How much carbon does a forest contain? Trees in a forest, alongside the fungi, animals and plants that live there in, capture atmospheric carbon dioxide and store it inside their tissues and in the soil as humus.

It is possible to estimate the amount of carbon stored in some portion (say 100 square meters) of a climax forest?

This should depend on the specific biome, for example Eucaliptus and Pine forests seem to contain less organic matter than broad-leaved tree forests in temperate regions.

PS: A slightly more speculative aspect of this topic is to evaluate weather reforestation can contribute to lower the amount of carbon dioxide in the atmosphere.

This question is very broad and this would require a lot of calculations, I will focus on the carbon dioxide in the trees, hopefully some other users can add details in respect to the organism and their carbon dioxide storage.

I found an article(R.Jandl et al.,(2007)) which did some calculations, this site does a really good job in explaning these calculations so I will cite that:

  As trees photosynthesise they use carbon dioxide (CO2) from the
  atmosphere with water from rain or irrigation and nutrients from the
  soil to form carbohydrates, which make up the tree’s biomass, but how
  much carbon is made by a tree in this process? Researchers at
  Ecometrica have worked it out! The amount of carbon stored by a tree
  depends on its size, which in turn is influenced by factors, such as
  species, local environmental conditions and the way it is managed. In
  an attempt to find a simple answer to this question, researchers at
  Ecometrica have broken down approximately how much carbon is stored in
  each element of a typical tree (the branches, the leaves, the stem and
  the roots) by percentage for a quick and simple calculation.

  They used standard forestry practices to estimate the amount of carbon
  contained within the stem, branches, roots and leaves of a mature
  sycamore (Acer pseudoplatanus), found near their office in Edinburgh,
  with a diameter of 52 cm and a stem height of 12 m.

  First they measured the various parts of the tree and, from these
  measurements; they calculated their volumes, which were then used to
  calculate the biomass (mass of living matter in plant tissues):  The
  radius of the stem at 1.3 m above the ground (r1 = 26 cm) and at the
  top of the stem (r2 = 20 cm), and The height of the stem (h = 12 m)
  They used known relationships between the biomass of the stem and the
  biomass of roots, branches and leaves to estimate the total biomass of
  the tree: Stem volume was estimated using the equation for the volume
  of a truncated cone:

  which gave an estimated stem volume of 2.0 m3 The wood density of sycamore is approximately 620 kg/m3, so using the equation:

  Mass = Density × Volume  the stem biomass was 1243 kg, or
  approximately 1.2 tonnes  The biomass of the roots, branches and
  leaves of a sycamore tree are known to be around 26%, 11%, and 1% of
  the total biomass, respectively. These proportions were used to
  estimate the total biomass of the tree without having to dig up roots
  or cut down branches.  In summary, the sycamore tree had a stem with a
  biomass of 1.2 tonnes, roots of 0.5 tonnes, branches of 0.2 tonnes and
  leaves of 0.02 tonnes, giving a total biomass of 2 tonnes.

  The carbon content of woody matter (stem, branches and roots) and that
  of leaves is approximately 50% of  their biomass. Multiplying the
  total biomass by the proportion of that biomass which is carbon gives
  an estimate of the total amount of carbon stored in the tree, which in
  this case was exactly 1 tonne! Each tonne of carbon equals to
  approximately 3.67 tonnes of CO2.

Then the further calulations really depends on the density of the trees in the forest (if you know the exact number let me know). There are a lot of atricles which gave some numbers the range is based on these articles somewhere around 30-400(and some even 1200 trees). I used the data from this article, which measured the optimal density for growing. I assumed that the climax forest is just naturally so I just picked 400 trees per acre (this is just guessing offcourse and I just generalized this for all trees, but I saw 400 in an other article):

Then we can just do some simple math for the carbon dioxide for the trees:

  total CO2 for the trees = 400 x 3.67 = 1468 tonnes

Let me know if someone can find the tree density of a climax forest


Inheritance of FEVR (Genetic Disease) If a woman has FEVR and is affected by the disease, what are the chances of her passing the disease to future generations. I read somewhere from a credible source like NIH(I couldn't find the link again, I am attaching another https://rarediseases.info.nih.gov/diseases/1613/familial-exudative-vitreoretinopathy#:~:text=Familial%20exudative%20vitreoretinopathy%20(FEVR)%20is,the%20blood%20supply%20to%20retina.), that the babies that the woman conceives could be affected by or carrying the FEVR causing genes, or may neither be carrying nor affected by them. Depending on the type of inheritance, which are autosomal dominant, autosomal recessive, or X-linked recessive, the chances of having a normal baby vary. The chances of having a healthy kid for autosomal dominant and autosomal recessive are 50% and 25%, respectively ( I am intentionally excluding the possibility of X-linked recession).
Therefore, if the inheritance is autosomal dominant, then, there is a 50% chance that the baby is healthy and not carrying the genes. And the successive generations created by the baby will not have the gene causing FEVR. Is my understanding correct?

The answer depends on (at least):

whether the woman is affected by the condition
whether the allele is autosomal dominant or autosomal recessive (excluding X-linked recession)
the frequency of the diseased alleles in the population
the presence or not of inbreeding

Below I assume no inbreeding.

The woman is affected and the inheritance is autosomal recessive. This means that the woman carries two disieased alleles and with certainty passes one of them to her children (i.e., with probability $1$). Whether the children will be affected by the condition depends on whether they get a second diseased allele from the other parent. Assuming that the frequency of the diseased allele in the population is $p$, this means that the probability of a child inheriting the disease is $p$.
The woman is not affected and the inheritance is autosomal recessive. The woman carries only one diseased allele, and passes it with probability $1/2$ to her child. The probability that a child is affected, i.e. that s/he has two diseased alleles is $p/2$.
The woman is not affected and the inheritance is autosomal dominant. In this case the woman carries no diseased allele, so the children are not affected.
The woman is affected and the inheritance is autosomal dominant. The woman carries at least one diseased allele, and could be carrying the second with probability $p$. In the former case she passes it to her child with probability $1/2$, in the latter with probability $1$, so the probability that the child inherits the diseased allele is $1/2 + p$. This is also the probability that the child is affected by the condition, since they will be affected regardless of the allele passed by the other parent.

Assuming very small probability $p$, case 4 gives us the probability $50%$, whereas the probabily in cases 1 and 2 is much lower. The numbers given in the question are calculated assuming Mendelian experiments, which are a heavy case of inbreeding (and even then not quite correct).
John H.Gellespie, Population genetics
Matthew Hamilton, Population genetics


Are ligand gated channels saturable? A major difference between simple diffusion and facilitated diffusion is that facilitated diffusion has a maximum transport and velocity; the rate of diffusion is limited, whereas in simple diffusion, it isn't.
Ligand Gated channels (like any protein 'channel') transports molecules through simple diffusion, so they should not be saturable, but how does that make sense ? The channels open by the binding of a specific ligand/molecule, can't they be saturated by this ligand just like carrier proteins are saturated by the substance/molecule which will pass through ?

If they were in fact saturable, how are they considered to be part of simple diffusion?

Yes, they are saturable, because they have a finite number of 'binding sites', depending on the particular example you are looking at. Then, once they join the substrate to be transported, they need to release it at the other side of the membrane, which takes time (in very short time scales, but time nevertheless). Therefore, the saturation rate and speed of transport depends on the number of transporters on the cell's surface, the gradient differential, and the number of binding sites.

Facilitated diffusion, which needs a transporter as you point out, is a form of passive diffusion, which implies that there is no energy cost to the cell to transport the solute (as opposed to active transport). This is the key difference: energy. It does not mean that it goes as fast as osmosis or any other type of passive diffusion/transport, because, the transport that goes across the membrane (small gas molecules, and other small molecules) will clearly be faster. Also, passive diffusion does not mean that there is no upper limit to diffusion, in fact, diffusion is always limited by the concentration difference of the diffusive molecule across the membrane, no matter if this is passive or active transport.

In short, it is simple/passive diffusion because it does not need energy. Whether is saturable or not is not what matters for this classification. In fact, all diffusion has a limit.


Identify this waterfowl species? I've been unable to find anything on the Google resembling this bird. I took the photo in Virginia Beach, VA around 2010, October, I think...
It appears to be between winter and summer plumage but I'm not sure. I tried looking on whatbird.com but couldn't find anything that really seemed to match up well.

Edit

I've added some more photos since people seem to question whether or not the white is snow, for some reason. Also note that most seem to have a red bill with a black tip, while the one with more white on its breast has a largely black bill with just a red band. Do bills change colors when plumage does, is that a thing, or perhaps it's just an anomaly or a gender trait?

I am not an ornithologist, but using identify.whatbird.com and a simple google search, this appears to be a Muscovy Duck. Try a google image search for yourself! Some of the birds pictured have more ostentatiously red or larger caruncles, but some look very similar to the birds you photographed. For example: http://www.birdinginformation.com/birds/ducks/muskovy-duck/

From muscovyduckcentral.com and identify.whatbird.com:
The domestic breeds can come in a variety of colors, but are primarily black and white with red and white bills. The males are larger than the females -- around 15 lbs for a male and only 8 lbs for a female. Females are duller colored than the males. Muscovy ducks are indigenous to Mexico, Central and South America, but are now raised in many different locations. They are considered a good duck stock because they are large, breed quickly, provide good pest control, and are quieter than many other duck breeds.


Significant presence/absence of plant species I have approximately 300 cluster of 200 different plant species and a presence absence matrix of all species versus clusters (since some species don't have clusters so they are checked if they are present or absent in other clusters). Now I want to find out if there is significant presences or absences of this plants in their clusters. At the same time I need to know which clusters have this significant presences. I want to know that if there is spesific software can do this or do I have to write code?

edit: it is not clear what i mean with significant presence and absence as i understand. by significant presence i mean "species being in the same clusters all the time. not one of them being in another cluster without the other." by significant absence i mean that "if leys say Y species never tooks place in clusters of which X species exist."

