like it's quite important exactly how many nucleotides are generated to form the overlap between the two broken strands. Too little, and no overlap is formed as the broken strands still form two disjoint sequences. Too much, and the broken pieces no longer fit together, there are parts doubled. It's like a puzzle where some pieces describe overlapping regions.
How does the polymerase know to add exactly the right amount of nucleotides?

Recombination is not my thing, but I’m sure it would help if you could provide a reference to the text you are reading — or an online source with a similar diagram to clarify your problem.


text:
How did Smith et al 2004 deal with missing HI [Hemagglutination Inhibition assay] values and HI values <10?
In the scientific paper "Mapping the Antigenic and Genetic Evolution of Influenza Virus's" Supporting Material, Smith et al write about determining antigenic distance Dij. However, I don't understand how one could calculate Dij from HI values of <10. Is it better to remove these data values or to change it to 9?
Also, regarding the missing data, how does one make a comprehensive antigenic map using shape space distance dij? I see that an error function must be minimized, but how does that give dij for all the missing data? Should missing data be ignored for the error function?

I don't know how Derek's group handles it (don't have time to look now) but conventionally HI assays less than 10 are called "9" for statistical purposes, and I assume that's how they did it. Have you looked at Henry Wan's antigenic distance web site (http://sysbio.cvm.msstate.edu/software/AntigenMap/about)? I think he talks more about his approach

You're clearly serious about this project, but asking on se.biology isn't the best problem-solving approach for this kind of in-depth question. Can you find a mentor in the field who can work with you specifically?

Thank you @iayork. I am a high school student and I am working on this project for a research competition. I appreciate your answering my questions for the past few months.

I'd like to help more, but this isn't my speciality, not to mention that I have my own group to run. Since you have good, specific and focused questions, you could just try writing to Derek Smith, who is a very friendly guy. Trever Bedford is enthusiastic and committed to open-source software and has a strong Twitter presence, and you might get answers from him too. Jesse Bloom is very knowledgeable and has open-source projects.

Alright, thank you @iayork. I will contact the people whose names you mentioned.


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What does (G+) (G++) in terms of male mutation rate and male-heterogametic XY-system?

What's the expression for $\alpha_m$ in case of male-heterogametic XY systems (G+)?

Derive the corresponding $\alpha_m$ expression of for (sic) male-heterogametic XY systems (G++)

I have absolutely no idea what they mean with G+ and G++ in the exercises. I have searched the whole Internet and the lecture slides for this but I think I am going crazy. Has it something to do with the gametes? Anyone who knows?
Thanks in advance!

I don't know what G+ and G++ mean. I don't know what $\alpha_m$ mean either. Can you provide some context that could help?

Please do not post text as images as images are not searchable and can pose problem to visually impaired users.

I think you need to provide more context.  When I saw G++, my first thought was the C++ compiler of that name.  I am unaware of any universal use for the term in biology.  It could very well be context specific.  It is common to use that sort of notation when describing alleles in a population, with the pluses following whatever variable name you gave to the allele.  So if we had an allele that we called G, and an individual had two copies of that allele, it would be common to see that individual referred to as G++, with G+ being used to refer to someone with only one copy.  I think it is quite possible that this is what the term means in your context but it is impossible to say for sure without more information on what the question you are being asked is in reference to.  Maybe it would help if you posted questions 1-4 or the blurb that precedes the problem set so we could see what you are actually being asked.


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What is the status of the "Free Energy Principle" as a theory of living organisms?
The free energy principle states that biological organisms maintain their order by minimizing a function called variational free energy (VFE).
While it is the case that the minimum to VFE also minimizes Helmholtz free energy under certain assumptions, VFE is distinct from Gibbs free energy or Helmholtz free energy and is borrowed from statistics (variational Bayesian inference). It measures the degree to which the approximate posterior deviates from the exact posterior.
It has been argued that the free energy principle explains many facts about brain function. However, I would like to learn about biologists' views on the broader claims as a principle that seeks to explain all aspects of the function of living organisms. I would be grateful for direct answers and for any references that discuss this issue.

I think the vast majority of biologists has never heard of this paper you linked (Karl, 2012; published in "entropy", a journal that I suppose few biologists ever read). So biologists's view are probably very inexistent for the moment. But maybe someone will be willing to read the paper for your post as the question can be interesting.

While this paper may not be the most popular (although it has been cited at least 300 times) this: https://www.nature.com/articles/nrn2787 is the "canonical" reference for the application of the free energy principle in neuroscience (since you used the tag). I am not (yet) an expert on the subject but I do feel that it is one of the most powerful theories in neuroscience at the moment. Some people feel uneasy as it explains too much.

Thanks, I‘m trained as a neuroscientist myself and I‘m roughly familiar with the applications of FEP there. However, FEP is often used as if it were a fundamental and universal biological principle, and I wanted to know whether this has been discussed within the biological communities. In particular, the distinction between free energy and its variational counterpart seems interesting.


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Contracting mouth muscles as reaction to taking in specific food items
When eating very specific food items, especially confectionery like (salty) liquorice, (it feels as if) the muscles of my mouth contract, right when it hits my tongue.
Does anyone know why this happens?
The process is similar to experiencing relatively high levels of sourness - suggesting it is a similar reaction - but, as far as I know, there is, apart from the glycyrrhizic acid in the liquorice plant, not a lot of acid in this type of confectionery. I imagine other possible causes could be sugar substitutes like steviol or Maltitol.


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What makes the flowers glow?

I had learnt in a plant biology course that, all the flowers are actually originating from leaves, with several mutations. I wonder what makes a flower sparkly like this.
Photos belong to a Phalaenopsis Orchid (White) (under direct sunlight) . But I believe this can be observed in many plants.
When searched for it, I saw one explanation on that they shine right after they are watered. But I observed this long after the plant was watered. So I guess this is not the case.
Also I've read about the pigments that absorbs different wavelenghts and give the plant its color. But I couldn't find an explanation about this sparkling view.
Another thing I read was about the shiny views of some flowers, like buttercup flower. It is said that this is originating from flat cell shapes. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5332578/). But again, this is different than what I am asking.
Biology is not my major (probably as you have already guessed :)), so I might not be searching it with the right keywords. So I will be glad to get some help. Thank you :)!
Edit:
Another photo, taken with flash light. The shiny view is only in the side leaves (petals and sepals), not in the middle parts.

hi new user and welcome! please provide name of the flower, and also any research you did to asnwer this question yourself

Hi, sure. Actually photo was just an example, I observe this in many flowers. Still, I will edit my question. Thank you :)

Also what lighting conditions &c.  From a quick look, the "sparkles" look like they might be small drops of water.  Have you looked at them under a microscope?

