Is there any way to make protein pass through cell membrane? Protein cannot pass cell membrane because it's a large molecule. Until now, is there any technique that can make protein pass through the cell membrane in vivo? I want to create a protein-drug that must be accessible DNA to reach it's site of reaction. How possible can i do it?

Various protein transfection methods are available.

The simplest one is electroporation. By using electric pulses, transient pores can be formed, so that proteins outside can go the inside of membrane.

Several protein transfection reagents are commercially available. I think the mechanism is similar to lipofection of DNA.

http://www.clontech.com/US/Products/Transfection_and_Cell_Culture/Protein_Transfection/Protein_Transfection_Reagent
https://www.neb.com/products/m2563-transpass-p-protein-transfection-reagent
https://www.thermofisher.com/order/catalog/product/89850

Fusion with the transactivating transcription factor (TAT) protein transduction domain from the HIV TAT protein. This 11-amino acid sequence help proteins cross plasma membrane.

http://www.nature.com/mt/journal/v8/n1/full/mt2003155a.html

I am adding a couple of methods here.

Liposomes

Liposomes were designed to deliver drugs to places where the effects are wanted. Drugs are enclosed in liposome vesicles, but when reaching plasma membrane, liposomes could fusion with plasma membrane and release drugs inside of liposomes, although all liposomes are not designed to fuse cellular membrane.  Lipo-fection of DNA is a bit different from this kind of liposomes because DNA is not necessarily enclosed in vesicles.

nanoparticles

This is relatively new. I do not have much knowledge about nanoparticles, but I know they are used to transfect DNA or RNA in vitro and in vivo. I do not know how popular nanoparticles for protein transfection are, but there are publications.

http://www.ncbi.nlm.nih.gov/pubmed/24859743


How was the guided daily amount (GDA) calculated? We are constantly shown nutritional information on food packaging stating this food contains "x" amount of your guided daily amount. A linked to the values is here. How were these values calculated? How do we know that men as a recommendation must not consume more than 2500 calories, 55g of protein 300g of carbohydrate etc...

The total calories are not in fact a recommended value - they are an example amount that is derived from some calorie intake that seemed reasonable to someone (I don't know the details). It does not mean that the government is recommending that you eat exactly 2000 calories per day.

The relative content is, however, a recommended value, based on presumably research. So, if you do take 2000 calories a day, then you know how much of it should be fat/carbs/proteins.

I think that there is some controversy about whether the recommended values were influenced by industry lobbying. Moreover, science is definitely not clear on what the optimal food content for a human is, which is why we keep having the different diet fads, oscillating from no-fat to no-carbs.


Is sexual desire stronger in men than women? Usually in popular culture it's considered men sexual desire is stronger than women. This seems to be congruent with the availability of sexual related items for men and women, such as magazines, movies, and more. Trying to understand if there is a biological connection to this, I found these paragraphs in some articles.

  Estrogen, progesterone, and testosterone are hormones that affect a
  woman’s sexual desire and functioning.

  When it comes to sexual desire, the most influential hormone is
  testosterone. Though it’s often considered a male hormone,
  testosterone — like estrogen– is present in both men and women, though
  the proportions differ between the sexes.

Hormones affecting sexual desire

and

  On average, in adult males, levels of testosterone are about 7 to 8
  times as great as in adult females.[7] As the metabolism of
  testosterone in males is more pronounced, the daily production is
  about 20 times greater in men

Testoterone

Is this greater production of testoterone in men related to a stronger sexual desire? Is there any research studying this, or studying differences between male and women sexual desire intensity in general?

Some of the work of Bob Trivers makes some sense to me. He talks about parental investment https://en.wikipedia.org/wiki/Parental_investment.
The "investment" of a man could be as little as paying for dinner, followed by a few minutes of sexual pleasure, and then he is free to go. The woman's investment for the same thing is the risk of pregnancy (or cryptic STD). Pregnancy is difficult, and before modern medicine, was one of the most common ways to die for women. Then she must feed a helpless infant with her own body, and tend to its needs for the next 15 years. We have social structures for the man to stick around and contribute. But these are not biological differences. The man can leave. The woman cannot. She bears virtually all the risks of sexual behavior. Of course, sexual desires vary by individuals, likely in a bell-curve that overlaps (I anticipate some PC doofus pointing out that some women have strong desires, and some men don't). But I would not be surprised at all, given the biological differences in risks and investments between men and women, that the peak of these overlapping distributions is higher for men than women. Also, evolutionary fitness is defined by the number of offspring an individual can produce. A man's strategy is fundamentally different than a woman's. A man who has 1000 sexual partners is likely to leave more surviving offspring than a man who marries the woman he loves, and stays faithful. A woman with 1000 sexual partners would not be able to have hundreds of children, and would likely put her health at risk.


Why was the Davson-Danielli model rejected? According to my textbook, Davson-Danielli's model of a phospholipid bilayer sandwiched between two layers of globular protein was incorrect. The nonpolar protein portions would separate the polar portions of the phospholipids from water, causing the bilayer to dissolve. Meaning, the Davson-Danielli model is not only incorrect, but it is also impossible.

I understand why the model is incorrect, but not why it is impossible. In my view, the nonpolar proteins would remain together in a micelle shape due to hydrophobic exclusion. Because of this, the phospholipid bilayer sandwiched on the inside would remain isolated from the water.

Why would a bilayer dissolve if the proteins were in contact with water and the phospholipids were isolated from the water?

I think that my confusion stems from many misunderstandings about the chemistry and structure of the cell membrane. In depth illustration of the error that my book mentioned would be most helpful.

The original figure that Danielli and Davson proposed looks like this (from the original publication):

It shows the phospholipid bilayer of the membrane (which is correct) embedded between two layers of globular proteins. The hydrophobic tails of the lipids are orientated towards each other, while the hydrophilic heads are oriented to the outside.

Although the membrane composition is correct (this was already published 1925 by Gorter and Grendel), there are some problems with the proposed model:

Membranes are not identical. The differ in thickness and the ratio of
proteins:lipids.
Membranes have distinct inside and outside layers (defined by the
membrane proteins which are present on the surface of the membrane)
Other than predicted by the model, the membrane proteins do not have
a very good solubility in water - in fact they are amphiphatic,
meaning they have hydrophilic and hydrophobic regions. The
hydrophobic side is anchored inside the membrane.
When the membrane proteins would cover the lipid bilayer, their
hydrophobic regions would be in contact with water, which
destabilizes this construct. Even if they would be oriented towards
the membrane, they would face towards the hydrophilic heads of the
phospholipids causing the same effect. Additionally the proteins
would also seperate the hydrophilic phospholipid heads from the
water. So there is no real stable solution in embedding the membrane
with proteins.


Decreasing signals in assay measurements I'm working with a calcium assay to study the effects of different virulence factors. The assay works, but from day to day the signals of cell lysis go down. Unfortunately, I haven't found an explanation for why this is happening.
The particular assay I use measures cell lysis. The virulence factors I use cause pore formation and lead to a calcium influx (from the buffer). Esterase proteins activate the fluorophore and need calcium. Increase in cell lysis leads to an increase in signal.
As I already mentioned my signals are dropping (from day to day). But I don't know why.
Have you got an idea of what could lead to such effects?
Here are some factors that might be involved.

The virulence factors lose their activity? (I don't feel like that this causes the problem because new stocks also show a decrease in activity, and also the signal from the positive control decreases. I would say it decreases in a similar ratio. The positive control is triton.
The dye loses its activity? The bottle is normally stored in a freezer. I just take it out for the assay. Before I use it, I place the bottle on a shaker for about 30 minutes. I just open the bottle for a few seconds and then put it then back in the freezer.
The plate reader is broken or the reading protocol has changed? I already checked the protocol and every thing is the same as in the beginning. Coworkers get the same results with the same plate reader as before. So I guess, this should not be a problem.
The buffer gets destroyed from the procedure? I store it in the freezer and take it out and put in a waterbath. After I used it I place it back in the freezer. I carry out this procedure every time, can this lead to negative effects? The medium contains calcium, can something happen with it (Calcium plays an important role in this assay)? A colleague already told me that he stores his buffer in the fridge not in the freezer, and he didn't got such effects. But perhaps it's not the only thing he does different..
The cell number changes? The negative control does not change over the experiments, and the signal from it is still higher than the values from the blank. But i will check that.
Could my cells cause problems? They look still good under the microscope.

Freeze-thaw cycles are often suspected of causing degradation in organic molecules 1,2. My first guess would be that your fluorophore is breaking down due to those repeated cycles. Alternatively, you might be getting precipitation of a calcium compound from the buffer you are freezing that your colleague is not.
Standard laboratory practice is to make aliquots of frozen solutions. Before thawing the solution for the first time, set up pre-labeled smaller containers (e.g. Eppendorf tubes) and then aliquot the amount you expect to use for each experiment. That way potentially sensitive compounds are only thawed twice.
References:
1: Kozikowski, B. A., Burt, T. M., Tirey, D. A., Williams, L. E., Kuzmak, B. R., Stanton, D. T., ... & Nelson, S. L. (2003). The effect of freeze/thaw cycles on the stability of compounds in DMSO. Journal of biomolecular screening, 8(2), 210-215.
2: US Food and Drug Administration. (2008). Guidance for Industry. Drug Stability Guidelines.


Why are bees attracted to Stag Hides in Lime bath A friend has some stag hides in lime-water solution. He noticed the stag hides were covered in bees of several different species. He also noticed that the nearby sheep hides in a similar bath have no bees. What attracts the bees to the stag hides? Alternatively, what repels them from the sheep?

There are a lot more bees when the sun shines. The bees principle seemed interested in the hairy side of the hides. There is a small stream and a dried up pond nearby, so probably other places if they just wanted a drink. There is no noticeable scum on the water of either container.

