text:
To what extent can bacteria actually see?
I found some popular articles (e.g. nbcnews and iflscience) that bacteria can "see," but I highly doubt it's in the same way as people do just from looking at the limitations in the vision of small animals like insects. So what exactly are bacteria capable of "seeing" or what are the limitations of their vision?

Can you please link to some of these articles?

Well I mean google can take care of that, for instance https://www.nbcnews.com/science/science-news/bacteria-have-ability-see-eye-opening-study-finds-n515141
or just http://www.iflscience.com/environment/bacteria-can-actually-see-acting-tiny-eyeballs/

@JohnJoe you are asking people here to help you and then say "google missing information". That is not very nice. Meanwhile, please post a quote that you need help understanding, right now question is unclear.

I'm not asking for people to verify the sources of what I said though. The way the articles phrase it is pop science anyway, not real science, so there's not even a point to referencing that information. However, the general topic is still relevant. Multiple news sources would not all lie about the same scientific subject, it is only that they do not portray it accurately.

Simple answer is that many simple organisms, including bacteria, carry light-sensitive molecules. One example is halorhodopsin (not bacterial but archaeic). This is a molecule, light-gated ion pump, that reacts to light, thus allowing organism to react to photons by changing concentration of certain ions inside the cell.
Study from Stanford described similar molecule found in bacteria.
In conclusion, if by "vision" you understand ability to react to light in the visible part of the spectrum, then a lot of organisms possess such ability. However, they lack other crutial parts of human vision.

I think that makes sense, thank you. So just to be clear, you're saying bacteria have the ability to sense simply "that" there is light in different levels almost like an on-off switch, but not the detail we see in larger animals? Can bacteria in any way distinguish either different frequencies of light, or, any kind of 2D or 3D structure?

@JohnJoe Most likely they don't. The most they can do is differentiate between high and low light. That too not by neural processing, rather by differential activity of light gated ion pumps.

Because bacteria are extremely small, the principles of optics prevent them from having lenses or other organs capable of determining the direction from which light is incident.  On the other hand, an entire spherical bacterium can potentially act as a lens, concentrating light from a given direction onto a corresponding position on the opposite side of the bacterium, and thus forming a very crude image.  Bacteria are certainly capable of responding to the frequency of incident light, if they contain molecules that selectively absorb light in specific frequency ranges.  And, they should be able to respond to the brightness or intensity of incident light, if those molecules return to their normal state shortly after absorbing a photon.  Of course, additional molecular machinery would need to be present in a bacterium to translate absorption of a photon into any sort of meaningful response.

@xusr, that paper makes a pretty convincing case that I was too hasty in rejecting the possibility that a relatively large, spherical bacterium could form enough of an image to "perceive" the direction of light.  The directional response to light described in the paper is, indeed, plausible.

Is there some way to combine both answers? They both have decent points.

I edited the answer accordingly.

Great, the only thing you're missing is credible references.

The reference given by @xusr, Cyanobacteria use micro-optics to sense light direction [https://elifesciences.org/articles/12620] is very good. If bacteria were large and spherical - on the order of a millimeter in diameter- and if their refractive index could be on the order of 2 rather than ~1.4 to ~1.6, then they would be able to form a high-quality image by this means: parallel rays from any given direction would come to a fine focus on the surface on the opposite side of the bacterium.  However, with a refractive index of 1.4, the focus lands far beyond the surface, hence a low res image.

I'm surprised at the focus on light in all these answers! To my knowledge, light is absolutely not the way that some 'bacteria' may be able to see.
Try looking on youtube for a macrophage (white blood cell) chasing down a bacteria.
You can see it actually following the bacteria - it's crazy. How on earth does it know where it is?
Chemical signalling, of course!! Sort of like a neurotransmitter. They secrete chemicals and follow the trail -  it could be really simple, such as, the transmitter converts to something else once it comes into contact with a phospholipid (of course indicating a cell membrane). I haven't researched that bit, but I hope it will allow you to direct your own train of thought/research.
Macrophages also have things called 'Toll-Like Receptor' proteins on their membranes, and they produce these things called 'pseudopods' that are essentially feelers/protrusions of the cell membrane. The Toll Like Receptor proteins recognise antigens by detecting Pathogen Associated Molecular Patterns that are common on the surface of pathogens/non-self objects (funnily enough). This is how your most basic innate immune system works- if the TLR protein on the pseudopod (wavy, baddie-finding arms) comes into contact with something it recognises as 'bad', it binds to it and draws it in for the white blood cell to engulf.
But it doesn't actually destroy/digest it at that point, because the TLR protein isn't perfect and sometimes there's some friendly-fire. A T Cell (I think T-Helper) comes along and 'double checks' that the macrophage hasn't picked up a friendly object. If it HAS picked up a friendly object, the T Cell will actually kill the macrophage for its mistake (usually).
OMG FRED, WHAT HAVE YOU DONE
Or at least that's how I like to imagine it goes down.

Chemical signals aren't exactly vision though, they aren't responding to photons.


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Can telegony happen in humans like in Telostylinus angusticollis?
Is it possible for a human male to transmit features of his phenotype via non-genetic semen-borne factors to his mate's subsequent offspring sired by another male? As it happens in flies (Crean et al., 2014).

Note that very few authors really use the term of telegony today. When talking about telegony, are you only referring to inheritance of genetic material or do you also refer to non-genetic material? Because the term is rarely used, I would like to invite you to add the definiton you want to sue in the post (by making sure to state wether or not you want to consider non-genetic elements too). You might want to have a look at wikipedia>telegony

Thanks for the edit. The question is clear now +1. I doubt we'll have much data on this. The 2014 paper you refer to does not talk about studies in humans so we very likely don't have any data prior to 2014. Note that as experimental manipulation would be unethical in humans, the question is probably hard to study.

There are also these studies. What do you think of these? https://www.ncbi.nlm.nih.gov/pubmed/29093734 https://www.ncbi.nlm.nih.gov/pubmed/23618818

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sort: votes


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Blood Pressure and Compliance
Need some insight into the relationship between blood pressure and arterial compliance(Change in Volume/Change in Pressure). Most text books suggest that systolic blood pressure has an inverse relationship with compliance.
I understand that systolic blood pressure is dependent on cardiac output, resistance and arterial stiffness(measured by compliance).
However, I still cannot understand the exact biophysical reason. It doesnt make intuitive sense right now

I wonder if you might add an explanation of what you mean by compliance here. Remember to also show your prior research when editing.

It's a part of the way we do things here, we encourage self-learning and people to show what research they've done when asking and where they got stuck. See the [ask] section of the [help] for clarification. Could you edit the question rather than leaving comments as they can't be guaranteed to stick around. Remember we also have a [medicalsciences.se] site.

Sure, thank you!!

I think it's pretty intuitive if you start with  the right understanding of the individual concepts.
First, the homeostatic goal of the cardiovascular system is to deliver a given flow rate for a given need. Flow (volume/time) is what delivers enough oxygen to tissues.
Second, compliance is best understood as the stretchiness of the system. A balloon has really high compliance: a little pressure in the system increases the volume. A sealed glass jar has very little compliance: it's going to stay the same volume even as pressures get high.
Third, the heart necessarily delivers all of the flow for a cycle in a relatively short time. It's not providing a constant flow, it's providing a pulsatile flow.
Where does all that blood go with each beat? It doesn't flow through the whole system during systole, it fills the proximal arteries, and they stretch to contain the volume, which then flows through the system for the rest of the cycle. If they're very stretchy, they will fill up without taking much pressure. If they're rigid and less stretchy, it takes more pressure for that same volume to be able to get into those same vessels.
Think of "systolic blood pressure" as "how much pressure the heart needs to push a sufficient volume of blood into the arteries". If the arteries are compliant, it doesn't take much pressure. If they are stiff (e.g. atherosclerosis) it takes more pressure.

So from what I understand. If the proximal artery is easily distensible, then it will need less pressure to stretch and hence systolic pressure will be low, right?

@user141356 Yes, that's right.

Thank you, I kinda get it now!!

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Exsanguination Time from Damage to Major Arteries
For a game project, I need to study how much blood loss is suffered when the major arteries of the human body are severed. I believe there are medical textbooks that have collected data on blood volume loss from the various arteries, but I'm not sure where to look to find this data.
If there were some table with a list of arteries, and the volume of blood lost every second, with estimates for how long a surgeon has before the patient bleeds out; that would be extremely convenient. I suspect that isn't the case.

EDIT: I searched further for data on the subject, and found something dramatically unusual. I would like to ask how credible this data seems: http://realfighting.com/unconsciousness_and_death.php
The data is said to come from a Dr Lorne David Porayko and a Dr Christine Hall.
The web page has a list of times for bleeding to death from if various arteries were severed under the conditions:

There is no compression of a lacerated artery underway. This was irrelevant for a lacerated vein due to the fact that a vein can’t be compressed
The subject is previously healthy with a normal haemoglobin concentration and has a normal VO2 max prior to being wounded.
If an artery is the target, the artery is incompletely transacted.  Completely transacted arteries go into vasospasm and retract into their perivascular sheaths which markedly reduces bleeding and even stopping bleeding all together in the case of smaller vessels. On this point Dr Porayko stated that this is the reason the Ghurkhas were trained to twist their knives in the femoral artery after puncturing it- to avoid a clean surgical transaction, thus preventing the vasospasm and retraction into the perivascular sheath, and instead to intentionally cause a hole in the vessel sidewall which is much more lethal.

The adventitia (a saran wrap like layer around the blood vessel) does not seal the wound ( The doctors stated that this usually does happen in survivors) and/or a clot does no form after blood pressure drops."