I am not quite sure what you mean by "significant presence". If you observe any non-zero number of plants of a given species in a cluster, then the rate at which this plant occur in this cluster is different from zero. No stats required to infer such thing. You should clarify your post.

Logistic Regression

It sounds like you would like to do a logistic regression with presence / absence as response and the nominal variable cluster as solo explanatory variable. In R you could for example do something like

# Dummy data
d = data.frame(
 presence = sample(0:1, 120, replace=TRUE),
 cluster =  rep(LETTERS[1:4], 30)
)

# Logistic Regression
m = glm(data= d, formula = presence ~ cluster, family = binomial(link="logit"))
summary(m)

You can find here another example of logistic regression in R

Phylogenetic signal and pseudoreplication

You might want to make sure to decorrelate your variable from the phylogeny to avoid pseudoreplication. There, the solution you might end up going with will depend on your genetic data. If you have a genetic PCA, you could go with using the first 2 axes as simple covariates in a type I sum of squares kind of model (which is probably the default of the logistic regression I performed above). If you have a kinship matrix you could use it with lmekin or MCMCglmm (see here for adding a kinship matrix). There would have many different statistical tools for such decorrelation depending on your data.


The parameter for setting the number of mismatches in standalone blast In a standalone blast search, is there a parameter that could be specified to fix the number of mismatches allowed in an alignment. I went through the parameters and I could only find parameters to set score.

-q => Penalty for a nucleotide mismatch (blastn only) [Integer] default = -3

-r => Reward for a nucleotide match (blastn only) [Integer] default = 1

What do I do if I only require hits with a maximum allowed mismatch or gap of 2 per alignment.

There is no direct option like that but you can set percentage identity filter with -perc_identity

However, this is only for reporting. BLAST will still perform all the alignments. That is why I suggested you to use bowtie.

EDIT-1 (getting long for comment)

If you want a word type of search then use the -n option. But it always starts from the 5'end which is quite justified in case of miRNA because the seed region is in the 5'.

Setting -n to 0 means no mismatch in seed region. -l option defines the seed length; I would advise that you use something like 10. -e refers to maximum mismatches in the non seed region but it is not the number of mismatches; it means maximum tolerated sum of phred score of mismatches (fasta files are assigned a default phred score of 40 at all residues. So, for 2 mismatches you have to mention -e 80).

EDIT-2

Yes. Increasing mismatch and gap penalties would make the search more stringent if you have already specified a cutoff on score.


Does soap kill human cells? I see many products, particularly hand soap and cleaning products, that claim to kill 99.9% or more of bacteria.

This makes me wonder, if the chemicals are potent enough to break down bacterial cell membranes, can they also break down human cells? If not, why not?

salamander is right about triclosan being the active ingredient in antibacterial soap, but the reason why it doesn't kill human cells doesn't have anything to do with the skin. From salamander's same source:

  Once they are in microbes cells, triclosan poisons a specific enzyme (enzymes are proteins that have particular functions, think of them as cellular machinery) that is used in making microbes cell membranes. Humans dont have this enzyme, so triclosan doesnt poison us.

The enzyme in question is called Enoyl-acyl carrier protein reductase (ENR), and is used by bacteria as part of their fatty acid synthesis. Eukaryotes use a different set of enzymes for fatty acid synthesis, so we aren't effected by this activity of triclosan.

For some more specifics about the interaction of triclosan and ENR, we can turn a study about the antibacterial mechanism of triclosan that was done soon after triclosan was first crystalized in situ with its target enzyme.

From Heath, et al (1999):

  Triclosan is a broad-spectrum antibacterial agent that inhibits bacterial fatty acid synthesis at the enoyl-acyl carrier protein reductase (FabI) step... The ubiquitous occurrence of type II fatty acid synthase systems in bacteria and the essential nature of the FabI reaction make this enzyme an attractive target for antibacterial drugs. Accordingly, triclosan is effective against a broad spectrum of bacteria, including multi-drug-resistant Staphylococcus aureus.


Cell Respiration and Oxidative Phosphorylation Why and how does the proton travelling through the stalked particle in the inner mitochondrial membrane, cause a conformational change in the ATPase?

The passage of protons through the FO (membrane) portion of the molecule (driven by the electrochemical gradient of protons across the respiratory membrane) generates torque at the interface between the a and c subunits. This mean that the ring of 10 c subunits rotates relative to the a subunit. The γ subunit in the stalk rotates along with the ring of c subunits, while the ring of α and β subunits in F1 is constrained to remain static with respect to the a subunit because of the interaction with the δ and b subunits (forming the peripheral stalk). So we have two portions of the molecule the "static" a-b2-δ-α3β3 part and the rotating c10-γ-ε part. The γ subunit rotates within the α3β3 part of F1 and drives a three-step cycle of conformational changes (via intersubunit interactions) which are linked to the phosphorylation of ADP.

There is a useful animation here illustrating the three step catalytic cycle being driven by the rotation of the γ subunit.

(image from Aksimentiev et al. (2004)
Insights into the molecular mechanism of rotation in the FO sector of ATP synthase. Biophys J. 86:1332-44)


Improving transformation efficiencies- induce supercoiling? From my limited knowledge of science, I know transformation can be one of the hardest step in cloning, and that a large amount of research/trial and error has been done to improve on this step. I've heard electroporation is the most efficient technique, though I have no reference, and of course the cell, media and duration all have vital parts to play in the process.

However, I've never heard of supercoiling as an important factor. Size of the plasmid plays a large part in transformation, so intuitively it makes me think supercoiling the plasmid prior to transformation would improve the efficiency. I thought transformation was simply DNA diffusing through holes, but are parts of the plasmid required to bind/interact with the host?

Why aren't we suggested we supercoil prior to transformation? I have several thoughts but I'm just guessing:

Is it because gyrase can disrupt the integrity of DNA?
Or is it that it's just an expensive enzyme and the gain isn't worth it?
Or perhaps supercoiling reduces efficiency of subsequent plasmid preps/transcription (though wouldn't the host's natural enzymes supercoil anyway?)

Here is a report that shows significant increase in transformation efficiency for large plasmids (transformation was by electroporation. However the paper has been cited fewer than ten times so clearly the technique did not catch on.

  Zhixing, Y and Nahon, J-L (1995) DNA gyrase improves DNA transformation of E.coli cells with large recombinant plasmids. Nucleic Acids Res. 23:3353-3354


Why does sequencing virus proteins take time? According to the below paper, the coronavirus spike protein sequence was available to scientists by end of february 2020 - the begin of march 2020 timeline. I had this question that why does sequencing of a virus protein take so much time (I am a software engineer, currently studying molecular biology to better understand the pandemic, hence I am seriously unaware!) ? The reason of asking is because, in case of another epidemic, we might need to spend again a lot of time to sequence the protein. This might be a real concern!
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7151553/#:~:text=At%20the%20time%20of%20the,remain%20identical%20or%20almost%20so.

Sequencing a viral genome requires isolation of the virus, propagation in cell culture, extraction of nucleic acids, and preparation of a sequencing library.  Once sequences are obtained, a genome can be assembled de novo using (untargeted) shotgun reads, and gaps in the genome can be spanned with (targeted) Sanger sequencing.  This process can take weeks to months depending on the availability of resources and the growth characteristics of the virus.
For details on how the 2019-nCoV genome was sequenced, see Zhu et al., published January 2020:
A Novel Coronavirus from Patients with Pneumonia in China, 2019


What is wrong with this analogy: Individuals are to alleles what governments are to individuals I'm an amateur when it comes to genetics, I'm hoping to learn something from the corrections. I am taking epigenetics into account (kind of); all 3 entities are susceptible to external physical influences.

Kind regards,

Frank

Alleles are passed down (to individuals) and created by individuals (although not fully under their control). But individuals are not passed out or created by the governments (I suppose), although individuals are influenced by the governments and they can influence governments, whereas individuals can not necessarily influence the allele of the gene they already have unless you take epi-genetics into account. Also, the creation of an allele is not entirely influenced by individuals due to independent assortment and chromosomal crossover, but individuals can more or less influence governments.


Raphide toxicity in Pothos plant Recently I found out that the common houseplant Pothos (Epipremnum aureum) is toxic to cats and dogs due to the presence of "insoluble raphides." I have a lot of these plants around my house and my cat drinks water from the vase that they are in (I put drinking water into the vase that he always drinks from). He doesn't chew the Pothos leaves, he only drinks the water, is it still dangerous? I tried several times to give him water in an ordinary bowl, but he prefers the water that's associated with the Pothos plant, so I thought that maybe the roots of the plant excrete something nutritious (but I guess that's not the case, apparently...).
Is it harmful for an animal (cat) to drink water that has a Pothos plant immersed in it?
Also, my other cat does chew on the Pothos leaves (he goes crazy for them). Is it possible to have immunity and not be affected by the toxic chemicals? I read that chewing is supposed to provoke stomach irritation, but I would think that if the cat that chews the leaves suffered from irritation he wouldn't keep getting excited about chewing the leaves...
So what is going on? Many thanks!

Perhaps someone else can answer this with more certainty, but I'd guess that because raphides are essentially sharp crystals that cause irritation-related symptoms, rather than toxic chemicals in the way one might usually think of them, that drinking the water wouldn't pose a problem (actually, I suppose the word "insoluble" might be a clue here). Raphides are defence against herbivory, and chewing raphide-containing leaves is what you want not to do (or not let your pets do).

Veterinary Toxicology p. 889 has more info.


Why does this genetic pedigree show an autosomal dominant allele at one generation but not another? Questions 186-188 of the GRE Biology Practice Test are prefaced with this genetic pedigree:

  Questions 186-188 refer to the following pedigree for the inheritance of a very rare human disease over three generations.