Photos of the stag hides:

Photo of the sheep hides:

Short answer: They are probably looking for minerals from the lime

Explanation:
Insects from time to time need minerals (salt) they can't get from there floral diet. Because they can't chew these directly of rocks, they suck these up from puddles or occasionally from human sweat. This behaviour is well known from butterflies, but also from honeybees

Notice BTW that there are indeed several bee species (Probably Apis mellifera, Bombus terrestris agg. and Bombus lapidarius), but also several flies including Eristalis cf. tenax, a hoverfly.

Why not from the sheep hides? I'm not sure, but the water around the sheep hides looks awfully brown, suggesting there are a lot of humic acids un the water. That might be less attractive to the insects.


What is this insect (Egypt)? I am from Egypt, and I found this insect in my house. It's slow when it moves, and I didn't see it fly. It's green (my phone camera didn't get the colors right).

This is some species of aphid.

Most people are familiar with the wingless stages of these insects that crawl on and eat plants. There are also winged 'alates'. For example, see the life cycle of the soybean aphid:

Due to the picture quality, I'm uncertain about the exact species. However, I can show you alates from some similar looking species:

Nasonovia ribisnigri (Currant-lettuce aphid)

 Source: influentialpoints.com

Aphis pomis (Green Apple Aphid)

 Source

Macrosiphum rosae (Rose Aphid)

 Source: Bernard Dupont

As you can see, these phenotypic characteristics (i.e., green body with black head, clear wings, black/green striped legs, green cauda and black cornicles) are present in numerous diverse species of aphids.

Perhaps you could comment on nearby crop plants or garden plants near your house or produce that you've recently purchased or brought into the house. Sometimes knowing possible host plant species can help narrow down possibilities.


What values to be taken for x-axis and y-axis? I did a lab on form and function in photosynthesis and I recorded the values of absorption spectrum in spinach chlorophyll extract. I have the following data and I need to draw a graph. I didn't understand what I should take for x-axis and for y-axis. Can anyone please explain this.

It doesn't matter really, but for aesthetics sake, you'd plot the wavelength on x and the absorbance on y. We tend to visualize such data as spectral or absorbance as "peaks" on the range of interest. There's a fairly good example here. It has something to do with convention: traditionally
 the independent variable on x and the dependent variable on y. There's a good answer on cross-validated on the matter, too.


What is this insect I found in my kitchen? So I found this bug crawling around near my kitchen sink. There were two others, but not any sort of swarm. I think they're some sort of insect larva, as they don't have a bunch of legs like a millipede or woodlouse, but I have no idea what kind. There also seem to be several shed shells nearby, if that helps.

As for location this is in the upper Midwest.

Here's the top of the thing, with screwdriver for scale

And here's the underside.

That is a larva of a dermestid beetle (Family, Dermestidae). https://en.wikipedia.org/wiki/Dermestidae Dermestid beetle larvae feed on dried material, and are the last insects to clean up a carcass. They are the bane of insect collectors, as they will eat a collection right off the pins. They leave nothing but dust and their shed skins behind.


What are cells not affected by hormones called? Cells that are affected by hormones are called target cells which have their own receptors that listen to signals. I'm unsure of the actual name of cells that are not affected by hormones, I tried searching around on pages relating to target cells and the endocrine system, but no one seems to actually give a name to these cells that don't have receptors.

How about non-target cells? I found several examples of that usage including:

A book section titled: 9.3 How are steroid hormone target cells differentiated from non-target cells?1
Containing the following line:

  Thus, estrogen will stimulate mRNA and protein synthesis in a target cell, but not in a non-target cell.

A book chapter titled: Target or non-target: Hormonal signal perception and response in the determination of cell performance2

References

1: Brown, R., Brown, R. E., & Brown, R. E. (1994). An introduction to neuroendocrinology. Cambridge University Press., p. 149.
2: Osborne, D. J., & Thompson, D. S. (1992). Target or non-target: hormonal signal perception and response in the determination of cell performance. In Progress in Plant Growth Regulation (pp. 237-247). Springer, Dordrecht.


Why are cells in blood smears undetectable after absorbing moisture? I'm a student learning how to prepare blood films and today I was curious about something, so I performed an experiment.
After preparing a thin blood smear and drying it (no staining), I took a look under the microscope (at a total magnification of about 200X... I have a cheap microscope). Even though it was zoomed out, the red blood cells were easy to distinguish. The cells were clear but they had dark edges.
Then, I blew some hot air onto the same slide, causing the dry smear to absorb some moisture. Then I let it dry once again.
I observed the same slide under the microscope once more, but this time, I could barely make out the red blood cells. They were certainly still there, but their features/borders were extremely hard to make out and distinguish.
I'm wondering what causes this. Are the cells absorbing moisture and thus changing their morphology? I couldn't find any answers online, so I thought I'd ask here.

It might be helpful if you are able to post a picture of what you're seeing, however, it sounds like the blood cells are lysing.
The water you introduced to the cells through the moisture in your breath is likely creating a hypotonic environment, causing the cells to intake a lot of water and then lyse, causing their appearance to become atypical.


Difference between pulse coupling and diffusive coupling In biological oscillators What are the differences between pulse coupling found among neuron cells and diffusive coupling found in cells that exhibit calcium waves?
Moreover, in both methods, is it a strict requirement that the cells have to be adjacent to each other or at a distance from each other.

I know this is not a mathematical forum, but can anyone answer the next question or at least point out some books/article where I can learn them.

How can we represent pulse and diffusive coupling mathematically?

Partial answer:

As for a book on the topic of mathematical modeling of coupled neural oscillators, you can start with:

Wilson, H. R. (1999) Spikes, Decisions & Actions: Dynamical Foundations of Neuroscience, Oxford University Press, Oxford UK. author's copy, amz


How do schistosomes find and attach to human skin? Schistosomes are parasitic flatworms that have a snail intermediate host and a human definitive host.

After developing in the snail, they (cercariae stage) escape into the water and can attach to the skin of a human. Then, it will penetrate the skin and migrate into areas of the human's body.

I have been unable to find any information on the mechanisms related to attachment to the human host's skin. More specifically, my questions are:

Do they attach to whatever they can find, and can only develop into the next stage if they (by chance) attach to the right host?
If they selectively attach to human host skin, how do they detect the skin? What makes the skin distinguishable to them?

Here is a great picture of the life cycle of these parasites, for reference.

Schistosoma recognize human skin by mechanical, thermal and chemical stimuli from host. Attachment of parasite to skin is  stimulated by L-arginine. Schistosomes specifically bind  to L -argine by chemotaxis. L-arginine guides this parasite towards site of penetration. The lipids on the human skin surface also serve as signal for host invasion.

It is also reported that parasite may use L-arginine to synthesize nitric oxide for blood vessel dilation so that it can easily penetrate into the host. Schistosoma may attach to L-arginine of surrounding tissues to escape the cellular immune response from host.

(Via: https://www.ncbi.nlm.nih.gov/pubmed/11860033)

These parasites enter the host through skin by producing several proteolytic enzymes to degarde the host tissue proteins including elastin, condromucoprotein, keratin, fibronectin, laminin and collagens.

Two distant serine proteases are responsible for digesting host tissue. One is Chymotrypsin-like protease which degrades protein with large hydrophobic side chains. And the second one is Trypsin-like protease which prefers proteins with positively charged side chains.

(Via: http://www.jbc.org/content/275/49/38667.full#ref-2)


Are all 23 chromosomes connected as one long strand of DNA? This has perpetually confused me. Is our genome made up of two long strands, each strand made up of 23 continuous chromosomes that bind together, or are they 23 free floating separate pair of chromosomes? I think it's the latter because I just learn that genes on different chromosomes assort independently, which would be hard if the genome was a long string, but I'm still not sure.

According to what I've learnt, we have 23 independent pairs of chromosomes. Each of them contains 2 chromosomes and different kinds of genes. The genes are connected in one strand. So it is the latter one. And the 23rd pair of chromosome is used to determine our gender actually. Females got XX and males got XY


Is there a model perennial plant species? Most of plant science is conducted on small annual species with short life cycles; predominantly Arabidopsis thaliana, but also a handful of others like Oryza sativa and Medicago truncatula etc.

Is there a model perennial species? And, if not, is there a good candidate that is relatively small but fast growing and able to be grown in lab/glass house environments that someone could recommend?

To my knowledge, Populus is one of the main model species when it comes to perennials and trees. It is for instance used in several sequencing projects, and to study accelerated breeding in strains that are promoted to flower at a very early age.

Excluding trees, other perennial species that has been described as model species are Panicum virgatum (Switchgrass) (see Lu et al. 2013. Plos Genetics) and Solanum lycopersicum (Tomato) (see Sato et al. 2012. Nature.

For a closer description, and arguments for Populus as a model species, see e.g. Taylor (2002. Populus: Arabidopsis for Forestry. Do We Need a Model Tree?. Ann. Bot.) or Jansson & Douglas (2007. Populus: A Model System for Plant Biology. Ann. Rev. Plant Bot).

  Here it is argued that Populus is rapidly becoming accepted as the ‘model’ woody plant and that such a ‘model’ tree is necessary to complement the genetic resource being developed in arabidopsis. The genus Populus (poplars, cottonwoods and aspens) contains approx. 30 species of woody plant, all found in the Northern hemisphere and exhibiting some of the fastest growth rates observed in temperate trees. Populus is fulfilling the ‘model’ role for a number of reasons. First, and most important, is the very recent commitment to sequence the Populus genome, a project initiated in February 2002. This will be the first woody plant to be sequenced. Other reasons include the relatively small genome size (450–550 Mbp) of Populus, the large number of molecular genetic maps and the ease of genetic transformation. Populus may also be propagated vegetatively, making mapping populations immortal and facilitating the production of large amounts of clonal material for experimentation. Hybridization occurs routinely and, in these respects, Populus has many similarities to arabidopsis.