They then suggested the following data:
Carotid Artery:
Approx 2-20 minutes
Jugular Vein:
Approx 15-60 minutes
Subclavian Artery:
Approx 2-20 minutes.  The doctors also noted: “this is a special circumstance anatomically because this vessel is protected by the clavicle and the first rib (sandwiched between them) if the Subclavian artery bleeds, the only way to compress it and repair it is to open the chest by thoracotomy.  You cannot compress it. Patients usually die on the scene or en-route to hospital.
Subclavian Vein:
Approx 15-60 minutes
Brachial Artery:
5-60 minutes.  The doctors also noted: “pretty unusual to see these without compression by EMS)
Femoral Artery:
5-60 minutes. The doctors also noted: “Pretty unusual to see these without compression by EMS)
Aorta or any part of the heart:
Approx 1-2 minutes.  The doctors stated that the heart conducts 100% of cardiac output.  Assuming transaction and that the hole does not seal. Ventricular holes do usually seal while the arterial ones do not due to the orientation of the muscle fibres.
Two other areas of note made by the doctors also included:
Popliteal Artery:
Located behind the knee, would be similar (but slightly less) to cutting the femoral artery
Inferior Vena Cava:
Can be attacked via a deep abdominal stab, similar to cutting the Jugular vein

Additionally, the Doctors shared anecdotes of patients who survived extreme blood loss, defying expectation:

One of the doctors has seen several patients with traumatic cardiotomies (a big hole in the
heart) survive for 20 minutes before being treated
One of the doctors treated a patient who had been stabbed in the abdomen, where the knife hit the inferior vena cava, his belly was full of blood, he was conscious, although in shock, an hour after the injury when he arrived in the ER. He survived.

The doctors stated that they have seen patients who have bled out nearly their entire blood volume, but yet are still awake and talking (although looking bad) for many minutes following an injury and  survive to tell their story.  Dr Porayko stated, “So it is a mistake to underestimate a person’s capacity to compensate for acute hypovolemia and anemia (hemorrhagic shock), even when very severe. This is especially true in the younger population.

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How long does it take for blood to travel from the lungs to the fingertips?
I've noticed that a pulse oximeter at my fingertip lags my breathing effort by a noticable amount.  I conclude that it takes some time for freshly oxygenated blood to travel from the lungs to the fingertips.
What lag time should I expect? Is there a chart or study which provides an estimate based on heart rate?
Is the lag greater for fingers, or toes? Presumably toes, being further from the heart and lungs, but perhaps the circulatory system has a larger carrying capacity and evens it out for the legs and feet.


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Check on 23andme what type of CYP2D6 substrate metabolizer I am
CYP2D6 is responsible for the metabolism and elimination of approximately 25% of clinically used drugs. Which SNPs do I need to check on 23andme in order to determine if I'm a poor or ultrarapid metabolizer of CYP2D6 substrates, and how reliable would the results be?
I've found one article on this topic, but I'm not sure how accurate it is, and it doesn't cite sources.
PS: why isn't this information more readily accessible to 23andme users, given the relatively large risks incurred by not knowing one's reaction to a large number of drugs?

Unless your polymorphisms have been tested against a particular drug, you can't extrapolate a starting dosage for it based only on your genotype.  It's better to actually take the drug, and change dosage based on observations.
See this paper
https://www.ncbi.nlm.nih.gov/pubmed/24935087

CONCLUSIONS AND RELEVANCE: In this meta-analysis of randomized
  clinical trials, a genotype-guided dosing strategy did not result in a
  greater percentage of time that the INR was within the therapeutic
  range, fewer patients with an INR greater than 4, or a reduction in
  major bleeding or thromboembolic events compared with clinical dosing
  algorithms.

.

why isn't this information more readily accessible to 23andme users,
  given the relatively large risks incurred by not knowing one's
  reaction to a large number of drugs?

Because no-way no-how does 23andMe want to be in the business of giving medical advice.  Nor should they be, because for most things, we have no idea how to convert genotype knowledge anything medically actionable.

This is the case for all genotype guided dosing strategies I'm aware of, even if the polymorphisms have been tested against a particular drug.  So far, clinical effect is always better.

That was my understanding too, but I phrased it like I did lest there be exceptions unknown to me.

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Publicly available genotype data?
I am a statistician and I'd like to test my new method on biological data. For this I am looking for genotype data for a number of individuals. That is, I am looking for something like this:

                    | Individual 1 | Individual 2 | Individual 3 | Individual 4 | ....
Chromosome 1 SNP 1  | AA           | BA           | AB           | BB           |
Chromosome 1 SNP 2  | AB           | AA           | AB           | BA           |
Chromosome 2 SNP 1  | BB           | AB           | BB           | AB           |
etc.

I don't really care about the species. Ideally I'd like to have data for complex and less complex genotypes (different number of chromosomes and number of SNP's).
Are there any publicly available data sets like this? I have been searching the internet, but I can't find any.

that's the stated purpose of the thousand genomes project.
the thousand genomes project has.. 1000 genomes.
its all downloadable.
http://www.1000genomes.org/

How about the allele frequency database?
http://alfred.med.yale.edu/alfred/index.asp
One of the main problems with SNP databases is that there are a lot of them so you can get lost quickly. This sight gives some overview on the available resources:
http://www.humgen.nl/SNP_databases.html
Hope this helps.

There is a vast amount of genotype data available at VectorBase's population biology browser, it is a database of insects which behave according to many mathematical assumptions - e.g. the non-overlapping discrete generations and homogeneous mating landscape.


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Meiosis pairing of chromosomes
How do the X and Y chromosomes synapse during the zygotene stage of when they have almost no homology between them?

There is 'homology' at the pseudo-autosomal region, a recombining region of the X and Y chromosomes.


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Behaviour of chromosomes and genes
I recently read a comparison between behaviour of chromosomes and genes - which had two statements understated -

Independent pairs segregate independently of each other
One pair segregates independently of another pair

I further found that the first one indicates segregation pattern of gene and the second accounts for chromosome.
But that bothers me, I am unable to compare chromosome and gene on this basis. I feel the two statements really confusing and it appears to me that both the statements apply both to chromosomes and genes.
Though, law of segregation for genes includes one pair of genes that segregate independently of each other but independent pairs too segregate independently of other pairs. As genes are present on chromosomes, what then defines their segregation differently.
Also, what does segregation of chromosomes imply? Does it include separation of sister chromatids in anaphase of meiosis as well as mitosis or separation of bivalents also during meiosis?
Is the question biased on independent assortment more than segregation pattern, please do correct me.
Those doubts appear absurd to me, but I hope that someone would help me, please.

Direct quote, please!
Please, when you are referring to something you've read, always add a link and attempt to offer direct quote. From your question it is a little hard to understand what is the original claim about. I suspect the following will help you though.
First, definitions
First, you might want to make sure, you know the definitions of

allele
locus

Segregation and recombination
There are two concepts you shall examine. Segregation and Recombination
Segregation
Segregation is the process by which hommologous chromosomes are independently separated into different cells during meiosis. The concept of segregation was first discovered by Mendel and expressed in his law of segregation

The Law of Segregation states that every individual organism contains two alleles for each trait, and that these alleles segregate (separate) during meiosis such that each gamete contains only one of the alleles.

Note that this law is partially (or mainly) wrong as it assumes that each phenotypic trait is affected only by a single locus with two alleles which is actually very rare.
Recombination
I am here describing recombination by its effects and by relating it to segregation. Recombination is the process that causes genes phyiscally linked on the same chromosome to not segregate entirely together. Recombination is caused by chromosomal cross-over, which are "recombination" between the "content" of the two homologous chromosomes. When chromosome segregate, it is actually the recombined chromosomes that segregate (in terms of the molecular machinery both process of segregation and recombination happen very much at the same time actually).
The concept of recombination has been discovered by Morgan with his fruit flies experiments. The Morgan is actually used today as a unit of recombination distance between two loci.
Source of information
You can have a look at any intro course to genetic such as these courses by Khan Academy for example.

Sorry for not providing link. I would try adding link next times.

@VidhiGupta No worries. We all go through the phase of learning to ask very good questions.

Definitely. This one is just the second question I have asked on this site and I am actually happy about it. Hope I would get an answer to my queries or maybe some more queries...

The difference is:

Different chromosomes always segregate independently
Different genes may or may not segregate independently

There are different mechanisms at work. The chromosomal segregation mechanism always separate chromosomes randomly (independently), as whole chromosomes are moved as a unit.
A different mechanism causes segregation of genes that reside on the same chromosome. It sends only large pieces of the chromosome to different daughter cells.  Each piece contains many genes, so within a piece, the genes don't separate at all, so do do not segregate independently.
When two genes are on different chromosomes, they segregate independently because their chromosomes segregate independently.  When two genes are on the same chromosome, they do not segregate independently since they may end up on the same segregating piece of their chromosome.

what about chromatid separation? Don't they segregate independently from each other.


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Identification of Bug/Insect (with picture)

What is this insect?
I’ve seen a lot of them indoors. The most distinctive characteristic is that single, orange dot in the middle of the back. The picture was taken in Louisiana, USA.

Further information: I’m currently located in Louisiana. I’ve seen a lot of them indoors and they’re quite small if you can see from the comparison to the baking soda box.

What is the approximative size in standard units (not everybody is used to the size of Arm Hammer baking soda box)? Can you get a better picture (a better view of the thorax may help)?

I'll try to get a better picture. They're quite small. This one was by far the largest at probably around a centimeter long. All the others I've seen were a fraction of the size.

It is a cockroach, probably a German cockroach nymph.
Cockroaches are well-known pests. According to the Wikipedia link above, there are about 4600 species of cockroaches, 30 of them are associated with human habitats. Cockroaches are extremely resistant and are able to survive in a wide range of environmental conditions.