It looks like the allele that caused the "affected" phenotype was dominant because Generation II showed a 3/4 probability of having the phenotype, and it looks like it was autosomal because it affected males and females roughly equally. This is confirmed by the answer to Question 186 ("Which of the following is the most likely mode of inheritance for the disease trait?") which is "(D) Autosomal dominant".

However, why don't the offspring 1, 2, 3, 4, and 5 in Generation III show a similar rate of expression?

Why don't the offspring 1, 2, 3, 4, and 5 in Generation III show a similar rate of expression?

Because there are only 5 individuals in that list. The entire generation III involves 8 individuals (all the offspring of one affected and one unaffected parent). The entire pedigree involves 12 offspring of an affected and unaffected parent.

When you look at III 1-5, you see 1/5 affected (0.20).

When you look at III 1-8, you see 3/8 affected (0.375).

When you look at all offspring of an affected and unaffected parent, you see 6/12 affected (0.50).

As you increase the number of offspring you consider, the proportion affected gets closer to the expected value of 0.5. Given a very rare autosomal dominant condition (i.e., I-2 is most likely heterozygous), this is exactly what would be expected. You may have to look at fruit flies, or some other prolific organism, to see it quite so clearly. Mendel looked at tens of thousands of pea plants, if I recall.

Generally, you shouldn't use the proportion of offspring that show a trait to rule out any particular mode of inheritance, especially if you're looking at a small number of offspring. You can state the probability of a particular child expressing a mendelian trait. That doesn't mean a small sample won't deviate from that probability.

You can read more about this in chapter 7 of Thompson & Thompson Genetics in Medicine.


Basic understanding of cell cycle (mitosis) phase Update

This is for a diploid cell (2n).

At G1, cell growth before the DNA is duplicated.

At S, DNA replicated. Chromosomes doubled!

At G2, cell growth

Then Mitosis; Prophase, Metaphase, Anaphase, Telophase, Cytokinesis

Could anyone explain if the chart is correct or incorrect?

# DNA molecules
A chromosome can have either 1 DNA molecule or 2, this depends upon what stage the cell is at that moment. It actually might help to know what chromatids are:

  A chromatid (Greek khrōmat- 'color' + -id) is one copy of a newly
  copied chromosome which is still joined to the original copy by a
  single centromere. (wiki)

This means that the number of chromatids is directly related to the number of DNA molecuels.

  Before replication, one chromosome is composed of one DNA molecule.
  Following replication, each chromosome is composed of two DNA
  molecules; in other words, DNA replication itself increases the amount
  of DNA but does not increase the number of chromosomes.(wiki)

We can now add another row which indicates the DNA molecules, chromatids are directly related to the number of DNA molecules thus from left to right:

 46        92         92        46

These are the basics, now in some more detail about mitosis:

So based on the number of chromatids and your chromosome number you can figure out the nubmer of chormatids and thus the number of DNA molecules:
Thus before replication (G1) = 6, then after S phase (G2) = 12, then metaphase = 12 and after cytokinesis = 6. Just as in your table so that part is correct!

# of chromosomes
You can read these from the table, however I think it's important to understand what is happening. In simple words chromatids and chromosomes are related in this sense:

  It is only when sister chromatids separate – a step signaling that
  anaphase has begun – that each chromatid is considered a separate,
  individual chromosome (source)

The phase in which the chromatids seperate is called anaphase, so after this seperation:

we consider the previoulsy chromatids as chromosomes. Thus anaphase and telophase contain the double number of chromosomes as the amount you started with. However anaphase and telophase are not mentioned in your table. So let's go back to the phases in your table. During metphase the chromatids are still connected to each other, meaning that we consider them as one chromosome (the same is true for G1 and G2, because we did not seperate anything). So that part of you table is correct too.

# genome copies

  The human genome is the complete set of nucleic acid sequence for
  humans (Homo sapiens), encoded as DNA within the 23 chromosome pairs
  in cell nuclei and in a small DNA molecule found within individual
  mitochondria.(wiki)

However read this question and the answers,  some say 1 genome per cell and some say two genomes per cell, this confuses me too so I'm not sure about this one, however based on the wiki it would say that 2n = one genome, which would make sense because the two pair of chromosomes are not equal and when saying you have two genomes per cell you are actually counting mitochondrial DNA twice.


What is the best way to block cigarette smoke from the body? Would it be better to hold your breath after smelling the presence of it or quickly inhale and exhale to get rid of it in your system(body)?

EDIT:
Changed from carbon monoxide to cigarette smoke.

You don't smell carbon monoxide in cigarette smoke. It's odorless. (And not exactly the part of cigarette smoke I would be worried about.)

You smell the other components of cigarette smoke. Which are not odorless.

Holding your breath and getting out of the smoke seems the way to go. Even better would be exhaling, then holding your breath until you are clear.[1]

Carbon monoxide, as well as other components of cigarette smoke like nicotine, are very good at getting into your blood stream quickly. Plus, when at rest, we inhale / exhale at only a fraction of our lung capacity. By (deeply) inhaling (your alternative course of action), you would just get more of the smoke into your lungs than you already have.

[1]: The trick with holding your breath is of course that, if you run out of breath while still in the middle of the smoke, you can't help but inhaling deeply...


Male Parenting from Evolution point From evolution point of view can we explain as to why mothers care about child rearing more than fathers? Is it Social phenomenon or genetic phenomenon?
Are mothers hard wired to take care of children more or they are socially forced to do so?

Because mother invest the most material and time into producing the offspring, so there is a stronger pressure on them to not waste it. Males can go impregnate other females so there is a stronger possible disadvantage for child rearing, few mates thus fewer offspring. Whereas a female can't have more offspring by finding other males while currently carrying offspring so they are forced to sink a lot of time and energy into the offspring. So evolution strongly disfavors females who waste those resources by abandoning the offspring.

Strong K strategists like human tend to override much of this becasue of how much investment the offspring need. So there is a strong pressure for the female to only accept mates that can provide a great deal of resources, including time. And males can seriously hurt the chances of their offspring surviving by abandoning them. But there is still more built in investment on the part of the female.

There is one other factor, A female knows who her offspring are, males do not, so the offspring they invest in might not be theirs, so there is a pressure to not put all their eggs in one basket so to speak, this is also why males tend to be more worried about physical infidelity (cuckolding) while females worry more about risk of abandonment (loss of support).

Now remember this is males an females in general, individual species can have different pressures. And remember that humans have very complex behavior so much of this just amounts to tendencies on average, not hard and fast rules.

More on the ethology of mating here. http://www.tandfonline.com/doi/pdf/10.1080/11250008409439461


RNA integrity and RNA fragmentation After RNA isolation and before following experiments, I know that RNA quality so called RNA integrity is so important. So why there is a RNA fragmentation kit? Do we need RNA intact or fragmented? (RNA will be used for biotinylation and RT-qPCR afterwards)

This paper uses a similar technique to you by purifying total RNA, synthesis of double-stranded cDNA containing a T7 promoter sequence, cDNA purification, in vitro transcription in the presence of biotin-labeled ribonucleotides and this transcription is possible with T7 RNA polymerase since the cDNA contains the T7 promoter region, and finally fractionation of RNA. This then allows target biotin-labeled RNA for short (~ 25 nucleotides) oligonucleotide arrays. The T7 polymerase performs a linear amplification, and the in vitro RNA obtained reflects the abundance of each transcript in the initial RNA.

Hence I assume you follow a similar protocol although I'm not sure why you do RT-qPCR on the fragmented RNA since that is unlikely to work if you are doing it using primers for specific regions as everything is fragmented. So I think you do a RT-qPCR before the fragmentation to test the expression levels of certain (known) genes (to see if you are getting the expected results) before you go ahead with fragmentation and look at the global RNA expression. If my assumptions are wrong, then it would be great if you added further details of your experimental protocols with the different steps and the exact orders of the steps followed and the results assessed and the experiments performed so that I can modify my response.


Do animal muscles atrophy slower than humans? Suppose I consider the silver back gorilla as an example.  I cannot imagine ever seeing one in the wild intentionally doing something akin to weightlifting like humans solely for the purpose of getting stronger (if I'm wrong about this, that would be fascinating to know as well).  However, last I checked a male silver back can easily lift several times its own body weight.  I used to workout heavily and used to hold my high school bench press record (330 lbs in the 160-171 lb weight class).  However, even then I would have struggled to do more than a few pull ups with a 170 lbs strapped to my waste.  Meanwhile, I've watched various types of monkeys and apes do handfuls of seemingly effortless pull ups at zoos as part of their play.
So do animals like gorillas have muscles that either start and stay stronger than humans or just atrophy much more slowly?  Or is it just a matter of constant use?  Or is it just a different proportion of fast vs slow twitch muscles as this study suggests?
I am skeptical of this last part because some estimates of gorilla strength suggest they can lift upwards of 10 times their body weight [e.g., https://storyteller.travel/how-strong-is-a-gorilla/].  I also recall reading a study in grad school of an orangutan pulling over 600 lbs with one arm clearly not straining according to the article (though I failed to find the reference while searching today, unfortunately).
If anyone has some useful references with quantitative data, that would be great as well.