There was a strong sunlight on them. I don't have a microscope :). So do you mean water droplets due to the air humidity ?

I'm not sure of the conditions in which the photograph was taken. That could be anything from wax on the leaf, or stomata.

I am adding a photo taken with a flash light. You can see that the shining part is only the petals (and sepals) not the middle part.

@GabrielFair this is something you can see with your naked eye in direct sunlight on daffodil petals as well as iris petals. I'm sure you can see it on many others but those are places I have seen flowers sparkle like this.

Could be water condensing from the air (dew), or it could be water released from the plants via transpiration: https://water.usgs.gov/edu/watercycletranspiration.html  But I'm just guessing...  Though Google Images has some similar pictures: https://www.google.com/search?q=water+droplets+on+leaves+from+transpiration&complete=0&source=lnms&tbm=isch&sa=X&ved=0ahUKEwi2u7iBu8ngAhUBqp4KHTVgBp8Q_AUIDigB&biw=1223&bih=952

@L.B. Yes it is exactly what I am talking about. I had thought that this was a very wellknown phenomenna through.

@jamesqf As you had Said, that sparkles really look like tiny water droplets (nearly microscopic). Actually they more look to me like some cyrstals, like a snow surface.  I have looked those transpiration photos. I couldn't catch a simular image though.. Those droplets are very big and seems to be at the surface of the leaf. Mine seems like they are at the inner tissue. It might be because they are very small scaled. I also searched it as "petal transpiration" but couldn't find a simular image yet.

@jamesqf - I knew this was an orchid when I saw the first picture. It is not water. It has to do with surface cell shape, translucency and light. It's not an uncommon phenomenon in flowers.

@anongoodnurse hi, as far as I understood from the article I mentioned in the question the flat cell shapes provides a mirror like or buttered/polished like shiny surface.But here, I think we can see some obvious particles. Might they be some plant mineral crystals? I had also thought of dust particles but these particles are very homogeneous and can be seen also at the back side of the petals, which I wouldn't expect to hold much dust.

@user6069929: I was thinking of this image in particular: https://image.shutterstock.com/image-photo/close-water-drops-on-pumpkin-450w-1027095193.jpg Looks almost exactly like yours.  But try some experiments, like brushing the surface of the leaf/flower, or passing a razor blade over it.

@user6069929 - I don't think so. See http://bulbnrose.x10.mx/Heredity/KayPetals1981/KayPetals1981.html; look at the photomicrographs. Especially helpful are scanning electron micrographs of orchid petals.

@jamesqf I see. Mine are not even that obvious. Moreover they are independent of the temperature or the time of the day. Also when I tap on the surface with my finger, it doesn't give a wet feeling neighter the pattern is distrubbed. But okay I will try those :) Thank you.

@anongoodnurse Thank you for the source. I have skimmed it, I couldn't catch the SEM Photos of Orchids (might be as I am not familiar with the names.., I couldn't Google it all). But, i.e. the one with conical cells which the light is reflected only from the tips and generates a spotted-like pattern. There it's written that the photo is in x160 scale. Mine are visible with bare eye. What would you say on that?

I have seen the phenomenon you describe to some degree in many flowers: violets, daffodils, but most prominently (in my mind) on orchids. Look up "scanning Electrom micrographs orchid petals; with what the paper discussed, it should correlate.


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Why is ATP used as a source of energy rather than glucose?
I'm struggling to pinpoint a misconception, but I don't think I understand why ATP is used as an energy molecule instead of glucose. I understand that glucose is respired, oxidised or combusted and produces energy in the form of ATP so I guess what I don't understand is why glucose isn't hydrolysed (like ATP is) when energy is needed instead of having to convert its energy to ATP first.

Please do not ask two separate questions in one question. The second is an elementary question the answer to which you should find out for yourself from any textbook of biochemistry, e.g. Berg et al. at NCBI Bookshelf. The first question has probably been asked before. The answer is historical. It was not possible originally to demonstrate synthesis of ATP experimentally with the ATP synthase, only the reverse reaction. Now the system is understood, references to ATPase are stupid and outdated. I suspect your textbook is the latter.

A similar question to your first has subsequently been posted, and as it received an answer (now two) cannot be deleted. I have therefore edited your double question so as to leave only the second part (even though I think you should try to answer it yourself.)

Perhaps I was a little unfair. Although the idea of ATP as an energy currency is described in textbooks, and you need to have progressed a little to follow it, the general question as to what molecules are suitable — and why glucose is not — is a little more subtle. I therefore decided to give my answer to it after all.

Well the mechanics of this can actually get pretty complicated, depending on how far into the biochemical weeds we want to go, but there are a couple of very simple reasons at the core... Well they actually aren't that simple, but they can at least be analogized in simple ways.  The first, and easiest to illustrate is this.  This is a glucose molecule:

And This is an ATP molecule:

If you want to get some energy out of an ATP molecule, all you have to do is break off one of those phosphate groups.  If you want to add more, you just stick another phosphate group back on.  This can be done without significantly changing the structure of the molecule itself.  That Adenosine base never gets touched.  Only the chain of phosphates is manipulated.  It is much more energy efficient to add and remove those phosphate groups than to add and subtract elements from a glucose molecule, as there is no way to effectively break it down without significantly changing its structure, which makes it harder to build back up.  We want a molecule that it is just as easy to add energy to as it is to pull energy out.  The glucose molecule just doesn't have a chain sticking off that's easy to remove and put back at will.  The CH2OH group on the end looks like an attractive energy sink on its face but getting the whole thing off isn't nearly as easy as it looks, and it doesn't contain as much energy as a phosphate group either, which brings us to the second easy to illustrate reason ATP is more attractive than glucose as an energy carrier.
If you look at that chain of phosphates, you will notice that they are each separated by an oxygen atom.  There are also a bunch of convenient hydrogens and OH groups floating around that make hydrolysis and dehydration very easy.  Where would you hydrolize the glucose molecule to produce a low energy molecule that can be converted back to glucose more efficiently than ADP can be converted back to ATP?  Just compare this process:

To this one:

The ATP hydrolysis looks more like the breaking down of polysaccharides into glucose than the catabolism of glucose itself, and this is at the core of the difference between the two molecules.  It is always easier to add and subtract links from a chain than it is to make direct modifications to one of the links themselves.  Glucose is great for energy storage.  You can pack a lot of energy into a glucose molecule, but once you get it out, it's very hard to put it back.  It's much easier just to throw out the waste and start over by making or eating another one.  We don't have this luxury with ATP.  It has to be able to drop off its energy load and go pick up more.  For this, the structure of ATP is much more appropriate than the structure of glucose.

