Why must DNA be packed into chromosomes during mitotic phase? Why does DNA have to be packed into chromosomes? Why can't DNA just divide itself evenly?

A chromosome is simply a length or segment of DNA. Bacteria have few structural proteins on their DNA, and they have one circular chromosome. In humans, before DNA replication, the nucleus contains 46 strands of DNA, i.e. chromosomes (22 chromosomes in two copies and usually two X or one X and one Y for males and females, respectively). All chromosomes are DNA that is bound by histone proteins that are organised in nucleosomes, approximately every 147 base pairs.

What you are referring to is a condensed chromosome in metaphase, which confusingly in humans is actually an X shape consisting of 2 identical chromatids, structurally condensed and joined at the centromere to form a duplicated chromosome.

The duplicated chromosomes must condense and join before the cell can divide because a tangle of 96 chromosomes as chromatin would be almost impossible to organise and separate properly. The joining of identical chromosomes and compacting process allows all the 46 compacted and duplicated chromosomes (i.e. 96 chromatids) to simply align along the spindle apparatus that forms in centre of the cell during mitosis, and have separation of the chromatids during anaphase so that each of the new cells has a full set of 46 chromosomes.


how many times can a spitting cobra spit its venom? exactly how many times can a spitting cobra spit its venom at a predator
it has a small venom sac, so I presume it can only spit once or twice only

I presume it can only spit once or twice only An unwise presumption.

  These cobras exhibited distinct control of venom flow with spits averaging 1.7% of the volume of the venom gland, thus enabling the cobras to rapidly expel over 40 consecutive spits ... There was no significant difference in the amount of venom spat between the first few spits and the 20th spit, however there was a significant (Student's t-test with unequal variance, p=0.017) decrease in the amount of venom spat between the 20th and 40th spits.

--Protein variation in the venom spat by the red spitting cobra, Naja pallida (Reptilia: Serpentes)


Measuring fitness / lifetime reproductive success (LRS) in Drosophila I am planning a fitness assay of Drosophila melanogaster. I'd like to get a good measure of lifetime reproductive success (lrs) but I don't want to count all the offspring produced over a lifetime by 100's of focal flies. The solution I am toying with is to count offspring production over the first few days or weeks. But before I commit to this I need to know if there is existing research material on the following:

Does early reproductive output correlate well with lrs? (this could be a low correlation if a fly trades early-life offspring production for late-life offspring production)

How much of a fly's reproductive output does one need to count before they have a good estimator of lrs? (does counting the offspring produced in the first day of life correlate well to overall lrs or do I need to count more - 5 days, 10 days, 50 days...)

I haven't done LRS but I don't see a reason why you couldn't make that measurement over only a few days, if you keep this method consistent through out all your populations. Just as a control you might have to do a complete LRS to see if you get any patterns in their egg laying behaviour, which I assume/believe is a decreasing pattern over time but just check the pattern of your WT and make sure your food is the same throughout all your experiments as changes in yeast % can completely distort your results as fly lay eggs like crazy when given yeast!! so use the same batch of fly food.

Although I'm no expert at this, if you look at female ovaries and do some molecular/phenotypic characterisations, you might get some interesting data if you are already observing a huge difference between your populations although you would have to look at the literature for this but having played around with these stuff a little, you find a surprising amount of data! This is in a way nice since you take the males out of the equation as the reproductive fitness could be compromised by either males or females in a population. To determine this you need to cross the males and females of your population of interest to WT flies and count the embryos (although this is slightly dangerous since if males are not performing well, females can lay lots of unfertilised eggs, blanks, and they are indistinguishable from fertilised egg so maybe count the hatched offspring and immediately discard them although that presents its own set of challenges and variables and to be honest its not likely to happen since you usually get this blanks in virgin females that have not yet courtshiped). If you observe lets say no changes in embryo numbers when your male populations are crossed to WT females but significant changes when females are crossed to the WT males, you would know the problem is with the males in your population.

Hope this helps!

EDIT: So I looked a bit further into this and came across this paper (http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0024560). If you look at Fig 6, I think it answers your question. I'm basically quoting the paper here. They measured the correlations between adult LRS and cumulative and short-time measures of fecundity and offspring production. Correlations of the short-time measures of fecundity and offspring production with adult LRS were highly dependent on the time of measurement. For young females the correlations were low, but when measured from older females, the correlations were much higher (up to 0.67 for short-time fecundity and 0.83 for short-time offspring production). For both short-time fecundity and short-time offspring production the highest correlations with adult LRS were reached when the female age was about 50 to 80 days. The length of the time frame had only a minor effect: the correlation of the 10-day measure with adult LRS was generally only slightly higher than that of the 2-day measure. The short-time measures performed well in comparison to the cumulative measures of fecundity and offspring production. So in short if you let your females age a bit and measure their fecundity, then it should be representative of their LRS.


Understanding the "Waterfall Illusion" Motion after-effect illusions, such as the waterfall illusion, refer to illusions where fixating a screen which shows stimuli moving in a particular direction  elicits the perception of motion in the opposed direction when subsequently looking at a static image.

Here is an example: Video Motion After-Effect

The explanation is typically that adaptation effects lead to a saturation of the firing rates of neurons encoding the viewed motion direction.

So far so good - but why do we then perceive afterwards motion in the opposite direction, and not in any other direction where no adaptation has happened?

The motion after-effect (MAE) is believed to be primarily due to adaptation of direction sensitive cells in the middle temporal area (MT) (Fig. 1.). The directional cells in this area of the cortex are selectively sensitive to motion in one direction. Hence, looking at a waterfall will selectively cause adaptation in those cells tuned to the direction of the waterfall. When one looks away, the MT cells responsive to opposite directions will become dominant, as their counterparts are momentarily shut down and one will see the waterfall running in opposite direction.

Adaptation thus apparently weakens the opponent input to the adapted MT cells, enabling an enhanced response to motion balanced stimuli. However, the possibility of adaptation occurring in MT neurons themselves cannot be ruled out (Mather et al., 2008).

The MT area is one of the principal visual cortical areas devoted to motion sensing and hence a likely culprit for MAE. However, fMRI studies have indicated that a lot more visual areas in the brain may be involved, either directly, or indirectly, including V1, V2, V3, VP, V3A, V4, and also MT (Mather et al., 2008).

Fig. 1. Two visual streams dominate vision: the dorsal 'where" pathway (containing the direction-sensitive MT area), and the ventral 'what' pathway. source: InTech Open

Reference
-  Mather et al., Trends Cog Sci (2008); 12(12): 481-7


What causes paresthesia from compression? Compression of a nerve causes loss of afferent and efferent information in it. What is the physiological basis of this?

Seems like it results from a loss of blood flow as the Vasa Nervorum is compressed. Vessels, like arteries or tubules within the kidney, are compressible since they have a vacuous lumen, while an axon is cellular and resists compression. I was thrown off a bit by an answer by a Bryan Krause to this question here, Neurons during Numb feeling, "the feeling of paresthesia is not from loss of blood flow", but, seems like that person was wrong.


Odds to clone a parent I was asking me something weird, and I thought you might validate or not my theory.

Hypothesis: A brother and a sister have one chance over 78 billions to clone one of their parent if they procreate

Here is my method:

I have 23 chromosomes from my mother, and 23 from my father. My father has 23 * 23 = 529 combinations of chromosomes in his "gametes". If my experience is willing to work, I need to have the exact opposites of my father chromosomes than my sister ones. That means that we can't have any of my father's chromosome in common with my sister. That makes approximately 1/529 * 1/529 = 1/279 841.

Then, if I decide to procreate with my sister, our child needs to have the 46 chromosomes back from my father. So the computation stays the same and I will have 1 chance over 279 841 to make it so.

1/279841 * 1/279841 = 1/7.8*10^10

My question is: Is my theory valid? If not why? If yes, that will make a hell of a story at parties...

Thank you for your scientific answers and have a nice day!

Assumptions

You are ignoring recombination and mutations. If you were to add these things, then this probability would be extremely smaller. In apparence, it would be infinitely smaller. It makes no biological sense to make such assumption but for the sake of the argument, let's assume only segregation happen. We will also assume that the parents are completely unrelated to start with (see @BryanKrause 's comment below).

For on given pair of chromosome

First, for a given chromosome number, both parents must each transmit a different chromosome to each offspring. This happens with probability $\frac{1}{2}$ per parent and therefore $\frac{1}{4}$ for both parents. Then, if the brother transmit the maternally derived chromosome, then the sister must transmit the maternally derived chromosome as well (and vice-versa). This occurs with probability $\frac{1}{2}$. So for a given pair of chromosome the probability to clone the parent pair of chromosomes (assuming no recombination and no mutation) is $\frac{1}{4}\frac{1}{2} = \frac{1}{8}$.

For the whole genome

The probability of this to happen for all 23 pairs of chromosome is $\frac{1}{8}^{23} = 1.69 \cdot 10^{-21}$, that is one chance out of a 1.69 thousands billions billions.

As you ask for the odds, note that for such low probability the odds ratio is pretty much equal to the probability.


Does all cells in individual has same mitochondrial DNA? I read that genetic code is universal except for mitochondrial DNA.

However, I want to clarify (generally speaking, regarding humans especially):

does all mitochondria in the same cell have almost the same mitochondrial  DNA?
does all cells in a single individual have almost the same mitochondrial  DNA overall?
does all the siblings in one family have almost the same mitochondrial DNA overall?

Thanks :)

In a homoplasmic individual, all mitochondria is the same. Therefor will be the same amongst cells and between siblings/mother. Unless some mutation occurs. A homoplastic individual either has all mutated mitochondria or all functional mitochondria of the same type.

A Heteroplasmic individial (more than one type of mitochondria) mitochondria occur when a mitochondria has accumulated sufficient mutations. When a hetroplasmic mother has children, the siblings have varying ratios to each other and the mother.