@PhysicalFatness pointed out that German cockroach nymphs look very much like your picture and it is likely the species that you've found. Don't be fooled by its name German cockroaches are found all over the world, not only in Germany.

You actually may be right. https://citybugs.tamu.edu/blatella-nymph/ It looks a lot like a German cockroach nymph.


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Optimization of Signal Peptides
We are looking at modifying the signal peptide of a receptor in a common immortalized human cell line.  The cell line already expresses an unusually high amount of the protein, but much of it is not surface expressed.
When we compared the sequence of the signal peptide in the cell line (in this specific case the first 19AA), we found 2 mutations vs the wild type (WT) sequence.  One obvious idea, which we will do, is to restore the peptide to the WT version.
But I've been curious about options that increase trafficking to the plasma membrane over WT.  When I've looked up groups that have actually done this, it's normally been with large screens against every possible mutation in the signal peptide.
Are there targeted approaches to choosing a small number of signal peptides to increase surface expression?
I'm playing around with swapping it out some viral peptides that are totally unrelated to see if we can get increased expression with a receptor that's still (semi) functional.

Is there any evidence for the idea that the signal sequence is the cause of the lack of surface expression? Do you know where the rest of the protein (not at the surface) actually is located?

From staining it seems to mostly be diffuse through out the cytoplasm, not really in puncta as I would have thought from miss-folding.  We also know that what is surface expressed is functional.

Further I'm interested in the general case if there is one, type-I transmembrane proteins if a type is needed.  I will say that interested in any particular modification, even if it's a signal peptide not found in the host (eg viral).  I'm trying to get my tech transfer guys to clear me asking about the specific protein.

I don't have an answer to the question but I'm intrigued by the problem. Do the mutations look like they might affect SP function? Meanwhile here is a paper on overall design principles that you may not have seen. It's old, but it's by G von Heijne.

@AlanBoyd Any von Heijne is worth reading regardless of application. That was the main source that lead me to ask the question.

Also, the mutation is a serine mutation so I think it probably changes things

You could upregulate the transcription of the receptor gene you are interested in. More receptors being produced = more receptors being expressed on the cell's surface.


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How do I tell whether a mass spectrum was made with ESI or MALDI?
I was working through a previous exam and came across the following question (with reference to the picture shown below):

"What MS ionization method was employed (MALDI or ESI)?"

I cannot seem to find the answer, so I'm guessing it is not possible to tell, but if there is a way to see which one was used, please enlighten me.

It is probably ESI because, as already mentioned, ESI produces multiply charged precursors while Maldi would generally produce fewer charge states and +1 most frequently. But, you can not say that MALDI wont give  multiply charged ions. So from just this picture you can not say for certain but can only make a guess.

I am not an expert in this topic but from what I have heard ESI generates multiply charged ions but MALDI usually does't. It is possible to find multiply charged species in the spectrum.

They all have a charge of four it seems to me? (Assume one Da mass difference, and then divide by .25, the m/z difference.) Is that how you are able to tell it comes from ESI, namely that they have a charge of four, not one? If you confirm I will upvote and accept your answer.

I was not actually looking at the spectrum that you attached.. I answered that in general ESi produces multiply charged ions. But when you commented, I noticed the spectrum and it seems that these are +4 charged ions of different molecules/peptides. Nothing else fits that neatly

This is the isotopic cluster of an ion, so chemically it should be of one kind of molecule/peptide and not multiple. Yes the analyte is in a charge state of 4, so most likely it would come from a an ESI.


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How does the composition of blood cell types in human blood change during our lifetimes?
I was reading the paper Age-related accrual of methylomic variability is linked to fundamental ageing mechanisms.
There they do additional checks to see that their results are not due to differing cell type composition in blood that happens as we age.
That made me wonder, how does the cell type composition of our blood change as we age? Is it known? (I guess we would get less hematopoietic stem cells, but I do not think they are in the blood themselves.)


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Among xerophyte plants, which one grow faster and consume water the least?
In an effort to select for the most suitable plants to possibly colonise desert and stop its expansion,
what would be the xerophyte plants that grow the faster and expand on surface, while using the less water and produce a maximum of biomass?

I don't think that there has been a comparison done among xerophytes as to which one grows fastest and which one the slowest. A list of fast growing trees can be found here and here.

Allan Savory recommends carefully managing grazing animals to promote grass growth. While his methods have been criticized, it hasn't seemed to damage our farm, where we raise cattle through intensively managed grazing, but our land isn't subject to desertification. I doubt you could solve desertification with a monoculture of xerophytes though.


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Are there anatomical differences between male and female mammal brains before action of hormones?
is there any evidences of these differences during development stages prior to hormone driven sexual differentiation? mice studies ?

Yes. Dewing et al. (20030 found that gene expression in mouse brains differs between male and female mice about 10.5 days after the mice had sex. This occurs before hormonal contributions to brain development. They identified about 35 genes that were appeared to show preferential expression in the female brain and another 16 that appeared to be show preferential expression in the male brain. Most of the genes identified were transcriptional regulators, signaling molecules, or involved with cellular differentiation. Of these 51, three were verified as showing female bias, and two of these were located on the X chromosome. Four genes were verified showing male bias, and two of these were located on the Y chromosome.
Similar results were found by Xu et al. (2002). They identified several of the same genes as Dewing et al., plus others that were linked to the sex chromosomes. They identified a total of six genes on the X chromosome that showed strong female expression bias during brain development. At least three of the genes were homologous between the X and Y chromosomes but showed different expression patterns between male and female brains at different stages of development.
The differences in genetic expression may cause some microscopic anatomical differences during brain development that is not explained by hormones (Bocklandt and Vilain 2007). They reviewed several studies that found differences in neuron growth, and density of vasopressin fibers in the lateral septum were more likely to be due to genetic expression than to hormonal expression. Bocklandt and Vilain did not identify the specific ages of the mice that showed these apparently gene-regulated differences but it is reasonable to speculate that these differences begin to appear in association with the differential gene expression.  Bocklandt and Vilain did not identify macroscopic differences between male and female brains prior to hormonal expression.

Citations
Bockland, S. and E. Vilain. 2007. Sex differences in brain and behavior: Hormones versus genes. pgs 245-266. In: Genetics of sexual differentiation and sexually dimorphic behaviors (D. Yamamoto, ed.). Academic Press.
Dewing, P. et al. 2003. Sexually dimorphic gene expression in mouse brain precedes gonadal differentiation. Molecular Brain Research 118: 82-90.
Xu, J. et al. 2002. Sex differences in sex chromosome gene expression in mouse brain. Human Molecular Genetics 11: 1409-1419.

interesting ! differences in gene expression but anatomical?

@Matoeil I've updated my answer to include what info I could find.


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Recommendations for textbooks on statistical and quantitative genetics, and genetic epidemiology
I'm looking for a textbook on statistical genetics, quantitative genetics, association mapping, and genetic epidemiology. My interests include, but are not limited to, complex trait analysis, and the mathematical and statistical aspects of these subjects.
I've found a lot of books, below are some that I'm considering:

"Genetics and Analysis of Quantitative Traits" by M. Lynch et al. (amazon link)
"Introduction to Quantitative Genetics" by D. Falconer et al. (amazon link)
"Statistical Genetics: Gene Mapping Through Linkage and Association" by B. Neale et al. (amazon link)
"Statistical Genetics of Quantitative Traits: Linkage, Maps and QTL" by R. Wu et al. (amazon link)

I haven't found anyone else posting this question. There are discussions about population genetics textbooks, but these books have limited information about quantitative genetics, etc.
If anyone has a favorite book, comments about the books above, or anything, I would greatly appreciate it.
Thanks in advance.
EDIT:
Another promising book:

"The Statistics of Gene Mapping" by D. O Siegmund (amazon link)

Related: Books on population or evolutionary genetics?


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Is this a bacterial colony?
On the physics StackExchange site people are trying to figure how and why these branching structures formed. The two questions can be found here and here. The latter had no cooling fans and was situated in an unventilated cupboard. There are many processes that could explain such structures without them being a bacterial colony, for example by Diffusion-limited-aggregation as explained in my answer here. To me it looks like this could be a bacterial colony. Is there any way to rule this out or say with precision that this is a bacterial colony?
I think some organic material and humidity could latch on to the irregular edges upon which bacteria could then grow in a warm environment.

What ways are there to tell from just a picture if this is a bacterial colony or  not?
What ways are there to tell if this is a bacterial colony or not if you have the structure at hand?
What ways are there to rule out or say that this is some kind of fungus or living thing if you have the structure at hand?

The second pic was taken by Wossname:

"the equipment is in a temperate climate in a non-aircon area of an
  office building near the external door. In high summer it would get to
  probably 40 Celcius and 85% or more relative humidity in my
  estimation. It's an area of the building that people most definitely
  don't loiter in during July/August. :)"

Unlikely to be living bacteria or other microorganisms as the environment is dusty plastic with moving air, so moisture would be at very low levels, probably too low to support bacteria.

@mgkrebbs In the image below there was no cooling fan or real airflow. It could have been humid and warm. Some organic material and humidity could have accumulated along the irregularities upon which bacteria could grow.

If it is a microbial colony indeed, I'd say it looks like a fungus rather than a bacterial colony. Not sure it's really a living thing though

@macco, the second pic was taken by me, the equipment is in a temperate climate in a non-aircon area of an office building near the external door.  In high summer it would get to probably 40 Celcius and 85% or more relative humidity in my estimation.  It's an area of the building that people most definitely don't loiter in during July/August. :)

looks crystalline to me

Microbiologist here, I agree with @Flo's comment. These do not look like bacterial colonies to me, the morphology is way too unusual. If anything they more resemble fungal colonies. However, I have my doubts  as to whether these structures are caused by living organisms. Have you got some microbiology guys at your institution? You could inoculate some agar plates with a small sample and see if something grows?