Animal muscle does atrophy and gain depending on use.
First, animal muscle does atrophy if the animal is too sessile. However in nature it is hard to be sessile. Consider how physically fit hunter-gatherer humans are in terms of their cardiovascular systems. If you are constantly active you don't need to "exercise" to build muscle - you are getting loads of physical activity. Walking 10km a day or more is normal for most humans without advanced technology. We used to see atrophy in animals a lot more, but with animal welfare laws we usually don't keep animals in tiny cages that prevent them from moving anymore.
Some animals are less lazy than humans: many animals will also instinctively stay active even when provided with the conditions to be sessile, but when forced to not be active we do indeed see muscle atrophy. This is especially true of less intelligent species, because the conditions to be sessile are too rare to waste "instinct space" on, but humans who have a much more broader range of behaviors with far more learning behaviors, so we can become very sessile. The downside of intelligence is that you can use it in self-destructive ways.
Just like humans, animals can also build extra muscle by doing the same thing over and over again: a draft horse will build different muscles than a race horse just because it is using them differently.
Many animals also have physiology that makes atrophy harder. Hibernating bears are known to have special adaptations to prevent atrophy because hibernation is defined as long periods of inactivity. But we only only see this in animals that have something like hibernation or have drastically different muscular systems.
So why is a gorilla so much stronger?
Well to start, wild male gorillas mass between 130 to 260 kg. Note that gorillas in captivity often become overweight weighing even more. They have short legs so we don't realize how much bigger than us they are. For scale, Andre the giant (a human far outside the normal range) masses about as much as a large but normal range male gorilla. But there are several other factors.
Humans’ muscles are weaker than other primates’ in significant ways. We have traded strength for much better endurance and fine control of muscles - we do indeed have a significant difference in muscle composition and possibly muscle fiber recruitment, although it is hard to test the latter - you can't tell a gorilla to contract one muscle as hard as they can. As a gain however humans have amazing endurance for any animal and far finer motor control than any other primate. An active human can have better endurance than almost any other terrestrial organism, humans can walk a horse to death, that is a human walking side by side with a horse can keep going long past the point the horse has died from exhaustion.
Gorillas are only stronger in some aspects, a gorilla upper body is certainly stronger, gorilla have large arms and a deep chest drastically increasing the muscle mass of the arms compared to a humans. But the best human could probably beat the best gorilla at kicking power, gorilla legs are comparatively small. To use Andre the giant again, Andre has a lot more muscle mass in his legs than a gorilla and the gorilla has a lot more in the arms, humans have long well-muscled legs. Like all things, genetics can set you up with better musculature, and you will keep it as long as it gets some use.


How are ketone bodies used? While searching for literature on ketone bodies, I can only seem to find how they are synthesized, but not how they are broken down.
I'm looking for the series of events with enzyme names and intermediates. Does anyone have this?

First, there are three ketone bodies: Acetone (top), acetoacetic acid (middle), and beta-hydroxybutyric acid (bottom), see the illustration from the Wikipedia:

The second and the third are taken up by heart and brain cells and then converted into Acetyl-CoA which is fed into the citric acid cycle where it is further metabolized. Acetone is mostly excreted. See here for some more information.

Aceto acetic acid is either converted into acetone and removed from the body or enzymatically converted into beta-hydroxybutyric acid by the beta-hydroxybutyrate dehydrogenase.
The third possibility is that it is converted into Acetyl-CoA. See the figure for the scheme:

For a more detailed explanation of this process (both, the generation and the metabolization of the ketone bodies) see here.


How can the phenotypic effects of a tumor suppressor mutation be silenced? I've been reading a little about the "two-hit" hypothesis for tumor suppressor genes here, which mentions that some genes exhibiting haploinsufficiency are exceptions to the hypothesis. I've read elsewhere on this site (namely the answer to this question) that suggests haplosufficiency as a means of "silencing" the mutation of the tumor suppressor gene such that the expression of the wild-type allele compensates for the mutant allele.

Are there any other mechanisms that contribute to incomplete penetrance of tumor suppressor mutations?

This is more of a comment

Mutation in tumour suppressor is a recessive trait and there is no active "silencing" of the mutation. If a tumour suppressor is a TF then a mutation in the DNA binding domain can have no effect if there is a complementary mutation in its binding site. This is just a theoretical possibility and I have not heard of any examples as such. I don't think any other mechanisms exist for "silencing" any loss of function mutation.


What does `knee atlas` means in an IEEE's paper? I am referring an IEEE's paper for my project which has a term called knee atlas, I am not getting the exact meaning of this term, does they mean it a processed image or something else? I am working in matlab and here is the paragraph of IEEE's paper:

    Six atlases were derived from 3-D DESS WE series from six subjectswith visually normal knee images ... The series for three of these atlases were selected from the public release OAI image dataset 0.D.1 and three were from the baseline pilot study. Trained human observers created the knee MRI atlases using manual segmentation.

The knee atlas is an MRI generated with the intent of identifying anatomical features, much like this.


why does the score matrix influence the E value (BLAST) When I align two HBB protein sequences wich have 80% identity, I used two kind of score matrices: Blosum62 and PAM30, to figure out the impact on my results.
I noticed that the bit score is higher when I used PAM30 instead of BLOSUM62, which makes sense because PAM30 is based on more closely related species.
However I don't understand why the E-values differs from each other:

PAMP62: Bit score: 251, E value: 8 * 10^91
PAM30: Bit score: 258, E value: 6*10^82

Question: I don't understand why the E-value changes when using an other scoring matrix?
thankyou,

Perhaps this BLAST tutorial by Steve Altschul will be helpful:  The Statistics of Sequence Similarity Scores

There is also the BLAST book by Mark Yandell and Ian Korf.


Where does fungus store excess food? Can anyone pin point, as to where and how, the excess food is stored in fungus (mushroom to be specific).
Like plants store as starch granules, so where does mushroom store?

From the Wikipedia article on fungi (under Characteristics -> Shared Features):

  They have a characteristic range of soluble carbohydrates and storage compounds, including sugar alcohols (e.g., mannitol), disaccharides, (e.g., trehalose), and polysaccharides (e.g., glycogen, which is also found in animals).


Do birds emit infra-red radiation? I'm an electronics engineering student and I am going to use a sensor that detects infra-red emitted by birds that invade rice paddies.

Do birds emit infra-red radiation?

Short answer
Birds emit infrared.

Background
Objects with a temperature higher than the background emit detectable infrared (IR). Endothermic (warmblooded) animals keep their body temperatures at around 37oC and given the relatively cool temperatures at the earth's surface, endotherms generally emit more IR than the background. Endothermic animals include the mammals and birds, but also some fish.

Infrared image of a hummingbird. Source: Nature Conservancy.

Note that dinosaurs were probably not ectothermic (coldblooded), but they are believed to have been mesotheroms, that is somewhere in-between ecto- and endothermic (Grady et al., 2014).

Also note your IR recordings will benefit from lower temperatures and reduced light-pollution from the sun, hence your recordings will be better at night than during daytime.

Reference
- Grady et al., Science (2014); 344(6189): 1268-72


Evolutionary advantage of F plasmid in bacterial conjugation Hi I would like to ask a question on bacterial DNA exchange, namely conjugation via F plasmid. It seems to me that all the F plasmid codes for is the sex pilus. What is the evolutionary advantage of the F plasmid? Does it code for anti-biotic resistance as well? Or enhances binary fission for reproductive success? Also, if conjugation transfers duplicated F plasmid from a F+ cell to an F- cell, why aren't all bacteria cells (that are capable of being F+/-) already F+? Is there a mechanism that somehow degrades your F plasmid?

Thank you in advance! I couldn't find the answers anywhere online.

F plasmids allow for the genetic exchange of material between cells, it's the closest thing to sex for most bacteria. Parts of the F plasmid are homologous to the chromosome of E. coli (mainly the transposons present on the plasmid) and through homologous recombination they can pick up bits of the chromosome. A lot of studies have been done where bacteria acquire traits such as galactose or lactose utilisation through these genetic exchange. They therefore allow fitness enhancing DNA to spread quickly through a population or species barriers [Ref].

Antibiotic resistance is not carried on F plasmids but there are many conjugative plasmids that do carry resistance genes (R plasmids). The F plasmid does carry a toxin/antitoxin system (ccdB/ccdA) [Ref]. If the cell loses the plasmid it will not be able to replicate its DNA because the toxin protein is very stable while the anti-toxin is rapidly degraded. So besides the evolutionary advantage there is also the possibility that it is simply 'selfish DNA' (see Richard Dawkins the Selfish Gene for details on this).

There are certain circumstances under which the F plasmid does not transfer such as low temperature so it is possible for a bacterium to lose the F plasmid and not get it back by conjugation. Maintaining a relatively 'useless' piece of DNA does have its metabolic cost so loss might confer a growth advantage.


Why animals can move and plants cannot in general? To clarify, I think the answer should be able to explain:

What are animals?
What are plants?
What's the difference between animals and plants (How do biologists differentiate them, if they differentiate them by moving ability of course it's simple, but we know they don't)?
How do those differences affect their evolutionary paths so that most animals can move around and most plants cannot? I know there are exceptions, but that's just the exceptions that show the rule.

Animals and plants are both classified as Eukaryotes, and as such can form large, complex, multi-cellular organisms. There are several major differences at the cellular level that distinguish the 2 Kingdoms (Animalia and Plantae). Without getting technical, the most crucial difference in relation to your question is that plants contain chlorophyll, and as such can generate their own food using sunlight.

This is very important when you consider that plants (by definition, those Eukaryotes that contain chlorophyll) have therefore evolved to be very efficient at converting sunlight to 'energy', whereas animals have evolved without this option and have to eat what food they need. So they have instead evolved mechanisms that allow them to forage, or even to hunt, for their food.

At some point, a unicellular organism incorporated chlorophyll, leading to multicellular plants in the course of evolution. The ancestor of animals evolved independently from the last common ancestor of plants and animals. Therefore, plants and animals are quite diverged, e.g. in mating 'rituals' (in plants this involves flowers and seeds - whereas in animals there are mating and gestation periods), and systemic changes, such as the immune system and the circulatory system (these are generally much more complex in animals than plants). All of which has stemmed from the difference in evolutionary pressures applied by the choice of food-source.

As you have pointed out, there are exceptions to all rules, so not all plants have chlorophyll, but as a rule it is the case! (Wikipedia: "Some plants are parasitic and may not produce normal amounts of chlorophyll or photosynthesize.").