When you produce oocytes, a selected number of mitochondria are transferred into each. During maturation, there is a rapid replication of mt-DNA, which can lead to a random shift in mutated DNA between the offspring and the mother. This is the mitochondrial bottle neck. Bottlenecks enforce mechanisms that omit cells or individuals, in this context mitochondria, ideally such that only the healthiest mitochondria are transmitted.

In a heteroplastic individual, different cells or populations can have varying amounts of of the mutant mitochondria (including complete homoplasmy).


Do Colorblind People Have Stronger Sensitivity in Their Other Remaining Cones? I came across this paper Color defect and color theory. The paper explained about how unilateral color blind (people who color blind only in 1 eye) actually see less bright in their color-blind eye (in graph : filled bullet) compared to the normal eye (in graph : white bullet). Especially to the scene that corresponds to the missing cone (in this paper, Deuteranopes. Missing cones = green)

I have 2 questions regarding this brightness loss in color blind people.

Green cones response are near the red cones response, and they are overlapping. How is it possible that Deuteranopes loss brightness in Green and Blue (which will make more sense if they also loss brightness in Red, thus loss brightness in the whole spectrum) but instead, still achieve the same amount of brightness in Red ? Despite Red and Green color-blind have the same color combination possibility (gamut mapping) that they can perceive ?
Could it be that color-blind people have stronger sensitivity in other cones (for example : stronger in red) and then this red opsin actually replace / fill the missing cones stimuli in retina, so their retina still able to perceive the same amount of brightness on that excessive cones ?

Kudos for Delta-S in Reddit for enlighten me. Original post is here.

The answer is no, color blind people don't have stronger sensitivity in their other remaining cones. This goes back to the Photopic Sensitivity Graph below.

As you can see, human vision are most sensitive to green. All responses of green cone are within the photopic sensitivity as well as most response of the red cones. And despite few responses of red cones are outside the Photopic sensitivity, the peak sensitivity of red cones is very close to the peak of Photopic sensitivity (560nm and 555nm).

Peak Photopic Sensitivity: 555nm
S cones peak  : 420nm
M cones peak  : 530nm
L cones peak  : 560nm

So, in case of Deuteranopic, depending on which wavelength is loss (defected) from their eye, if it closer to the red response then they will likely to experience luminance loss as well. However, if the green cone that is defected is far from the red response, the red cones still have possibility to maintain the luminance they can achieve.

Unfortunately in the paper, it's not mentioned which sensitivity wavelength was defected from the unilateral participant. It is only mentioned "result indicate that she was deuteranopic".


Cheap enzyme assay for a high school lab At the moment, I'm designing an experiment for a high school lab with no financial resources. I need to assess the impact of a variety of factors on a specific enzyme's reaction with its respective substrate and determine the rate of reaction. Normally this would require some combination of an assay kit and a plate reader. Though cheaper versions of the former are within my budget, the latter is not.

What are the cheapest ways you can think of to:

1) Get access to enzymes and the substrate;

2) Make them react in a controlled manner;

and 3) Assess the rate of reaction from the resultant substance?

There is the classic potato starch/iodine/amylase experiment:
http://dailynexus.com/2016-08-31/chemistry-101-the-classic-potato-iodine-blueblack-experiment-finally-has-an-explanation/

From memory, when you add iodine to a small piece of potato, the potato starch reacts to produce a dark blue/black colour.  The amylase enzyme in human saliva can break down the starch and remove the colour, which is effected by spitting into the test tube.

You might need to try titrations to work out how to do number 3.


Species Identification - small insect: is this a bed bug? I found this bug in my apartment in Chicago.  We had bed bugs in our house the previous year (but we thought we got rid of them).  This bug was very small - maybe 2 millimeters in length.  These photos are all of the very same bug (just different lighting).

This is a really old thread but just in case someone happens upon it, this isn't a bed bug.

I am not an expert but it looks like it's likely a book louse or psocid.
See comparison photos of unfed first instar bed bug nymphs vs. psocids/booklice here: http://bedbugger.com/2008/03/04/booklice/
It's all about the shape of the head and body.


Do we consume DNA and proteins of other organisms? When we eat raw meat, e.g. chicken or fish, we are actually consuming the DNA, proteins etc. which are present in their cells.

Wouldn't this affect our cell functions as this DNA might enter our cells?
It is known that we get energy by eating them. Is it glucose or ATP or some other form of energy that is produced from them?

Yes, we are eating the DNA and proteins of an organism when we consume and digest its cells.

However, consuming the "raw flesh of hen or fish" in your example would not cause harm strictly due to the consumption of their DNA.

DNA has two basic components - a structural 'backbone' of alternating phosphate molecules and sugar molecules (called deoxyribose) and a nitrogenous base (a group of atoms that includes nitrogen) on each backbone unit. These basic components of DNA are common to the all organisms that contain DNA, like the hen and fish in your example.

When you digest the DNA in your food, specialized molecules (in this case nuclease, which digests DNA) produced by your digestive system break down DNA into its components. These components can then be rearranged to create 'human' molecules, such as human DNA.

In other words, you don't integrate fish or hen DNA directly into your human DNA; you break it down and rearrange it into human DNA, then integrate it into your body.

To answer your second question, we get energy by breaking down the proteins, carbohydrates, and fats (known as macromolecules) of other organisms. Much like DNA, these three macromolecules are broken down into their singular components. For carbohydrates, this would be glucose.

These components are then further broken down into energy (as a force) which powers cellular machinery to 'recharge' ADP (the 'discharged' version of ATP) back into ATP, a specialized molecule which can 'bring energy' to other parts of the body to power your body's processes.

ATP is not energy per se - energy is defined as the "capacity to cause change" (Campbell Biology, pg. 160) and do work. Energy is therefore a property rather than a distinct molecule.

Summary:

When we consume DNA of organisms, it does not inherently damage us as we break it down and rearrange it into completely 'humanized' molecules.
Glucose and ATP aren't energy per se - they are just molecules that contain lots of energy. ATP 'brings energy' to other parts of the body; glucose is broken down into energy to 'recharge' ATP. Energy is not a molecule - it is a property.


SNPs in DNase hypersensitive and histone marks sites I am investigating a role of SNPs in DNase hypersensitive sites and in the DNA regions of histone marks and have some questions about it.

SNPs in DNase hypersensitive sites might mean that those SNPs are in enhancer regions and might influence TF binding affinity what can influence a transcriptional output. Is it correct?

SNPs in histone marks sites
I have the number of SNPs that fall in the peaks (chip-seq) for the following histone modifications of healthy patients:
H3K27ac,H3K4me1,H3K4me3 (represent the active chromosome)
H3K27me3, H3K9me3 (represent the repressed chromosome)

Histone modifications represent if the chromosome is active or repressed. A SNP might change the binding affinity of a histone. It means that if I have a SNP in data for active chromosome (H3K27ac,H3K4me1,H3K4me3), it might change the status of a chromosome, namely turn it into a repressed one or it might induce a histone not to bind at all(it means that this region is still active,no?) Is it right? I am not sure I understand the possible influences of a SNP histone marks sites.

First off let's define some concepts.

DNAse hypersensitive regions are DNA regions which are in an open chromatin conformation (i.e. euchromatin). This means that those regions are more active at the genomic level (i.e. higher gene expression, gene regulation and higher TF binding) and are less prone to form nucleosomes.
Histone mark sites are DNA regions known to bind certain type of histones and therefore also influences the chromatin conformation leading to the same effects described previously. The critical point is that the histones you are listing do not primarily bind a specific DNA sequence (as described by @mdperry) but rather DNA sequence marked by epigenetic modifications such as methylation and acetylation.

Now for your first questions, SNPs in DNAse hypersensitive regions might influence the chromatin state and therefore yes might influence gene expression and gene regulation. Will those SNPs also influence TF binding? Well they might indirectly via chromatin modifications. They will not directly act on TF binding if not located in a sequence known to bind TFs (TFBS). DNAse hypersensitivity is not a synonym for transcription factor binding regions/sequences.

For your second question, SNPs in histone mark sites are a little bit more difficult to interpret. They might, or might not, provoke chromatin changes by influencing the binding of histones but not in a direct way. CpG islands are, for example, DNA regions known to be greatly under the influence of epigenetic marks and therefore mutations in those specific regions (e.g. a C -> T mutation) might influence the relative methylation/acetylation state and therefore the binding of histones. SNPs might therefore influence gene expression via chromatin changes which leads to higher/lower TF binding but again not in a direct way. Here again a SNP would influence TF binding directly only if the mutation is located in a TFBS.

As you can see my answer is full of "might" and the reason is that it is very difficult, at the current state-of-the-art, to determine the exact impact of a SNP on the 3D conformation of the chromatin and therefore predict the effect on specific gene expressions.

An advice would be to try to co-localize your SNPs with known TFBS either predicted In-silico or measured via CHiP-SEQ experiments and merge that with the information about DNAse hyperactivity and histone marks you already gathered. For example a SNP in a TFBS in a DNAse hyperactive region is very likely to have a greater impact than a SNP in a TFBS in a non active region.

I am sorry I cannot be more specific but this is a very active research area in genetics and there is still a lot to understand, especially for the interactions between all the players influencing the chromatin conformation.


Which synamorphy evolved last I know that if species are on the same height level, they existed at the same time and indicates extinction. Does that apply to synamorphy? Did hair and eggs with shells evolve at the same time or did one evolve last?

A cladogram does not indicate time. That would be a calibrated phylogram. We can tell from the above cladogram that the two synapomorphies "Hair" and "Eggs" with shells are the two most recent, and happened after all the other ones because cladograms do indicate the relative timing of events. However, knowing a bit about mammals, "Hair" is the more recent than eggs with shells. Actually, eggs with shells should be on the same internode as "Amniotic eggs" in this cladogram, because Montreme mammals had eggs with shells, which were lost in the most recent common ancestor of Marsupials and Eutherians (Primates and Rodents/Rabbits are both Eutherians). So "eggs with shells" came first.