Why was this answer downvoted? It appears to be correct and is close to what I would have written.

Lol I have no idea.  Maybe they wanted to answer it.  Maybe they didn't like my simplification.  Maybe they thought this question just shouldn't have been answered at all for one reason or another.  Downvotes without comments can mean anything and often indicate an opinion too poorly thought out for me to even bother wondering about.  If there is a real, concrete problem to be addressed, it should be pointed out.  Otherwise I just tend to ignore it and briefly assume some sort of misanthropy on the voter's part before forgetting it altogether.

To understand this answer to the question one needs to have an elementary acquaintance with glycolysis and the concept of free-energy change in chemical reactions. This can be obtained from biochemical texts such as Berg et al. on-line.
Energy Currency
If biochemical energy is stored predominantly in a particular molecule, that molecule acts as “currency” which can be used for a variety of biochemical requirements. The general idea is that the (negative) Gibbs Free Energy change of the conversion:
                            Loaded-Purse —> Empty-Purse

is used to drive some chemical reaction or process such as ion transport, light emission, muscle contraction etc. that requires energy. For a chemical reaction, this would be:
                    Low-energy-compound —> High-energy-compound

There needs to be some way of recharging the unloaded-purse with energy.
In cellular metabolism ATP is the loaded purse and ADP — and sometimes AMP — the empty purse. The question is why ATP, and not glucose.
Desirable Properties for an Energy Currency
Here are some. You may be able to think of others.

It can be used in a wide variety of chemical processes in the cell.
It can store and release energy in amounts that are sufficient for most reactions, but not too large to be wasteful.
Its removal and regeneration will not disrupt important metabolic pathways.
It can be made available to different types of cells and organelles in a variety of circumstances.

How do the candidates fulfil the requirements?
If we look at glucose as such, it immediately fails the test on count 2, because the energy released by its oxidation to carbon dioxide and water is much more than is needed to drive most chemical reactions: approx. 30x that for the hydrolysis of ATP, which turns out to be of a more suitable magnitude.
But, let’s not give up on glucose yet. We could take just one of the intermediate steps of glycolysis where a suitable free energy change does occur. A prime example is the oxidation of  glyceraldehyde 3-phosphate. In glycolysis the energy change is used to phosphorylate the oxidation product (phosphoglycerate), but in a different universe we might imagine glyceraldehyde (with or without the phosphate) to be the energy currency, and the free energy of its oxidation coupled to other reactions.
This has one chemical problem: what is happening to glyceraldehyde (and glucose as a whole) is oxidation — not hydrolysis as the question states — so it would only be suitable for driving reduction reactions. It fails on count 1.
“High energy” redox intermediates have their place in metabolism — NADH etc — but this is clearly limited, which is why the energy of their oxidation is used to regenerate the more general currency. In practice this is ATP. Although one can argue whether Nature could have adopted some other molecule which had a high negative free energy of hydrolysis, that is not the question here. (It does in some cases.)
There is no real need of either of points 3 and 4 to rebuff the glucose argument, but there is no harm in addressing them. Could an intermediate in the oxidation of glucose be used without disrupting the process of glycolysis? Perhaps — ATP is used for RNA synthesis. But what would be the advantage anyway? Glucose is not the only cellular source of energy — Why not an intermediate in the oxidation of fatty acids? And if you accept that the currency would have to be an intermediate, the availability of glucose is less relevant, because  the purse would not need remaking all the time, just refiling, in a similar way that adenosine synthesis is low compared with the phosphorylation of ADP.
Reference
There is a specific section in Berg et al. on ATP as an energy currency.


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If the effect of increase CO2 in the air has a negative effect, why doesn't decreased CO2 have a positive effect?
I recently asked a question about whether there were studies on the effects of reduced CO2 level air and got what sounds like a good answer:
Are there studies on the effect of reduced CO2 levels on human cognition?
The answer posted to the above question states that there is no reason to expect low inhaled CO2 levels to even make a difference in the relative levels of CO2 in the lungs, with are ~100x higher than in the ambiant air. This seems like a rational argument.
But with further thought that argument seems inconsistent. If average CO2 levels in the air are around ~400ppm, just 3x that number, ~1200ppm, is known to be associated with drowsiness and complaints of poor air quality (if my research is correct).
If the argument above holds, that reducing CO2 levels in the air from ~400ppm to ~0ppm, isn't going to significantly affect the ratio of CO2 in the lungs, then why doesn't that argument hold also with a seemingly small increase of 3x CO2 levels in the air (as compared to the 100x levels in the lung already)?

The US Navy has tried to replicate the (highly dubious) results claimed by some recent "Green" buildings research (which is the stuff you're referring to, even if you don't say it explicitly). The Navy replication study failed to find any differences whatsoever in their replication. Non-replicable research gets published in psychology all the time, alas. Also the "Green" building research contradicted decades of prior research on the matter.

Thanks, that's a really good reference, that's the kind of stuff I was hoping to find with this question, you should post that as an answer. I am interested in the references to the decades of prior research. I'm not an expert in this field, so I look to places like wikipedia and stack exchange to cue into it, and I've been seeing contradictory publications.

3X atmospheric CO2 does not have appreciable cognitive impact.
Indoor air typically is already much higher in CO2, especially in a room full of people, because they are all breathing out CO2. It would not be unusual to find 2-3X atmospheric CO2 inside.
In the answer to your previous question, I referred to much higher concentrations that do have appreciable impact. For example, at 100X normal atmospheric concentration, the concentration in the air is similar to the normal concentration in the lungs, such that CO2 builds in the lungs and dissolved levels increase in the bloodstream.

So is a site like this is publishing incorrect information? https://www.dhs.wisconsin.gov/chemical/carbondioxide.htm, they state that: "1,000 - 2,000 ppm: level associated with complaints of drowsiness and poor air."

@davidparks21 They're being super safe for safety's sake. They aren't publishing incorrect information, they are publishing guidelines for keeping building air overturned. If CO2 levels inside are rising to 1000-2000 ppm, probably the building air isn't turning over much. There could be lots of other things in the air, and particular individuals who already have breathing problems (i.e., the CO2 in their blood is already high) could have symptoms.

I see a variety of numbers published that are hard to disentangle here. On this wikipedia page: https://en.wikipedia.org/wiki/Carbon_dioxide#Toxicity, I note two quotes, (1) "In concentrations up to 1% (10,000 ppm), it will make some people feel drowsy and give the lungs a stuffy feeling.[115]", which seems to support this line of reasoning, and (2) "A study of humans exposed in 2.5 hour sessions demonstrated significant effects on cognitive abilities at concentrations as low as 0.1% (1000ppm) CO2 likely due to CO2 induced increases in cerebral blood flow.[121]", which seems to question it.