Just scrape some material off and get it sequenced.

These look like crystallization structures when liquids dry up. But if it were to be a living thing, I'd go with fungal colonies. In my opinion, the best methods to tell is to scrape off a small piece, flood with KOH, and observe under a microscope, if you see filaments then it is definitely a fungus, and alternatively you can inoculate an agar (Sabouraud agar could work, or LB agar) to see if something grows. If its a fungus, it can take from 4 days up to 3 weeks to grow depending on the species and the growth conditions provided.
Good luck.
Here's a ref that might help you.
Microscopic potassium hydroxide preparation:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3994805/


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Curious about Brazzein
What is in compound "Brazzein" that it makes it 2000 times more sweeter than sugar?
Can anyone please explain the science behind it?

Does someone care to answer?

If you are pressing people, nobody will care to answer. A common thing here is that we expect people asking questions to try and find out the answer first and then explain in their questions what they already know or at least what they tried to find an answer. This is a stack exchange site, not google.

@skymninge I know that but at least they should initiate something!

No, actually what I meant to say is that it is you who should initiate something.

Brazzein is not even a sugar - its a protein that comes from Oubli, a West African climbing plant.
While I think nearly every living thing from bacteria up to large animals can perceive some carbohydrates as a food source, the mechanisms vary over the tree of life.
Because of this the taste of sweetness in animals varies a lot.  Aspartame, a non carbohydrate sweetener does not register as sweet in all the primates.  Brazzein and aspartame as capable of activating one or more of the human taste receptors.  Receptors are just proteins which sense a stimulus.  They can be activated by other compounds - this is how most pharmaceuticals work.  Sweeteners which are not glucose/sucrose can bind more tightly or affect the structure of the receptors, causing them to send a sweetness signal. Often these compounds also register with other sense receptors and so the sweetness is accompanied by other tastes as well.  It sounds like Brazzein is a clean taste, less likely to have such side effects.
I've not dug fully into this - its clear that some human sweetness receptors are known, but I'm not sure they are all known.


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What is the close and related genome used for in Gene models?
all
I am a little bit confused about using the related genome or reference genome.
When we have a reference genome, we can do alignment. Also we can do the assembly.
Can you give some more reason why a related genome can help to improve gene model ?
And if we do use a related genome, what kind of problems or caveats may occur there ?

can you please be more specific, like what species you have in mind and if you are talking about RNA or DNA?

Why a related genome helps:
1) Alignment of the reads first and assemble next.
 2) The gene-space is already predefined ( the genes and their co-ordinates are already known), so if your assembly is fragmented or missing a portion of the gene information, that can be accomodated with reference genome.
Limitations: Rather than assembling your own genome, you are forcing the reference genome to be part of your genome assembly. If at all, any differences are there, they are washed out, when you do a reference assembly.


text:
Can plants survive indefinitely without external supply of gases at compensation point?
During photosynthesis, there is a point at which the light intensity is such that the rate of photosynthesis exactly matches the rate of respiration called the compensation point. What this means is that the plant can essentially utilize the $\ce{CO_2}$ produced during respiration for photosynthesis and the $\ce{O_2}$ produced during photosynthesis for respiration. But, does this mean, that a plant which has been given an initial supply of $\ce{CO_2}$ and $\ce{O_2}$ and then subsequently put into another gas (still in compensation point light intensity), say nitrogen, can survive indefinitely? (or as long as it's life span).

If the plant is growing the system will fall out of equilibrium due to more carbon going into biomass than oxygen.

Another concern might be that depending on how much neutral nitrogen there is, the oxygen/CO2 might diffuse into the nitrogen, lowering the available amount.


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What evolutionary advantage do viruses have in host specificity?
Warning: I have almost no knowledge of biology past the high school level.
Viruses generally have three components: the DNA, the virus protein coat, and an outer membrane "decorated" with these surface marker glycoproteins. I am thinking that a virus would want to infect as many hosts as possible, so that it would reproduce as much as possible, why would a virus just infect one group of organisms.
What evolutionary advantage do viruses have in host specificity?

Tell me if there are issues with this question, I will reply as soon as possible

It is true for any living creature, that it would be great for it if it could thrive in all environments. Any creature would do better if it had a greater ecological niche while remaining as competitive in each of these niches. However, competition, predation and other biotic and abiotic factors lead species to specialize in specific niches. Of course, some species are more generalist and some are more specialist but I won't go into these details.
When it comes to parasites, such as viruses, the story is the same. A host is an environment. Being less specific would be great but the immune system is no easy detail to get around. Viruses are often quite specific to a given species, just because it evolved to be efficient for a given host but tend not to be that efficient in other hosts.
Note that parasites are not only species specific but also often tissue specific and specific to the specifics genetics of the host (e.g. malaria).
Somewhat related posts:

Why do parasites sometimes kill their hosts?
Why aren't all infections immune-system resistant?

Thank you @DeNovo for helpful comment

Good answer. I'd note that, not only are viruses often specific to a given species, they're often quite tissue specific.  I think there are several Q/A pairs that may relate to this question. The one you linked, and also this, though asked about bacteria. The basic question (why doesn't some group of organisms just take over everything everywhere) is very similar.

Thank you! Helps the day before my bio test ;)

I would more specifically address the advantage/benefit, in that even though a virus may be host specific (or not, since it really doesn't matter in terms of gain), even the most virulent of viruses throughout history have not killed off entire species, save the 'virus' of being man (whole other story), yet for some reason some within a species survive! They may have a specific protein, are a carrier - the list is long and not entirely understood. In any case, they often handoff whatever adaptable mutation they have to their offspring, thereby making them immune to such viruses. Survival of the fittest?

Viruses infect a cell via a receptor. Without the specific receptor infection is not possible. A virus will mutate to enter a cell via another receptor (HIV-2). So, I say viruses are receptor specific.


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How is a substance classified as a vitamin?
From wikipedia

A vitamin is an organic compound and an essential nutrient that an organism requires in limited amounts.

There are many essential nutrients to an organism. Glucose for example. However, not all of them are classified as vitamins. Is there a clear, non-arbitrary definition of vitamin? If not, who decide what ought to be called a vitamin?

I completely rewrote your question. I removed one of the two questions (which you might want to ask on a separate post). I think the question is good but you already got a close vote but it needed a lot of reformatting and needed is scope to be reduced. Feel free to roll back if you don't like my edit.

@Remi.b  Hm, I posted an answer to the original two-part question just as you edited it.  If we keep the question in this new form, feel free to edit the answer ...

Thanks for changing my question. I'm not native English people, so my english skill is not up to scratch. Before edited, I asked two questiom - 1. Why vitamin D is classfied even it can be naturally synthesized.

And Why vitamin A B C D E K are classified and named as 'Vitamine'

1) Vitamin D is a bit of an umbrella term that actually refers to a whole group of related molecules. One of these, vitamin D$_3$ (cholecalciferol) is formed spontaneously from ergosterol in the presence of UV radiation, which happens in the skin when exposed to sunlight. Cholecalciferol is then converted to calcitriol, the active form, in the liver. Here is some information on the metabolic pathway.
2) Actually, if you consider the definition carefully, only a few molecules are essential for human growth and nutrition, in the sense that they cannot be replaced with something else, and are required in small amounts. For example, the majority of amino acids can be synthesized by the body from other amino acids, and are therefore nonessential. The remaining amino acids are essential nutrients because there is no synthesis pathway -- but they are required in large amounts and not considered vitamins. This distinction between "large" and "small" might sound strange, but it is important since it tells you if the nutrient is consumed for energy/growth (like amino acids) or has some "supporting" role, such as antioxidants, cofactors for enzymes, or hormones (like the vitamins).
That said, it is sometimes a bit fuzzy if a nutrient is essential or not. Vitamin D is a borderline case: it should perhaps not be called a vitamin, since it can in fact be synthesized by most adults in adequate amounts. However, vitamin D deficiency can occur if one does not get enough exposure to sunlight, and this can cause the disease rickets. Some researchers have suggested that this is one factor behind evolution of lighter skin in northern human populations, since dark skin pigment reduces UV radiation needed for vitamin D synthesis.

Thanks for your answer.I usally takes some supplements for my immune system  and I wonder why some supplements are not classified as Vitamine - Especially Coenzyme Q10 and Omega-3-fatty acid. Your answer give me more clear view than my thoughts.

You're welcome! Btw, coenzyme Q10 is not an essential nutrient; omega-3 fatty acids are essential, but not considered vitamins since they are required in larger amounts.

Please keep reading the Wikipedia article, it clarifies substantially in the next several lines, for example (emphasis mine):

An organic chemical compound (or related set of compounds) is called a vitamin when the organism cannot synthesize the compound in sufficient quantities, and it must be obtained through the diet

and also:

By convention the term vitamin does not include other essential nutrients, such as dietary minerals, essential fatty acids and essential amino acids

Glucose, as an example, is something that is both used in relatively large quantities by humans, and can be synthesized by humans (from carbohydrates and other energy sources).

Wikipedia actually has a really good definition of an essential nutrient:

An essential nutrient is a nutrient required for normal physiological function that cannot be synthesized by the body, and thus must be obtained from a dietary source. Apart from water, which is universally required for the maintenance of homeostasis, essential nutrients are indispensable for the metabolic processes of cells, as well as the proper physiological functions of tissues and organs. In the case of humans, there are nine amino acids, two fatty acids, thirteen vitamins and fifteen minerals that are considered essential nutrients.