Cellular specific mass (in grams-dry-weight per pico liter)? What is the cellular specific mass, in units of pgDW (pico-gram dry-weight) per pL (pico liter)?

I suspect there is some variability between cell types, but this variability must be limited. Perhaps bacteria and mammalian cells are different, but the number shouldn't change much among bacteria. This is just intuition, I could be wrong.

So, what is the cellular specific mass, for different cell types (assuming there is limited variability, so this is not an infinite table)?

Density of a variety of cell types is rather well known. It can been measured directly by examining buoyancy (tendency to float) in liquids of known density, and also by microfluidic methods. But the results depend on the osmolality of the solution in which the cells are kept, since cells tend to "swell" (take up water) in low osmolality (hypotonic) medium.

Using a microfluidic technique, this paper reports a density of 1160 $\pm$ 1 pg/pL for E.coli at 290 mOsm, and 1139 $\pm$ 3 pg/pL for red blood cells. At comparable osmolality and using a gradient centrifugation method, this paper gives a density of 1095 pg/pL for E.Coli. So the results clearly differ a bit depending on experimental conditions (possibly the medium composition was different). For budding yeast, this paper estimates a density of 1103 $\pm$ 3 pg/pL, compared to 1113 pg/pL by gradient centrifugation.

In all cases, cells are heavier than pure water (1000 pg/pL), and larger eukaryotic cells seem to be slightly more dense. As macromolecules are more dense than water, this would suggest that eukaryotes have lower water content.


What spider is this? Is it dangerous to humans? What is the species? Is it dangerous to humans?

I chanced upon this beautiful one near our water well. It stood at a height where an adult could accidentally walk through the web and the spider would land on one's face.

As a test, I dropped a piece of leaf onto its web, and the spider jumped to action, checking what it was and it took out the leaf from its web.

Size: Web, almost circular 50 cm diameter. Spider, about 8cm.
Location: Malabar region, Kerala state, south of India

This is most likely a spider from the genus Argiope, which has a few members native to India. See here for a list, I think this is most likely
Argiope pulchella, see the image from the Wikipedia:

Wikipedia also says that these spiders hunt insects, but are not dangerous for humans.


What's the name of this caterpillar? It was found in the state of Virginia, on the east coast of the United States.

I think it might be a species of Fritillary. Below is a picture of a Marsh Fritillary.

Marsh fritillary. Source: Butterfly Conservation.org

I do not think it is a woolly bear or giant leopard moth, just because the hairs seems too sparse for a woolly bear and it lacks the distinct red striping of the giant leopard moth caterpillar. It does not seem to be arctiinae to me.


Can SIRS occur without Sepsis from Infection? I am thinking this figure

It suggests me that there has to be Sepsis that infection can lead to SIRS.

I am thinking particularly the pathogenesis of Cryptococcus neoformans where

respiratory tract $\to$ pulmonary infection $\to$

asymptomatic and nonspecific pulmonary signs in normal patients
progressive systemic disease in immunocompromised patients

and the last row.

Can SIRS occur without preceding or simultaneous Sepsis?

According to the classification of sepsis, it is SIRS with a suspected or known source of infection. By definition therefore, sepsis without SIRS is not sepsis but SIRS can exist without sepsis. In all fairness though, SIRS can exist if you run for a while (elevated heart rate and respiratory rate by themselves qualify for a diagnosis of SIRS).

Sepsis is however not the same as a bacteraemia which may be caused even by brushing your teeth (although the bacteraemia in this case is transient).


How can I label cryotubes in a way that eliminates the problem of legible hand-writing? My lab stores biological material (tissue, cells, plasma, serum) in a -130 C, liquid nitrogen freezer. The cryotubes that we use to store a samples are labelled by hand which frequently creates legibility problems.

Its my understanding we can't print out stickers to use as labels because they will degrade in the cold. The solution of putting barcodes on the tubes has been suggested but its undesirable because in addition to the cost and logistic complications; we would have to choose between thawing and refreezing all of our samples to transfer them to new tubes OR live with the nightmare of having both labeling systems in use at the same time; one which humans can read and one which humans cannot.

The ideal situation would be a small, portable machine that can physically label the tubes for us. I'm envisioning:
 - an adjustable clamp to hold the tube in place; ideally with sensors that would infer the shape, size, and position of the area that can be labelled.
 - a very-fine tipped pen attached to a motor that would mimic a printer's line-by-line printing action; this would have to take into account the shape and size of the area that can be labelled
- rollers in the clamp to adjust the available space for labeling
 - a screen/keyboard interface that would display how the label will appear

Does anything like this exist?

Do you have any other suggestions about how to deal with the problem of legible hand-writing on cryotubes?

Please advise if there is a more-appropriate SE site to post this question

This is indeed a problematic point. I have been using machine printed labels for a while now (sometimes with some extra scotch tape around it to prevent it from falling) off, which worked pretty nicely.

However, there is a printer available on the market (though I haven't tested it yet) which claims that they can print on any tube. This printer is called Tubewriter, which is probably also worth a look. The backside is the price, Fisher Scientific lists them around 40.000$, which will make them unavailable for most labs, except for cell banks etc.


determining meaning of basic biological keywords about C. elegans First of all I have to say that I have no biology background since I'm a undergraduate computer science student. Nowadays, for my research I need to use some of the databases related with bioinformatics (modENCODE and NCBI-GEO). Currently, I'm searching RNA-Seq data and I have found the following one in modENCODE website which is stored in NCBI-GEO database.RNA-Seq data

In the description part of it, it is written that:

  Synchronized L1 worms cultured at 25degC for about 91 hrs to a point
  at which ~100% worms are resistant to 1% SDS treatment. Illumina
  sequencing of C. elegans dauer daf-2(el370) sample 2-1 DauerDAF2-2-1
  polyA+ RNAseq random fragment library This sample is available through
  the modENCODE DCC (www.modencode.org) as: DauerDAF2-2-1 Local library
  name: DauerDAF2-2-1 Quality values are ASCII encoded Phred + 33.

Regarding with this paragraph, I want to ask that, what is C. elegans dauer daf-2(el370) . I've searched on the internet and I have found that dauer is kind of development stage of C. elegans. However, I could not find any information about the daf-2(el370) part (Actually all I found was that daf-2 is name of a gene of C. elegans). Actually, my primarily concern is whether this RNA-Seq data contains the C. elegans' whole transcriptome or it contains only mRNAs related with daf-2 gene.

Have you discovered wormbase yet? It will become your new best friend. In worms gene names reflect the loss-of-function (lf) phenotype. Daf means "abnormal DAuer Formation," so daf-2 was the second daf gene identified (ref). The mutations are called alleles and each worm lab has their own allele designation. e was for England and in that lab's strain list the daf-2 allele was the 1,370th on their list. So daf-2(e1370) designation means that the strain carries a lf mutation in the daf-2 gene, and the specific allele is one that was isolated in Cambridge, UK. I believe that allele is temperature-sensitive (ts) dauer-constitutive.
So at 25⁰C 100% of the animals were dauers. That is when they harvested RNA. It is the entire transcriptome. It sounds like you may be familiar with modENCODE Data Warehouse. You can still ask questions about modENCODE datasets at help@modencode.org. While the modENCODE Data Coordination Center was mothballed at the end of the NIH funding period, there are a few people who still field queries like yours, to the Helpdesk. Also, moving forward the new ENCODE DCC has taken over curation of archival modENCODE metadata.


How prominent is the gene-centric view of evolution among professional researchers? Richard Dawkins famously advocated a gene-centric (as opposed to organism-centric) viewpoint on natural selection, most notably in The Extended Phenotype. However, I have also heard "on the grapevine" that most professionals in biology and related areas do not take the gene-centric viewpoint altogether seriously.

My question is simple: how prominent is the gene-centric view of evolution among professional researchers in biology and related fields?

What do you mean by gene-centric view of evolution

I am not totally sure you know what really means the gene centric view of evolution. Everybody agrees that selection (also) acts on genes and that selfish genetic elements exist. I think that what one calls the gene centric view of evolution is nothing but the modern synthesis of evolution (following the work of Ronald Fisher, Sewall Wright and some others such as Motoo Kimura).

Or maybe by gene centric view you refer to the concept of level of selection.

Some people however argue that because of the gene centric view of evolution, we tend to underestimate the importance of some parameters in evolution and some are willing to rename the evolution theory into Extended Evolution Theory according to new insights about how parameters such as developmental bias for example influence the evolution of populations.

Modern snythesis of evolution theory

You will find more information in this recent article that you may appreciate reading if it is not too complicated. I personally endorse the "No, all is well" opinion. It is important to understand that those who criticize the gene centric view in this article are NOT saying that selection do not act on genes neither that selfish genetic elements do not exist (thinks that R. Dawkins talk about in his books). They totally agree with those things. They just argue that the fisherian view of evolution in not enough and that according to recent findings we may want to rename our theory. The "no, all is well" opinion totally agrees with the importance of these new insights that do not come from what one may call the gene-centric view of evolution but they just don't think it is worth renaming the theory for that because our knowledge in evolution is just growing as it has always been growing and it doesn't seem that we are currently living a revolution in our understanding of evolution. I think that the main revolutions that happen to occur in evolution these days mostly have to do with the methodology of testing rather than with the theory itself. These revolutions have to do with increased computer power, better statistical methods and faster and cheaper sequencing.

Level of selection

Now, by gene-centric view of evolution you may refer to the concept of level of selection. To my knowledge everybody agree that selection occurs at different levels. Again, NOT everybody agree on the relative importance of selection acting at different level. The vast majority of research focus at evolution at the gene level, sometimes implicitly only.

To conclude, we all agree on the theoretical principles (I think) but not everybody agree on the relative importance of the different mechanisms. In saying this, I don't mean that everybody agree with everything that is written in R. Dawkins books!