Bryan is right, I think. The level of CO2 is used as a measure of indoor air quality because it is convenient, not because CO2 is toxic at these concentrations. There are probably confounding factors in studies which find a correlation between CO2 level and effects on cognitive function at 1000ppm. Studies controlling the level of O2 and other confounding factors have found have found no dose-response for CO2 under 2000ppm.


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excitatory-inhibitory synapse ratio
For each inhibitory synapse, how many excitatory synapses are in the brain?
It is the same ratio along the animal kingdom or nervous system areas?

E/I synapse ratio probably isn't the most informative measure, because you leave out the release probability of synapses, the postsynaptic efficacy of a synapse, the level of presynaptic activity, the spatiotemporal correlation of inhibition and excitation, the meanings of excitation and inhibition in different parts of the animal kingdom, the temporal features of rapid neurotransmitters vs slower neuromodulators, etc etc.

I'm aware that at a dynamical level E/I balance could be very different than E/I balance at the anatomical level. For my purposes, I want to have an estimation of the E/I ratio in terms of connectivity alone.


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Volvox Cellular Reintegration
A couple of days ago, I answered this question over on worldbuilding.SE with some information about volvoxes, and commenter Liam Proven pointed out that one of the claims I made was dubious.
I had first read about the volvox in a book that described their basic biology and life cycle (the book may have been Flatterland by Ian Stewart, but I no longer have a copy to verify). One detail I vaguely remembered was that since volvoxes are essentially colonial organisms, individual cells do not immediately die when the volvox disintegrates, but rather some of these cells can rejoin the cytoplasmic matrix of other colonies, similar to sponges.
Now, I read this a long time ago, and my memory is admittedly foggy, and I never had any university-level training in biology. It's entirely possible I'm conflating this with something completely different I read elsewhere, so Liam's comment sent me searching for more info.  And even if I am remembering correctly what I had read, it's possible the original author was mistaken.
The best article I could find on the topic was Cytoplasmic Bridges in Volvox and Its Relatives by Hoops, Nishii, and Kirk, but it doesn't appear to support my recollection (it talks mostly about the inversion process in embryos).
So I thought I'd bring the question to a wider audience. Do individual volvox cells reintegrate after disintegration, or do the mother's cells simply die?


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Does hybridizing a specific flower affect the offspring?
If among several flowers within a plant, there is a specific flower that is slightly larger or brighter or has an extra petal, will this trait be possibly passed on to the offspring? In other words, does picking a specific flower to hybridize matter and impact the offspring or does the offspring inherit the general traits of the whole plant and any flower has the same impact? Just wondering if when hybriding a plant, I need to be selective on which flower to choose.


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Do large animals experience a meaningful delay when moving their most distant appendages?
According to the Physics Factbook, nerve impulses travel at speeds anywhere from 1 meter per second up to around 100 meters per second. Blue whales reach up to around 30 meters long.
For a full-size blue whale, this means that a nerve impulse to move the tail muscles could take from 0.3 seconds to 30 seconds to reach the tail. While I'd imagine factors such as myelination and other adaptations function to keep this closer to the 0.3 second measure above, this is still a best case scenario, and would certainly be a noticeable delay were it a human being.
Do large organisms experience meaningful delays when moving their most distant appendages?

Humans have a delay of around 0.3 seconds for moving arms (training helps for many situations). Part of that is the transmission speed, but there's also the serial problem - neurons arranged in a sequence gain considerable delay. That's why we have so many "automatic" systems that don't rely on inputs going from e.g. leg to the brain, get processed and transmitted back. You usually don't notice because your brain lies to you all the time - there's some real fun experiments that cheat your brain to thinking reactions happen before their stimulus (e.g. pressing a button to light a bulb).

Yes, larger animals do experience larger delays in movement.
There have been studies of size difference vs sensorimotor delays in terrestrial mammals, https://www.ncbi.nlm.nih.gov/pubmed/30158304

That graph is for innate reflexes of a needle to the hind versus a kick-time. Perhaps no one dared to prick a blue whale.
Elephant vs shrew, heartbeat of 30 vs 1500 BPM, elephant 50 times slower than the shrew. Larger animals compensate with a better ability to predict physics and kinematics using their larger brain.
There are other kinds of movements which have more complex neural pathways that the graphs of pin-prick reflexes, that are even slower compared to size, you can study the physiology of eye to hand response in humans which varies from 120ms to 270ms for different humans.
It does have an effect on survival for example with a mongoose versus a snake, the mongoose has more versatile and faster reactions.

There are also weasel attack videos on the web.
some graphs here

Good presentation. Would benefit from a
#Yes, larger animals do experience larger delays in movement.
Introduction

"heartbeat of 30 vs 1500 BMP" I think you meant "BPM (beats per minute)"?

It may be valuable to point out that (most) invertebrates have a far slower conduction velocity than vertebrates due to the former not employing saltatory conduction.

It's a shame humans are not on the pain reflex graph, and that there's no non-human data for eye-hand reflex.


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Why can't complex multicellular organisms reproduce by regeneration?
My textbook says that regeneration isn't  possible in complex multicellular organisms.
But why? Why can't specialized cells be present in the bodies of complex multi cellular organisms which can proliferate and ultimately make a whole new organism, when (for example) cut in two?

What textbook are you using?  Regeneration most assuredly is possible in many complex multicellular organisms, such as the Asteroidea of the Echinoderms.

The book means to say in most organisms

I was doing some research on this myself and from what I had found, the body has hox genes that direct the formation of body parts. So now the obvious question is that if a body part contains stem cells and hox genes, shouldn't it be able to regenerate a new body? Well, perhaps. But the problem is that as organisms become more complex, the process of the creation of their bodies also becomes more complex. For example, in the fruitfly, if the labial gene function is not expressed, the mouth and head that develop outside the body do not get involuted and that prevents the salivary gland from forming.
So the answer about why multicellular organisms can't regenerate so easily simply seems to be because the process of creating a multicellular body has for some reason become an extremely complex, intertwined process where various body parts creation is dependent on other body parts creation. So in the evolutionary process it's entirely possible that the stem cells noted that there's no point trying to regenerate a body part, and therefore they just don't.
Here's an anomaly. There's a jellyfish that can reverse aging and go back to infant stage. I think it's able to do so because it has a simple body structure.
Another possible reason could possibly be the presence of unstructured proteins which are more abundant in multicellular organisms.

The jellyfish you mentioned is turritopsis dohrni if I remember correctly. When I was young, I wanted to be like that jellyfish. Now I know that im too 'complex' (instead of simple) to be that.

An evolutionary reason for the lack of regeneration in long lived animals is cancer. The waiting undifferentiated cells (stem cells) are another potential source of cancer.