How fast do lipids on the inside and outside of a lipid bilayer exchange? Biological membranes normally have different composition of lipids on the inside and outside (ref 1, ref 2).  This is maintained both by how new lipids are added to membranes, and by specialized enzymes (flippases).  Certain lipids being on the "wrong side" is an important signal (eg for apoptosis).
My question is: how fast do lipids from the inside and outside exchange spontaneously?  In a patch of membrane with no enzymes, how long until half the "inside" lipids have flipped to the outside and vice versa through simple diffusion?
I did a search but couldn't find any specific paper that measures the spontaneous exchange rate.  I'd be very interested in a definitive answer - could be just order of magnitude, but based on real measurements.
UPDATE This is important for figuring out the inside/outside composition of membranes in real scenarios when they're no longer being maintained in an asymmetric state: for example enveloped viruses, but also microparticles, dead cells, etc.

A cursory search seems to show at least a few papers using sum-frequency vibrational spectroscopy to measure rates of flip-flopping/transverse diffusion in lipid bilayers.
This paper in particular ("1,2-Diacyl-Phosphatidylcholine Flip-Flop Measured Directly by Sum-Frequency Vibrational Spectroscopy") cites an activation barrier of 79 kJ/mol which corresponds to a rate on the order of 10^-4/s.
There is also this review which seems to have more information on the topic: http://dx.doi.org/10.1021/acs.accounts.6b00435.


Down syndrome in subsaharan populations What is the rate of occurrences of Down syndrome in subsaharan African populations? Is it the same as in white European populations?
An interesting hypothesis came to my mind:
Could it be that Down syndrome is the result of interaction of different dominant or recessive Neanderthal or Denisovan genes that European and Asian populations cary in small percentages?

See UN > stats Down Syndrome per country.

What the data says

I have not made a proper statistical test (as I am too lazy to reformat the data in anything convenient to perform a statistical test) but the prevalence seems to be consistently around 0.12499% all around the world with very very little variance. I doubt there is any significant difference in the frequency of birth that have down syndrome.

As @Markonionini rightly noticed, these estimates of prevalance are slightly far fetch extrapolation and the UN specifically advice to consider them with caution. It is probably the best data we have though.

The hypothesis seems improbable to me

Do you have any good rational behind your hypothesis? Down Syndrom is typically caused by de novo mutations and not due to standing genetic variation (Veltman and Brunner 2012) so your hypothesis seems rather implausible to me.


Why is 5S-rRNA is different from other rRNAs in place of transcription and usage of RNA polymerase? While transcription of rRNAs happens in nucleolus mediated by RNA Polymerase-I, we see that 5S-rRNA is transcribed elsewhere by RNA Polymerase-III. What is the cause and why?

The three RNA polymerases (RNAPs) are very similar to each other, yet not identical. As described in this article, there are subunits that are specific for each type of polymerases.

  In addition to providing unique substrates that polymerase-specific subunits bind to give each of the RNAPs their specific functionality, the two largest subunits also shape the active site cleft of the enzymes where the transcription reaction occurs.

The results of the linked article also claim that even though the cleft loops are conserved regions, there are significant length differences between the three polymerases.

Also rRNA gene is similar to the tRNA genes and they differ from other genes in the recruitment of the polymerases. "Traditional' promoters are located upstream the start site, while 5s rRNA gene and tRNA genes have one and two boxes respectively that recruits RNAPIII.

  The 5s rRNA and tRNA genes have promoters within the coding region of the gene.

source: http://mol-biol4masters.masters.grkraj.org/html/Gene_Structure5C-Eukaryotic_Promoter_Structure_for_RNA_Polymerase_III.htm

Here are two images form the linked page:

Edit:

In this article it is described that 5s RNA genes have translocated severeal times throughout evolution, and on of the mechanisms for this could be analogous of the second class of SINE elements, that contain internal RNAP III promoters, and are derived form tRNA (this could also indicate the similar structure to tRNA genes).

From this good review Evolution of multisubunit RNA polymerases in the three domains of life
 I'd like to take one short quote that might help:

  ...The structure and function of some of these factors are conserved across the three domains, whereas some non-homologous factors show an intriguing level of structural and functional similarity, suggesting that convergent evolution has led to alternative means of facilitating the same process.


Homework problem:Introductory genetics The problem is as following:

Primary Ciliary Dyskinesia (PCD) is caused by an autosomal recessive gene. 50% of patients with PCD also have Kartagener Syndrome. Josh has Kartagener Syndrome. What is the chance his brother or sister also have this syndrome?

A  0%
B  6.3%
C  12.5%
D  25%
E  50%

Is this problem actually solvable without knowing the alleles combination of the parents? The answer states C, but perhaps I´m missing something here.

Ok, Josh has PCD. That gives three possible genotypes for parents:- ( let the alleles be P and p)

1) Pp x Pp
2) Pp x pp
3) pp x pp

In (1), the probability for next child to be pp is 25% and to have the disease is 12.5%.

In (2) and (3), the probability of any parent to be pp is rare as the p allele is quite rare (discussions with swbarnes2 in comments). So the real probability will be only slightly higher than that of case 1 i.e. 12.5%


problem with natural selection I fail to see how natural selection can build any kind of new functionality.

New functionality in a design requires sacrificing a complex series of meanwhile useless steps before the new functionality works and becomes advantageous.

For example, if I want to upgrade a stationary chair to a wheelchair, there are many intermediate steps that must be done (which are not advantageous) before the added functionality becomes advantageous.

If a human being sits there and tries to intelligently assemble the wheelchair in such a way that it will be advantageous at each step, he will not be able to do it. it just doesn't work like this.

Can someone fill me in as to how this works and whether there have been experiments that demonstrate this, for example, having someone assemble a simple functional design with the limitation that every few step adds advantageous functionality.

This is fundamentally a teleological argument.

The error is in assuming that the intermediate steps were a precursor to the present functionality. For example, interpreting an 'intermediate' bird wing as a fully functional wing, intended for flight. In fact, there is no prerequisite that present characteristics or functions have evolved from intermediates that were intended FOR that characteristic or function.


Biological key file format I am in the process of creating biological key software tool for use on android devices. I would like to know if there are any established file formats for storing biological key data.

Thanks

I searched a bit and could not find any such format, but I am not a specialist in taxonomy.

From what I understand, the structure you want is that of either a tree or a DAG (Directed Acyclic Graph). Both are straightforward to store in a variety of formats.

One possibility is to use a format similar to other biological data that has a similar data structure. For example, Gene Ontology is a widely used dataset that has the structure of a DAG and has a number of formats including XML listing the parents and additional data of each node in the graph. See here for their formats.


How can I get started in molecular biology? I have a background in computer science and math and am interested in learning molecular / synthetic biology - what resources do people recommend?

First develop a background of basic highschool chemistry, basic biochemistry and basic genetics.

What is molecular biology: Molecular biology has 2 definitions. A broader definition is molecular basis of life. That is indistinguishable from biochemistry. The second definition is how does genetic information flows through
 molecular mechanism. The secod one is a more specific definition of molecular biology and how it differs from biochemistry.

Its good to develop some background in biochemistry and genetics because concepts of molecular biology comes from biochemistry and genetics.

A quick start through biochemistry:

Lippincott's illustrated review on biochemistry.
Harpers's illustrated review on biochemistry
Organic chemistry by Solomons and Fryhle (especially stereochemistry portion).

then go through gradually more detailed book, such as biochemistry by Lubert Stryer.

Parallelly go through Genetics book such as

Principle of genetics by Hartl and Jones
Gene IX by Benjamin Lewin
Principles of genetics by Snustad et al.
iGenetics by peter J. Russell
Concept of genetics by Benjamin pearce
Genomes 3 by T A Brown
Principles of gene manipulation and genomics by RM Twyman and Sandy B Primrose.

Each book has a different perspective. it will help a clearer picture of different concepts.

Some basic molecular biology books:

Molecular bioloy- principle of Genome function: by Nancy Craig et al.
Molecular biology by RF Weaver.
Fundamental molecular biology - Lizabeth Allison
Princiles of molecular biology by Barton and Tropp.

For a more cellular approach and bigger picture see cell biology based molecular biology books viz.

Cell biology by Pollard, Earnshaw et al.
Cell biology by Gerald Karp
Lewins' CELL by Plopper et al.
The Cell- a molecular approach- by Geoffrey M. Cooper.


Does the second law of thermodynamics cause aging? What is the current understanding as to why organisms age and die? In the following explanation on Ask an Engineer, entropy is not even considered (despite it being answered by an engineer). Unless you consider

  accumulation of damage to an organism over time

as a result of entropy ?

In the end, is the eventual death of any organism a result of how the laws of universe? In the paper Aging of the brain, entropy, and Alzheimer disease, the author states that

  Increasing entropy, manifest through a complex network of interacting ARCs, is seen as the fundamental driving cause of neural and cognitive decline in the elderly

where the abbreviation ARC stands for age-related changes.

Second law of thermodynamic and ageing

The second law of thermodynamic applies to closed system. Organisms are not closed system. The second law of thermodynamic is a fundamental principle of our universe and any biological processes do follow the principles of physics. However, stating that biological ageing is (partially) caused by the second law of thermodynamic suggests a big misunderstanding of what the second law of thermodynamic is.

To have a better understanding of the second law of thermodynamic, check up the wikipedia article or one of the many other sources of information on the subject and ask questions on Physics.SE if needed.

Ageing and its evolution

The evolution of ageing (or senescence) is a big subject and has already been subject of a large number of questions on Biology.SE. Have a look at the questions tagged . Below are two examples of post that will interest you:

Why do we age? or Do we have a theory of senescence?
Why does evolution not make our life longer?

There is also a wikipedia page on the evolution of ageing.

Note btw that biological immortality and negligible senescence do exist.