(from Taylor, 2002))

  With the completion of the Populus trichocarpa genome sequence and the development of various genetic, genomic, and biochemical tools, Populus now offers many possibilities to study questions that cannot be as easily addressed in Arabidopsis and rice, the two prime model systems of plant biology and genomics. Tree-specific traits such as wood formation, long-term perennial growth, and seasonality are obvious areas of research, but research in other areas such as control of flowering, biotic interactions, and evolution of adaptive traits is enriched by adding a tree to the suite of model systems.
  ...
  The development of Populus as a model system for tree and woody perennial plant biology has been largely driven by the rapid development of genomic and molecular biology resources for this genus, as discussed below, culminating in the completion of a draft sequence of the Populus trichocarpa (black cottonwood) genome (106). This information will facilitate studies on the comparative biology of Arabidopsis and Populus as representatives of two angiosperm extremes, enabling discovery of mechanisms conserved among eudicots.

(from Jansson & Douglas, 2007)


Bumblebee (?) identification These bumblebees live on my balcony, in ventilation holes in doors and windows. I'm trying to find the exact name of the species, but I can't find any that look exactly like this. Their top segment is completely black and the bottom one is completely orange. I'm not 100% sure that these are bumblebees, but they behave like bumblebees, I mean, they fly horizontally and like nectar.
The location is in the southern part of Germany (Bavaria). The insects are ~20mm long, similar to the size of a honey bee.

The closest match is probably Bombus lapidarius, but Bombus lapidarius only have orange "tails", most of their bottom half is black.
It looks very similar or even identical to Bombus alpinus, but the problem here is that Bombus alpinus usually live in the mountains (and I'm in 300km from the closest mountains) and they are considered to be almost extinct in Germany.
Do you have any idea what they are called?

Your pictures are quite blurry, but I think this is an Osmia, ie a Mason bee (and not a bumble bee). I think you can see a tendency of the “horns” that female Osmia bicornis (red mason bee) have on their heads on your pictures, so this is my guess. Females are much larger and generally darker than males on the thorax and head, and often quite black there while overall red on the abdomen.
Another option is O. bicolour, where females lack the “horns”of bicornis.
See eg this picture:

Head picture of female O. bicornis, to see the “horns” clearly (if it is indeed this species):

(Pictures from artportalen.se)
Another possible species in the same genus is Osmia bicolor (two-coloured mason-bee), which is more clearly divided in black-orange, see e.g.:

This species has an interesting biology, in that it is specialized on using snail shells for egglaying and preparing larval cells stored with food.


Immunity to one's own microbiome It seems that a human bite can be very dangerous, because of the myriads of bacterial species found in saliva.  This leads to several questions that, perhaps, may have the same single answer.  But, I'll boil it down to a single question per the comment.

Is there a mechanism by which the body "tames" their own oral bacteria that could otherwise be dangerous pathogens, so that the bacteria don't cause pathology but also don't arouse a typical immune response or inflammation?

No doubt this question has been explored often, but I haven't been able to find a clear answer.

One way to identify mechanisms by which the body tames the microbes in the mouth is to observe what happens when those mechanisms are impaired:

  Deviation from symbiosis among the bacterial community
  leads to “dysbiosis”, a state of community disturbance. Dysbiosis
  occurs due to many confounding factors that predispose a shift in the
  composition and relative abundance of microbial communities.
  (Dentistry Journal)

1) Immunity

Normal innate, cellular and humoral immunity helps to prevent oral flora from causing infections.

a) When the immunity is impaired due to a disease (HIV/AIDS, cancer...) or long-term treatment with antibiotics, steroids, immunosuppressants or chemotherapeutics, a part of normal flora, such as the yeast Candida, can overgrow and cause oral thrush.

  Host defense against infections with Candida spp. depends on rapid
  activation of an acute inflammatory response by innate immunity,
  followed by an incremental stimulation of specific immune responses
  mediated by T-cells (cellular immunity) or B-cells (humoral immunity). (Immunology of oral candidiasis, J Pharm Bioallied Sci.)

Picture 1: Oral candidiasis (source: Wikipedia, creative commons license)

b) Impaired immunity can result in osteomyelitis of the mandible, caused, for example, by the Actinomyces bacteria:

  Systemic factors such as diabetes mellitus, agranulocytosis, leukemia,
  severe anemia, malnutrition, or alcohol abuse affect immune
  surveillance and lead to impairing the osteomyelitis

  Actinomycotic druses and filaments were detected from the sequestrum
  of the fracture site (Rapidly Progressing Osteomyelitis of the
  Mandible, Case Reports in Dentistry)

2) Saliva

Saliva helps to prevent mouth infections by flushing microbes into the gut and by the antimicrobial substances.

  Among such protective factors, the flushing effect of saliva flow is
  the most important one...(Antimicrobial function of human
  saliva--how important is it for oral health?, Acta Odontol
  Scand.)

  Importantly, saliva is crucial for defense against microbial species,
  as it is rich in antimicrobial compounds such as hydrogen peroxide,
  lactoferrin, and lysozymes...disruptions in saliva secretion increase the frequency of oral
  conditions such as oral candidiasis, gum disease, and tooth decay
  (caries), as well as respiratory tract infections (The power of
  saliva: Antimicrobial and beyond, PLoS)

Impaired saliva excretion due to a disease (salivary stones, Sjögren's syndrome, untreated diabetes, radiation injury) or drugs (antihypertensives, antidepressants, tranquilizers, diuretics, antihistamines...) can result in dry mouth (xerostomia), which increases the risk of oral thrush and other mouth infections.

3) Lack of substrate for microbial overgrowth

Clean healthy mouth does not contain enough food for microbial overgrowth.

On the other hand, in untreated diabetes mellitus, the abundance of glucose in the saliva promotes the overgrowth of the yeast Candida (oral thrush):

  A dry mouth coupled with a higher amount of glucose in the saliva can
  also make for favourable conditions for thrush.
  (Diabetes.co.uk)

Mouth full of food debris due to poor hygiene can promote bacterial overgrowth:

  Periodontitis is caused by certain bacteria (known as periodontal
  bacteria) and by the local inflammation triggered by those bacteria.
  Although these periodontal bacteria are naturally present in the
  mouth, they are only harmful when the conditions are right for them to
  increase dramatically in numbers. This happens when a layer of
  bacteria and food debris, known as plaque, builds up and is left
  undisturbed on the teeth...(What is periodontitis, European
  Federation of Periodontology)

The bacteria from normal oral flora often involved in periodontitis: Porphyromonas and Streptococcus (Lumenlearning.com).

4) pH

The normal pH in the mouth is 6.2-7.6 (Journal of Indian Society of Periodontology). When it falls under certain value known as critical pH (~5.5), acids derived from bacterial fermentation of dietary sugars start to dissolve tooth enamel and cause caries. The bacterium Streptococcus mutans is a part of normal oral flora, but is commonly involved in caries (Lumenlearning.com).

5) Low susceptibility of mouth mucosa for certain microbial toxins

Certain microbes, such as Staphyloccocus aureus, which are a part of normal mouth flora do not likely cause infections in the mouth, even when they appear in the mouth in much greater amounts, for example, in food poisoning and even if these microbes can cause severe diarrhea (Centers of Disease Control and Prevention). This is because the mouth mucosa is not susceptible for the toxins secreted by these bacteria, while the stomach or intestinal mucosa is.


How to linearize target vector by PCR In my bio class, we learned that you can use restriction enzyme or PCR to linearize a plasmid. Linearizing by restriction enzyme seemed visual and intuitive but how do one linearize a vector using PCR?
I know how PCR works(at least I believe I do), since I watched couple of videos on YouTube explaining them.

But it is not connecting to me how PCR can be used to linearize a "circular" DNA. I have seen videos where a straight double stranded DNA was separated into single strands and using PCR to produce multiple copies with appropriate primers.

But if a plasmid, the circular DNA is not "straight" or linearized in the first place how do you perform PCR on it? Because if they are in a circular state during PCR the strand would never separate in to linear strands. Wouldn't you just have two sperated strands that are circular? E.g a small ring of single strand DNA and a bigger ring of single strand DNA. They are still in circular state after the strands split from each other. Please correct me if I am spitting out nonsense. I just don't see the visual here.

If you use PCR, the products from the reaction will be linear pieces of DNA. Yes, you'll have two templates that are circular after the first denaturation, but when you anneal the primers and perform elongation you'll be making linear fragments. The exponential nature of PCR means that these linear fragments will far exceed the template after several cycles.

PCR can also be tuned to be selective for shorter fragments. If you use the proper protocol for PCR of the entire plasmid, your PCR products will be a complete copy of the plasmid that is linear.


Carbohydrate in egg white I looked up online to find which type of carbohydrate is found in egg white, but the only information I found is the quantity of sugar. I would like to know the exact name of the carbohydrate found in the egg white in order to draw the sugar molecule.

The one I found is Ovomucin,though it's not a pure carbohydrate.

Ovomucin is a highly glycosylated protein and approximately 33% of ovomucin is made up of carbohydrates.

Nutritional Values of Egg White Proteins paragraph of
http://ps.oxfordjournals.org/content/92/12/3292.full
So you can see it's mostly a protein.

Ovomucin is a trypsin inhibitor found in raw egg white.
Ovomucin is responsible for the gel properties of fresh egg white and is believed to be involved in egg white thinning. Ovomucin is composed of two subunits:

α-ovomucin - carbohydrate-poor with a molecular mass of 254kDa

β-ovomucin - carbohydrate-rich with a molecular mass of 400-610kDa

Souce: Wikipedia


Is flowers nectar secreation influenced by bees/pollinators? Nectar secretion by flowers is influenced by many environmental factors e.g. water supply and air temperature [1].