Not all complex organisms are incapable of regeneration!
The most famous example is probably the axolotl - a salamander that is able to regrow whole limbs or even parts of essential organs like the brain or heart. While it's not yet know how that is possible, there are a lot of researchers looking into it (the genome of this species was fully sequenced last year).
Another example is the regeneration of zebrafish fins, which - while less impressive - is by now pretty well studied.


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what is the characterization of mutant bacteria and how is it done?
I have a task to characterize protease producing bacterial mutants but I have failed to understand what it is and how it is done

Hi, and welcome to the biology stack.  This is clearly a homework question.  While those are okay, they have to follow the guidelines for homework questions.  Please [edit] to show what you've tried, and where the confusion specifically lies.  Thank you!


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What are the advantages of sexual reproduction over asexual reproduction?
What are the advantages of sexual reproduction over asexual reproduction?
How does variation influence ecological and evolutionary success?

The question is unclear. You might want to rephrase. As you say, sexual reproduction is good for life because it's a method of reproduction, which allows for survival, which life requires by definition. But that's just tautological. Do you mean to ask what the benefits of sexual reproduction are over asexual methods for an organism in an ecological/evolutionary context? Or would you like to know the biological, cellular and molecular mechanisms which occur exclusively in sexually-reproducing species that allow for variation? Please clarify.

I meant to know the benefits of sexual reproduction over asexual reproduction

Genetic variation -- a variation in alleles to enable organisms to avoid passing on mutations/traits that reduce fitness and possibly create new combinations of alleles that lead to traits that actually increase fitness. You might also want to take a look at population genetics and microevolution to see how this plays out at a larger scale.

Please consider using a search engine for these kinds of questions. This question has been addressed nauseatingly often. PS: The main advantage of sexual reproduction is the introduction of a LOT of genetic variation which is not achieved through budding/regeneration/fragmentation (asexual reproduction). Variation is fundamental to evolution and as such has a protective, prophylactic effect against parasites and disease. Unique offspring are produced each time. The downside is that it's more energy-costly, takes a lot of time, requires two organisms (parents) and produces fewer offspring.

@SPr I was just wondering what else was it good for rather than the points you mentioned. The points you mentioned are addressed often to this question. I was wondering if there were any other reason. All the websites I entered , ultimately only mentioned that it's good for production of complex organisms, makes lot of variation which helps both adapt and speciate. Not anything else.

You are misunderstanding the core advantage. Sexual reproduction is not "good for production of complex organisms" - this is a misunderstanding. It's an effective strategy to introduce genetic variation between individuals of a species. It occurs in many simple organisms too. Variation is very, very important in evolution. A lineage with steadily high levels of variation between successive generations can escape diseases, be resistant to parasites, is protected from major genetic mutation events, and has the additional benefits of sexual selection. These all lower the chances of extinction!

One question at a time please.


text:
Spermatozoa and sperms
Does  spermatozoa and sperm have different meaning?If they are same why do wikipedia have 2webpages ? But most websites mention them as the same thing.I am confused .Thank you in advance

In broad way we call it sperm but the motile sperm is precisely called spermatozoon and plural form of spermatozoon is spermatozoa. A non motile male gamete is sperm but not spermatozoon but there is a term for that too its spermatium.

Not just in humans most animals have sperm, in fact non-motile sperm cells would be the basal condition.


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Biological Nitrogen Fixation
I just studied Biological Nitrogen Fixation and saw it's reaction but i do not understand why there is 8 electrons and 8 protons are involved and Hydrogen molecule is formed side by side along with 2xAmmonia... According to me there should be 6electrons and protons because it needs 2electons in each step from Nitrogen to Di-imide and 2electrons from Di-imide to Hydrazine to give out 2xAmmonia

The reason why two additional electrons are required is to reduce two additional hydrogen ions to one molecule of hydrogen gas, as any text book account makes cleaer e.g. Berg et. al.  Are you asking why this latter occurs, when it seems unnecessary? The absence of an explanation in such texts tells its own story.


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Can crossing over between X and Y chromosome of sex chromosomes take place?
Can it? If no, what would happen if it did?

What effort have you put in yourself to try to answer this question? Failure to show your own effort will result in your post being voted down and closed. Please update!

Yes, it can, but it is rare, and typically only in the pseudoautosomal region, meaning those sections on the X and Y chromosome that have homologous genes.
The reason it's rare and more difficult is that the DNA does not match as well, so the chromosomes have trouble interacting along the length of the chromosome.  Furthermore, there are less recombinant zones available.

Sources:

Kauppi, Liisa, Marco Barchi, Frédéric Baudat, Peter J. Romanienko, Scott Keeney, and Maria Jasin. 2011. Distinct properties of the XY pseudoautosomal region crucial for male meiosis. Science 331 (6019): 916-20.
Hinch, AG, N. Altemose, N. Noor, P. Donnelly, and SR Myers. 2014. Recombination in the human pseudoautosomal region PAR1. Plos Genetics 10 (7): e1004503.

So even if it does, there won't be any effect? The offspring will be as normal as any other child?

Typically, yes.

Yes, I believe it can, however, crossing over between non-autosomal chromosomes can occur. I think it depends upon what regions came to cross over, in terms of how it would affect an individual, as the y-chromosomes surpisingly has few sex related genes, and individuals only use one (X), male or female, I do not think that it would produce a really mutated individual.


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Which statements are true regarding an energy pyramid?
The number of producers is greater than the number of primary consumers.
The amount of energy at the primary consumer level is greater than the amount of energy at the secondary consumer level.
The number of primary consumers is less than the number of secondary consumers.
The amount of energy at the producer level is less than the amount of energy at the primary consumer level.

Sorry, we're not here to do your homework for you.


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How much energy takes C4 photosyntesis to make glucose?
Wikipedia has a kind of contradiction that I would like to understand:
According to this link

The C3 pathway requires 18 ATP for the synthesis of one molecule of glucose while the C4 pathway requires 20 ATP. [...]

According to this other link:

[...]. The C3 pathway requires 18 molecules of ATP for the synthesis of one molecule of glucose, whereas the C4 pathway requires 30 molecules of ATP.[...]

Also, I don't understand much of this, I was just curious. I found this link (not sure if reduction also means generate glucose):

However, the C4 pathway of CO2 reduction expends more energy (5 ATP and 2 NADPH) than C3 pathway (3 ATP and 2 NADPH) (Hopkins 1999).