Can plants break down cellulose for energy? I know humans and other animals start using their own proteins as food when starving. This made me wonder if a plant that is deprived of sunlight, after using up its sugar reserves and other carbs, could break down parts of its own woody structure in order to feed the rest of itself.

Googling yielded no useful results, which leads me to think the answer is no. I've never heard of plants themselves possessing cellulase, only certain animals.

Additionally, I would imagine that cellulose is not easy to transport, so it would have to be decomposed by the region of tissue surrounding it - which obviously couldn't last for long before that region died due to cannibalizing itself.

Plants do not produce extra cellulase to break down cellulose for an energy boost when they are grown in dark conditions (that I know of). But remember, cell walls are the structures maintaining turgor pressure in the cells, so breaking them down would be very costly to plant survival. A couple notes: plant cell walls have more components than just cellulose, and they ARE dynamic. In dark-grown conditions, plants elongate (etiolation) during which time, enzymes (expansions) break down cell wall bonds to allow the cells to elongate the stems of the plants. Elongation is an evolutionary advantage to find light when things get shady.

To read more about what the cell wall is made of, and the function it provides to the cell, try watching the Khan Acadamy video about cell walls. Light signaling is an entire field in Plant Biology (example). Read more, if you are interested in how immobile plants handle shading from other plants or periods of darkness. Plants do break down proteins for reuse! Read more about plant vacuoles if you're interested in how they recycle and break down some molecules and proteins when needed (related to your question's parallel to animal cells; although, not cellulose breakdown to replace photosynthetic sugar output).


Evolution from Mating types to different sexes Imagine a lineage of multicellular organisms that had mating types and evolved their mating types into sexes. What are the possible mechanisms that might have brought this lineage to evolve sexes from mating types?

To my understanding of the definitions of sexes and mating types, the only diffenece between the two is that sexes imply gametes of different sizes. Is it correct?

Another important reason to have mating types is to prevent self-fertilization or self-polination that produces less capable offspring. Because of this requirement, mating types may evolve also for species that produce both types of gametes, or does not differentiate them into male and female gametes. Fertilization is only possible if gametes have different mating types.

It may be more than two mating types, but if there are only two, they are probably similar to "sexes" even if gametes do not look different.


Real-time PCR result interpretation I performed real-time PCR and I was looking for expression fold changes for 2 genes and I had two sample pools, one treated and the other not treated (for each gene). The problem is that my housekeeping gene (UBQ 30) got a fold change on the treatment. Therefore, what is the correct interpretation and data treatment?

I mean, is it correct to use each control and treatment I got for UBQ CT values to normalize the other two genes corresponding CT, as housekeeping genes are "by definition" expected not to change? (and that is why indeed they are used to normalize)

or should I rather make a mean of my whole UBQ CT-s and normalize all other genes CT values with that mean?

You should try another housekeeping gene like GAPDH since the very definition of these genes is that they shouldn't change with your treatment


Which method of seed dispersal is the most common among the seed plants? The five most common methods of seed dispersal in the plant kingdom are:

wind (anemochory): tumbleweeds, dandelions, maples
animals:(epizoochory) externally - burs / (endozoochory) internally - fruits
water (hydrochory): aquatic-water lily/terrestrial-mangrove trees
gravity (barochory): apples, coconuts
ballistic (ballochory): impatiens, geraniums

source: https://en.wikipedia.org/wiki/Seed_dispersal

As far as which one of these five is the most common, this site says that animal dispersal is more common than wind but nothing in relation to the other methods listed above.  Each method likely is most common in it's most well suited niche, but which one is the most common (in the widest range of species) overall?

This paper from Herrera (1989) investigates the role of endozoochory in Angiosperm diversification, and it has a table that can help answering your question, since it deals with all seed plant families:

As you can see, among Gymnosperms there is no question: endozoochory is the most common mechanism of dispersal.

Unfortunately, things are a bit more complicated among Angiosperms. Exclusive endozoochory is not the most common mechanism (27.1% versus 72.9%). However, if we take into account that the plants that perform endozoochory are actually the sum of the first and second ("mixed") columns, the total is 50.9, which is more than 50%. Of course, there is a mathematical possibility that another method, together with the "mixed" column, also surpass 50%.

Finally, it's worth mentioning that the authors are calculating the frequencies of endozoochory only. If one adds epizoochory to that number (zoochory = epizoochory + endozoochory), the frequency of zoochory is even higher.

Source: Herrera, C. (1989). Seed Dispersal by Animals: A Role in Angiosperm Diversification?. The American Naturalist, 133(3), pp.309-322.


Trying to identify the tree in this picture. Shot from the Nepenthe restaurant, Big Sur, California I'm trying to identify the tree in this picture. This was shot from the Nepenthe restaurant, Big Sur, California.
Any help is appreciated!
Thanks,
Robert

It's difficult to make out the leaves in the photo, but the tree in the foreground appears to be a coast live oak (Quercus agrifolia).  The tree has hairy lichen growing on its branches.


How can toddlers expend seemingly boundless energy when they eat so little? A toddler's food intake seems very little: only milk and water and some solid food. Therefore, from where does this energy come?

They don't eat little. Consider the volume of milk / food they consume as a ratio of their weight. Quite the contrary they are ravenous machines and their consumption is much higher than an average adult. All cellular energy comes from the hydrolysis of ATP, and the production of ATP comes from the breakdown of glucose. The glucose comes from a sugar found in breast milk, called lactose.


Why is ACE2 not used as drug against covid? Can ACE2 be produced and used as drug against covid? I read it is the receptor molecule. If it is in the organism the virus should bind to it and could not attack cells anymore? Is that right?

There's a Cell pre-print by Monteil et al. (DOI: 10.1016/j.cell.2020.04.004) which argues that human recombinant soluble ACE2 protein can competitively bind to SARS-CoV-2 virus and reduce its ability to infect and replicate:

  Here, we report that clinical-grade human recombinant soluble ACE2 (hrsACE2), which has already been tested in phase 1 and phase 2 clinical trials (Haschke et al., 2013, Khan et al., 2017), can reduce viral growth in Vero E6 cells by a factor of 1,000-5,000. Moreover, we show that human blood vessel organoids and kidney organoids can be readily infected, which can be significantly inhibited by hrsACE2 at the early stage of infection.

Though it is not perfect, in that other factors and receptors may be implicated in infectivity:

  Our data now show that this clinical-grade human ACE2 molecule - but not mouse soluble ACE2 - can significantly inhibit SARS-CoV-2 infections and reduce viral load by a factor of 1,000-5,000. However, as observed in antibody neutralizing experiments of many viruses, the inhibition is not complete, though clearly dose-dependent. This may be due to the fact that there might be other co-receptors/auxiliary proteins or even other mechanisms by which viruses can enter cells, as had been initially proposed for SARS (Jeffers et al., 2004; Qi et al., 2020).

One person is right to comment that these are in vitro studies. In other words, they treat cell cultures on the functional equivalent of a Petri dish: Vero cell lines or simulations of human tissues (organoids), and they see what happens.

The in vitro studies are useful and important but it is a big step from those to 1) treating people in vivo — designing a drug that can actually and safely target the virus where it infects respiratory and renal tissues — and, 2) making and distributing that drug in quantity, cheaply, safely, etc.

But the larger point of these studies is to show that scientists are definitely thinking about the mechanisms by which the virus infects cells, and to see if there are ways to interfere with and limit the virus, by doing so.

Like your thought to use ACE2, some researchers have looked at other viruses, like poliovirus and HIV, to see if there are similar soluble ligands that they can bond to antibodies and deliver safely to humans, as a general therapeutic idea.

They found that HIV-1, which uses binding to the CD4 receptor as a means to infect T cells, could develop mutational resistance to soluble CD4 and use other mechanisms to cause infection. But by adding a second receptor CCR5 to the immunoglobulin, other researchers were able to limit the ability of HIV-1 virus to evolve resistance to both receptors, which provides some possibility of this approach as a vaccine, down the road.

These issues all complicate use of receptors as a way to "fake out" the virus. But it is an avenue being explored, especially for this virus during a time of emergency.


Why are there no artificial wombs yet? If the conditions within the womb are mimicked, and proper amniotic fluid with constantly recycling nutrients is maintained, is it not possible to obtain an artificial womb? Is there anything missing? I think, artificial womb, if possible, could open new ways to study human anatomy and development and further the research studies. Starting with test tube fertilization, one could observe the entire process of growth of a zygote to a fetus.

It is impossible at present to reproduce all the conditions of a womb.

A womb is more than a warm fluid-filled home for nine months. A few days after fertilization, the trophoblast portion of the conceptus attaches itself to the uterine wall where it develops into a placenta and umbilical cord while the rest (the epiblast) becomes the baby.

Throughout the pregnancy, the mother delivers oxygen, nutrients and hormones through the her blood flow to the placenta, while carrying away waste. The womb also prevents infection of the placenta and amniotic fluid.

In addition, the placenta contributes to amniotic fluid production. Production and reabsorption of amniotic fluid is a very dynamic process; it isn’t just there. It is estimated that more than 95% of amniotic fluid turns over on daily basis, and the fluid composition changes throughout pregnancy.

While cell cultures of the womb's endometrium have been grown, there is nothing artificial which is close to this kind of environment yet, nor is there likely to be in the near future.


DNA to Binary Distance Computation If I represent DNA as binary values, what is the best way of computing distance between them.

So :
A = 00,
T = 11,
G = 01 and
C = 10

Hamming Distance between ATGC and TAAC is 3, however their binary representations give a different answer:

Hamming Distance of 00110110 and 11000010 = 5.

Whats the best way of distance computation if the DNA bases are represented in this way?

The best way is to choose a distance that represents what you want it to rather than necessarily relying on the Hamming distance.