For vitamins, this appears to be a definition by exclusion: everything that is an essential nutrient but not a mineral, amino acid or fatty acid is considered a vitamin. Specifically:

Vitamins are organic molecules essential for an organism that are not classified as amino acids or fatty acids. They commonly function as enzymatic cofactors, metabolic regulators or antioxidants. Humans require thirteen vitamins in their diet, most of which are actually groups of related molecules (e.g. vitamin E includes tocopherols and tocotrienols).

I think the reason why food like glucose is excluded from this list is because no particular form of food is necessary in and of itself: as long as you're consuming carbohydrate or fatty acid, the human body can produce energy through carbohydrate catabolism or fatty acid catabolism. So it isn't one particular nutrient that's necessary, just "anything that can be used as an energy source".


text:
Where does Darwin state his "principle of multiple utility"?
I have never heard of Darwin's 'principle of multiple utility', but several papers refer to it. For example, from Darwin at the molecular scale: selection and variance in electron tunnelling proteins including cytochrome c oxidase

Such a high degree of conservation is probably the consequence of many parallel and concurrent aspects allied to the construction, manifold functions and demolition of cytochrome c oxidase as illustrated in the molecular scale view of Darwin's principle of multiple utility (Darwin 1872) shown in figure 7.

Also, from the pape, Engineering enzymes.

Another source of biological complexity arises from Darwin’s principle of multiple utility. The principle originally applied to organisms recognizes that any one trait in an organism is subject to be selected by multiple forces.

The citation to "On the Origin of Species" in these paper provides no page numbers. Neither do any of the other papers that mention the principle. I searched the sixth edition of "On the Origin of Species" for terms such as utility, multiple, roles, etc., but found nothing that sounds like such a principle.
It seems to me that anything described as a Darwinian principle would be extensively discussed in the literature. That does not seem to be the case with this so-called 'principle of multiple utility'.

I also can't find anything specific from Darwin himself. The phrase is used in a number of places, but almost always by the same two authors (Dutton and Moser), who invariably refer unhelpfully to (Darwin, 1872). A couple of other papers use the phrase and cite Dutton and Moser. I believe that this is a paraphrase that D&M came up with, not an actual principle that Darwin spelled out.

I agree with @iayork, and the earliest reference I found was in 1991 with no citation to anything. Origin does talk about biological complexity, and specifically has explanations for why we should not expect all life to be "complex" (according to a particular definition of complexity), but if Darwin talks about the multiple utilities of a particular trait that must be in later work, not in Origin.

I agree with both of you, @iayork and Bryan Krause, that Dutton appears to have coined the term 'principle of multiple utility'. Accordingly, I emailed him to ask for a more precise citation to Origin of Species.

@Nick Gall It would be great if, once you receive Dutton's answer to your email, you could report his answer here! Thanks

@Remi.b Absolutely, with his permission of course.

I heard back from Prof. Dutton and Prof. Moser, who referenced the principle in their joint paper. Here is the gist of their response. Basically, they claim to have gotten the principle George McLendon.

I wrote to Prof. McLendon. This is the gist of my question to him. Basically, I think Wallace's "principle of utility" mutated into the "principle of multiple utility".

I just checked my copy of The Origin of Species and it's been released in 1859. The book Darwin released in 1872 was The Expression of Emotions in Man and Animals, so I would assume that's the book they refer to - maybe they mixed up the reference. Unfortunately, I have not read it, but that might be worth to check out.

The 6th edition was published in 1872 as The Origin of Species.


text:
Does the amplitude of action potentials vary among species?
I would like to ask if the amplitude of action potential in animals(for example zebra finch or other bird) differs from the amplitude of action potential in humans which is approximately 70mV.


text:
Efficacy of sonic kangaroo deterrents
Bender (2003) tested the efficacy of sonic kangaroo deterrents. Their device is static (and apparently ineffective).
Has there been any rigorous testing of the whistle-like 'kangaroo deterrent' devices fitted to the front of vehicles?


text:
Dimensional analysis Question
So I'm new to the dimensional analysis world and I'm little confused and the answers I'm getting are not convincing :(
if the concentration of hemoglobin in a 5ml sample of blood is 34 g/dL. and red blood cells are 31.45 hemoglobin, what is the mass of red blood cells in the sample?
So.. any thoughts on how to do it?
Thank you so much

It doesn't seem like you need the 31.45 hemoglobin number (which is good because no units are given:
5ml * 34g rbc /dL * 1 dL/ 100 ml = 1.7 g rbc
would fall out from unit analysis

Thank you!! hemoglobin's unit is percentage. 31.45% so should i just multiply your number it with that?

Shigeta's equation should have used "hgb" instead of "rbc".  To turn 1.7g hgb into rbc, you multiply it by the .3145 hgb/rbc value. Note the dimensional units work out.


text:
How much of your stock solution should you take to make the 1000 cells/mL mixture?
You need a solution containing 1000 buccal cells/mL. You count that you have 125 buccal cells in 50uL, from a total solution of 8 mL. How much of your stock solution should you take to make the 1000 cells/mL mixture? How much solvent if you would like a total volume of 5mL?
I don't even know how to approach this!!!
Help??

You should try to find the concentration of your stock solution which contains the same amount of cells as required and then dilute it. Have you tried anything yet?

welcome to cell culture & dimensional analysis
125/50µl or 2.5 cells/µl is your concentration (better way of expressing it)
2.5 * 8000µl = 20,000 total cells you have. 1000µl in 1ml that's why the 8000µl
20,000 cells / 1000 cells/ml = 20mls final culture volume to reach desired concentration
20mls - 8mls = 12mls   so you need to add 12mls of medium / saline / whatever to your 8mls to dilute it to the correct concentration.
when you ask about solvent to ADD to make 5mls. Prob with this question is you don't state the desired concentration. So assuming its still 1000 cells/ml kinda go backwards,
1000 cells/ml * 5mls = 5000 cells is what you want to get
to get it:
5000 / 2.5 cells/µl = 2000µl or 2mls of your culture.
So take 2mls of your culture and mix it with 3mls of solvent / medium  (5mls - 2mls).
I'm quite certain chris below is not correct.

OMG! You should be a teacher!!
It's crystal clear now!
I'm in love with this answer :)
Thank you very much. I wish you luck and success
I sincerely do

Oh, come on, thats simple math.
First calculate how many cells you have per ml: 50$\mu$l are $\frac{1}{20}$ of 1 ml. So multiply 125 with 20 to get the concentration per ml: $125 \times 20 = 2500 \frac{cells}{ml}$
If you want to know how many cells you have in total, multiply by 8 (for the 8ml you have) and you come to 20.000 cells in your 8ml solution.
When you want to know, how much of your solution you need, you calculate: $\frac{2500 \frac{cells}{ml}}{1000 cells} = \frac{1 ml}{x}$.
This can be transformed into $x = \frac{1}{2,5} ml = 400 \mu l$.
So you need 400 $\mu$l for each ml of your final cell solution. So if you want to have 5ml with 1000 cells/ml you need $5 \times 400 \mu l = 2000 \mu l = 2 ml$ of your cell solution. To reach 5 ml add 3 ml of your solvent/media.


text:
Transportation of bacteria
I would like to take an apparatus containing bacteria to another country (Bolivia) from the U.S.. How do I determine whether I am allowed to do this?
The bacteria are:
http://www.atcc.org/Products/All/49787.aspx,
http://www.atcc.org/Products/All/53774.aspx,
http://www.atcc.org/Products/All/51573.aspx,
http://www.atcc.org/Products/All/700550.aspx
Also... What is the best way of transporting bacteria from one country to another?

there are some regulations w.r.t pathogenic strains.. you have to get a certificate issued that says that the sample that you are carrying is non-pathogenic non-hazardous etc

@WYSIWYG Can you give me the contact information of someone who could help me with that?

it depends on the laws of different governments. Ask someone in the customs.

Please go through this link http://www.dehs.umn.edu/bio_pracprin_std_ship_guide.htm and this pdf ( www.ncsu.edu/ehs/dot/Bio_shipping.pdf ). Since all of the microbes are Biosafety level 1, you shouldn't have much problems.

@okarin  That's actually bad advise.  I would actually recommend that you ship them ahead of yourself.  Not al microbes are Biosafety level 1, and their BSL level is not actually what is considered (risk level by CDC in the US, IATA has set standards as well).  You need to determine if your bacteria are UN2814, UN2900, or UN3373.  IF they are not pathogenic (not just to humans, but animals) but are GMO then they will be UN3245. Remember dry ice by itself is considered a hazardous material.  Post specifically what you're moving and I'll give you an answer.

@TheLastWord That's a good link to what needs to be covered, but your later comment is not entirely correct, and might cause confusion as BSL is not directly correlated with Risk Group Classification

@AtlLED What do you mean by post specifically what you're moving? Is there information that you need other than the names of the bacteria?

@okarin names of the bacteria, are they GMO (transformed with a plasmid counts unfortunately), the transport media, and transport temp.  Ie. NEB 10b's transformed with HIV-env in a glycerol stock transported on dry-ice.


text:
Buy bacteria for experiment?
Where can I buy paracoccus denitrificans? I need it for an experiment. I cannot find online where I can purchase this.