My question is: do bees (or any other pollinator) influence it too?

I can imagine every bee's visit takes away a certain amount of nectar from the flower. Then following the flower nature, it should produce nectar again (if there are the right conditions, e.g. enough water).

[1] https://www.jstor.org/stable/2468960

In short, yes, it seems many flower species have mechanisms to replenish nectar after removal. For example, in Luo et al. 2014 Journal of Pollination Ecology,  9 of 11 species of plants they studied in the Colorado Rockies showed significant additional nectar production after some nectar was experimentally removed. Furthermore, the magnitude of this behavior was greater for flowers known to be heavily visited by bees:

https://www.researchgate.net/publication/268523373_Stimulation_of_flower_nectar_replenishment_by_removal_A_survey_of_eleven_animal-pollinated_plant_species


Stem Cell Replication Reading from the internet, I've come across quotes that said stem cells have the potential to replicate indefinitely. However, there are other sources that say cells that are specialised will have their telomeres shortened each time the cell undergoes cell division until it renders them unable to reproduce.

I would like to ask if stem cells that replicate in terms of self-renewal will have their telomeres shortened as well to a point where they can only renew themselves a set number of times before they cannot undergo cell division anymore.

Thank you.
[P.S. I'm no biology student, just a curious person seeking answers, hence do forgive me if this is supposedly a basic question. I've tried looking online for answers but it seems quite difficult to get a satisfactory or targeted answer.]

Telomere shortening is intrinsic to the process of replicating linear DNA (termed the end-replication problem). Adult stem cells that rapidly proliferate express the enzyme telomerase which is capable of lengthening shortened telomeres, thus allowing theoretically indefinite replication.

Further reading: Telomeres of Human Chromosomes


Changes of permeability and driving force during voltage clamp An action potential can be understood in terms of voltage changes, and these are fundamentally a function of relative permeability changes, mostly for Sodium and Potassium ions. If for instance the relative permeability of a cell strongly changes in favor of Sodium, the membrane potential approaches the equilibrium potential of this ion, leading to the depolarization of the membrane.

I understand that voltage clamp methods allow us to assess these permeability changes by "clamping" the membrane potential, and equivalently keeping the driving force constant:

$I = g * (V_m - E_{eq})$

with $V_m - E_{eq}$ being the driving force.

Related to that, I have two questions:

(1) Say we are approaching the Na+ equilibrium during an action potential peak, being closer to the Na+-equilibrium means a smaller driving force, hence the ion flux is an interaction driving force x permeability. Hence why the strong emphasis on permeability if the driving force is as relevant?

(2) When we clamp the voltage, say below the Na+ equilibrium at -20mV, we will have a constant influx of Na+. While I understand that this influx consists of only few ions entering the cell, doesn't clamping over a longer period of time change the concentration because the pumps can not keep up with the constant influx of cations, adding up over time?

Relative ion permeabilities determine the equilibrium for a given configuration of ion channels. You can easily understand what is about to happen to the voltage of a cell if you know the permeabilities: if the equilibrium voltage is more positive than the present voltage, then the voltage will increase over time. The rate at which it increases depends on the membrane time constant, which depends on the capacitance of the cell (which is based mostly on membrane area, and stays relatively constant) and the resistance; the resistance is, again, based on permeability.

So permeabilities tell you A) Where you are going, and B) How fast you are going there. This is all relevant if you are living in "voltage land": you can actually ignore currents completely and just think in terms of voltage. This is the situation in 'current clamp' recording and for the most part I would say is the easier way to understand the 'big picture' for a neuron.

If, however, you want to think about currents themselves, then you typically clamp the voltage. Clamping the voltage also keeps the driving force constant (at least over the time scales on which voltage-clamp experiments make sense). In that case, you are right, you can't ignore driving force, however, in that case you are usually setting the driving force (by setting the voltage), and measuring the current. "Driving force" is then only necessary to figure out the permeability.

If you voltage clamp a cell at a depolarized potential for a long time (minutes), eventually yes the ion concentrations will change. Voltage-gated sodium channels tend to inactivate pretty quickly, so you actually won't get much sodium current when you voltage clamp at -20 mV for a long time, at least not in the soma, but you might get more current out in the distal processes that are not clamped well and other ions like calcium. Cells do not hold up well under long-term voltage clamp, however. I believe the main culprit is calcium toxicity, though it might vary by cell type and other particulars of the recording configuration. You can also kill a cell by just disrupting the membrane and making it more leaky: the concentrations change faster than the pumps can keep up with and you get excitotoxic cell death.

I usually recommend Purves' Neuroscience as a basic textbook, and the Methods in Enzymology volume on Ion Channels edited by Rudy and Iverson for patch clamp techniques and related practical wisdom.


Preserved alpha complementation over evolutionary time? Has the result of alpha-complementation ever happened via mutation through evolutionary time, and been preserved in modern day organisms?

In other words, has a functional gene product ever been split or terminated by mutation, exhibit alpha-complementation, and has since been preserved as a quaternary protein? This could be found out by comparison of proteins in closely-related species, but don't know of any specific examples. Has such a thing ever happened?

Yes, there are cases where one gene has become two. Or, at least, where multiple  functions carried out by a single protein, the product of one gene, are carried out by distinct proteins, the products of different genes, in another species.

One case I have personally worked with is the bacterial SelB protein. It is essential for selenoprotein biosynthesis and has a dual function as an elongation factor and RNA binding protein. In eukaryotes, these functions are split between two proteins coded for by different genes. The Sec specific elongation factor EfSec and the RNA binding protein SBP2. See here [1] for more information.

Chimeric transcripts are also examples of this. One I happen to know of is the protein secp43 which in the mosquito A. gambiae is encoded by genomic sequences found on two different chromosomes [2]. Essentially, by two different genes.

The problem is that although we can easily find such cases of one protein's function being shared between multiple proteins in other species, or of one protein being coded for by multiple transcripts, it is hard to reconstruct the evolutionary history that gave rise to the current situation. So, whether the current situation has arisen because of alpha complementation or other causes is hard to know.

REFERENCES:

1) Lescure A, Fagegaltier D, Carbon P, Krol A., Protein factors mediating selenoprotein synthesis. Curr Protein Pept Sci. 2002 Feb;3(1):143-51.

2) Chapple CE, Guigó R., Relaxation of selective constraints causes independent selenoprotein extinction in insect genomes. PLoS One, 2008, 3(8):e2968.


Where does my extra blood volume go after giving birth? I'm pregnant. I've learnt that during my pregnancy my blood volume will increase by 50%. https://www.ncbi.nlm.nih.gov/m/pubmed/4075604/

So I'm wondering, what does my body do to decrease my blood volume after I give birth? Where does all that extra blood go? I would imagine I lose some during labour, but I seriously doubt it's all of it.

The extra volume of fluid is due to the fluid retaining effects of high oestrogen secretion in a pregnant human female. After this high level of oestrogen subsides the extra fluid is mainly eliminated as:

urination
some is lost during parturition (labour)
lactation to some extent as well

Reference:A Textbook of Medical Physiology (South Asian Edition) Guyton and Hall


Which plant is this? I'm curious what plant this is! I found it at 37°52'23.2"N 122°16'55.3"W (north of Oakland, California, USA).

It looks a lot like Queen Anne's Lace, but yellow and with more slender leaves. I believe it's Sweet Fennel (Foeniculum vulgare). It's in the Apiaceae family, which has a lot of edibles: carrots, parsley, fennel, anise, caraway, celery, chervil, cicely, cilantro, cumin, dill, parsnips and more. Black swallowtail butterflies lay their eggs on this, so often you can find a really fine caterpillar on them; bees like the flowers as well.

Apiaceae has 3,700 species spread across 434 genera; it is the 16th-largest family of flowering plants. It has a few poisonous plants, like water hemlock (white flower) and poison hemlock (also white). Wild parsnip has a very similar yellow flower but it's sap is wildly irritating in the medical sense (it will cause pain and blisters); its leaves are very different.

If you crush some of the slender leaves between your fingers, it should smell like fennel (a common spice, e.g. in Italian sausage), or if you aren't familiar with that, a bit licorice-like.

Sweet fennel (left, up to 6 feet tall)        Wild Parsnip (right, 3-5 feet tall)


What is the term for a given interpretation of a fossil record? There exists a term, that I have heard and forgotten it appears, for taking a described species in paleontology and creating a version of what it was like in life.

For example, a prior [insert this term here] for T Rex had it upright and dragging it's tail, while a more recent [insert term again] has shown a much more horizontal and rigid body plan.

I know you 'describe' it formally when you identify it from remains, and 'mount' when you set up a specific set of remains. But what is it when you interpret those remains to a specific form?

The term you are looking for is reconstruction (as in
Forensic facial reconstruction).

You can find it used on the wikipedia articles for Fossil cave and for Transitional fossil or in the post In reconstructions, how are various shapes of facial features determined from skull only? for examples.


Is Pork more prone to carrying higher loads of parasites than Beef? My friend told me that pork is dangerous due to containing worms.
I told her that beef contains worms too and that's why we cook it.
We went to steak restaurant and ordered "medium" beef.
And that makes me think a lot. Why I can order medium beef? It's still rare inside.
I have never heard people ordering medium pork.
Is pork more prone to worm investation than beef/cows?
What sort of worm we have anyway?