If you simply want base-by-base difference then calculate that (this may help) but you may also want a difference that depends on the likelyhood of mutating between different bases in which case you want to define a function that translates the mutation into a score for each transfer, i.e. you might want to score a deamination from 5-methylcytosine to thymine as the most likely occurrence. Expressing the relative likelyhoods of different mutations is not an easy problem but there are a number of widely used options.

The important thing is to ensure you represent the underlying biology not ensure that you have the fastest implementation. Decide on this first, then on the algorithm that gives you the best speed (also, deciding on that algorithm is on-topic for Stack Overflow not this Stack Exchange).


Is there an antagonistic association between Penicillium and Aspergillus? Some Aspergillus species appear to like walnuts. My question concerns the association of Penicillium and Aspergillus. No sooner does Aspergillus colonize a walnut (or some other challenging carbon source) than Penicillium seems to move in, eventually killing the Aspergillus colony.

A totally unscientific guess is that Aspergillus is a good colonizer and Penicillium a good opportunist and that this is a common pattern with these two species. Is there any science in this direction? I do recall a sort of well-known picture from an old text in which Penicillium is shown more or less strangling a species of Aspergillus. I didn't think about it much at the time.

The image attached is not very incriminating but the theme is the same. Penicillium are the green hand-like structures strewn about the clover-like Aspergillus. Foot-cell of the latter cropped.

This seems like a simple question but a quick search doesn't reveal a lot, I think in part because this would generally come up as a contamination issue.

It is hard to find any articles on the association between Penicillium and Aspergillus species, although they are both considered two of the most common mold species found indoors.

  In this study, the most prevalent spore types detected in both the indoor and outdoor air samples were generally from the Penicillium/Aspergillus group [...] these ﬁndings are qualitatively similar to those observed in other geographical locations, conﬁrming the ubiquitous nature of these fungi.

Although these genera seem to be found commonly, it also has to do with environmental factors, and the relative humidity of the area as well.

  Geographical location, climate, and short-term meteorological
  conditions are responsible for outdoor types and levels of fungal
  spores.

As for the association and apparently colonization/opportunistic behaviour of the genera, it seems like there are not any associations between the two, unless perhaps environmental conditions are subject to changing, and different mold species have different moisture/temperature thresholds, although again these mold groups tend to be generalists and do well at a wider range of environmental conditions than other fungi.

  A laboratory procedure was developed in which viable peanut seeds were wounded and inoculated with field soil containing natural populations of fungi, then incubated under different conditions of seed water activity and temperature. [...] A. parasiticus colonized peanut seeds at lower temperatures than A. flavus, and cool soil temperatures relative to temperatures of aerial crop fruits might explain why A. parasiticus is found mostly in peanuts.

  Other fungi, dominated by the genera Penicillium, Fusarium and Clonostachys, colonized seeds primarily at water activities and temperatures suboptimal for section Flavi species and A. niger.

  Eupenicillium ochrosalmoneum frequently sporulated on the conidial heads of section Flavi species and showed specificity for these fungi. The inoculation of wounded viable peanut seeds with soil containing natural populations of fungi provides a model system for studying the infection process, the interactions among fungi and those factors important in aflatoxin formation.

Any associations with different fungi species and their different structures, including, for example, with the conidial heads of Aspergillus seem to be currently under study:

  The genus Penicillium comprises species that mostly colonize plant matter. However early reports suggest that several species are capable of parasitizing Aspergillus and sporulating on the conidial heads of the host. More recently Eupenicillium ochrosalmoneum and E. cinnamopurpureum, [...] have been observed sporulating on the heads of Aspergillus species belonging to section Flavi during the colonization of peanut seeds.

  Little is known about the host specificity underlying these Aspergillus-Penicillium associations. [...] all species spread across Aspergillus colonies by means of aerial hyphae that grew from head to head. Additional studies are required to clarify whether Eupenicillium and Penicillium species are parasitic or simply epibiotic on their hosts.


When does DNA replicate actually? I read on Wikipedia that when the cell enters prophase during mitosis , the DNA has already been duplicated , that is the DNA is replicated in the chromatin form , but here I see the picture which shows the already condensed DNA ( now chromosome ) divide into sister chromatids. When does DNA divide actually ?link to wikipedia -https://en.wikipedia.org/wiki/Prophase

According to This paper and most biology textbooks, S-phase or synthesis phase is literally defined by the beginning and ending of DNA replication.  The first picture does not accurately represent the nature of DNA replication and is instead a model to help people track DNA copies during stages of cell division.  DNA is replicated as chromatin and condenses to "double" chromosome form.  You can see some micrographs of DNA condensation in this paper.  You'll see that they don't condense as single chromatids, but they are already replicated.


Does a presence of ants on a plant mean that the plant has been infested by aphids? Ants protect aphids from their predators (such as ladybirds):

  Aphids and other hemipteran insects secrete a sweet liquid called honeydew, when they feed on plant sap. The sugars in honeydew are a high-energy food source, which many ant species collect. In some cases, the aphids secrete the honeydew in response to ants tapping them with their antennae. The ants in turn keep predators away from the aphids and will move them from one feeding location to another. (source: wiki: Ant)

Does a presence of a large amount of ants on a plant in my garden (especially fruit trees, willow trees, flowers, vegetables) mean that the plant has been infested by aphids?

It's easier to spot the ants rather than the relatively smaller aphids so I am wondering if I may use this as a trigger for using an anti-aphid pesticide before the aphids start causing visible damage to the plants.

Simple answer is no:

$Ants \neq Aphids$

However, they could be used as evidence that aphids are there depending on the reliability of the coexistence. Ants and aphids are independent entities and do not rely on each other so can exist in non-overlapping populations. Applying this idea to the correct species of ant and aphid is, of course, important for it to work as an indicator - it will only be true in those combinations where this "aphid protection" occurs.

I can't find any information on the reliability of the relationship, especially not knowing which species you are looking at. If there was a high positive correlation of ant density and aphid density then one would expect the presence of ants to be a good indicator to the presence of aphids. If the correlation is low there is a higher chance of a false positive (where a false positive = when you see ants, conclude there must be aphids, and there are no aphids).


Giving diuretics to insipidus patient I read in Tortora and Derrickson that giving diuretics to diabetes insipidus patients may in fact alleviate the symptoms of the disease.  How is this possible?

Wikipedia has your answer:

  It seems paradoxical to treat an extreme diuresis with a diuretic, but the thiazide diuretics will decrease distal convoluted tubule reabsorption of sodium and water, thereby causing diuresis. This decreases plasma volume, thus lowering GFR [glomerular filtration rate] and enhancing the absorption of sodium and water in the proximal nephron. Less fluid reaches the distal nephron, so overall fluid conservation is obtained.

The source for that is an editorial from 2004 that has some good other sources, including what appears to be the 1959 original paper finding this seemingly-paradoxical result.

  Thiazide diuretics inhibit the NaCl co-transporter (NCC/TSC) in the renal distal convoluted tubule (DCT). The DCT is water impermeable and considered to be part of the diluting segment. Therefore, the water-preserving effect of thiazides is unlikely related to a direct effect on the DCT. In fact, the most widely accepted hypothesis suggests that the antidiuretic action of thiazides is secondary to increased renal sodium excretion. The renal sodium loss causes extracellular volume contraction leading to lowered GFR and increased proximal tubular sodium and water reabsorption. Hence, less water and solutes are delivered to the distal tubule and collecting duct and are lost as urine.


What is the name of this plant? (found in a rock) I found it in Western Turkey.It was growing on a rock so what's it?

I have been looking into this for days, but this plant is difficult to identify without its flower. I reached out to a botanist at Dartmouth, who suggests that it is either one of two species-- a nasturtium (Tropaeoleum sp.) or a geranium (pelargonium). The leaves are what are called peltate, meaning shield-like with the stem attached directly underneath.

Source:

Botanist at Dartmouth
http://etc.usf.edu/clipart/48400/48426/48426_peltate_leaf.htm

On further research, specifically of peltate leaves, this plant looks more like Umbilicus rupestris, which is commonly found in southern Europe and grows in damp rock crevices!

Source:

http://en.wikipedia.org/wiki/Umbilicus_rupestris


Spread of a benign virus in a population over time This is a somewhat difficult (for me) population dynamics question and I wonder if someone with experience in this area could suggest a reasonable approach?

My simplifying assumptions: As a gross oversimplification, let p(k) be the world's population at generation k, and assume a smooth exponential curve that models p(k) from $k=0$ at 10,0000 B.C.E to generation $k=600$ in 2000 C.E. A generation is 20 years, and in acc. with this Wiki there are about 4 million individuals at $k=0$ and 6070 million at $k=600.$
(Of course the exponential model is bad, as world population growth appears to have been sluggish before recorded history.)

Now assume a benign virus infects 120 individuals in $k=0.$ It benignly infects all individuals who have at least one infected parent. Perhaps unimportantly, it also continues to infect 30 new individuals per million in each generation (because its found in the soil), but would not infect those already exposed.

Call infected individuals II and non-infected NI. They are indistinguishable without clinical tests--which are not done, since the virus is harmless. Since II individuals are almost certain to mate with NI individuals, in earlier generations, the number of II will grow very quickly. For a time the growth rate of II will exceed that of p(k). At some point it will be unlikely that an II individual will encounter an NI mate, however a few NI persons will still pair with NI mates--for a while.

My question is, after 600 generations, what is a reasonable estimate of the percentage of II in the population? Is is possible that there would be any NI individuals left? Or would we have some sort of dynamic equilibrium between II and NI in which (I think) the former would strongly dominate?

FWIW, the population growth model is $p(k)=4e^{0.012 k}$ with $p(k)$ in millions.

To many, many decimal places, the percentage of II in the population is 100%.