ATCC- you can get most bacterial strains and cell lines there.
Find P. denitrificans here:
www.atcc.org/products/all/13543.aspx

You said see this but didn't link to anything. Did you mean to include a link?

yep.. it didnt work.. see the edit

Sorry about that. I have accepted it.


text:
Over what range do Thyroid Stimulating Hormone (TSH) levels tend to fluctuate over the course of a day?
I understand that the majority of doctors consider the TSH test "the gold standard" for measuring thyroid function (examples stating that literally are here and here).
The reference range for what is a healthy TSH is under debate, but no matter what range is considered there tends to be a proportionately large difference between the top and bottom (eg 0.3 to 3.0 μIU/mL).
However I've never seen anything indicating over what range TSH varies over the course of a day, or a few days. It's also unclear as to how much error there tends to be with a test result, even if tested from the same sample.
How much fluctuation in a TSH result is normal over the course of a day?

I wrote an answer about the circadian rhythm of TSH for a question over on Health.SE: How does one's TSH tend to vary over the course of a day. That answer also has some information on how this is different in people with hyperthyroidism and hypothyroidism.
The paper Physiological variations in thyroid hormones: physiological and pathophysiological considerations has a section on circadian and seasonal rhythm and a table with some values. Quoting from the paper:

There is a clear circadian variation in circulating TSH concentrations in animals and in humans. TSH concentrations are low during the daytime, increase in the evening, and peak shortly before sleep.  Amounts decline slowly during sleep. Table 3 summarizes studies of mean, nadir, and peak serum

This is table 3:

A chart is available in figure 2 of the paper Modulation of Endocrine Function by Sleep-Wake Homeostasis and Circadian Rhythmicity
As for test error, it's important to note that TSH itself is not used for or at least should not be used for diagnosis of Hypothyroidism and hyperthyroidism. T3 and especially T4 need to be measured.

Heh, only now do I realise that it was actually you asking the question on Health.SE. Oh well, maybe it also helps someone here :-)


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Identification of a beetle found in a basement in Virginia, USA

Beetle found in basement in Alexandria, VA, USA
Approximately 5cm (2 inches) in length.

That is a female Eastern Hercules beetle. Dynastes tityus https://bugguide.net/node/view/4462 Family Scarabaeidae, Subfamily Dynastinae. One of the largest of the beetles in the South-East U.S.


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Help identifying a moth
It looks like it might be an emerald moth but its hard to tell from the discoloration in the wings and it is too high up for me to get a better look.
When: July 23rd 2018
Where: Central Illinois

It looks like an Imperial Moth (Eacles imperialis):

Source: https://www.butterfliesandmoths.org/species/Eacles-imperialis
As shown on the distribution map at this link, they can be found in central Illinois.


text:
Book-recommendation: Ethology
I am looking for a book that covers the following topics in ethology:

Behaviour

Sensory filtering, reponsive-ness, sign stimuli, learning and memory, instinct, habituation, conditioning, imprinting.

Role of hormones in drive

role of pheromones in alarm spreading; crypsis, predator detection, predator tactics, social hierarchies in primates, social organization in insects.

Navigation and Biological Rythms

Orientation, navigation, homing, biological rhythms, biological clock, tidal, seasonal and circadian rhythms.

Methodology

Methods for studying animal behaviour including sexual conflict, selfishness, kinship and altruism.

Do you have any suggestions?

Hope you don't mind that I edited your question. I think it looks better like this and will attract more attention and better answers. Good design is essential for a good communication. There is probably still room for improving your question if you want to give a try.

Thanks a lot I will take care in the future for he same.

I can suggest three books, none of them cover all those aspects, though:
1) The Foundations of Ethology, Konrad Lorenz. The best introduction I know for the field of ethology. Lorenz is called by some "the father of ethology".
2) Sociobiology: The New Synthesis, Edward Wilson. The deepest study of animal societies I know of.
3) Evolutionary Ecology, Eric Pianka. If my memory is right, it says something about the Navigation and Biological Rythms part.


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What were the main discoveries in Biology?
What were the greatest achievements in Biology? Can you please provide a short list of discoveries that you would consider as being the most important discoveries of the history of Biology.

I edited the post to match my answer (as I misread the question to start with). The post is now on-topic I think and I am voting to reopen.

Here are a few things coming to my mind

Discovery of cells by Robert Hook
Discovery of bacteria by Antonie Philips van Leeuwenhoek
Discovery of antibiotics by Alexander Flemming
The basis of heredity by Gregor Mendel
Evolution (On the origin of species by C. Darwin)
Watson and Crick discovery of DNA structure
Vaccination
The concept of ecosystem

yes they were incredible :D but i meant UN discovered things in biology which would be awesome :)

OP says would be, not what were

It always amazes me that a Canadian like you has trouble with these things, being so 'close' to the US. I have to visit Canada some day to pick up the flavor of it. Nonetheless, nice list +1 I would even recommend editing the question in line with your interpretation, because your interpretation is less pob (but still is), while the original question is definitely going to be closed.

@Christiaan I definitely misread the post indeed. I edited the post as you invited me to do. I feel quite proud when you call me "Canadian". In reality I have lived in Canada (Vancouver, BC) for the past 1.5 years but grew up in Switzerland.

That explains everything haha. Both very nice and interesting countries.  I'll vote to reopen. But it may still be pob...

@Christiaan Actually, in this context, the OP's would be is equivalent to what were. If you were to rephrase the "would be" expression, it could be something like "what would you consider to be some of the greatest achievements". People commonly use the two interchangeably in colloquial speech here in the US. Although if you want to to be technical about it, the OP 'should' have said "were", but this is SE Bio, anyway, not ELU :)

@AleksandrH - touche :)

Oh indeed! I like to think that this is why I understood the post the way I did. Thanks @AleksandrH

I don't understand the 2 down votes I received. Comments are welcome.


text:
Competition with other individuals of the same species vs. adaptation pressure from predators
It is often said "You don't need to outrun the cheetah, just the other gazelles", thus emphasizing that greater part of the adaptation pressure comes from competing with other individuals of the same species and not directly from predators/parasites (which are seen as more indirect forces similar to the living conditions imposed by the environment (climate, geophysical factors, etc.))
My question is:
Isn't there a difference between competing with other individuals of the same species for food, habitats (i.e. resources) and competing with them in avoiding being eaten?


text:
Why might food spoil faster in Ireland than the US?
An American is staying in my house for the summer and claims that food (specifically, bread and milk) spoils a lot faster here than at home in California. Is there a significant difference in chemical content (preservatives etc.), or other factors, that might explain this?

There are way too many factors that we can never consider for this kind of question.  Does California represent all of the US? What part of California?  What part of Ireland?  What's the humidity and average temperature of each region?  What are the agricultural and chemical preservative regulations?  Is it a matter of how you store the food in your homes?  The quality of your cooling method?  The way people in the household handle the food?  Too many variables.

@KeeganKeplinger, this seems like a good answer, to me – these are are "factors that might explain", which is what he asked for. Why not post it as an answer?

I would think added preservatives are the most likely candidate, for example, Azodicarbonamide is frequently added to bread in the US, but banned in Ireland and most of the rest of the EU. Since it has a preservative effect it is a reasonable candidate for a specific causal factor.
But as Keegan points out there are an awful lot of possible factors so it's impossible for us to say with any certainty.

Going to accept this answer because it tells me one potential reason that I didn't know before. I realise this question was a bit too open-ended and vague, but my knowledge of this stuff is rather limited.

There are more factors than we can ever consider.
As far as region: does California represent all of the US? What part of California?  What part of Ireland?  What's the humidity and average temperature of each region?  What are the agricultural regulations?
As far as cultural/methodical differences: how do you store the food in your homes? The quality of your cooling method? The way people in the household handle the food?

That's a fair point. I expected this answer because I didn't know how to specify the question. I appreciate the feedback.


text:
What is a zygote?
During fertilization, the nuclear membrane of the pro-nucleus of the ovum and sperm degenerate. Is the cell is stage called a zygote?
After the dissolution, mitosis occurs and two cells are formed.Or is the cell is stage called a zygote?
I'm confused as i knew a zygote was single-celled.

A soon as fertilization occur, the "thing" is called a zygote. It means that a zygote can be a single cell. I don't know where are your difficulties but you might appreciate checking the definitions of: Morula, Blastual, gamete, gametophyte, spermatophyte, plasmogamy, karyogamy. You will easily find all these informations on wikipedia. Did I answer your question ? Where you thinking about a specific species that have an unusual reproctive system like some fungi ?

Oups.... did I write can be a single cell. I'm sorry. It is a single cell. After division, it is no more a zygote.

Conventionally, a zygote is considered to be formed the moment that a spermatozoum, penetrates the cell membrane of the ovum and yields its genetic material into the ovum. Effectually, however, there is a lag between the instant of fertilization and the fusion of the male and female pronuclei. In mammals, the duration of this lag period is ~12 hours. There are also additional actions that must be completed before the first mitosis as in most mammals, including humans, the ovum is actually in the second metaphase of meiosis at the time of fertilization.


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How to parse SCOP parseable files PDB residue identifiers?
I am trying to parse the SCOP parseable files, specifically dir.des.scop.txt ver 1.75. But, I have been facing problems with the PDB residue identifiers in the file. This is a tab limited file and the PDB residue and chain identifier is the 6th column which. An example of this identifier is A:1-28,A:77-837 for domain d1kk8a2.  Hence forward I'll represent that as domain_id (pdb_id chain&range). This particular example is straightforward, which means the domain d1kk8a2 consists of residues 1-28 and 77-837 of chain A of the corresponding PDB entry 1kk8. But some of them are unintuitive and like d3ckra1 (3ckr A:-2-385), what does the negative entry for the start mean? And this example d2p83b1 (2p83 B:61P-385), there is a P in the range (61P-385).
If you go to pdb website and search for the corresponding entries, then go to the sequence tab, you will see the alignment of the PDB chain and the corresponding SCOP domains. The ranges shown there correspond to the entries in SCOP, but it is difficult to make sense of it. Can someone please explain or provide some pointers. Thank you.