Trichenellosis from pork occurs in about about 5 people per year since the 1980's in the US. it has a 0.2% mortality rate there. We can say that 1 American/ 1 European dies from pig meat every 20 years. That's a fair concession. Worldwide the death rate is in the 100ds per year from pork, compared to 3 million who die from the fat in beef and chicken and lamb and excess sugars, and 1.35 million attributed to cars.
The other pork parasites are less dangerous and have less than a 90 cases per year in the USA, mostly people coming from epidemic areas. https://www.oie.int/doc/ged/d9157.pdf
Beef can transmit tuberculosis, E-Coli, BSE/CJD and sarcosystosis. E-Coli from unsanitized beef kills many times more people than pork born diseases, i.e. 100 times more people in the US die from E coli from beef, it is one of the main vectors and a lot more difficult to control than via pork. E-Coli is uncommon from pork. Worldwide many thousands of people die of E-Coli from beef every year.
There were an estimated 147 000 new cases of zoonotic tuberculosis and some 12 500 people died of the disease in 2016. Beef are the main causal agent. All animals have tape worms and other worms.
Beef, Lamb, Pork, chicken, and milk all increase the risk of heart attacks and strokes because animal fat can increase cholesterol dramatically, and eating beef from one region can make you more susceptible to heart attacks than pork from another region, because the fat content can vary a lot. Far more people die of heart attacks than animal parasites these days, about 1 million times more rich people die from animal fat and sugar related disease than from pork parasites.

No pork parasites are counted on this list of parasite deaths, globally it's perhaps 50-350 per year.

About 99.999 percent of people that die from meat, die from the fat and other high sugar diets, and it doesn't matter if it's pork or beef. (source WHO)... 5 million people die every year from tobacco, and 2.5 million die every year from Alcohol, especially in very poor countries.
The income levels of people that die from parasites and alcohol are very low, something like 99.9% of parasite deaths are poor people and 90% of alcohol deaths.
So you can concede that alcohol kills many poor people, but that animal parasites from pigs kill 10,000 times less people than alcohol. Pork kills a million times less people in the west than cars or fatty foods.
Details:
There are three important parasites found in pigs which pose
a risk to humans who ingest raw or undercooked pork
products. These parasites are Trichinella spiralis, a nematode
or roundworm, Taenia solium, a tapeworm, and Toxoplasma
gondii,


Is there a name for the evolutionary loss of vestigial structures? Consider a biological structure which no longer benefits an organism, such as the eyes of an organism whose population now lives in total darkness.  I can think of three reasons why such a structure might disappear:

0) Random changes to the structure over time wouldn't be corrected by selection favoring the functional version of the structure, leading to a wider variation where most versions of the structure no longer effectively function.

1) The resources the structure demands could be better spent on structures which are actually being used; e.g. human eyes require a lot of blood that could be used elsewhere.

2) Perhaps the existence of a very complex structure leads to biological problems which would no longer be an issue if the structure were not present; e.g. human breasts plus breast hormones frequently leads to cancer.

Are these three examples reasonable means by which a feature would disappear?  Are there any other possible reasons?

Is there a general name for the phenomenon of evolutionary removal of vestigial features due to those features no longer being useful to a population?

This phenomenon can be (and has been) described as regressive evolution (the loss of a phenotypic trait). There are several reasons why this occurs:

Neutral mutations which become fixed through genetic drift.
Positive selection of regressive mutations that are beneficial.
Pleiotropic antagonism: positive selection for one trait may have the consequence of disrupting another trait which isn't strongly selected for.

The eye degeneration example you chose is a good one because it is well studied in cavefish (which evolved from sighted surface fish and have degenerate eyes). Normal eye development is under the control of the Pax6 transcription factor. Expression of another transcription factor, Shh, reduces Pax6 expression. Shh expression along the embryonic midline is responsible for splitting the eye field bilaterally. Overexpression of Shh in surface fish leads to eye degeneration and, indeed, it was found that cavefish have an expanded Shh expression pattern.

Cavefish have also undergone a behavioural shift to bottom feeding and have become less aggressive to focus more on finding food. As it happens, the expanded Shh expression also causes a widening of the jaw and amplification of taste buds, both of which aid in scooping and sampling the river bottom. Furthermore, increased Shh expression during brain development influences a decrease in aggressiveness and a shift to foraging behaviour.

This is an example of pleiotropic antagonism: positive selection for jaw enhancements and behavioural changes via expanded Shh expression, which increase fitness in cave environments, can explain why the eye degenerated.


Physiology of tricuspid and bicuspid(mitral) valves The tricuspid and bicuspid valves are atrioventricular valves. Both are valves that prevent backflow of blood pumped from the atria to the ventricles. However, the former has 3 "flaps" while the latter has 2.

Despite searching the internet, I could not find a biological explanation for this difference.

Might this be just a relic of evolution or some sort?

During embryogenesis at the level of an atrioventricular canal there is so called endocardial "cushion" tissue. This tissue bulges to the left side more than it does to the right and contribute to the fusion of the valvular ring to a one leaflet, while from the remaining part of the ring develops the second leaflet:

AVEC = atrioventricular endocardial cushions

As has been stated, the cushion tissue bulges more to the left, thus on the right side where the tricuspid valve is forming the leaflets does not "merge" and develop into three-leaflet valve.

Interestingly, this left side "suture" might sometimes fail to develop with resulting three-leaflet mitral valve.


Why does the cloned cat, CC, exhibit mosaic fur color? Since fur color in this cat is from a sex-dependent gene, I see how calico cats occur. However, I don't fully understand why it happens in cloned cats.

When the cat is cloned, the DNA is taken from a somatic cell in donor and put into the egg of a surrogate. Wouldn't the DNA from the donor already have one of the X chromosomes inactivated to a barr body? Since one of the X chromosomes are inactive, wouldn't there only be a single color expressed?

There are mechanisms through which the X-chromosome that has been turned into a Barr-body can be re-activated. This happens during cloning, but is also seen in some cells that turn into cancer cells. This paper discusses a lot of intriguing lessons we've learned from transplanting nuclei from one cell to another in frogs and mice.

Interestingly, though the succes rate of cloning is surprisingly low (see this paper), but it is equal for male and female clones. This implies that the failure to turn a Barr-body into an active X-chromosome does not contribute significantly to cloning failure.

Of course, if the Barr-body gets re-activated again and turns into a normal X-chromosome, that means that later in embryonic development it can get de-activated again (at random, as is normal in cats), leading to mosaic phenotypes such as the calico. The inherent randomness in this process (at least in some animals, such as cats) means that the calico pattern of the clone is highly unlikely to resemble the calico pattern of the original.


A suggested ancestor of cyanobacteria consumed manganese. Why not magnesium? Joseph Kirchvink and others have suggested a theory that a precursor to cyanobacteria consumed manganese (I believe in the form of Mn2+ dissolved in water). Why wouldn't dissolved Mg2+ work equally as well? It was more abundant and is the central ion of the porphyrin ring in chlorophyll.

There is no conclusive proof of why those organisms chose Mn over Mg (for obvious reasons). I'll just give an opinion on how Mn could be beneficial over Mg.

Even in the photosynthetic organisms present today, $Mn^{2+}$ is the ion used for oxidation of water while $Mg^{2+}$ is used to just get electrons by input of photons (from Kirschvink, 2015, if you're talking about this). When electron is removed from $Mg^{2+}$ (from 3s orbital), the formed $Mg^{3+}$ quickly oxidizes $Mn$ in the oxygen evolving complex (see this answer for more details). This suggests that $Mg^{3+}$ is much more unstable than $Mn^{3+}$, maybe too unstable for enzymes to use it to catalytically oxidize water.

Another point could be energy requirement. The third ionization enthalpy of magnesium ($ Mg^{2+} \rightarrow Mg^{3+} + e^-$) is 7732.7 kJ/mol. On the other hand, the third ionization enthalpy of manganese ($Mn^{2+} \rightarrow Mn^{3+} + e^-$) is only 3248 kJ/mol (which is still higher than other elements nearby it in periodic table, but thats another point). Now, though this energy is available today via sunlight for magnesium, it was most probably too large an energy input (keeping in mind the environmental conditions, like low sunlight due to excess sulfur dioxide in atmosphere, Kirschvink, 2015). Thus, manganese may have proved to be more beneficial than magnesium. As time passed, slowly there would have been enough energy available to oxidize magnesium, so it (sort of) took over manganese in the race.

Again, this is just a speculation. The real reason can remain elusive for a long time (until very strong, conclusive evidences are found).


What is a lip? (upper lip and lower lip) Everyone knows what a lip is but I'm asking from a technical and anatomical standpoint.

Actually what we call "lip" is "vermilion" in medical terminology. But I want to ask if my understanding is right or not regarding to surface anatomy of the lip.

Lip consists of two parts called upper lip and lower lip. And upper lip and lower lip consists of two parts: skin (cutaneous) part and vermilion part  (vermilion is a special kind of skin also but we do not call it skin).

Thus:
Lip = upper lip (upper cutaneous lip + upper vermilion) + lower lip (lower cutaneous lip + lower vermilion)

This is a diagram that depicts the upper lip portion:

Source: http://elementsofmorphology.nih.gov/anatomy-oral.shtml

Questions:

Am I right so far? Did I miss any points?

Is the term "upper lip" ever used for the skin (cutaneous) part only? (especially in surgical terminology and reconstruction surgeries)

Are the "upper cutaneous lip" and "lower cutaneous lip" terms established terms in medicine? Are there any other names or latin names for those?  (I also see the usage of "cutaneous upper lip" and "cutaneous lower lip")

Source

  The upper lip extends from the base of the nose superiorly to the nasolabial folds laterally and to the free edge of the vermilion border inferiorly. The lower lip extends from the superior free vermilion edge superiorly, to the commissures laterally, and to the mandible inferiorly. Around the circumferential vermilion-skin border, a fine line of pale skin accentuates the color difference between the vermilion and normal skin. Along the upper vermilion-skin border, 2 paramedian elevations of the vermilion form the Cupid bow. Two raised vertical columns of tissue form a midline depression called the philtrum. The philtrum is located between the paramedian elevations of the vermilion and the columella above. The labiomental crease passes horizontally in an inverted U-shape across the lower lip, which intraorally corresponds to the depth of the gingivolabial sulcus.