To answer this you need to make some assumptions about mating structure. I assume mating is panmictic here for simplicity. Ditto sex ratio, but I'm assuming equal number M/F (and equal risk of environmental infection). Finally, I’m assuming NI and II are at equal risk of soil-borne infection (and infections to II are simply wasted), rather than the environmental reservoir somehow seeking out a fixed proportion of NIs, which I think is probably what you meant. I’m also applying the soil-acquired infection to generation 0 here (so they have a chance to become infected before they mate). Finally, II and NI are more traditionally called $I$ (for infectious) and $S$ (for susceptible) in this type of model, so I've followed that convention below.

Unless I’m missing something the population size makes no difference: the chance of a child acquiring infection does not depend on the number of children, and the background rate of environmental infection is proportional to population size, so it all cancels out. I'll therefore stick to proportions from here on, which means $I$ and $S$ are proportions below, not absolute numbers.

Each generation, the proportion of matings between two $I$s is $I^2$, between two $S$s is $I^2$, and between an S and an I is $2·S·I$. So the proportion of Is in the next generation is $I^2 + 2·I·S$. Or, more simply, $1-S^2$.

So:

$S(0) = \frac{3,999,850}{4,000,000} = 0.9999625$
$S(1) = S(0)^2$
$S(2) = S(1)^2$, which is ${S(0)^2}^2$

More generally,
$S(n) = {S(0)^2}^n$

So at generation 600:

$S(600) = {S(0)^2}^{600}$

$2^{600}$ is a very large number. So it shouldn’t be too surprising that everyone is infected by this point.

We can mess around (technical term) with the equation:

$S(n) = {S(0)^2}^n$

...to solve for (for example) how many generations it takes for 50% of the population to be infected:

$$\begin{alignat}{1}
0.5 &= {0.9999625^2}^n \\
\log(0.5) &= \log(0.9999625)\times2^n\\
\frac{\log(0.5)}{\log(0.9999625)} &= 2^n\\
\log_2\left(\frac{\log(0.5)}{\log(0.9999625)}\right) &= n
\end{alignat}$$

So 50% of your global population is infected by generation 15, only 300 years into the simulation.

  however a few NI persons will still pair with NI mates--for a while

The probability of anyone ($S$, or $I$) mating with an $I$ individual is directly proportional to the $I$ proportion of the population, so the chance of this happening just keeps going down faster and faster.


How fast do cancer cells divide (compared to normal cells)? This question suggests that we have, on average, 50-70 billion cell divisions per day. I just read that cancer cells divide more often and are therefore more prone to radiation.

I am wondering, for a specific type of cancer, how fast cancer do cells divide (approximately) compared to normal cells. Does the ratio of cancer mitosis rate to the normal cell mitosis rate varies a lot?

I checked bio-numbers but there's not much data there.

Tumors can be benign (they don't bother you at all eg: a mole which does not change) and malignant (also called cancer).

The difference is based on:-

Degree of differentiation - How much the tumor cells resemble the normal cells
Rate of growth - In general (over generalised) benign tumors are slow growing while malignant tumors are fast growing
Spread to nearby tissues - Benign growth don't cross tissue planes as defined by basement membranes/fascias, while malignant tumors invade across tissue planes
Metastasis - Spread to a remote location in the body through blood, lymph vessels, transcoelomic (peritoneal, pleural, pericardial spaces) routes - This is ONLY seen in malignant tumors.

Coming specifically to rate of growth, these factors must be considered:

What is stated above in 2 is the general case:

Malignant tumors a.k.a cancers grow fast
Benign tumors are slow growing
That being said some benign tumors grow faster that malignant tumors. Eg: Fibroid - grows very rapid under the influence of estrogen as in pregnancy

The rate of growth of malignant cancers depend on their degree of differentiation (look point 1 above).

Well differentiated cancers grow slow - Cancers that are very similar to normal cells are considered to be well differentiated
Poorly differentiated cancers grow faster based on the "poorness" of differentiation,i.e. the worse the degree of differentiation, the faster the growth. Totally undifferentiated (unidentifiable as any tissue type) are called anaplastic cancers and these grow the fastest

The rate of growth of cancers may vary over time

Due to excessive division probability of mutation is high and a sub-clone may emerge with faster rate of division thus a previously slow growing cancer could suddenly start growing fast
Due to the same process some cancers may suddenly decrease in their growth rate and may eventually even vanish! (become necrotic and get cleared away)

This is taken from Robbin's Text book of Pathology,Ed.8, chapter 6

Edit 1:
To know the numbers you need, you have to find out the rate of increase in volume (by measuring size at two points in time) and divide it by the approximate volume of one cell. This will give you the number of cells that has newly divided within the two measured points (growth in interval). Which can then be converted to cell divisions per second.

As pointed out, the rate is going to vary extremely, based on the cancer type.


The probability of indirect human fertilization? What is the probability of conception in situations when sperm isn't directly ejaculated into the woman's vagina, like:

The man's or the woman's hands come into contact with sperm, for example when removing a condom. (Perhaps after washing them,) the hands later touch vagina, for example during foreplay to another intercourse.
The man and the woman taking a bath together, the man ejaculates into the water.
The man ejaculates on the woman's body, perhaps on or around vagina but not inside. (In this case it could also make a difference whether the woman has shaved pubic hair or not.)
The man ejaculates during receiving oral sex, (perhaps the woman rinses her mouth), the couple kisses, the man performs oral sex to the woman.

In all these situations, it seems possible that a tiny amount of sperm is eventually transferred into vagina indirectly. And since just a single cell is enough to fertilize, it seems that there is non-zero probability of conceiving.
How much care need to be taken to prevent conception in such situations? Does simply washing sperm away with water (+ soap perhaps) eliminate it?

If you think of similar situations that are similar, please don't hesitate to add them.

I don't have answers to all of your questions, but here is one example of a highly unusual conception via the gastrointestinal tract: http://blogs.discovermagazine.com/discoblog/2010/02/01/ncbi-rofl-thats-one-miraculous-conception/.

To cut a long story short, a woman born with a congenital defect that caused her to have no vagina was stabbed in the abdomen when her boyfriend found her performing fellatio on another man. She was taken to the hospital and patched up but a few months later:

  Precisely 278 days later the patient was admitted again to hospital with acute, intermittent abdominal pain. Abdominal examination revealed a term pregnancy with a cephalic fetal presentation. The uterus was contracting regularly and the fetal heart was heard. Inspection of the vulva showed no vagina, only a shallow skin dimple was present below the external urethral meatus and between the labia minora. An emergency lower segment caesarean section was performed under spinal anaesthesia and a live male infant weighing 2800 g was born…

The article concludes that:

  A plausible explanation for this pregnancy is that spermatozoa gained access to the reproductive organs via the injured gastrointestinal tract. It is known that spermatozoa do not survive long in an environment with a low pH (Jeffcoate1975), but it is also known that saliva has a high pH and that a starved person does not produce acid under normal circumstances (Bernards & Bouman 1976). It is likely that the patient became pregnant with her first or nearly first ovulation otherwise one would expect that inspissated blood in the uterus and salpinges would have made fertilization difficult. The fact that the son resembled the father excludes an even more miraculous conception.”


Do bacteria with flagella self-rotate? The bacterial flagellum uses rotation for generating forward motion, just like a helicopter main rotor does. Helicopters must utilize a secondary rotor to avoid self-rotation due to preservation of angular momentum. Alternatively they can have multiple rotors rotating at opposite directions. But all flagella rotate in the same direction.  Does this mean that the bacterial cell rotates in the opposite direction?

If so, what is the typical frequency of such rotation? Shouldn't the rotation disturb sensing and nevigation in the environment by the cell?

My opinion as a physicist would be that yes, they do.

Assuming a sperm-like structure with a single flagellum at the centre of a long, thin cell of uniform density. They would rotate around the axis of travel.

However, for other cells, this could be mitigated in several ways:

If the cell was submersed in or floating on a liquid, it is likely that the effects of Archimede's Principal would be sufficient to keep it in a fixed orientation (this is how ships and submarines stay upright despite rotors that all go in the same direction - the least dense parts of a body always attempt to restore themselves to the highest position).
Fluid in the cytoplasm could act as ballast, providing a counterrotation force thanks to the gravitational effect on it.
If the cell happened to be particularily masseous in relation to the force the flaggela were providing, this would make any rotational force negligible.
If the flagella were located away from the axis of travel (through the centre of gravity - ie to the sides) the torque would have less of an effect.

As for the navigational aspect of your question, if these cells do auto-rotate, they will have done so throughout their evoloutionary histories and therefore in all likelihood will have evolved navigation methods capable of dealing with this.

I will however put a disclaimer on this, I am not a biologist and am weighing in from the point of view of a physicist.


What is the relationship between snails/slugs and clams/mussels? Slugs and clams are both phyla in mollusca, but how can I tell which features they inherited from an ancestor? Basically, I'm curious about how excatly these organisms are related but can't find any information and do not know where to look.

The Tree of Life web Mollusc page  shows that gastropods (snails/slugs/etc.) and bivalves (clams/mussels) are two of the major groups within Mollusca:

You can click through to get more detail on the individual groups (but there isn't much more information about the defining characters, date of divergence, etc.). At the very least, these technical names for the taxa (and of the Conchifera, their parent taxon) should help you search for more information, e.g. a Google scholar search on "bivalvia gastropoda divergence", which gets to Investigation of molluscan phylogeny using large-subunit and small-subunit nuclear rRNA sequences ("scaphopods are more closely related to gastropods and cephalopods than to bivalves") or Phylogenetic relationships of annelids, molluscs, and arthropods evidenced from molecules and morphology. (You do have to be careful in reading the phylogenetic literature, as it's rapidly evolving; the latter paper is from 1996 and may well be superseded.)