And this link:

ATP consumed in C4 plants
  C4 cycle ( which involves regeneration of PEP from C3 acid) - requires 2 ATP per CO2 fixed.
  C3 cycle ( which is common in C2,C3,C4 cycle)- requires 3 ATP per CO2 fixed.
  Total - 5 ATP per CO2 fixed.
  Thus to form a hexose or to fix 6 CO2 6*5= 30 ATP

All emphasis mine.
So... Does C4 requires 20 or 30 ATP per molecule of glucose? I think I found more evidence over 30 than 20, is that correct?

Yes,C4 plants use 30 ATP molecules to make one molecule of Glucose.See since you have stated in your question that you know very less about biology and got some similar vibes from looking at your profile so I'll sum it up in a nutshell but hopefully this might help.In flowering plants,all of them follow a basic pathway know as the C3 cycle to make glucose from CO2.Now,in that process about 18  ATP is used.But apart from CO2, there's O2 also present in the atmosphere which interferes with the compounds taking part in C3 cycle and instead of CO2 participation O2 participates in the reaction and the consequence is that glucose is not produced and the plant wastes some energy in the form of ATP.
Now to prevent that from happening,some plants evolved themselves and made some chemicals which bind only with CO2.But the thing is that they also require energy to function and for each molecule of glucose produced they require 12 ATP this making net amount of ATP required to be 30 in a C4 plant.You can in a way visualise this C4 pathway that the plant placed some guards in the form of chemicals that combines with CO2 and makes sure it reaches its destination and to prevent traitor O2 molecules to disrupt plants from making glucose.But we all know that that guards would require some fee and so that fee is 12ATP.And visualise C3 pathway as some some sort of glucose making factory which makes glucose from CO2 and the production cost from raw materials is 18 ATP.

Thanks for your answer. Since it seems that you know about this, could I make a not much related question? Does CAM photosynthesis is the same as C4 but instead of absorbing CO2 during the day it does during the night to avoid competitors (other plants) and lose of water due transpiring?

See CAM pathway is found in xerophytic plants.Now,for eg: in deserts,there is a very high chances of water loss.So what they do is that they use some similar compounds as C4 plants and use it to store CO2 in the nighttime as there is chances of high water loss during daytime.Now in the day time,they use the stored CO2 to perform photosynthesis and manufacture glucose via the normal C3 pathway.


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Typical DNA replication times
Just out of curiosity (I am completely strange to biology), as I have been unable to find this info on the internet:
How long does the whole DNA replication process take? (say, the replication of a whole chromosome)
Approximately, how long does the DNA spend in a single helix structure during replication?
I am curious about the time scales of these processes, from the moment the polymerase starts cutting the double helix till the moment there are two double helices perfectly formed (one of them a copy of the other). How long can this take? miliseconds? seconds?

A mammalian cell takes about 8 hours to replicate all of its DNA in its S phase; a yeast cell would take about 40 minutes.
Some other information that you seem to not have quite the right information about:

The DNA polymerase does not unwind/split the DNA—that is the job of DNA helicase. The DNA polymerase cannot bind to the single-stranded DNA until the helicase unwinds the double-stranded DNA ("melts"), or the dsDNA is artificially melted in a test tube via high temperature.

The dsDNA is not fully separated before it is copied. There are tens of thousands of sites—origins of replication—across the genome that unwind and begin replicating every time the cell replicates its genome.

"...DNA replication in most eukaryotic cells occurs only during a specific part of the cell-division cycle, called the DNA synthesis phase or S phase. In a mammalian cell, the S phase typically lasts for about 8 hours; in simpler eukaryotic cells such as yeasts, the S phase can be as short as 40 minutes."
"An average-size human chromosome contains a single linear DNA molecule of about 150 million nucleotide pairs. It would take (0.02 seconds/nucleotide) x (150e6 nucleotides) = 3e6 seconds (about 35 days) to replicate such a DNA molecule from end to end with a single replication fork."
"...Approximately 30,000–50,000 origins of replication are used each time a human cell divides."

–Molecular Biology of the Cell, 6e, Alberts, et al.

Thanks for the answer and the extra info!

I think your view of DNA replication is a little off-target in relation to strand separation (which produces what you call “single helix structure”). The strands of the DNA are separated continually as replication occurs and then they are copied quite quickly by DNA polymerase. They are not separated completely and then copied. (And DNA polymerase doesn’t cut anything.)
But here are some typical times from on-line text books, where you can read more about the subject:
Bacterial cells
According to the text book The Molecular Biology of the Cell:

“It takes E. coli about 40 minutes to duplicate its genome of 4.6 × 106
  nucleotide pairs.”

And this has been discussed in an answer to a previous question.
Animal Cells
According to the text book, The Cell:

…human cells in culture, which divide approximately every 24 hours.

However, as explained out in the section cited, S phase — when DNA synthesis occurs — only takes about 8 hours. (Thanks to @rotaredom for pointing this out.)

Good answer, though I feel like your last quote doesn't address the question.  I know this isn't the most authoritative source, but this suggests that replication time is around an hour in humans.

@David if it's dividing every 24 hours, most of that time is not spent in the S phase.  The cell has to grow in order to sustain proliferation; hence a long amount of time must be spent in G1.  And it takes some time to get through G2 and M, of course.

Thanks @rotaredom. Have edited my answer, still keeping it to the minimum so that people will go to read the sources for themselves.


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Effect of the same caloric intake of different macronutrients on body weight
To gain weight, caloric intake > caloric expenditure.
To lose weight, caloric intake < caloric expenditure.
But what is the effect of the type of macronutrient ?
That is to say :

does the same caloric intake of carbohydrate, protein, lipid have the same effect on body weight ?
Does X amount of carbohydrate caloric intake > caloric expenditure or X amount of protein caloric intake > caloric expenditure or X amount of lipid caloric intake > caloric expenditure lead to weight gain ?
Does X amount of carbohydrate caloric intake < caloric expenditure or X amount of protein caloric intake < caloric expenditure or X amount of lipid caloric intake < caloric expenditure lead to weight loss ?

Just a warning, this would seem to be a reasonable scientific question, and there are studies addressing several aspects, but it gets to people's personal beliefs about food and body weight, which are very charged issues. I've found researchers, clinicians, public health officials, and members of the public in general have very strong opinions on this. Depending on who you ask, you'll hear the data are conclusive (on one side, or the other) and people on the other side are charlatans, shills, and hacks.