This includes vermilion as well. Dont forget the mucous part inside mouth.

This whole is lip.

As for upper cutaneous lip or cutaneous upper lip, it wont matter, both are same and are used interchangeably. And quite frequently
used is upper cutaneous lip.
As for latinisation, you can use labium for lip, no such specific word for upper or lower lip, is know to me. But, you can try superior cutaneous labium and inferior cutaneous labium, if you want.


Can a same gene stretch from one chromosome to another separate chromosome? Can a gene continue on from one chromosome to another separate chromosome? For example, can part of an eye colour gene be on one chromosome and the rest of it be on the next chromosome?

Usually not (as described in the other answer, non-contiguous pieces of DNA are not considered as a part of a single gene). However there are some cases of trans-splicing in which the spliceosome can splice together RNAs arising from different genomic locations. But these are rare and do not have a direct effect on distinct phenotypes such as eye colour, to be classified as genes. Not much progress has happened in this aspect of transcriptomics, actually.


Calculating the ripeness rate in fruits I need a way to calculate avocado ripeness rate in my experiment so I need a quantitative way, I'm not sure if calculating the cellular respiration for the avocado will result in ripeness rate for the fruit, if that's true I need references if you got.
And if you got another better quantitative ways to get the "rate" of the fruit ripeness.

Generally, ethylene production is used to gauge fruit ripeness.  This paper (PDF download) outlines an experiment measuring ethylene production from Hass avocados at different temperatures over several days.  It appears they used gas chromatography to measure both ethylene and CO2 concentrations.


Book for artists' renderings of extinct species? I'm looking for a collection, in print or online, of pictures of ancient extinct species (i.e., imagined from fossil remains). Is there a good single resource for this? I'm interested in animals of all kinds, barring dinosaurs, and invertebrates. I'm not interested in recently extinct species but rather the very distant past.

With a quick search I was surprise that I could only find

Animals of a Bygone Era: An Illustrated Compendium
Extinct Species
Extinct Animals of the British Isles
Extinct Birds

It looks like there is an open niche to someone who like biology of extinct species and illustrations!

Note all will be of interest to you. None of them seem to offer good quality computer based illustration but rather pencil drawings.


Viruses selected by evolution I had a conversation with a family member who is a bio-computer-scientist and he talked to me about what his colleagues (biologist) are doing and I feel confused about it.

They work in Chile and are studying plants that live in the desert.

If I understand correctly his team is trying to explore the idea that some viruses might actually be good for the plants they are infecting and might have been "selected" and are now "part" of the species.

The way I understand it is that they collect samples of plants and somehow by analyzing their DNA notice that these plants are all infected by some kind of virus and they tell themselves that maybe if all the plants have the virus it's because it's good for the plants.

My questions are:

1) Does any of this make sense?

2) If it does how would the selection process happen ? Combining my (old) high-school knowledge and Wikipedia I see a virus as a piece of DNA that goes into a cell and then uses the cell's tools for it's own purpose, but it is not part of DNA. So how can it be treated as part of the plant ?

3) Do you know any good references (preferably for an enthusiast layman) about this subject (i.e. the potential good of some viruses and maybe potential applications in bio-engineering) ? I find especially fascinating the idea that maybe evolution isn't just the result of mutations but also of "contamination".

Welcome to Biology.SE!

About your title

Let me first react to your title: Viruses selected by evolution.

Evolution is any process of genetic (and eventually phenotypic) change in a population through time. Selection (Natural Selection for example) is one of such process. Genetic drift is another such process. So, evolution doesn't select viruses unlike your title suggests. Viruses are selected and therefore evolution occurs. When saying "viruses are selected", it means some viruses have a higher fitness (fitness is a function of both survival and reproductive success) than others.

Species interactions

Generalities

Species interact. Species actually interact a lot. One can classify species interactions into categories. Here is a table of possible biological interactions (comes from wiki), where a + indicates "beneficial", a - indicates "detrimental" and a 0 indicates it has no effect on fitness.

Note about symbiosis - comes in reaction to @Gerhard's comment

Different authors use the word symbiosis differently. From wikipedia:

  The definition of symbiosis is controversial among scientists. Some believe symbiosis should only refer to persistent mutualisms, while others believe it should apply to any type of persistent biological interaction (i.e. mutualistic, commensalistic, or parasitic).4 After 130+ years of debate,5 current biology and ecology textbooks now use the latter "de Bary" definition or an even broader definition (i.e. symbiosis = all species interactions), with the restrictive definition no longer used (i.e. symbiosis = mutualism)

Blurry limits

Generalities

It may seem pretty obvious that two species should have either one type or another type of interaction. However, the reality is often more complicated than that. An interaction might fall under one set of environmental conditions and fall under another category under another set of environmental conditions. In addition to that, it is not uncommon that due to selection on the host genes due to the presence of a parasite, the host evolve so to tolerate the presence of the parasite up to the point of actually having a lower fitness in the absence of the parasite.

Example

Parasites often have different life cycle of alternance of generation. That is a parasite sometimes need several hosts such as the parasite causing malaria for example that need both mosquitoes and a primate.

Consider for example a snail which is infected by a parasite. Let's assume (I think it is a real world example but I am too lazy to find out a reference) that the parasite need the snail to be eaten in order to reproduce in the body of the predator. In order to improve the chance of its host to be eaten the parasite is selected so to diminish the thickness of the snail's shell. In response to that, there is selection (which intensity depend also on the proportion of infected snails in the population) for having thicker shells. But now, snails that are not infected have shells that are so thick that the can't move as fast as they'd need to forage. So, by the end infected snails may have a higher fitness than non-infected snails. And therefore the interaction between the snail and its parasite is not a parasitic interaction anymore but a mutualistic interaction.

Can viruses have non-parasitic relationship with their host?

Well... why not? There is nothing so fundamental about viruses that would prevent them to have mutualistic relationship with their host. Actually I am aware of a few relationships. For example, female parasitoid wasps (parasitoids: parasite that kill their host). parasitoid wasps lay their egg in other insects larvea (host), the egg (and later the larvea I think) develop in the larvea (host), eat the larvea (host) and once the host is dead, the individual metamorphose to its adult form and fly away to find a mate a parasite the next larvea. Some lineage of those wasps have viruses in their ovary that infect the host to reduce the immune defence of the host to protect the growth of their egg (Flemming and Summers 1991). This is an example of mutualistic relationship between the wasp and the virus.

Sequencing to know if the plants are infected

You said

  they collect samples of plants and somehow by analyzing their DNA notice that these plants are all infected by some kind of virus

Most likely, they make a PCR (amplification of DNA, that is increasing the number of copies of a given DNA sequence) on viral DNA and look for a signal. In other words they are not sequencing (=reading) the plant DNA but only seeking for viral DNA. If they find viral DNA, then the plant is infected if not, the plant is not infected.

What is unclear to me from your text

From your post, it is unclear to me yet how your "family member" plans to decide the type of interaction there are between viruses and plants. Knowing the frequency of infected plants won't tell you much about the interaction between the plant and the virus.

They will likely have to make growth experiment and try to measure the fitness of infected and non-infected plants.

EDIT - Following the first comment

Knowing that every plant individual is infected doesn't tell much of the virulence of the virus. The frequency of infected is not an information that can help understand the "type of biological interaction" (paratism, mutualism, etc..). One will need to actually make growth experiment and measure fitness (or measure phenotypic traits that are known to be good proxy for fitness).

  One question about your answer is : can we really speak of a virus as a species and especially does your table really apply in this situation ?

The concept of species is not a natural category. It is a man-made, unclear, sometimes useful, category. Typically, it is hard to even talk of species for organisms that don't have sexual reproduction (which is the case of viruses). I wrote this other answer today about the concept of species, you may want to read it. Here is another post on the subject. Btw, talking about semantic issue, viruses are often not considered as alive. All those semantic issues don't have any impact on our understanding of biological processes.

But yes, the table applies to viruses as well. This table is indifferent to the concept of species. Consider just two genotypes (two individuals), one plant and one virus, the existence of the virus has (or has not) an impact on the fitness of the plant (and vice-verse) and therefore, you can classify the relationship between those two genotypes (individuals) into one category of the table. As a reminder, the nature of those relationship may depend on the environment. Typically, a photosynthetic endosymbiote might be very beneficial to the "host" if there is some sunlight but might be quite detrimental in the absence of sun light.


Could someone recommend a book for surveying species? I'm trying to get/renew basic knowledge of species. Could someone recommend a book for surveying "important"/"representational" species? I am looking for a book with good illustrations and that covers most "important"/"representational" species.

I am currently reading The Tree of Life: A Phylogenetic Classification, and it is thicker than I want to read as a first book in this kind.

Judging from your response to Gurav in the comments, it sounds like introductory zoology and plant biology texts would fit the bill.

For zoology, we teach from Hickman et al's Integrated Principles of Zoology. It outlines the major phyla, their defining characteristics, with plenty of specific examples scattered throughout. There are nice little problem sets throughout, and it goes into a solid amount of detail for a first or second year zoology course.

For plants, I've used Graham et al's Plant Biology, which takes a similar general approach. Though it's perhaps a bit broader, and less species-focused.

Both of these books outline the major relevant groups, and use 'representative' species to illustrate various biological points throughout. They might be a good place to start!


Proportion of amino acids from a random polymer of U and C A protein synthesis assay was carried out in vitro. A
  polyribonucleotide containing U and C in proportion 1:5 (positions of
  U and C are random) was used as a template. Which amino acids and in
  what proportions will be incorporated into the synthesized polypeptide
  molecules?