Question in gel chromatography experiment Here I am trying to do
gel chromatography to separate vitamin B12 and Bovine Serum Albumin (BSA)
in this experiment, I am using sephacryl s-100 HR gel column
my question is can I use Phosphate buffered saline with sephacryl s-100 HR gel column
also since the Bovine Serum Albumin (BSA) is colorless I need some kind of Protine detection reagent to see this protein (I need something other than Coomassie brilliant blue)

Within reason, you can basically use any buffer you like with Sephacryl S-100, provided that is suits your purpose in terms of protein/enzyme stability, and phosphate-buffered saline sounds ideal.
There are sometimes a small amount of positively or negatively charged groups associated with a gel-filtration resin, introduced during the manufacturing process, and it is recommended to have some salt present (100mM KCl used to be recommended) in order to counteract anion-exchange and/or cation exchange effects.  In addition, at very high salt concentrations (1M ammonium sulphate or higher), proteins may bind to the resin by a hydrophobic interaction. Furthermore, one or more of your target molecules may be unstable at extremes of pH.  NADH, for example, is unstable in acid.
In other words, you want to set up the experiment where the target molecules are stable, and where separation on the column is by 'molecular sieving' only.
A very common method of measuring protein concentration is to measure the A-280 of each fraction (the absorbance at 280nm). The has the big advantage of being reasonbly sensitive AND is non-destructive (you can fully recover the sample after the measurement).  All you need is access to a spectrophotometer and a quartz cuvette!
In addition, with (pure) BSA the method may be made quantitative as the A(1%, 280),sometimes called the E(1%,280), is known. From memory I think this is about 0.68 for BSA.  That is, a 1mg/ml solution of (pure) BSA will have an absorbance at 280nm of 0.68.  (The 'rule of thumb' for impure protein preparations is that a 1mg/ml solution has an absorbance of 1. But note that many compounds absorb at 280nm, including DNA)
You can, if you wish, calculate the A(1%, 280) from the amino acid sequence of the protein of interest. The refs (Perkins; Gill & von Hippel) are given below.
It should be possible to detect B12 by a similar method, perhaps even at 280nm, but an absorbance spectrum may yield a more sensitive/specific wavelength.
You don't give the pH of the PBS (!important), or the dimensions of the Sephacryl column.
Long, narrow columns work best, but you probably already know that.
Some Refs
Gel Filtration by Reiland (Methods in Enzymology, 1971).  A great article
Protein Purification: Principles and Practice by RK Scopes (Springer Advanced Texts in Chemistry) 3rd Edition
Sober, E. K. & Sober, H. A. (1970). Molar extinction coefficients and E (1%, 280) values for proteins at selected wavelengths of the ultraviolet and visible region. In Handbook of Biochemistry. Selected Data for Molecular Biology, 2nd edn. Sober, H. A., Ed. pp C-71 - C-98. The Chemical Rubber Company, Cleveland, Ohio.
Perkins, S. J. (1986). Protein volumes and hydration effects. The calculation of partial specific volumes, neutron scattering matchpoints and 280-nm absorption coefficients for proteins and glycoproteins from amino acid sequences.  Eur. J. Biochem. 157, 169 - 180. [Pubmed]  [pdf]
Gill, S. C. & von Hippel, P. H. (1989). Calculation of protein extinction coefficients from amino acid sequence data.  Anal. Biochem. 182, 319 - 326.  [published erratum appears in Anal. Biochem. (1990) 189, 283].


What kind of caterpillars are these? My niece found some caterpillars that we can't identify. Anyone know what these are? They were found in Massachusetts. The look kind of like Luna Moth caterpillars to me, but I'm not sure.

Most likely it is Polymopheus moth caterpillar, known as Antheraea polyphemus  from the giant moth family.

yellow-green, and the setae become relatively less prominent with each molt. The translucent yellowish-green to green, full-grown (fifth instar) caterpillars are 60 to 75 mm in length. They have yellow mid-segmental lines that run from the sub-dorsal scoli (setae-bearing, wart-like bumps) touching the spiracles and to the lateral scoli on abdominal segments 2 to 7.

Reference

The species is widespread in continental North America, with local populations found throughout subarctic Canada and the United States. The caterpillar can eat 86,000 times its weight at emergence in a little less than two months.

Reference

The adult wingspan is 10 to 15 cm (approximately 4 to 6 inches). The upper surface of the wings is various shades of reddish brown, gray, light brown or yellow-brown with transparent eyespots.

Reference

Adult male moth

Adult female moth


What is the copy number of a given gene in GRCh37? sorry for the naive question, but how do I determine what the copy number is in GRCh37 for a gene with multiple CNVs? (e.g. DRD4).

A very naive approach would be to simply ask how many copies of the sequence in question are in the hg38 sequence, at some level of homology. You could do this using a tool such as BLASTN (which has a web interface that you can use to search against a human genome) or, if you have the sequences downloaded somewhere where you can work with them, using a tool such as minimap2 (which will be faster) as long as you're comfortable using command-line tools.
If you choose to do this, you will have to be comfortable setting thresholds for what counts as a copy of the gene in question.
A more involved solution would be to obtain DNA sequencing reads for the sample you're interested in and use them to quantify the copy number of the gene based on the number that map to a given sequence of interest. An older approach would be to use microarrays.
I am guessing that since you are interested in the reference genome that you are not interested in going to that kind of trouble.
Is this a homework question? If so, you should add the "homework" tag.


How do female hormones cause blood to clot? On most female-hormone supplements you get a warning that is something like this:

  The use of a combination hormonal contraceptives (CHC), like NuvaRing, is associated with increased risks of several serious side effects, including blood clots, stroke, or heart attack. (Nuvaring)

The use of a CHC, like NuvaRing, is associated with increased risks of several serious side effects, including blood clots, stroke, or heart attack.

It also goes onto state that smoking can increase these risks.

What makes these hormones so dangerous (prone to clotting)?
If a person is naturally high in these hormones are they at a higher risk of blood clots?
Why/How does smoking affect the hormones - or is the increase risk just due to the natural risk of smoking?

These combination contraceptives contain two substances: Estrogen and progestin (a synthetic progesterone). Both are used together to overcome the negative effects of single substance drugs as acne or sickness.

The risk for blood clots has been known for quite a while (see reference 1 and 2) and is generally caused by raised levels of clotting factors (especially VII and X), increased plasma fibrinogen, increased platelet aggregation in the blood and reduced activity of antithrombin III (which inhibits coagulation). This can happen as well in pregnancy when the factors are naturally elevated (that's the way these contraceptives simulate pregnancy to the body). The paper shows this nicely for two of the factors of the blood coagulation cascade (factor VII and X):

This risk is relatively rare, it affects only about 1-5 in 10.000 women, but is still not negligible. The risk is much higher in persons with defects in the blood coagulation cascade. Compared to this, pregnant women have a risk for blood clots of 5-20 per 10.000 women (for details see here).

Blood coagulation is really fine tuned to ensure proper function when necessary but no blood clotting when not. Basically activating and deactivating hold a balance, as depicted in figure 1 from reference 3:

Smoking now disturbs this balance by inhibiting fibrinolysis and promoting the accumulation of fibrin and pushes it more to the site of coagulation. What causes the problem here is the elevation of clotting factors in combination with the disturbance of the balance between activation and inhibition of clotting. See reference 3 for the details.

This effect seems to be limited to high concentration single estrogen and estrogen/progestin combination preparations, while there seems to be no such effect in progestin single preparations (although data is limited here). There is also a significant difference in the type of estrogen used. See references 4 and 5 for more details.

The mechanism of how this works is relatively straightforward. The estrogen binds to the estrogen receptor on the cell surface and forms a receptor-ligand complex. This leads to signalling inside the cells which finally results in changed gene expression. Additionally the complex can be internalized by the cell. Inside the cell this complex can bind to the so-called "hormone response element" and also regulate the expression of genes. This is explained in detail for Factor XII in reference 6 (and works like this for other parts as well). See the image for illustration (from reference 7):

References:

Relation between oral contraceptive hormones and blood clotting
Use of combined oral contraceptives and risk of venous
thromboembolism: nested case-control studies using the QResearch and
CPRD databases
Hemostatic effects of smoking and oral contraceptive use
Coagulation effects of oral contraception.
Lower Risk of Cardiovascular Events in Postmenopausal Women Taking
Oral Estradiol Compared With Oral Conjugated Equine Estrogens
Molecular basis of estrogen regulation of Hageman factor XII gene
expression.
Estrogen synthesis and signaling pathways during aging: from
periphery to brain


Evolution (Reductionism) My recent post was tagged as unclear so I wanted to re frame my question. Though I am a layman, I would love to read books and find the stuff, if I get an overall picture of intelligence factor. My question is, how come evolutionary mechanism of protecting ones species made them adapt to their environment ?

The answer comes by the genetic mutation, the switch genes and so on. But how are these cells intelligent to cause such mutation ? For instance, cells don't have intelligence of their own, so presented a situation where in you have to see, but have no eyes, or have to walk but have no legs, how come cells know that they have to work against gravity and develop such structures and hollow bones in birds to make the flight easier ? Does it mean that nature is intelligent ? How come matter itself create gravity, space etc., on one side, and creating beings to overcome it ? Isn't the matter altogether ? If that's the case, imagine a thought experiment, where in we all have dangerous predators which are 4D beings. So since our cognitive and visual percepts  are just designed to perceive 2 dimensions at a time, we being 3D creatures. So over thousands of years, since we have to live and survive, would we develop a vision that can see 3D ? It would be amazing then. It then means that there is an intelligence factor in nature that tells the creatures how to change !

Please do answer, and again repeating I want to hear, how Genes know that they have to work against gravity, or develop a particular efficient thing, that can solve the problem. Otherwise it's as if Genes permute infinitely, and then develop all possible models, and only those which serve the purpose will stay.

Please do clarify.
Thanks !

I think we may be missing a piece from Darwin's original hypothesis.

An outline of the first 4 chapters of Origin of Species form the kernel of the Theory of Evolution:

1: Variation under Domestication
2: Variation under Nature
3: Struggle for Existence
4: Natural Selection

Really you can't reduce evolution to less than variations; competition (struggle) ; selection.  that's about as far as you can go and still call it evolution.  Even genetic algorithms which don't use living organisms at all have these 3 steps.

