How do big cats perceive objects, specifically vehicles? Right so we have been on safari in South Africa recently and before encountering big cats (lions) we have been told to hold still and not reach out beyond the boundaries of our safari vehicle because the cats would see it as uninteresting "object", unless something sticks out or moves.

Having a bit of background in biology I tried to map this to a more "scientific" explanation but wasn't successful so far. How would you describe the cognitve perception of vehicles by big cats (or lions specifically)?

It's basically the same as humans, they include higher predatory associations and less logical and word associations. The neural circuits study all the images received from the eye and compare new objects to previously learnt categories: Bird/Log/Horn/flailing upside down limb/face/car/rhino... You can feel your own neural networks at work when you focus on an unidentified detail (bird/branch/rock) and class them into right and wrong results. Moving objects occupy a moving class of their own, i.e. in your garden, they are a potential threat or a prey.
When the truck is rolling along normally, the cat has extensively studied this kind of object already and has made these associations: Glass windows he can't get into, faces inside glasses, rubber tires, slight smell of humans, major smell of petrol and artificial stuff, indestructible, square and round bits, sees it every day from all angles and has interacted with trucks plenty of times. He rarely gets any food from safari trucks, they all look a bit the same. A truck occupy the same prey opportunity as birds in trees which can just fly away.
The brain behaves differently towards known objects and movements and new, unknown animate objects, the unknown animate things result in: the capture of attention.
When there is an arm waving out of the window, the cat's brain is receiving an unidentified living thing attached to the truck, perhaps some kind of living meat! A living thing, a prey. Is it a leg of lamb? is it inside or behind the box? Can he get into this truck? Is it a bird? The cat will be interested in the unidentified, new kind of living thing until he has figured it out.
general reading.
visual cortex of monkeys and cats.
Activation of the hypothalamic feeding centre upon visual prey detection
other research.


Does meosis takes place in cell cycle? Cell cycle is as follows- g1,s,g2,m( mitosis). Does this m stands for mitosis only or does this "m" stands for meosis also

This is a question of convention really.

When people discuss the cell cycle, they usually refer to diploid cells (for diploid animals). So in your context, M stands for mitotic phase and does not directly apply to meiosis.

In meiosis, you could say that the cell also undergo a M-phase (actually two in a row, see footnote) but then the cell cycle becomes irrelevant as you get 4 haploid cells (gametes) that cannot duplicate by themselves anymore, effectively breaking the cycle.

Footnote

The M-phase in the cell cycle is a simplification of the process of cell division as this phase can be further sub-divided into a Prophase, Metaphase, Anaphase, Telophase (PMAT for the purists) followed by cytokinesis. In meiosis, you have a slightly different PMAT process during meiosis I (i.e. 1 cell -> 2 cells) followed by another PMAT (2 cells -> 4 cells). You can find additional information here.


How do fish communicate? Fish, as far as I know ( of course there may be exceptions) , don't have any vocal organ...but they are proven to be social...so how do they manage to communicate with each other...on land, organisms like the honey-bee have their "tail-wagging dance"; ants have pheromones...so, what about fish?

Be glad to answer your questions.
fish also sounds. The difference is that they are put in different positions by the body to sound.The sound of fish is about 20HZ. Difficult to discern the human ear. But you can rely on instruments to imitate and perceived. Of course, some fish also relies purely on action to exchange summarize a sound.Some fish by ultrasonic communication with dolphins is very similar (dolphins are not fish).

2 colors.
Some fish by changing the body color transfer information, are located in the tropical shallow water.

3 flow.
Some fish to pass through the water with their fins flapping shaped courtship information.

4 pheromone.
Release pheromone few fish, mostly deep-sea fish.。


HIV and effectiveness of inhibitor cocktail over single inhibitor I'm looking for clarification on the answer to this question. It's in my biochemistry class but I figured this is more Biology than Chemistry, so I'm asking it here.

The question is:

  One of the more effective treatments for HIV-positive individuals has been for them to take
  protease inhibitor cocktails. Certain proteases are required for the virus to mature and these inhibitors prevent them from functioning. A cocktail of inhibits means that numerous inhibitors are used at once. Why would a cocktail be more effective than a single inhibitor?

My answer to this is that there could be more than one mutation of the virus, and with each mutation a variation in specific protease. So, the protease cocktail would defend against a wider range of the mutated virus.

Is this correct? Is there an answer that might involve describing epitopes?

Your answer is correct. HIV-1 encodes a single homodimeric aspartic protease, with each monomer containing the classic Asp-Thr-Gly motif, and the dimer's active site being formed with the two monomeric active sites creating a cleft where the proteolysis takes place. In it, water acts as a nucleophile in conjunction with the aspartic acid residue to hydrolyze the peptide bond in the protein's target.

WikiMedia: Aspartyl protease mechanism.png

A number of HIV-1 proteins are synthesized as polyproteins, and protease is required to cleave them in the appropriate spot(s) so they can assume their mature forms. This is a very big deal, because without these cleavage events HIV-1 cannot complete its replication cycle, and so becomes non-infectious.