  А. 1Phe : 5Pro : 3Leu.

  B. 1Leu : 1Pro : 1Ser : 1Phe.

  C. 1Phe : 5Ser : 5Pro : 5Leu.

  D. 1Phe : 25Pro : 5Ser : 5Leu.

  E. 5Leu : 5Pro.

First thing I am not sure is whether only U and C is there. I have tried solving this sum taking both the conditions into consideration . I also tried solving it from options but could not succeed.

The first thing to mention is that this is the type of experiment that Marshall Nirenberg performed in order to break the genetic code, and for which he got the Nobel prize in 1968. We stand on the shoulders of giants.

If the ratio is U:C, 1:5, then it is easy to calculate the probability of encountering each of the 8 possible codons composed by just U and C. So for example:

the probability of UUU is (1/6)3

the probability of UUC is (1/6)2*(5/6)

and so on.

Here's a Table that gives all of the values and demonstrates that the answer is (D).


Amino acids in human cancer cells expose dextrorotation? I would like to know if the amino acids in the human cancer cells are dextrorotatory or levorotatory.
I mean the majority of them.
They expose levorotation just like the amino acids in the normal cells or they are different?

I mean in general. Maybe some particular types of cancer are significantly different from the rest.

I'll try to make the question more on-topic: The amino acids in cancer cells are also levorotatory, just like the amino acids in the normal cells?

This book: Breaking the Cancer Code: A Revolutionary Approach to Reversing Cancer says "We know that tumor cells grow in dextrorotation" - so I wonder where the author(s) know that from. They must be speaking about amino acids inside tumor cells, when they say "tumor cells"

I took a 30 second look at the book you mentioned. The authors just made this up, just like 95% of the book.

The authors are not wrong, they didn't want to write something useful and made a mistake, they're just bullshitting: They're making stuff up, letting it sound a tiny bit scientific and try to sell a lot of books.

If you want to know more about something, usually Wikipedia is a good place to start, and if you're not sure how to distinguish between science and pseudoscience it might be a good idea to read a bit about recognizing pseudoscience.

Now to answer your question: cancer cells are almost the same as normal cells, and they contain mostly levorotatory amino acids. The main difference between a cancer cell and a normal cell is that the cancer cell has one or more mutations that cause it to divide a lot more than normal cells. The DNA, proteins and small molecules in the cells are mostly the same as in normal cells, that's why it's so hard to specifically kill cancer cells.


Reaction centre in Photosystems of higher plants In photosystems of higher plants, there are about 250-400 pigments (number wise) in a particular photosystem. Out of which,approx 170-180 pigments are of chlorophyll a molecules. And any one of them behaves as a Reaction centre in a photosystem.

My question is:

What are the factors and laws which decide which chlorophyll a molecule will work as a reaction centre?
What's the difference in chlorophyll a molecules present in reaction centres of PS I and PS II since they have different threshold energy. Is there any structural difference?

Someone else too had asked your question no. 2. here Photosystem 1 and 2; P680/P700; Chlorophyll a/b

The answer basically quotes Molecular Biology 4 ed. by Lodish as follows.

"The chlorophylls in the two reaction centers differ in their light-absorption maxima because of differences in their protein environment."

[I could've just commented this but I can't locate add comment option on your post. Am new here.]


Do the two catalytic cores of DNA polymerase III operate in the same direction? This diagram is from Molecular Cell Biology by Lodish, 2000 which states:

The other core-polymerase molecule, which elongates the lagging strand, moves with its β-subunit clamp in the direction opposite to that of the fork movement.

Again the images provided in Principle of genetics by Simmons, 2015 and Cell Biology by Karp, indicate that the catalytic cores are directed in the same direction. The following diagram is from former book.

Which one is correct and why(please provide citations)?

The DNA polymerase-III holoenzyme moves in one direction (along the fork). One of the DNA polymerases works on the lagging strand but the enzyme is oriented in the same direction as the one that is working on the leading strand. For details see this review (it is old but this fact is also old enough).

The second diagram shown in your question is an accurate representation of what happens. This, statement is confusing (and misleading):

  The other core-polymerase molecule, which elongates the lagging
  strand, moves with its β-subunit clamp in the direction opposite to
  that of the fork movement.

Both polymerases move in the same direction but elongate DNA in opposite directions. The opposite elongation direction, as shown in the second figure, is facilitated by looping of the lagging strand.

You can simply google "DNA polymerase-III holoenzyme" and you'll get many sources that will corroborate this.


Relationship between genetic diversity within and between species Here is a quote from Wagner (2008)

  A second line of evidence [against neutralism] comes from the relationship between the mean number of polymorphic differences between alleles within a species, $\pi$, and the number of fixed differences between genes in two species, $d$. For neutral mutations, a positive association between $\pi$ and $d$ should exist, because the neutral theory predicts that both quantities are linearly proportional to the rate at which neutral mutations arise. Recent genome-scale data shows instead that this association is in fact negative.

What do "the mean number of polymorphic differences between alleles within a species" and "the number of fixed differences between genes in two species" have to do with each other?  Why should there be any relationship at all?  And by "two species", are they talking about Eastern Yellowback Whooping Finches versus Western Yellowback Whooping Finches, or any arbitrary two species, like E. Coli versus Muskrats?

I found this related question, but it doesn't say anything about different species.

Metrics of interest
The two metrics you are interested in are

$\pi$ - the mean number of differences between two randomly sampled (with replacement) alleles in a population
$d$ - the mean number of differences between two randomly sampled (with replacement) alleles coming from two different species

Consider two sequences

ATCGTCAAT
ATAGTTAAT

There are 2 pairwise differences between these two sequences (positions 3 and 6).
The whole point here is to understand that two individuals in the same population coalesce at a given time in the past just like two individuals coming from two different species. The number of pairwise differences is just equal to the rate at which mutations accumulate multiplied by the coalescence time. Let me develop this idea with a few equations below.
Neutral Expectations
Let's do the math! We will do two important assumptions below.

Every mutation makes a new allele (it is an infinite allele model)
All mutations are substitutions (no indels, no gene duplication, etc...)

Intro to Coalescence Theory
Let's first make sure you understand the concept of coalescence. Imagine you were to look at an evolving population backward in time. A coalescent event, is an event by which two lineages become one (looking backward in time). For simplicity consider a case of an asexual population (but future calculations don't do this assumption). In an asexual population, two siblings coalesced the previous generation, as in the previous generation the genes they are carrying were in a single individual (their parent).
We will see below how to calculate coalescence time between two randomly drawn individual from a population and how we can make inference about genetic diversity from this coalescent time.
Rate of accumulation of neutral mutations
The rate of accumulation of neutral mutation is also called the fixation rate of neutral mutations. Let $fix$ be this fixation rate. Consider a panmictic diploid population of constant size $N$. At a given locus of interest, the mutation rate is $\mu$. The number of mutations occurring every generation in this population is $2N\mu$ (The $2$ comes from the fact that in a diploid population, there are two homologous copies of every gene in each cell). If the mutation is neutral, then every single individual in the population has the same probability to end up being the parent of the whole population in a long time in the future. In other words, starting to look at this problem from the future and looking backward in time, any individual in a distance far enough in the future descends from a single individual in the present. As a consequence, the probability of a new mutation to reach fixation is $\frac{1}{2N}$. Multiplying the probability of fixation by the rate at which mutations occur in the whole population we obtain $\frac{1}{2N} 2N\mu = \mu$. In other words the rate of fixation of new neutral mutations is simply equal to the rate at which mutation occur.
Key equation:
$$fix=\frac{1}{2N} 2N\mu = \mu$$
$d$ - number of pairwise differences between randomly sampled (with replacement) alleles coming from different species
Consider two species which common ancestor lived $T$ generations ago. Each lineage accumulated mutations at rate $\mu$ (and explained above) and therefore the expected (average) total number of pairwise differences is $\bar d=2\mu T$. The probability of having exactly $d$ pairwise differences comes from a Poisson distribution with rate $2\mu T$ ($P(D=d) = Poisson(2\mu T)$).
Key equation: $$\bar d=2\mu T$$
$\pi$ - number of pairwise differences between randomly sampled (with replacement) alleles coming from the same population
Here the calculations follows the same logic as above $\pi = 2 \mu T$. The whole issue is that $T$ (the coalescence time) is unknown for the moment and we need to calculate it.
Let $P(T)$ be the probability that two randomly sampled (with replacement) individuals from a diploid panmictic population coalesce exactly $T$ generations ago. The probability of coalescing in a given generation is simply the probability for drawing the same individual, that is $\frac{1}{2N}$ and the probability of not coalescing in any subsequent generation is $1-\frac{1}{2N}$. Iterating over the generations we obtain
$$P(T) = \frac{1}{2N} \left( 1-\frac{1}{2N} \right)^T \approx \frac{1}{2N}e^{-\frac{T}{2N}}$$
, where $e \approx 2.7$ is Euler's number. The above approximation is accurate for large $N$ (say larger than 100). In case you are interest, you will find on this Math.SE post, an explanation for this approximation.
The expected value (average) $\bar T$ of this distribution is $\bar T=2N$ (and the variance is $var(T) = 4N^2$). As a consequence the expected number of pairwise differences between these two individuals is $\pi = 2 \mu 2 N = 4N\mu$
Quickly speaking, these calculations can be extended to calculate the coalescent time between $k$ randomly sampled alleles. The expected coalescent time is then $\bar T = \frac{4N}{k(k-1)}$ and therefore some algebra shows that the total expected time (along all branches) is $4 N \sum_{i=1}^{k-1}\frac{1}{i}$ and the expected number of segregating sites is $4 N \mu \sum_{i=1}^{k-1}\frac{1}{i}$.
Key equation: $$\pi = 4N\mu$$
Conclusion
It is clear from the above that $\pi = 4N\mu$ and $d=2\mu T$ are correlated as they are both linearly related to the mutation rate. As it is said in your quote

For neutral mutations, a positive association between $\pi$ and $d$ should exist, because the neutral theory predicts that both quantities are linearly proportional to the rate at which neutral mutations arise

The quote goes one saying

Recent genome-scale data shows instead that this association is in fact negative.