Most people don't have an issues with Variation any more.  At one time it was thought that individual variations were not important, but now most people understand that one water bug might have significant individual differences from other water bugs and its not just people who look at each other and marvel at individual traits.

The struggle for existence was difficult for people to accept at the time, but its simply that most living things don't make it.  Darwin had noticed that each spring that a typical bird pair might have 3-4 eggs in their nest but if you do the numbers it tells a story of how much of a struggle life can be even if we don't see it on a walk in the woods.  If all eggs reached maturity and reproduced, a single pair of birds would generate enough birds to cover England in about 40 years.  That's just a squeak under 3.5^40 without death from old age.

The struggle for existence hints how competitive Selection is.  In their breeding lifetime, to have a static population of birds, a breeding pair produces 2 breeding offspring out of perhaps 14 eggs lain.

It's a given that genes don't know that they have to do anything, but if they don't work well they will not be seen again. Their host dies from a developmental issue, falls and hurts itself doesn't display the right plumage, isn't fast enough to catch its food, is so slow that it gets eaten, its seed falls on soil it cannot germinate in, etc etc.

The list is endless as to the things that can go wrong in the wild and would cause an individual to be removed from the gene pool and they don't produce offspring. All of the important qualities that genes need to have is mysteriously embedded in what we call the environment - the earth, the air, the water the behavior of other living things decide whether most genes make it or not.

If you need any more evidence that intelligence has nothing to do with evolution, then look at human beings... not getting along well with other living things well now - is that smart?

An example of selection
Since it was requested, let me expand and give a very simple example of random selection that I've always liked (Disclaimer: maybe because I made it up as far as I know!).

Take a box of 100 coins.  We want all 100 coins to be heads up, but we can't individually flip any of the coins over: we can only shake the box.  Note that when we shake the box - nothing is thinking or acting consciously.  Genes do permute randomly and, for all reasonable approximations of infinity, infinitely, but they tend to stick around when something works.  This makes evolution seem unnaturally quick to respond.

Method 1: shake the box, looking every time. There are 2^100 combinations.  Getting terribly lucky we'd have to shake the box 2^97 times before we accidentally caught a box of all heads up coins.  That's random chance.

Method 2: if we remove the coins that are heads up every time we shake the box, we'll be shaking the box 8 times or so.  That is similar to a strong selection case in evolution: the coins which are heads up are like traits which have an advantage so they stay around.  Its striking how efficient this can be and how many tremendous changes can happen in a short time if there is selection and advantage.

Note that we have plenty of bad traits here (tails up); they show up all the time - with great frequency.  They just don't stick around because the struggle for existence is so challenging.

You can further get an idea of weaker selection if you can imagine that instead of the heads always staying heads, you have a little stickiness on the tails of the coins.  80% or 60 or 52% of the time these coins stick and stay as heads.  It still will not be long before you find that the coins are mostly heads.  10 20 or 30 shakes of the box rather than 8.

Where do new traits come from then?
So taking all this and thinking about how new traits like eyes which had not been
seen before, the same blind and random process applies.  It is better not to think of humans and human traits - we're the product of over a billion years of selection and evolution!   Think how primal traits at the bacterial level emerge.

Below is a picture of salt pools in the San Francisco Bay.  Evaporation increases the salt concentration in the pools and as they become inhospitable, halophilic (salt loving) bacteria take over.

The pools are colored because these bacteria have an ancient mechanism which allows them to harvest light to pump the salt out of their bodies and help create energy as well.  The light is harvested in one well documented case by a retinol molecule which absorbs blue light.  Retinols are a variation on vitamin A and must be quite ancient.

Yet a similar molecule, retinal, is used in human eyes as the light sensor there.  A similar protein holds those light sensing molecules in both human and halophile as well. While the structure of the eye and the nervous system that processes information into the brain all came later, you can see at one point the interaction with a bacterium with light became so useful that once it evolved, it has stayed in the gene pool since the days of bacteria to be the light sensor.  Vitamin A is the product of a biosynthetic pathway that very easily makes a variety of molecules.  The light sensing genes that used them evolved once, but variations on it sense light in our eyes today.


What are mast cell membranes made out of? What are mast cell membranes made out of?

What would weaken or strengthen them?

Web searches bring up a lot of information about mast cells but very little on the membrane. And the Wikipedia page is not clear as to whether or not additional calcium or sodium fluoride would improve/weaken mast cell wall strength.

Although the Wikipedia page on dermatographism refers to "weak membranes" it cites no source for this, and like Chris, I haven't found any mention of this in a quick look at the literature.

Histamine is usually released from mast cells in response to specific stimuli by a degranulation reaction (internal vesicles fusing with the surface membrane to release their contents) and I would guess that abnormal degranulation is a more likely cause than cell lysis.

In a recent paper (Ralph, JW (2013) Evidence for a role of neural pathways in dermographism. Brit. J. Dermatology 169, 1357–1374) a case is reported of a man who combines dermatographism with a syndrome called "stocking-glove neuropathy". This latter syndrome results in a pattern of loss of sensation in the lower arm. When the dermatographic reaction is triggered in this patient the resulting weal does not extend into the affected part of the arm, suggesting that neural activity is part of the trigger for dermatographism. In other words, in those suffering from dermatographism, sensory nerve activation would somehow result in cross-talk into the pathway for stimulating mast cell degranulation.


Can humans go to hibernation? Like squirrel undergoes hibernation during unfavourable periods if we induced the hibernation causing pitutary hormones in the human blood stream, can humans go to hibernation?

Humans cannot hibernate. There are a number of reasons why we would not expect them to do so.

Hibernation is thought to be an evolutionary adaptation to cold temperatures, and food scarcity, (perhaps also predator avoidance). Humans evolved in tropical regions with an abundance of food, and are also considered apex predators. There was thus no evolutionary pressure.

If we were to induce sleep with the relevant pitutary hormones. Humans would likely die, if they do not have any life support.


Does a full tear of the gluteus minimus tendon has any functional implications? From what I read on Wikipedia, all functions of the gluteus minimus are mirrored by the gluteus medius. Additionally, the gluteus medius is larger than the gluteus minimus (see comparative images here), which leads me to believe that the gluteus medius is stronger than the gluteus minimus.

Subsequently, I would tend to guess that a full tear of the gluteus minimus tendon does not have any functional implications. I.e., a human might have a full tear of the gluteus minimus tendon without any limitation of their movements. Is my guess correct?

You’re correct that the gluteus minimus is redundant in function with the gluteus medius, but an isolated gluteus minimus tear still causes functional problems because of the associated inflammatory response and subsequent pain deemed “greater trochanteric pain syndrome,” as the greater trochanter is the insertion site for hip abductor muscles like the gluteus minimus and medius:

  MRI Web Clinic — May 2004,
  Gluteus Minimus Tear & Trochanteric Bursitis,
  Michael E. Stadnick, M.D. (mirror)

    Clinical History: 70 year-old female with chronic left hip pain...What is your diagnosis?

    Diagnosis: Gluteus minimus tear of the left hip with associated trochanteric bursitis.

    Discussion: Lateral hip pain is frequently a challenging diagnostic and therapeutic problem. In the past, the presentation of chronic lateral hip pain with tenderness over the greater trochanter was attributed to trochanteric bursitis. This symptom complex, called greater trochanteric pain syndrome (GTPS), can mimic other serious causes of hip pain...Abductor tendon (gluteus minimus and gluteus medius) tears are becoming increasingly recognized as a frequent cause of pain at the hip. In fact, tears of the abductor tendons, instead of trochanteric bursitis, are likely the most common cause of GTPS.

    In a large majority of patients, trochanteric bursitis or distension will accompany an abductor tendon tear. The frequent coexistence of trochanteric bursitis and abductor tendinopathy has led some authors to suggest that bursitis may in fact be a result of the underlying tendinopathy.

    Early descriptions of abductor tendon tears at the hip emphasized involvement of the gluteus medius tendon as being most common. However, subsequent papers have revealed a roughly equal frequency of involvement of the gluteus minimus and medius tendons.


Specific location where nerves converge I'm looking for the "earliest" specific site where the 3 following nerves' sensory signals "converge":

Trigeminal nerve
Median nerve
Superficial peroneal nerve

By "earliest", I really mean the first location in the sensory pathway (to the brain) at which these 3 nerves' sensory signals converge.  And by "converge", I mean "feed into each other". My understanding is that, with sensory nerves, all tactile reception roads lead to the somatosensory cortex, and so, I would imagine all the nerve signals converge/merge into one another at some point.

I would imagine the location I'm looking for is the brainstem, probably the pons, but I'm not a biologist and am looking for either correction or confirmation here. This uneducated guesstimate comes from two sources:

Wikipedia - which states that the cranial nerves feed into the pons; and
The fact that the median and peroneal nerves are spinal nerves, which ultimately feed into the medula, which then turns into the pons.

Am I right or way off track?

Please note: this is not homework!

By reasoning, we can make the following distinction:

the trigeminal nerve is a cranial nerve.
the 2 others are peripheral
nerves.

Cranial nerves take their origin into their respective nuclei, and bypass the dorsal columns (main spinal tract for sensory information). Peripheral sensory nerves stem from the spinal roots, and from there go up through the dorsal columns. This would bring you to the thalamus, where all sensory information is regrouped. However, somatosensory information from the face and the rest of the body happen to travel through different thalamic nuclei (ventroposterolateral for the body, ventroposteromedian for the face, If my neuroanatomy is not too far behind me...). This leaves us with the internal capsula (fibers that link the thalamus to the cortex), but I do not think much signal integration occurs there.

In conclusion, the first anatomical level of convergence between the 3 above-cited nerves would indeed be the somatosensory cortex.