WikiMedia: HIV-replication-cycle.svg

Protease inhibitors act by "sticking" in the binding cleft, obscuring the aspartate and preventing binding of the target proteins. However, these small-molecule inhibitors are very specific to HIV-1 and the amino acid residues that compose the binding cleft, otherwise they could potentially inhibit one or more of the many aspartyl proteases our body makes naturally. While it is not very likely that a destructive mutation in the Asp-Thr-Gly motif would result in a replication-competent virus, other more conservative mutations may occur in the binding cleft that still allow the target to bind and be cleaved. However, depending on the exact protease inhibitor being used, a single mutation, even if it's conservative, may still be enough to dramatically decrease the inhibitor's binding efficiency and allow protease to maintain some or all of its functional capacity. This is why cocktails of inhibitors are used: they each depend on different amino acids for their binding, so if mutations arise at some point that do affect the activity of one inhibitor, others may still be unaffected. Evolutionarily-speaking, the inhibitors put a tremendous selection pressure on the virus, which combined with HIV-1's naturally "sloppy" replication process, leads to mutants appearing in relatively short periods of time.

There are two kinds of epitopes in the adaptive immune system: those recognized by antibodies and B cells, and those recognized by T cells when presented in the context of MHC. Antibody epitopes are generally found on the surface of a pathogen or a pathogen-infected cell (when speaking in the context of infectious diseases), as proteins or other compounds capable of raising an immune response that are only located completely inside of the pathogen or infected cell are not available for binding. T cell epitopes, on the other hand, are linear peptide fragments (and sometimes other molecules, like glycolipids) generated by internal processing in the antigen-presenting cell, and are usually pretty representative of the complete contents of the cell, native and foreign. Native epitopes generally don't produce immune responses - when they do, autoimmunity occurs. Foreign epitopes are recognized by circulating T cells, and help prime an immune response against the infected cells. (As a side note, since HIV-1 infects a subset of T cells, it is a way for them to escape immune detection). Mutations in the protease protein may affect some of the epitopes it produces, but those mutations are just as likely to increase visibility to the immune system as decrease it, so overall there's no net gain or loss.


Does a breastfed infant gain immunoprotection due to intramuscular vaccination of the breastfeeder? There is a claim that infants gain immunoprotection from breastfeeding.  I am especially interested in specific protection against pathogens the breastfeeder (not necessarily the mother) has been vaccinated against intramuscularly.

While I know, that IgA and IgM may be present in breast milk and provide passive protection against foodborne pathogens, it is unclear to me, whether there would be any synthesis (and transport to breast milk) of those antibodies without contact between the pathogen and a mucosal membrane of the breastfeeder.  Answer to my previous question suggest that there would be no IgA production as signals received by B-cells in a muscle will lead mostly to IgG synthesis.

I am not asking about the transplacental transport of IgG, only about breastfeeding.

Vaccinating the mother or a breastfeeder to provide immunization for the baby through breastfeeding is not proven nor recommended by health authorities.

If a mother is vaccinated intramuscularly or any other route, it will anyway pass IgA and IgM, and to a much lesser extent IgG antibodies to the baby through breastmilk but it is not proven to confer specific immunity against all pathogens.

And as per your other question, a child from a mother who hasn't had any infection/vaccination with Hepatitis A and hasn't passed any IgG through the placenta will not be conferred immunity against Hepatitis A even if it is breastfed from a woman who had the infection or was vaccinated against Hepatitis A.

There are other ways a mother's breastmilk can induce immunity (cell immunity) this is currently under research and it has been proven to confer immunity in animal models in recent studies but is still not a medical recommendation in humans (studies in pups regarding passing immunity through foster breastmilk for candida albicans , tuberculosis and helminth infections).

What is already proven is that breasfeeding and vaccination of the baby does provide with a more robust vaccination response so that is why breastfeeding and vaccination to the baby at the same time are encouraged.

Maternal Milk T Cells Drive Development of Transgenerational Th1 Immunity in Offspring Thymus

Pre-conception maternal helminth infection transfers via nursing long-lasting cellular immunity against helminths to offspring


How do cockroaches resist the effects of ionizing radiation? Cockroaches are very hardy insects. It is known that, among other things, they are able to withstand bursts of ionizing radiation that would kill a human being.

The explanations of this observed resistance I've seen include cell division not being that fast in cockroaches, and the relative simplicity of these insects compared to other organisms. I know that microbes are able to resist radiation by having "tough" DNA (more G-C base pairs) and ready repair systems. Do cockroaches also have mechanisms like these, or is it really as simple as them being, well, "simple"?

Off the top of head as a medical professional I can imagine the following mechanisms (everything is just speculative reasoning):

Insects don't have blood. Instead, they have hemolymph whose primary role is not oxygen transport (they have an additional tracheal system for this purpose), but rather that of nutrients. Thus they don't need (and don't have) an intense proliferation of blood cell precusors -- these (bone marrow, spleen) are the most susceptible to radiation in a human and animal body.
Insects have a rather primitive immune system that is mostly humoral[a]  and much less cellular[b] compared to the immune system of animals and humans. This eliminates the next common weak place in the body: lymphatic nodes, thymus, again spleen and bone marrow etc.
Insects have generally a much primitive and in many cases also rather decentralized nervous system: the ganglia are organized in a sort of a cord and even though the capital ganglia are usually larger, these dominance is not as prominent as in case of CNS and PNS in animals and humans. Therefore this system is much more tolerant to losses.