Such negative relationship between $d$ and $\pi$ cannot be caused by neutral processes. Therefore selection must be involved somehow.
Imagine for example that two species are both selected at different optima (opposite selection pressures). In such case, you would see purifying selection within species reducing the probability of a new mutation to reach fixation to a value lower than $\frac{1}{2N}$ and therefore reducing the rate of fixation $fix$ so that $fix<\mu$. However, such opposite selection pressure among species will yield the species to diverge more than expected by random processes that is $\pi > 4N\mu$. Such selective pattern could explain the observed negative relationship.
More information
This post offers book recommendation on the subject (population genetics).


Is there a correlation between incidence of type 1 diabetes and vitiligo? Does the data indicate that if you have one, the probability of you having the other is higher than that of someone who doesn't have the one?

It has been associated with polymorphisms with the CD4 gene, which is usually implicated in type I diabetes. The wikipedia article for vitiligo also mentions studies for the NALP1 gene. NALP1 is expressed at high levels in T cells and Langerhan cells, white blood cells that are involved in skin autoimmunity.


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)

For statistical genetics, take a look at:

Likelihood, Bayesian, and MCMC Methods in Quantitative Genetics. Daniel
Sorenson and Daniel Gianola. (2002. Springer).

Warning: heavy on math (calculus). If that doesn't scare you, it's excellent guide to non-frequentist statistical methods applied to problems in genetics.


How do CO₂ and carbonic acid (H₂CO₃) work in buffering the blood? Been struggling with this for the past few days even after reading half of the acid base tutorial here, if someone could help me that'd be great.

What I don't understand is how HCO3- is supposed to buffer the blood. I know that HCO3- is a base and can accept H+, but the way that the HCO3- came to fruition is by donating a H+ to the surrounding water, so there's a net zero change in H+ thus no buffering action took place. Let's say a HCO3- accepts a H+, now the CO2 produced by H2CO3 → CO2 + H2O leaves the blood because the PvenousCO2 gets higher than the CO2 pressure in the air in the lungs, and you exhale. Now you're in the exact same situation as before the CO2 got attached to H2O.
Still the text calls it as an buffer, with a very large buffering capacity as well. How does this work?

To me it seems that buffering blood using HCO3- makes as much sense as using HCl, Cl - can accept H+, right? Nevermind that HCl is a very strong acid.. Surely no one would think of using HCl to buffer blood.

What do you mean by "there's a net zero change in $\ce{H+}$ thus no buffering action took place"? The property of a buffer system IS to prevent drastic change in pH.

Buffer capacity, a measure of how much a buffer system can sustain a change in $\ce{[H+]}$ (aka. pH), (mostly) depends on two parameters -- the concentration of that buffer, and how close the desired pH is to its pKa. $\ce{H2CO3}$ has pKa's of 6.4 and 10.3. Given that the pH of blood is about 7.4 and better to stay that way, the base/acid pair, $\ce{[HCO3_^{-}]/[H2CO3]}$ (pKa=6.4) (plus a whole bunch of various proteins such as albumins in blood, all of which has its own pKa) does provide a good buffer capacity around that pH.

True, $\ce{CO2}$ is constantly removed through respiration, but it is also constantly generated by cellular respiration, making $\ce{H2CO3<=>CO2 + H2O}$ a "volatile equilibrium" and keeping both $\ce{HCO3_^{-}}$ and $\ce{H2CO3}$ in high enough concentration to sustain its buffer capacity.

HCl has a pKa of about -7 so it would make a good buffer around pH of -7. In an aqueous environment, all HCl molecules will 100% dissociate, and no $\ce{H+}$ will ever bind to $\ce{Cl-}$ because water itself will first "hijack" the proton as  $\ce{H3O+}$ (pKa=-1.74) before $\ce{Cl-}$ by about five order of magnitude.

---EDIT---

You may be thinking that when cells release $\ce{CO2}$ to the blood, $\ce{H2CO3}$ would be the first product, and in order for $\ce{H2CO3}$'s conjugate base to work as a base to absorb any extra $\ce{H+}$, first it must release a $\ce{H+}$, resulting in no net change in free $\ce{H+}$ and hence no capacity in balancing extra or insufficient $\ce{H+}$ to maintain the pH. Indeed, if $\ce{H2CO3}$ is the ONLY chemical species in the blood when it would not be a buffer. A buffer requires at least two species -- a potential proton donor and a potential proton acceptor, both of which in high and comparable concentration. pH is a measure of external free $\ce{H+}$, a result of final proton balance of all the acid and base in the blood, dictated by the Henderson–Hasselbalch equation. Thus when $\ce{H2CO3}$ is released in the blood, the blood's basic pH will causes most of $\ce{H2CO3}$ to become $\ce{HCO3_^{-}}$, releasing free proton. Again IF that's all the $\ce{HCO3_^{-}}$ in the blood after being made from $\ce{H2CO3}$, the blood's pH will drop, but there is already abundant amount of $\ce{HCO3_^{-}}$ in the blood, helping the system to reach new equilibrium. Of course, the buffer capacity of blood is not infinite. If there is so much metabolic acid being produced that it shifts the ratio of $\ce{[HCO3_^{-}]/[H2CO3]}$ toward excessive acid, acidosis would occur.


What are the differences among food poisoning, gastroenetritis and diarrhoea? I have now studied a major chunk of my microbiology course without understanding the basic difference between the three. The terminologies seem to be confusing. Is it a necessity for food poisoning to be cause by bacterial toxins? My texts include Shigella, which causes dysentery under food poisoning. What are the operational definitions for them? Is food poisoning more of an epidemiological term? I understand that they aren't clear cut identities and there is significant overlap. But could someone please help out?

First of all, diarrhea is a symptom, generally defined as passing large amount of loose stool. Diarrhea has countless causes, which include gastroenteritis and food poisoning (although not all types of gastroenteritis or food poisoning cause diarrhea).

Now the other two terms. Strictly speaking gastroenteritis refers to the inflammation of stomach/intestines, but clinically, it is most often used to refer to infection of stomach/intestines. Gastroenteritis is most often caused by viral infections e.g. rotavirus, noravirus, enterovirus, adenovirus... but can also be bacterial in origin.

As for food poisoning, is usually defined as illness (usually gastrointestinal symtoms, including nausea, vomiting and diarrhea) caused by "poisoned food". Food poisoning can be caused by the presence of a microbial toxin (which can sometimes be heat-stable ie not inactivated by boiling/cooking). Examples include S. aureus enterotoxin, B. cereus enterotoxin, shigatoxin... There can be an overlap, when ingestion of food causes an infection of the gastrointestinal system, but gastroenteritis is not necessarily foodborne.

Hope that clarifies things.

References for further info:
Food poisoning
Basics of acute viral gastroenteritis


Short-term Lamarckism in asexual single cell organisms I was reading through the Karr et al. (2012) whole-cell computational model. One of the things they did was to induce single-gene disruptions in their model. They observed several to be fatal, but:

In some cases (Figure 6B, fifth column), the time required for the levels of specific proteins to fall to lethal levels was greater than one generation (Figures 6C and 6D).

As far as I understand this is because when a single-cell divides, daughters get not only get a copy of the mother DNA, but also have their initial levels of proteins and RNA set to those of their mother (or similar, with some statistical fluctuation).
To me this screams of Lamarkism: if an organism during its lifetime came in contact with an environment that caused a greater expression of some protein that in had at birth, its children will also have a higher initial expression of the same protein. In other words, the trait of "level of this protein" seems to be being passed down in a Lamarkian way. Is my understanding correct, or am I missing the point?
If my understanding is correct, then what are some standard methods to account for this short-term Lamarkism in mathematical models of evolution?

Notes

I am primarily interested in mathematical (or other formal) treatments of this. I have a background in mathematics and some work in mathematical modeling for population biology and evolutionary game theory. I have no background in biochemistry or microbiology. I would appreciate answers or references that cater to this awkward background but I am not adverse to plowing through some microbio if it is for something awesome.

Similar partial arguments can be made for non-single-cell and sexual organism by considering hormone expressions of the mother during pregnancy, as in this answer. I am satisfied with an explanation for asexual single-cell organisms, but bonus points if it can also say something about non-single-cell and/or sexual organisms.

Follow up question on modeling the mechanism behind this: Macromolecule levels in daughter cells after fission

This phenomenon is well known and can be observed in several species. In fact, if you look at the time it takes for E. coli to change its transcription program in order to react to the environment (signal->transcription->translation), you will find it can be longer than its ~20 minute doubling time. You can indeed think of it as a form of Lamarckism. However, it is part of a field that has been booming in the last ~10 years, known as epigenetics.

Epigenetics is a field of research that deals with hereditary information that is passed by non-genetic mechanisms, i.e. not in the DNA sequence. This includes several mechanisms including passing of proteins/RNA, chemical modifications of DNA (methylation) and chromatin (histone modification). It turns out that epigenetic effects can be observed in virtually all species (including human) and affected phenotypes can be significant (leading to disease, for example).

This is a very interesting field of research and is very wide, so I would recommend reading a bit. Specifically regarding protein/RNA passing, I believe this is somewhat less deeply studied, perhaps due to the fact that the effect decreases exponentially (due to dilution), can be limited by protein/RNA stability and some measurement difficulties. However, I think I recall mathematical treatment of this in Prof. Uri Alon's book. You can also catch his systems biology course online on youtube, which I think touches on some of this material.


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

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

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

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