What is the focus distance of a 3D screen? I've thought long and hard about wheter this is the appropriate section for this question, because I guess it's kind of an interdisciplinary subject.

My understanding of stereopsis (please, correct me if I'm wrong), basically depends of the way we cross our eyes when we attempt to see objects at different distances.
The more "our eyes are crossed", the greater the difference between the images we receive in each eye, which it's more effective to look at closer objects. In order for an object to be in focus, it needs to be at the point where the vision of the eyes intersect (including "at infinity" for very far away objects).

Now, with this mindset, how would such a gadget as Oculus VR work?
It consists of two separate screens (one for each eye) attached directly on an helmet-like device strapped to the user's head. It is capable of convincing 3D representations and has similar features which make it of close interest for gaming and similar applications.

So, my question is: in order to deliver such an illusion of depth, do the users' eyes need to be focused at the screen's distance, or at the represented objects' distance?

Sorry for the long question :P

Thanks in advance!

There are a number of aspects to the perception of a 3D world. While looking into how cinema and TV 3D systems work recently, I found the following Wikipedia articles useful on how the illusion of a 3D world is generated:

Stereoscopy
Depth perception

The articles on 3D Television, 3D film and Head-mounted displays have some coverage of the issues with 3D display systems, since they do not work the same for all individuals.

Generally 3D display systems ignore convergence and accommodation as a mechanism for generating depth and instead depend on parallax and the brain being able to assemble an approximation of the 3D scene without the information from those cues.

In head-mounted display systems such as the Oculus Rift the image focus is usually at infinity.


Metabolism of different saccharides Learning about carbohydrates, I wonder what the differences there are in terms of metabolism, and overall health between the different types of saccharides. In other words, does the body use polysaccharides, such as starches the same, or similar to how it would use a disaccharide like table sugar, sucrose?

It piqued my interest because people seem to put sugars and other types of carbohydrates into totally different categories, and one is seen as "healthy", the other "unhealthy".

If you can digest (break down) the polysaccharides to useable monosaccharides, then they can be incorporated into glycolysis (or some other metabolic pathway!). The metabolic pathways around glycolysis are complex, but here is a representation of some of them:

As you can see in, in the top right corner, sucrose/starch, but also other sugars like nucleosides, can enter the overall simple sugar metabolic pathways. How and what exactly happens to the complex sugars will depend on how they are broken down (if they can be broken down at all) and they will have their own more or less complex metabolic pathways associated with that.


Why do changes in preload not cause changes in end systolic pressure? I am trying to understand why changes in preload do not cause concomitant changes in end systolic pressure. If you have preload enhancement than this should lead to an increase in cardiac output..increased cardiac output at a constant heart rate I would think would lead to increased end systolic pressure. Why doesn't this occur?

Preload is defined as the volume of blood that stretches the ventricle at the end of diastole. Therefore, when preload is increased, the end diastolic volume is increased. In simpler terms, there is more blood in the heart just prior to contraction. Even though there is more blood being ejected from the ventricle during systole (that is, there is an increased stroke volume), the increase in preload alone will not affect the end systole volume or pressure.

When preload is increased while afterload and inotropy are held constant, the cardiac muscle fibres will still shorten to the same length. This means that the end systolic volume is unchanged, therefore the end systolic pressure is unchanged. This is best visualized by a pressure-volume loop. On the first example on the diagram below, you can see that the end systolic pressure and volume at point 3 are unchanged with increased preload:

Since cardiac output is equal to the product of stroke volume and heart rate, with increased preload the cardiac output is increased due to the increase in stroke volume. The reason why the end systolic pressure is unchanged with the increased cardiac output is because the end diastolic volume is increased.


Location of TFBS in genome I have an annotated set of SNPs and I would like to explore the difference in the binding affinity of the transcription factor (TF) if I have a SNP in my locus. As my SNPs are annotated (I know wether it is in an intron variant, downstream gene variant, missions variant, etc...) I might explore the binding affinity of those SNPs that are categorized as intron variant, downstream variant,upstream_gene_variant, non_coding_transcript_variant, 5_prime_UTR_variant and not take into consideration SNPs that are "missense variants". The reason why I want to do so is that transcription factor binding sites (TFBS) might be located before gene and after it.

What do you think about it? Can a TFBS be located in the exon of a gene? What are the locations of the TFBS regarding the exons,introns, 5' UTR etc?

I would link your data with the ENCODE dataset. This dataset provides locations of TFBS. It is also accessible via the UCSC genome browser.

For the actual question TFBS are located pretty much everywhere, including exons (as described here), introns and of course intergenic regions (e.g. enhancers, silencers, control locus regions - here a reference).


What are the mechanism binding histone code with alternative splicing? There are some bioinformatical considerations showing that there is a significant correlation of some between histone code and alternative splicing; but what are the hypothesis about the underlying mechanisms? Is there any experimental insight in the problem?

According to literature, histone marks seem to be affecting splicing both directly and indirectly.

The indirect regulation appears to be due to biophysical hindrance, where a certain chromatin structure would cause Pol-II slowdown, allowing the splicing machinery to do its job.

The direct regulation seems to be essentially dependent on H3K36me3 and H3K4me1, marks that are recognized by MRG15, which in turn recruits the splicing regulator polypyrimidine tract-binding protein to splice sites.

Ref: Luco, R. F. et al. Regulation of alternative splicing by histone modifications. Science 4 Feb 2010


Find how much times blood is filtered in the kidney? The blood that circulates in our body is about 1/12 of our mass. If the kidneys filter 7.5 liter of blood a hour, then how many times does it filter in the kidney the whole blood of a person will mass 60kg?

Here's what my teacher did:

1/12*60=5 liter blood

0.55*5=2.75 liter plasma of blood.

The plasma is filtered 60 times is 24 hours. (how did she find that?)

24 hours ->60 times the plasma filters

1 hour -> x

x=2.5 times

Do you understand her explanation? What should I do next?

I'll try to dissect your teachers answer for you:

  1/12*60=5 liter blood

no explanation required here

  0.55*5=2.75 liter plasma of blood.

only the plasma is filtered in the kidney (the 45% cell content remains in the blood stream), so out of the 5 l blood, only 2.75 l need to be filtered.

  The plasma is filtered 60 times is 24 hours. (how did she find that?)

the kidney filteres 7.5 l per hour so if the whole blood plasma has 2.75 l, then in one hour the whole blood is filtered 7.5/2.75=2.73 times. In one day the whole blood is filtered 2.73*24=65.5 times (the numbers are slightly rounded).


Does the red blood cell in frogs undergo amitosis? It is a notion particularly popular among Chinese high school Biology textbooks, that the red blood cells in frogs can undergo amitosis (not mitosis), a claim which I have not been able to find reference. A search on Pubmed led me to this article, which states:

  The nucleus of the frog erythrocyte is not a regular ellipsoid; ... a single nuclear invagination located at one end of the long axis is frequently seen in the phase microscope.

However I have also been unable to find more recent researches on the nature of this observation, and whether it is related to amitosis. Can you help me find some?

Unlike mammalian blood cells, blood cells in Amphibia are nucleated (as the paper in your link explains) and can perform cell division (here is an old paper from Acta Haematologica, 1954: https://www.karger.com/Article/Pdf/204534).

Your question is: is this division a regular mitosis or the so called amitosis? According to Barni et al., 1995, amphibian blood cells can perform amitotic cell division:

  The proliferation of haemopoietic cells, detected by the anti-BrdU labelling index, was accompanied by absence of mitotic cell division and the appearance of cells showing features of amitosis (e.g. nuclear constrictions with bundles of electron-dense chromatin)

Source: Barni, S., Fraschini, A., Prosperi, E., Vaccaronel, R. and Bernini, F. (1995) ‘Possible occurrence of amitotic cell division during haemopoiesis in the Urodeles’, Comparative Haematology International, 5(3), pp. 183–188. doi: 10.1007/bf00368042.


Why don't membrane proteins move? I understand that based on their tertiary structure, intrinsic proteins have hydrophobic non-polar R-groups on their surface and that they 'interact with the hydrophobic core of the cell membrane to keep them in place'.

But how does the hydrophobicity of both the protein and the cell membrane prevent the protein from moving?

Proteins can move around the membrane.
Most proteins do move within the membrane. The membrane is a liquid crystal and has fluid behaviour. Specifically, this is due to the membrane being in a gel-state. This gel state allows phase behaviour which means that the protein is able to move around on the surface. This results in an effect that is often referred to as the fluid mosaic model.
Proteins tend not to move out of the membrane.
The protein doesn't leave the membrane as a result of the transmembrane helix being very hydrophobic. This hydrophobicity and the hydrophobicity of the lipid tails means that they self-associate. A better way of describing it is that they fiercely dissociate from the water. A molecular dynamics simulation showed that even in simulations the membrane will readily self-assemble as a result of the hydrophobicity.
This is achieved by a few properties of the TMH sequence. There is a large amount of hydrophobic residues like leucine. At either end of the helix are large aromatic residues called the aromatic belt. Further is the electrostatic satisfaction offered by Gunnar von Heijne's famous positive inside rule and the recently identified negative-outside rule present in helices with evolutionary pressure to optimise anchorage.

(Image source: Baker et al., 2017)
Cymer et al. published a study showing the free energies associated with each part of the transmembrane protein helix (figure below). The overall ΔG for a transmembrane helix in the membrane is ~-12kcal mol−1. This means that the association of the helix in the membrane is typically spontaneous.

(Image source: Cymer et al., 2015)


Good model for comparative genomics in relation to temperature adaptation Can anyone suggest any highly related bacterial or parasitic species which live at very distinct temperatures, which might be a good model for comparison of genomes in regard to temperature adaptation. For example, related pathogens of which one species infects warm blooded animals, and the other infected cold blooded animals? So far I have come up with one possible example: Salmonella enterica is a pathogen which infects warm blooded animals, whilst Salmonella bongori infects mainly reptiles.