PDB residues are described by the residue number and an insertion code. Residue numbers can be any number, including negative values. In 3CKR the first residue has nr. -6, followed by -5, etc. This might indicate that there are additional residues at the beginning of the sequence, relative to other PDB entries. In 2P83, the first residue has the number 61P. Take a look at https://lists.sdsc.edu/pipermail/pdb-l/2004-March/001513.html for an explanation why PDB residue numbers have insertion codes.

Thank you very much for the helpful answer. I would like to get the residue numbers associated with each PDB protein chain. I was able to get the sequences from this location ftp://ftp.wwpdb.org/pub/pdb/derived_data/, but I could not find the corresponding residue numbering.

I think you need to get a PDB file parser and parse the information out of there ...


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methods for targetted deletion of genomic regions?
I would like to know what are currently used methods for targeted deletion of genomic regions in mammalian organisms or cell lines. I have heard of Zinc-Finger nucleases as a recent genetic engineering method, but I don't know if there are other methods, more efficient or better tailored, for the deletion of specific regions.

please consider setting for an answer. thank you

I can only provide you with a few pointers from memory, as an ad hoc search for "review of dna cutting techniques" was not prolific.
Please consider the provided information with precaution and only for pointers to help you do literature research.

cre/lox system and variants (best known), belong to SSRs (Site specific recombinases)
various Restriction enzyme based systems (see Homing Endonucleases)
meganuclease based tools
aptamer based
based on hybridizing n-mer probes which yields a reactive species nicking the DNA at the probe's-site when introduced to certain chemicals such as oxoacids
light twizzers and lasers /purely proof of concept (perhaps already commercialized?)
ZFNs and variants / protein based-probes . http://en.wikipedia.org/wiki/Zinc_finger_nuclease

There are definitely published reviews on this exhaustive topic, notwithstanding the dozens of books.
I would estimate that there are at least 10 commercial methods, and almost 100 methods in total when theoretical and proof-of concepts are included.
Naturally (literally!), the vast majority of methods will be based on the noncovalent interaction of an n-mer "homing construct"/probe a)attached to an nuclease or b)an
attachment site for a nuclease or c)participate in the reaction for the formation of a reactive chemical species to break the sugar-phosphate backbone.
I would speculate that most other methods are likely not practical in terms of either efficiency and/or affordability.
To learn about the applicability of the respective methods relating to your field of research, and be provided with an overview of the pros and cons of the methods, you will still need to find a good review paper.


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Can you consider a human as alive, or is it the cells on the body that are alive?
Sorry if this question seems strange, but in the recent time I have been interested in the question of what life is and how you can define life.
My question:
How long can individual cells live on a human body from the point the human dies? When a human dies, legally he is dead, but how is the medical explaination? Can a human be partly dead, that the heart and brain has stopped, but the cells on the body are still alive?
When you talk about a human life, is it one life or could you consider each cell on the body as a living piece and the whole human body itself including the consciousness is just a container for the cells?

Or: "Is Henrietta Lacks still alive?"

This is a question of emergence

I'd love to see answers to the specific questions 'how long can individual cells live in a human after death' (in normal circumstances - HeLa excluded :P) I'm thinking alveolar squamous epithelium might do fairly well  in terms of maintaining oxygen supply.

Humans are social animals.  If you entirely isolate a human from all human contact (e.g., solitary confinement in prison, or lone shipwreck survivor on deserted island) for years at a time, usually the person will go insane, to some degree.  So, can you say that an individual human is alive?  Certainly, no individual human can reproduce, thus failing one of the usual criteria for life.

After heart dies, unless oxygen and nutrients can be supplied, cells will die within a short time.

Muscles of patients with motor neuron disease will undergo degeneration. For maintaining muscles even in a living person (meaning not brain dead), nerves are essential.

Life of multicellular organisms consists of life of all important unicellular organisms (which are called cells, and not just organisms because they can't live long when the "big" organism dies). But this question also might boil down to the meaning of the word "life" and then it's not biology.

The definition of life is the main issue here. That is one of the great philosophical questions in Biology (and not only Biology) and is way beyond the simple Q&A format of this site. However, most definitions of life can be boiled down to1:

A self replicating entity that interacts2 with its environment.

Or, even more simply [1]:

Life is self-reproduction with variations

In both cases, the answer to your question depends on which level you are focusing on, your resolution if you like. If you take a human cell and apply either of the definitions above, it is alive. A cell is capable of autonomous reproduction, and metabolizes substances harvested from its environment. The same holds true of you look at the human body. However, the definition will not hold for a part of the human body, for example an arm or kidney.
Consider also that a human cell is capable of making more copies of itself, more individual cells. A human body is also capable of making more copies of itself, more human bodies. They can, therefore, both be taken as alive.
There are even more complex examples like Dictyostelium discoideum an amoeba that can exist (and be alive) either as a single cell or as a colony sporting different cell types and rudimentary organization. However, the organism is alive in both of these stages. In one case, you would consider the cell to be the fundamental unit of D. discoideum life, and in the other you could consider the colony.
So, to answer your question both a human cell (as long as it is alive, actively metabolising and capable of reproducing) and the entire human body can be taken as alive. That my cells are alive does not lessen the fact that I am too. It is just a matter of perspective.
References

Trifonov EN., Vocabulary of definitions of life suggests a definition. J Biomol Struct Dyn. 2011 Oct;29(2):259-66.

1 Yes, I know this is a simplification, I just don't want to be drawn in to a long winded discussion on what the definition of life is. My answer is applicable to any of them really.
2 Metabolism can be seen as a form of interaction.


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What factors are known to affect evolution?
My understanding is that the possible mechanisms of evolution are:

Environmental changes
Cultural/mating preferences
Population Immigration
Genetic Mutation

Am I missing anything? I've heard that population shifts within a existing populaces will effect evolution, but imagining the most simplicity scenario, it's hard to see why the would make a difference.

It's not really clear what 'factors of evolution' you are referring to... there are many factors that play a role in evolution - availability of nutrients, availability of reproductive partners, space,... Could you clarify a bit what kind of factors you mean?

@Armatus: "availability of nutrients" would be an environmental change. I'm not sure about "availability of reproductive partners", though I believe that if the availability partners was stable, it would not be a factor, and I already stated in the question that it is unclear to me if "population shifts" beyond population immigration play any significant role.

@Armatus: My list is based on this video, the "Five Fingers of Evolution" - though I've edited it's meaning to make more sense to me; for example, "Environmental changes" I believe are called adaption, which to me is less clear the saying the changes are a result of the environment changing. If it's still not clear what I mean, please attempt to be more description on were exactly things are clear, and unclear. Thanks!

I'll have an attempt at an answer in a moment :)

If I understand right, it may be good to change your question to "What mechanisms can cause evolution" and also quote that definition - that evolution is merely any change in the gene pool. On the other hand, you are answering your own question - it's all in that clip which you linked. Maybe you could include that in the question and more specifically ask something you don't understand in the video?

+1 @Armatus: Yes, mechanisms is more clear, I've updated the question. Also, I agree that evolution is genetic change, though currently genetic change unless previously tied to a known trait is meaningless.

@Armatus: As for the video, I found the use of 'mating' to mean non-genetic bias, not genetic, which to mean upon reflection seems a likely mechanism, and would be it's own; meaning there's a delay in the genetic mating bias generational stabilization of a genetic mating bias. Population shift role in evolution appear unimportant if selection within the shift is random; non-random shifts would another mechanism.

+1 @leonardo: Thanks, so are you saying environmental changes are not the mechanisms of change when the only change done within lab setting is within the environmental factors, and a minority genetic trait within the genome of a populous shifts due to the change? If so, then what is the mechanism in those circumstances? As for the meaning of evolution, "Evolution is any change across successive generations in the inherited characteristics of biological populations."

@leonardo: Thanks, I've updated the question attempt to pull content from the comments into the body of the question. So, yes, in fact I would say that environmental factors "edited" the genome of our species, and most species for that matter. Species don't make up genes to adapt to change, genetic traits either becomes more or less used. Just because environmental change dynamically and passively, does not mean environmental changes are not the one to the mechanisms of change in my opinion.

The first version of the question was vastly superior. In the current form, it’s much too long, needlessly detailed, contains errors, and no longer is a question. I’d suggest reverting to something much closer to the original form.

why would you find out more here than on wikipedia, which has 1000 lines on it, with all references.

Evolution is defined as a change in the allele frequency of population through time.  The Hardy-Weinberg model predicts that the allele frequency of a population will not change (i.e., evolution will not occur) if the following conditions are met:

no natural or sexual selection
no gene flow (immigration or emigration from the population)
no mutatation
no genetic drift (changes in allele frequency due to random events)

So we can conclude that if any of the above conditions are not met then there is a change in allele frequency and thus evolution, and thus that factor is the cause of evolution.

+1 @DQdlM: Awesome! Knowing now that Hardy-Weinberg appears to be the source of the logic was a huge help, and you're answers was within my range of plain-English. Taking a step back from "bio-lingo", would it be correct to say that the "inputs" for natural selection are only mutation(s) and/or statistically significant changes in the way the organism interacts with the environment? Also, assuming mating was completely random, why would emigration affect evolution? Meaning it would appear that other conditional changes would be the source of the evolutionary change, not emigration. Thanks!

@blunders natural selection requires heritable variation and a survival or reproductive advantage based on that variation.  The ultimate source of all variation is mutation but note that the thing that evolves is a population, so you can change the allele frequency by having individuals enter or leave a population.  This would be an evolutionary event unto itself but would also potentially add more heritable variation that natural selection could act upon.