This is a hard question because you will find sources that claim that calories from protein have less effect on body weight gain when compared to the same amount of calories from carbs or fats. Likewise you will find other sources that state that a calorie is a calorie regardless of its origin and hence consuming 2000 calories of protein would have the same effect on body weight when compared to consuming 1200 of carbs, 500 of fat and 300 of protein for example.
A proposed mechanism for protein calories having less effect on body weight gain is "thermogenesis" or in order words that some of the energy from protein calories is lost when processed by metabolic pathways after consumption, but this is not globally accepted by the scientific community. Here is an article from the International Journal of Obesity that discusses the subject. I would suggest being VERY picky with the references you find on the subject since there is a lot of info floating around in the web in sites without any scientific backbone.
Something that can be assured though is that different calorie proportions origin-wise cause different results for other variables different from weight such as body composition. In addition to this, there are several studies adressing the apparent statistical find that protein rich foods increase satiety and hence facilitate body weight control; however, the latter is not related to calorie intake count but rather to other factors that decrease hunger physiologically or psycologically.


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Does human brain produce nicotine?
I had a discussion with a high school student about the effect and production of nicotine. He mentioned that nicotine is naturally produced in our brain so when the person takes to smoking, the brain stops producing its own nicotine and starts craving it from an external source. According to him, this is how nicotine addiction develops. How true is this?
The students also claimed that nicotine in cigarettes is harmless. I have already seen the answer about how toxic it is to humans, but I would love to know:

What's the lethal dose for nicotine via ingestion (not inhaling)?
How does nicotine compare to other toxic substances - for example, cyanide or any other known poison? Is it more toxic or less toxic?

THANK YOU

No, the human brain does not produce nicotine. The brain has nicotinic acetylcholine receptors, but the endogenous agonist for these receptors is acetylcholine, not nicotine; they aren't named "nicotinic" because they are for nicotine but just because nicotine happens to act on them. Many other human receptors are named similarly, based on discovering the molecular basis for sensitivity to exogenous compounds.
The human LD50 for nicotine is reported between 0.5-13 mg/kg depending on age and other factors, but LD50 is only appropriate for evaluating acute toxins; many substances, including nicotine, are most often encountered in small chronic amounts, but concentrated availability of nicotine in insecticides or vape juice can be a plausible source for sufficient doses for acute toxicity. Studies of nicotine toxicity in relationship to smoking are going to be based on much smaller doses over many more administrations.

Thank you very much for your answer. Could you please provide some info on your educational background? I want to show your answer to my students and I don't want them to say "you cannot believe random people on the Internet". Thanks one more time.

@treehugger My educational background shouldn't be relevant; I do have a PhD in a biological science but I could also say I'm an astronaut and the head of state of a major country; since I am ultimately a person on the internet you should use other information to decide whether to believe me. Your question is fairly basic, so I've left some links to Wikipedia articles. Of course, Wikipedia is not an ideal source, but you can follow sources on each of those linked pages to reputable scientific publications.

@treehugger I understand, I'm just trying to give you another perspective. As a scientist, I'd much prefer a ninth grader learn how to find and evaluate scientific information from credible sources rather than appeal to authority of an individual. They should learn to be skeptical of their own intuition, skeptical of unsourced claims, skeptical of sources with other motives or unclear provenance, and learn about how scientists themselves reach their conclusions. All those skills are much easier to learn as a high school student than as an adult - we adults tend to be quite stubborn.

No nicotine is a special type of drug which is never secreted by the brain. Each person has their immunity -- it's based on what amount you take and how your body responds towards it because for some there is a small amount require to become toxic but for some, it can't. As compared to cyanide it is less toxic because cyanide is very harmful

Needs a citation.

The answer is poorly written. Needs links and references.

https://cvi.asm.org/content/11/3/563

It is a good link and there is a lot of explanation and a lot of knowledge in it


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Is there a way to chemically detect the presence of Fungus in a sample?
I would like to know if there is a way to chemically or somehow detect the presence of Fungus in a sample?

What kind of sample?

What kind of fungus?

Relevant literature: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3968782/

You could test for the presence of chitin, which is a fundamental component of fungal cell walls.  There is precedent for this: https://apps.dtic.mil/dtic/tr/fulltext/u2/a036986.pdf
Chitin is not only present in fungi though, it is also fundamental to insect and crustacean exoskeletons, and the occasional plant species (e.g. Aegagropila).

Don't insects have chitin as well, and aren't insect parts generally found at some level in many foodstuffs?


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Probability of carrying an autosomal recessive trait given both parents are carriers
I recently came across a question that asked for the probability of having a child with an autosomal recessive trait, namely cystic fibrosis. From various parts of the question, we can conclude that the father is definitely a heterozygous carrier and that the mother's parents are both heterozygous carriers. In this situation, the only way to produce a child with cystic fibrosis is if both parents are heterozygous carriers, and this will happen with a probability of $\frac{1}{4}$.
The part that causes confusion is figuring out the probability that the mother is a carrier.
One student reasoned that a cross between two heterozygous parents will produce a 1:2:1 genotypic ratio, so $\frac{1}{2}$ of the progeny will be heterozygous carriers. Therefore, the probability that the mother is a carrier is $\frac{1}{2}$ and the probability of producing a child with cystic fibrosis is $\frac{1}{2}*\frac{1}{4}=\frac{1}{8}$
Another student also referenced the 1:2:1 ratio but reasoned that since the mother is phenotypically normal, that the ratio is actually just 1:2 because there is no chance of being homozygous recessive. Therefore, the probability that the mother is a carrier is $\frac{2}{3}$ and the probability of producing a child with cystic fibrosis is $\frac{2}{3}*\frac{1}{4}=\frac{1}{6}$
These two answers are also found at this other question.
The last solution proposed is the most interesting. This student referenced the Monty Hall Problem, which is indeed somewhat related to this problem (read more about the Monty Hall Problem). Using the same ratio as above, we can conclude that there is a $\frac{1}{4}$ chance that the mother carries no alleles for cystic fibrosis and a $\frac{3}{4}$ chance that she does. The fact that she definitely does not carry two alleles does not change this probability. Therefore, the probability that the mother is a carrier is $\frac{3}{4}$ and the probability of producing a child with cystic fibrosis is $\frac{3}{4}*\frac{1}{4}=\frac{3}{16}$.
Out of these proposed solutions, which one is correct? And why are the others incorrect?
EDIT: To be clear, the solution I initially considered to be correct was the second one.

Solutions 1 and 2 are not contradictory.  1 is appropriate if you do not know the mother's phenotype, 2 is appropriate if you know she is not affected.

Using the same ratio as above, we can conclude that there is a 1/4
  chance that the mother carries no alleles for cystic fibrosis and a 3/4
  chance that she does. The fact that she definitely does not carry two
  alleles does not change this probability.