Examples for which there are publicly available genomes, and which have been used in previous studies would be preferable.

As a starting point I would suggest you look at genomes of thermophiles and hyperthermophiles (organisms that thrive at upwards of 40 °C and 60 °C respectively), which are often found near underwater volcanos or hot springs.

For instance, one could do a genomic analysis of the archaean Methanocaldococcus jannaschii, comparing it to mesophilic species of Methanocaldococcus or Methanococcus. This organism is well studied, and genomic information for this organism is readily accessible.

Some studies have been done comparing the genomes of mesophiles and thermophiles. For example, Zheng and Wu (2010) found a correlation between GC content in coding/noncoding regions and temperature conditions.

At the other end of the spectrum you could examine psychrophiles (organisms that grow at low temperatures, −20 °C to +10 °C). However, few of these organisms are obligate psychrophiles, meaning many can thrive at higher temperatures as well and thus may not be suitable for your purpose.


Do all IgG autoantibodies lead to autoimmune diseases? If there is a presence of autoantibody in our blood, does that mean that we are going to have an autoimmune disease? Are there some autoantibodies which don't cause tissue and organ damage?

As usual with biology, it's not that simple. There are autoantibodies present even in people without any signs of autoimmune disease. The immune system is a complex network of positive and negative regulatory cells and molecules - looking at a single component is unlikely to determine the state of the system. This is a major reason that it has been so difficult to figure out how to selectively act on the immune system to stop or prevent an autoimmune disease without compromising normal immune function.
Here's an article that expands on some of these aspects: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2703183/
For example, note "Despite the physiological elimination (negative selection) or functional inactivation (anergy) of high-affinity, self-reactive T and B lymphocytes in the thymus and bone marrow, respectively, there is compelling evidence that low-affinity, potentially autoreactive cells persist and that low-affinity reactivity to self-antigens is required for survival of T and probably B lymphocytes in the peripheral immune system."
It's also important to keep in mind that affinity of Abs and receptors for antigens usually depends on additional 3rd party molecules involved in the interaction, and that a single molecule may present very differently in different situations (for example, damage or inflammation may alter some self molecules into a previously unseen configuration that stimulates self-reactivity).


Do action potentials cause the neuron to heat up as well as its environment? I have read that we might be yawning to cool our brains down, so then a thought occurred to me. If we need to cool down our brain, then our brain but heat up for some reason. The only reason I could see would be the action potential causing some sort of temperature increase. My query is how exactly would a neuron heat up, if it does do so in the first place?

While it is possible that action potentials themselves result in waste heat, there are other processes within the neuron likely to contribute much more to energy lost as heat. The action potential itself uses energy that's been stored in chemical and electrical gradients that are the result of numerous sodium-potassium pumps which require the energy in ATP. There would be some loss of energy in the operation of these pumps.

But far more heat is likely generated by the mitochondria within the neurons. These are the structures that convert most of the energy in the breakdown products of carbohydrates and fats into the ATP the Na-K pumps require. Generous estimates put the efficiency of this production at roughly 50%. That means about half the energy from the food-stuffs used to create the ATP is lost as heat.


How can heart disease cause excessive sweating? According to google:

  What can cause sudden sweating?

  Excessive Sweating. A person with
  excessive sweating has a condition called hyperhidrosis. ... In
  adults, the most common cause of hyperhidrosis is emotional stress.
  However, excessive sweating is also caused by heart disease, lung
  disease, diabetes, and shock.

Sweating is seemingly unrelated to the heart conditions. By what mechanism can a heart disease cause excessive sweating?

The answer lies in compensation. Take myocardial infarction, for starters. MI, if large enough, severely weakens the heart, and hence, at the same level of stimulation, it can no longer pump blood effectively, causing what is called Heart Failure (inability to pump enough blood). This causes an excess stimulation of the sympathetic nervous system (or more technically, neurohumoral mechanisms) in an attempt to compensate, which by its effects on heart contractility and rate increases the amount of pumped blood to match the need. This sympathetic outflow also causes increased sweating, nervousness, dry mouth etc. Sweating, nervousness are cardinal signs of acute MI.

Additional point: This compensation can only work in certain cases, say for example where the heart failure is due to blood loss with a healthy heart. But in cases like MI, this compensation is not an optimal response, rather it worsens the case, since increasing the workload on an ischaemic heart (ischaemic levels of atherosclerosis being the commonest cause of MI), further damages the wall leading to chronic heart failure and disease. This is the Broken Compensation Model for chronic heart failure. This is why we use Beta Blockers to abrogate the sympathetic system's (or more technically, the neurohumoral mechanisms') unwanted compensatory efforts, and the observed efficacy and increased longevity substantiates the validity of the model.

References:

I added them in a bit of a haste. They might not be the best references available, but they are considerably credible. Pathophysiology of heart failure, ventricular remodelling and the involved neurohumoral mechanisms are well-studied, and you shall get several papers on it on pubmed or google scholar.

Books

Robbins and Cotran: Pathological Basis of Disease 9th Edition
Hutchison's clinical methods 23rd edition

Papers and links -Heart Failure pathogenesis

Kemp CD, Conte JV. The pathophysiology of heart failure. Cardiovascular Pathology. 2012 Oct 31;21(5):365-71. (General overview of the pathogenetic mechanisms underlying)
CVphysiology.com(A relatively less technical review)
Kırali K, Özer T, Özgür MM. Pathophysiology in Heart Failure. InCardiomyopathies-Types and Treatments 2017. InTech.
http://bestpractice.bmj.com/best-practice/monograph/61/basics/pathophysiology.html

Papers and links -Sweating as a symptom of MI

National Heart Lung and Blood Institute
Bruyninckx R, Aertgeerts B, Bruyninckx P, Buntinx F. Signs and symptoms in diagnosing acute myocardial infarction and acute coronary syndrome: a diagnostic meta-analysis. Br J Gen Pract. 2008 Feb 1;58(547):e1-8.
Gokhroo RK, Ranwa BL, Kishor K, Priti K, Ananthraj A, Gupta S, Bisht D. Sweating: A Specific Predictor of ST‐Segment Elevation Myocardial Infarction Among the Symptoms of Acute Coronary Syndrome: Sweating In Myocardial Infarction (SWIMI) Study Group. Clinical cardiology. 2015 Dec 1.
https://www.sciencedaily.com/releases/2005/11/051122183817.htm
http://www.webmd.com/heart-disease/news/20051115/sweating-prompts-heart-attack-care#1


Why don't we speak of medial and lateral rotation of the forearm? And pronation and supination of the upper arm? Why don't we speak of medial and lateral rotation of the forearm?

I notice we speak of forearm supination and forearm pronation, but why not medial and lateral rotation.

It seems to me that if we take the diagram of the human with palms forward, which I understand to be the neutral position one is meant to start from.. then forearm pronation looks to me like a medial movement. So why not medial rotation?

And similarly with upper arm.. why don't we speak of pronation and supination of the upper arm?  We speak of medial and lateral rotation of it..

Pronation and supination involve a change in relationship between the ulna and radius.

  When you rotate your hand from palm ventrally (as in anatomical
  position) to palm facing dorsally you have moved your hand from a
  supinated position to a pronated one. This movement of supination to
  pronation occurs when the distal head of the radius rotates on the
  capitulum , the bone rotates along its long axis, and the proximal
  head of the radius flips over the ulna. (Duke Medicine)

and:

  Pronation and supination are rotational motions that exist exclusively
  in the forearm. The mechanical bases for these movements are the
  existence of two forearm bones and the presence of two coupled
  trochoid joints—the proximal and distal radioulnar joints (PRUJ and
  DRUJ). (Clinical Gate)

Image source: Wikimedia, CC licence

During medial or lateral rotation of the upper arm (without additional rotation of the forearm), the humerus rotates, but the relation between the ulna and radius does not change, so there is no pronation/supination.

It is more practical to use supination/pronation for the forearm/hand, because you can have a forearm/hand in various positions where medial/lateral or internal/external does not make sense: for example, when you rotate your forearm/hand with your arm extended toward the side. Saying that, medial/lateral and internal/external rotation of the forearm is also commonly used (search: "medial rotation of the forearm"). So, you can use any of these terns according to what's more practical and less confusing in a given context.


Is it possible to get (an estimation of) reaction rates from the Michaelis constant? I want to apply the Gillespie Algorithm to a biological system so I need to know the reaction rates for the relevant reactions. However, for all those reactions, I only know the Michaelis constant $K_M$ and the maximum rate $V_{max}$ (see Wikipedia). Is it possible to derive (an estimation of) the reaction rates $k_f$, $k_r$ and $k_{cat}$ (see image below) given $K_M$ and $V_{max}$? If so, how can it be done?

$K_M$ is a ratio and for QSSA it is $\dfrac{k_{cat}+k_r}{k_f}$ and for equilibrium approximation it is $\dfrac{k_r}{k_f}$.

It is clear from the formula that you cannot obtain all the constants simulataneously. If you know two (in case of QSSA) you can get the third.


What do we mean by distribution of species? What is meant by distribution of species in the following context?

  density-independent factors tend to limit the distribution of individuals and therefore of species.

Welcome to Biology.SE!

  Species distribution is the manner in which a biological taxon is spatially arranged.

In the specific sentence you suggest, it seems that the term species range would have eventually be a little bit more appropriate though. The species range is the delimitation over space where individuals are found. The species range is just the maximum value in every possible direction of your species distribution.

Note however, that we often don't care too much about such semantic details (the sentence sounds correct to me).

Next time, please specify where you get the citation from 1) because context often matter and 2) because it is a copy right issue to not cite your source.

Same as above in simple terms

The term species distribution (and species range) describe the geographical locations of individual of the population (of a species). We are talking about a single species here. The term distribution takes the same definition than it does in statistics if you are used to it.