The answer is actually partially wrong. I agree that under all of the above conditions, no change in allele frequency can occur. However, this is true even if you drop the last condition (random mating). In absence of random mating (and in presence of the other conditions), genotype frequencies may change through time (and differ from Hardy-Weinberg's predictions) but allele frequencies would still remain constant.

@Remi.b thanks for your comments. I agree with your feedback so I have edited the answer in response.   Thanks.

You have to leave random mating. First, releasing random mating will change genotype frequencies SO it is evolution. eg : aa = blue Aa=green AA=brown, if not random mating, this biological feature will change its frequency, so population evolved. Moreover, you think human/mammals but many species also reproduce using clonality (so no "mating") which change again the evolution of both genotype and allele frequency. By the way, "random mating" includes 2 factors of evolution: reproduction modes (clonal vs sexual) and mating mode (selfing, inbreeding, panmixia, outcrossing).

Please, delete your edit and reintegrate "random mating" as it is the major factor to explain evolution (eg  http://ebd10.ebd.csic.es/pdfs/Duminil_etal_2007_AmerNat.pdf  ; Charlesworth (2003, p.  1052):  “The  mating  system  is  probably  among  the factors  with  major  effects  on  variability,  clear  enough  to be discernible even in the presence of other factors.”

I downvoted for the removal of random mating. As sol noted, it is critical to the understanding of evolutionary change in a population.

@Bugmo I already had "no sexual selection" in the answer so the whole random mating issue is covered.  Nonetheless, it does appear to have caused confusion so, I agree it is best removed.

In the real world this boils down to does it have heritable characteristics and does it reproduce? If yes to both it will evolve. good answer though

@KennyPeanuts You might want to add something like If one were to use another definition of evolution (see [How to define “evolution”?](https://biology.stackexchange.com/questions/11400/how-to-define-evolution) for a discussion), of course the below list of mechanisms that are driving evolution would be different. to deal with users that are bothered by the quite standard definition you're using. +1

What is evolution?
The first step is to remind ourself of the definition of the term "evolution". Evolution is most often defined as "any change in allele frequency in a population". I will assume that you are willing to use this standard definition.
If one were to use another definition of evolution (see How to define “evolution”? for a discussion), of course the below list of mechanisms that are driving evolution would be different.
Forces that drive evolution
Categorizing the processes that affect allele frequencies might be subject to issues of semantics. Without going into the details, we generally recognize 4 forces that drives evolution

Natural selection

Natural selection refers to the deterministic change in allele frequency due to a differential in fitness among different genotypes. Sexual selection and artificial selection are typically considered as part of natural selection (although that may vary from author to author)

Genetic Drift

Genetic Drift refers to the stochastic sampling process of individuals

Mutations

A mutation refers to any spontaneous change (substitution, indel, chromosome duplication, etc...) in an individual's genotype.

Gene flow  (aka. migration)

Gene flow refers to the transfer (migration) of DNA sequences among populations.

KennyPeanuts's answer, random mating and hardy-weinberg equilibrium
In his answer, @KennyPeanuts also talk about random mating. Random mating refers to the condition where the probability of two individuals to mate depends only on their respective fitness. Many people phrase random mating as absence of mate choice but it actually refers to the absence of variation for mate choice in the population.
Hardy-Weinberg states that under the above four conditions and random mating, then the frequency of the genotype that has the allele $i$ derived from the mother and the allele $j$ derived from the father, where $x_i$ and $x_j$ are the frequency of these alleles is $\cdot x_i \cdot x_j$. This means that for a bi-allelic locus, the allele frequency of the genotypes AA, AB, BA and BB are $x^2$, $x(1-x)$, $x(1-x)$ and $(1-x)^2$, respectively where $x$ is the frequency of the allele A. For the heterozygotes (AB and BA), we often care little which of the two allele is inherited by the mother and which is inherited by the father (assuming there are genders) and we therefore call AB both AB and BA genotypes (which can eventually be confusing). As such, the frequency of the AB genotype is $2 x(1-x)$.
The condition of random mating ensure that there is no deviation of genotype frequencies from the Hardy-Weinberg's expectations and it ensure that there is no change in genotype frequencies from the first to the second generation considered (after one generation, the equilibrium genotype frequency is immediately reached). Random mating is therefore not a condition for evolution to not occur.

Evolution: change in the frequency, not of "allele frequency" but of heritable biological feature,

The usual so called "population genetics definition" of evolution refer to change in allele frequency. It is a very standard definition. You might want to put emphasis on the phenotypic trait that which variance is at least caused by genetic variance but the detail definition gets a little trickier.

"Science sans conscience n’est que ruine de l’âme" Rabelais (Pantagruel) and “The enemy is the gramophone mind, whether or not one agrees with the record that is being played at the moment.” Orwell (Essays)...So, you might have one locus, two alleles A & B, let's say f(A)=0.5, f(B)=0.5, if at generation t, you have all diploid (but works with polyploid also) individuals [AA] and [BB], the next generation t+1, all individuals are all [AB], you HAVE evolution while "allele frequencies" have not changed. You get it? In popgen, mass thinks in alleles but as Ewens 2004 tells, genotypes only matter

...and that's one of the multiple point you miss by saying "Evolution = change in ALLELE frequencies", so replace by "change in heritable trait (can be genotype, phenotype) frequencies". Pop gen comes from information sciences. This definition includes also heritable but non mendelian traits, which changes in frequencies are also evolution.

I am repeating a very standard definition. I am well aware of its limitations. A definition is completely arbitrary and it may or may not fit the intuition. You are free to use the definition you want. In no way am I claiming that this definition is the only, pure and perfect definition. It is just a simple and very standard one and I think that when someone asks what causes X everyone would expect the person answering to use the standard definition of X. Your citations of Rabelais and Orwell are really off-topic btw.

Note that your definition is slightly unclear as many of the considered traits take continuous values and therefore, one cannot consider a frequency without making arbitrary grouping of those values. Also, your definition depends upon the concept of heritability and the heritability of trait themselves vary through time, among environments and among populations. Also, the (sometimes arbitrary) grouping of individuals into populations will affect heritability of traits.

Your definition will likely run into problems when considering things like reaction norm (and reaction norm of the slope of the reaction norm), developmental noise, niche construction too. So do not think you found the holly grail with your definition!

Don't be gripped in the vice of an excessively rigid definition which ultimately will make the concept open to challenge. Repeating a definition because it is "standard" is not scientific but dogmatic. Moreover, a parsimony approach tells us that there is no need for this term added: "allele" to this definition, if not to enclose the thought. Finally, where did you see that this definition is standard? I quote you a reference book in gen pop that says the opposite, what are your sources? Dear Black knighnt, read more books and original articles before throwing Holy Hand-Grenade of Antioch.

Let's not extend this discussion too much. I have justified the use of this definition, not because it matches better the intuition than other definitions but for the fact that it is what people usually mean. I have also highlighted why your definition was in no way better. I don't think there is much interest to keep arguing on it, esp. if you start calling me "black knight" or naively accuse me of not reading many original articles in the field.

If you want to discuss the definition of evolution you should have a look at the post How to define “evolution”?. I will likely not answer to further comments of the kind here.


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Single channel micro arrays
What does single channel microarray mean?
When is it used?
 Thank you for your case in advance.

@PlaysDice - please avoid answering questions in comments - see the meta discussion here for more background. Thanks.

Single channel refers to the system used to detect the labelled probes.  A single channel array, as shown in this slidedeck (slides 6-8) uses one type of molecule for detection.  In the example, (slide 8) the optical label is phycoerythrin.   Contrast that to a double channel array (e.g slide 7) that uses a "green" or "red" molecule used to label probes.  Detecting two different labels requires two channels, one to detect red and one the the green.   The key to using two (or more) labeling molecules is to ensure that your detection system can discriminate between the light spectrum emitted by each of the labels.   Many modern microarray readers have designs that handle multiple labels.
When you see single channel results, they often have colors.  The color is a pseudo color representation of the intensity of the emission of single-color label, which is due to how much probe has bound to the array at that spot.

Adding to this: When using only one color to mark the sample, you can only use one sample (direct comparisions are not possible, since they can not be discriminated). The intensity of the signal here is used to measure the strength of expression, which can also cause some bias.


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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.

Why do you want to change the cell membrane?

I'm trying to understand potential causes of Dermatographic Urticaria.

Why this happens is unknown (at least after a short look into the literature), but it seems, that anything, that causes stress to the skin can cause this symptome.

Add more information on the context of the question to get a better answer

Cell membranes (not cell walls) are composed of a double layer of phospholipids. The lipids are orientated in the way, that the hydrophilic part of the molecule is oriented to the outside and the inside of the cell and the hydrophobic tail to the inside of the membrane.
See the figure from the Wikipedia:

Embedded in the bilayer are transport proteins, receptor and so on. Calcium and sodium fluoride have no effect on the integrity of the membrane.

So mast cells are the same as all cells in regards to membrane and wall?

@brannon there are no cell walls in animal cells.  They r found in plants and fungi. See d wikipedia page on call walls.

Eukariotic cells only have membranes made of phospholipids. Their protein content and also the flexibility varies between the different cell types. But in general, the overall composition is the same.

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.


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Effects of having too much vitamin D?
I saw there was another question about vitamin D; however, I do not believe this is a repeat.
What are some of the effects/side effects of having too much vitamin D in your body?

That is a rare condition that can only occur when taking too much doses of vitamin D. It has nothing to do with sun exposure.
High levels of vitamin D stimulate hypercalcemia and all its negative consequences. It can also exacerbate liver and kidney chronic diseases.
Reference: Katherine Zeratsky, What is vitamin D toxicity, and should I worry about it since I take supplements?