Yes it does.
Money Hall is about 1) picking, 2) the revealer, knowing where the prize is, reveals something, then 3) you pick again with the new information.  That's not really what this question is.
Lets say there are 4 doors; one affected, 2 carrier, and one not a carrier.  You do not pick anything (which is why this isn't really a true Monty Hall).  If you know the mom's not affected, that's the equivalent of Monty opening the affected door, no mother.  Now the odds are clearly 2/3 carrier, 1/3 not, where before they were only 1/2 for carrier.  Eliminating a door changes the odds for the others, that's the point of Monty Hall.  Eliminating a phenotype does change the odds of the genotype.

Monty Hall does not apply here because there is no decision point past where information is given: the information is already known that the mother is normal phenotype, and the probability for each child of the mother's parents is independent; in the Monty Hall problem, it is known that exactly 1 of the doors contains the prize. Because this sum is known (that only 1 door has the prize), if you know the contents of one door it changes the probability of the others. That is, the occurrence of the prize/goat is sampled without replacement: the thing behind each door is dependent on what is behind the other doors.
2/3 is the correct probability for the normal phenotype mother to be a carrier. Therefore the probability for a child to be homozygous recessive is (2/3) * (1/2) * (1/2) = 1/6.

The part of Monty Hall that appears to relate is that removing a possibility does not mean the remaining possibilities are all equally likely. The way I understand it, the incorrect third solution is saying that removing the homozygous recessive case does not mean the remaining two heterozygous and one homozygous dominant cases are equally likely.

@DarinMao Monty Hall is about adding information about one of the possibilities when you are asking which contains a prize. That is, it is not only known that the probabilities behind the doors are equal, but also that the sum occurrence across all doors is also known (and equal to 1 in the standard Monty Hall problem). Therefore, knowing one door the probability of the other doors changes. That is not true for the mother and her possible sisters, however: her probability is 2/3 regardless of how many sisters she has and regardless of how many of them are or are not carriers or homozygous.


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What are the (statistically) normal pH levels in the most-outer part of human sexual organs?
What are the (statistically) normal pH values of the outer skin/epidermis of human sex organs (groin/crotch) in the male and female? e.g male testes, female vulva, male glans, the enveloping epiderm, etc. I was trying to find information to no avail.
Edit:
I googled different terms, like anatomical ph index map of the body, and couldn’t find any ph data about specific anatomical structures.
When I googled, I read through reiterations that the body has neutral ph mostly. Again, nothing anatomically specific.
Due to the ‘unique’ per structure microbiome, it does make sense to foresee a different ph, more to the acidic scale.

Hi and welcome to Bio.SE! Could you provide a clearer indication of where you've already searched and what information you did learn along the way? We as that question askers not only do background research of their own, but that they also demonstrate it. Please update your question using the edit button and add additional detail about your research process thus far.

Can you explain why you would expect the values to differ from those in the skin at other parts of the body? This would provide context for your question. Otherwise it appears rather strange and is likely to be ignored.

@David I don't know if this is related or not, but recently a rumor began circulating on the Internet saying that women's vaginal areas are more acidic than the stomach. I wonder if that is why this question is being asked. Ironically, I was just thinking about asking this question... Beat me to it lol

@L.B. — "A rumour began circulating on the internet". I vote to close.

@David still would be interesting to know if there's any merit

@L.B. — I would imagine that three days' silence tells its own story.

@David, the question makes no attempt to ask about a personal medical question, so voting to close as such doesn't seem appropriate. It also doesn't seem strange for someone to ask this fairly straightforward question given the different environments, bacteria, etc. that these sex organs are associated with compared to the rest of the body. I vote to keep open, and I ask that you more patiently judge people's posts.

Hi, @theforestecologist I used google with difference keywords, for instance, I just can’t seem to find a ‘map’ of some sort of the human ph index presuming such a map even exists in biology books. I just can’t find any ph data about specific anatomical structures.

@Ryan, for the sake of making your question more robust and assuaging other users' concerns, I recommend editing your question by including a rationale for why you think the pH is different. I would think a slightly more drawn out form of your last comment (perhaps with an additional explanation of why you think the groin would have different pH) would suffice. Thanks.

@theforestecologist — In relation to your request, may I say that I read your original personally offensive comment before either the moderators or you removed it. You should therefore know what is required before I respond to that request or any future comments you might make on my posts.

I might suggest googling "normal vaginal pH", "normal urethral pH", and "normal skin pH". This will get you better google results than your prior search strategy.


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Oil absorbed into human skin -- where does it go?
For example, I apply petrolatum to my dry hands twice a day as in winter I am usually in a 20-30% RH environment.  Within an hour, the petrolatum seems entirely absorbed.
According to [1], petrolatum and the other oils tested there "do not reach the viable cells of epidermis, saturating only the uppermost horny layers of the skin."
So my question is: Where does the oil go?   I do not believe I am shedding unseen skin layers fast enough nor transferring the oil to other objects fast enough that I can repeat and apply twice a day, without the oil going deeper than "uppermost horny layers" and being excreted internally. (Via lymph? blood?)  Also, I rarely wash my hands with soap.
[1] Confocal Raman microscopy for investigating the penetration of various oils into the human skin in vivo.
Choe C, Lademann J, Darvin ME.
J Dermatol Sci. 2015 Aug.
https://atlasofscience.org/oil-penetration-into-the-human-skin/
Accessed 2/8/2019


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Is this a Loranthus Europaeus?
Location: Austria, Vienna Ottakringer Wald
Date: Feb 8
I found something beneath a tree with epiphyta , which I thought to be Viscum album but is vividly yellow instead of white and I found no leaves.

My search of subspecies of Viscum album initially revealed:

Viscum album subsp. austriacum (Wiesb.) Vollmann. Fruit yellow; leaves 2–4 centimetres (0.79–1.57 in). Central Europe. On Larix, Pinus, Picea.

But then I began to think it shouldn’t be V. album. In illustrations of V. album there aren't the thin stalks between berries and branches as in my specimen.

Perhaps Loranthus europaeus?

You are quite right: it's Loranthus europaeus. Vienna was the prime example in our botany lectures where to see that plant without a fuzz.
c/p from the Flora of Vienna:
"Auf Eichen, vorzüglich auf Quercus pedunculata und Qu. sessiliflora, selten. Im Eichenwalde von Schönbrunn, auf dem Gallizin, hinter Neuwaldeck, hin und wieder; viel häufiger auf dem Bisamberge {A}. ... auf den grössern Donau-Inseln z. B. ... in der Lobau {C}."
"Häufigkeit des Vorkommens: häufig bis sehr häufig"
(Confused about the contradicting "rare" and "frequent to very frequent" statements, but anyway.)
Here are some more pictures.

The first „selten“ only applies to the case of quercus. He/she lists „locations“ in order of ascending probability.

I suspect your are right, but I can't be sure. Would have assumed to be the probability/frequency to be in brackets after Q. sessiliflora if it would relate to frequency on the host.