Imagine you have a population of oak trees. You can position every single individual tree over space Consider the drawing

Each individual is represented by a circle. The blue line represents a river.

Description of the species distribution: There are no individuals south east of the river. There is a clutch of high density at the north west of the study area.

Description of the species range is given by the red circle

The difference between species range and species distribution does not matter much for your purpose. The point is that you understand those terms are concepts describing the geographical locations of individual of the population (or the species if you prefer)


Is poison venomous and is venom poisonous? I know the difference between poison and venom AND poisonous and venomous.
But I just want to know if an ingested venom would do harm to humans and if an injected poison would do harm to humans.
I really think that poison is both poisonous and venomous AND venom is both venomous and poisonous.

I think you are both confused about terminology, and asking a very broad question. An organism that produces venom is venomous. Poison is not venomous, the black mamba is venomous. Venom is not venomous.

According to the Wikipedia article on venom,

  Venom is a form of toxin secreted by an animal for the purpose of causing harm to another.

A toxin is a poisonous substance produced by a living organism. The article goes on:

  Venom is injected into victims by means of a bite, sting or other sharp body feature, which differentiates it from poison (that is absorbed, consumed or inhaled).

However, a toxin is a poison, and poisons are defined (by wiki) as

  substances which cause disturbances to organisms, usually by chemical reaction or other activity on the molecular scale, when a sufficient quantity is absorbed by an organism. (emphasis mine)

So, the definitions are kind of circular.

From what I understand of your question, you are wondering whether a venom would still be dangerous if it were, for example, ingested rather than injected, as well as whether a poison would still be dangerous if injected rather than ingested (or inhaled, or whatever), and this is where the "Too Broad" category gets applied. There are thousands if not millions of different types of toxins in the world, ranging from full proteins to peptide-based to small organic molecules to completely different structures, such as lipopolysaccharide (LPS, the component of Gram-negative bacteria that causes septic shock). Some may not survive the digestive tract, others might. Some can act through the skin, others can't be absorbed. Inhalation is the next best thing to injection, but probably not for every single one of them, so it's impossible to make broad statements about their efficacy and median lethal dose via different routes of exposure. The exact same thing applies to the "poisons" category - while something that is damaging when absorbed cutaneously, such as methyl mercury, is probably just as damaging directly injected into the bloodstream, it's impossible to say that with certainty about all poisons.


How is insulin transported in vivo in mammals? What is the mechanism for transport of insulin in mammalian cells?

The process is described here. This is my summary, plus a few extra details:

The primary gene product of the INS gene is preproinsulin. As the N-terminal signal sequence (pre-) emerges from the ribosome during polypeptide elongation the signal sequence binds to a signal recognition particle which arrests elongation until the nascent chain has engaged with the translocation apparatus in the membrane of the endoplasmic reticulum (ER). The preproinsulin polypeptide is translocated across the ER membrane in a cotranslational process, and the signal sequence is cleaved off by signal peptidase.

The proinsulin molecule folds in the ER lumen, assisted by various chaperones and, in particular, by protein disulphide isomerase, which ensures that the correct disulphide bonds form. The correctly-folded proinsulin polypeptide is exported from the ER in COPII-coated vesicles which deliver it to the Golgi. At this stage the proinsulin is cleaved by furin-type proteases (pro-hormone convertases; cleave at pairs of basic residues), removing the internal C-peptide (pro-) and after a little C-terminal trimming, leaving the insulin A and B peptides covalently attached via disulphides. This is mature insulin.

The mature insulin leaves the Golgi in secretory vesicles. Since insulin secretion is regulated, these vesicles do not fuse with the cell membrane constitutively, they are stimulated to fuse by a Ca2+-dependent signalling pathway. Vesicle-membrane fusion is mediated by SNARE proteins. At this stage the insulin has been released from the pancreatic β cell. Notice, however, that the insulin has been extracytoplasmic since it was translocated into the ER: all other steps in the transport process are achieved by rounds of vesicle formation and fusion.


How the genome assembly be done after k-mer counting? As far I know, before assembly of a genome, all k-mers from read should be counted.

But after that, how the genome assembly be done?
Is there any other thing needed along with k-mer counts?
How the standard value of k is determined for a particular genome assembly? or is it fixed for all kind of assembly?

I just want to know the basic concept that how this actually been done. Explanation with flow char or algorithm is much more appreciated.

I went through some similar question, but those did not help me too much.

There are multiple ways of doing genome assembly.
The term you are probably looking for is "De Bruijn-Graph based assembly". Using this you can find a lot more different explanations of how it is done.

Another frequently used method is "Overlap Layout Consensus assembly", which in fact is not based on k-mer counting.


Beetle with long, slender iridescent green body and orange legs I recently saw this beetle while on a trip in central Texas, USA (in a rural area just before sundown). The body was about 2-3 inches long (compare to nearby chair leg and floorboards) and had a long body. It was very vivid green, and its upper legs were very bright orange (which made me wonder if this is aposematism). Its antennae had very uniform half-circle arcs (instead of the uneven parabolic shape often seen in cockroaches and similar common insects) and didn't seem to bend besides being rotated ~5 degrees up and down.

It carried itself pretty high off the ground, perhaps half an inch between the belly and ground-level. It seemed to move fairly fast, but not as fast as a cockroach. It didn't fly in the few minutes I observed, and didn't seem like it could fly since the shell appeared solid, but I might have mistaken well-fitting sheaths for fused ones.

What is the most likely species? Is it poisonous?

I'm going to guess it's an Plinthocoelium suaveolens, based on the image found here, which I show below:

I found this link through a Texas beetle page here and is the best I can do from the image provided.


What would cause bands to appear lower on a nonreduced SDS-PAGE gel? I have a protein gel and I'm comparing the reduced with the non-reduced gel. On the reduced gel, I have a few shorter bands but these bands appear with low intensity. In the non-reduced gel, I'm seeing more of the shorter product? What would case the protein to run "smaller" in the non-reduced conditions?

The major effect of changing the redox environment of a protein is the formation or breakage of disulfide bonds. Under sufficiently reducing conditions no disulfide bridges will be present, while under oxidizing conditions your protein will form disulfide bridges if it has the ability to do so.

Disulfide bridges can significantly change the tertiary structure of a protein and change the behaviour of the protein on a gel that way. Generally, disulfide bridges should make the protein more compact and make it run faster on a gel.

It is therefore plausible that your faster band is the protein with disulfide bridges, which will appear to run like a smaller protein as it is more compact. The slower band then is the protein without disulfide bridges which can adopt a more extended conformation.

I'm assuming you're talking about native gels here, as denaturing gels usually contain DTT or beta-mercaptoethanol in the sample buffer to reduce any disulfide bonds and avoid this effect altogether.


How to find the location of a gene, starting with the gene name and the DNA sequence of nucleotides? I'm not a professional biologist, I'm just trying to analyze some actual data. Where should I look up the location of a gene and nucleotides it consist of? How can I find it in DNA? Is there an algorithm that can be used?

To find the genomic location of a gene when you start with a gene name;

Use the UCSC Genome browser. This has a number of advantages. There are a number of species to choose from. It provides a representative image of the gene and regulatory elements that surround it. It can display a lot of extra information if you want to see it. The disadvantage ot the UCSC Genome browser is that the information density may overload non-professional users.

To find the genomic location of a gene when you start with a DNA sequence;

Use the search tool that links to the UCSC browser.

The alternative option is to search for your gene ID or sequence in NCBI Gene.

To search for a DNA nucleotide sequence using the link above, select Reference genomic sequences (refseq_genomic) from the pull-down tab in the Database field. Limiting the search to a species using the Organism field is also wise.

Both of these sites provide the information you are after. Taking time to read the help instructions will be useful.


Epithelial cells and Rhinovirus If you injected a tumor with epithelial cells infected with the Rhinovirus, would this still evoke an immune response as it would with the respiratory system? Secondly, what is the specific reason the Rhinovirus is only attracted to the epithelial cells in the respiratory system.  Do these cells give off a specific chemical signature in which the virus is attracted to?

Infecting tumor cells with viruses to provoke an immune response used to be  termed (tumor / immune ) 'xenogenization'.  The approach may now fall under the general headings of tumor immunology, immune modifiers or tumor vaccines.   Xenogenization been explored for decades (with only moderate success).  Some modern approaches include adding immune stimulating genes to the viral 'vector' (e.g GM-CSF) to try and improve an immune response.  Xenogenization is usually intended for use with the patients own (autologous) tumor cells.   Other approaches that use viruses include delivering genes that preferentially act in tumor cells or "tumor antigens".  Some of these modified viruses may have been engineered to have low, or no, ability to replicate in the body.   Note that some viruses, such as influenza or rhinoviruses are not (generally) able to circulate in the bloodstream (viremia) to infect distant tumor cells.  Instead, the goal of using such viruses is to provoke an immune response against tumor antigens expressed on the 'original infected' cells at the site of injection and hope that the immune system goes on to attack distant masses/metastases.


Terrestrial locomotion of bats and pterosaurs Bats and pterosaurs have skin attached to their forelimbs that aid them in flying and when they are on land, they use all four of their limbs to walk in a quadrupedal posture. Can these organisms be considered as true quadrupeds? Is there a different term used for this type of locomotion?

Quadrupedal means walking on 4 limbs, so yes bats can be considered quadrupeds. The scientific name for how an animal walks is gait. However, keep in mind that the same animal can have different gaits, think of a horse that can walk, gallop, etc. It seems that not all bats walk the same way, this here might be of interest, where they tell about a paper published in Nature in which they find a very different gait in Vampire bats, compared to 'normal' bats. In this paper they say that normal bats: "...shuffle  awkwardly from  a  sprawled  position." So I don't think they have a real name for a 'normal' bat gait.

For flying pterosaurs, it is hard to tell, we've never seen one walk.