1.-3. Therefore, the only sensitive part of insects is the intestinal epithelium which gets renewed on a regular basis (similar to that of humans, also a known target of radiation), but...

Insects (and generally the arthropodes) are known to have exoskeleton. This potentially serves as a good "armor" for vulnerable intestine cells, filtering out the most heavy particles (like alpha- and in some respect also the beta-particles).
EDIT: This seems not to be real protection, see the discussion in comments.

Therefore it is not a surprise that insects generally show much higher resistance against radiation.

EDIT:
As it was correctly added in the comments, there are also gamets, that are most sensitive to radiation (because they bear only the half of the normal genetic information and cannot repair mutations). Even though the lesions in gamets do not lead to immediate death, the potential sterility can easily cause the extinction.

However, cockroaches (and insects generally) are known to be r-animals, meaning that they favor the quantity (r) over quality (K) of their off-spring. This strategy is optimal when dealing with radiation-induced changes in gametes: the high number of offsprings compensates for the genetic imperfections in gametes.

[a] -- meaning that is has secreted peptides in their hemolymph that protect them
[b] -- there are phagocytes, somewhat similar to tissue magrophages in humans, but the rest of the cell chains in immune response in vertrebrates, like T- and B-cells, are completely missing. Those are responsible for the mediation and amplification of the immune response in vertebrates and are the cells that are most susceptible to radiation damage.


Hybridization in Darwin's finches is rare or frequent? I've talked to a couple of researchers today and read recent articles on the subject of hybridization of Darwin's finches. I'm confused about the consensus in the scientific community.

First, I was reading about hybridization in systems where adaptive radiation occurred. I came across this Honeycreepers paper: Knowlton, J. L., D. J. Flaspohler, N. C. R. Mcinerney, and R. C. Fleischer. 2014. First Record of Hybridization in the Hawaiian Honeycreepers: 'I‘iwi ( Vestiaria coccinea) × ’Apapane ( Himatione sanguinea). The Wilson Journal of Ornithology 126:562–568.

In this paper they are saying:

  The Galápagos finches, for instance, hybridize frequently both within and across genera (Grant et al. 2004, Grant and Grant 2008).

But in the resources they cite, here is what I found:

  Rare hybridization between the species, occurring partly as a result of misimprinting on song (Grant
  and Grant 1998)

From Grant, P. R., B. R. Grant, J. A. Markert, L. F. Keller, and K. Petren. 2004. Convergent evolution of Darwin's finches caused by introgressive hybridization and selection. Evolution 58:1588–1599.

  Hybridization was rare at the level of individuals: only
  a few percent of all offspring are hybrids

From Bell, G. 2015. Every inch a finch: a commentary on Grant (1993) 'Hybridization of Darwin‘s finches on Isla Daphne Major, Galapagos’. Philosophical Transactions of the Royal Society B: Biological Sciences 370:20140287–20140287.

  Hybridization was always rare.

From Grant, P. R. 1993. Hybridization of Darwin's Finches on Isla Daphne Major, Galapagos. Philosophical Transactions of the Royal Society B: Biological Sciences 340:127–139.

  Hybridization occurs rarely (less than 2% of breeding pairs) but persistently across years, usually as a result of imprinting on the song of another species.

In Grant, B. R., and P. R. Grant. 2008. Fission and fusion of Darwin's finches populations. Philosophical Transactions of the Royal Society B: Biological Sciences 363:2821–2829.

Did I miss something, or is hybridization rare and not frequent? Maybe frequently is so vague that it includes, rare?

I actually just had to read a Grant & Grant paper, so hopefully, I can get this right. My understanding is that hybridization events have repeatedly seen to occur, but the events themselves usually do not repeat within a lineage, i.e. once a lineage becomes partially hybridized, it is unlikley to continue to breed with adjacent populations.

Due to the reproductive barriers that come from song patters of hybridized individuals (Grant & Grant, 2009), Repeated hybridations are unlikely to occur within a lineage, even when in the presence of a species with which hybridization can occur.

Grant, P.R. and B.R. Grant. 2009. The secondary contact phase of allopatric speciation in Darwin's finches. PNAS 106 20141-20148


Where does the inverse seconds unit come from in the association constant? I'm working to determine Kd(s) kinetically by generating association and disassociation curves.  Kon (association constant, or on-rate) is in inverse seconds multiplied by inverse molar.  I get that the molar comes from concentration, but where do the seconds come from?

First order association reaction:

$$\ce{A + B <=>[k_f][k_r] AB}$$

Rate of association (units: concentration per time) = $k_f\times[A]\times[B]$
 Since [A] and [B] are concentrations and LHS is conc. per time the units of $k_f$ has to be such that it gives conc per time when multiplied by conc2 ([A] ×[B])  Which is conc-1 × time-1

Rate of dissociation (conc. per time) = $k_r\times[AB]$
 Therefore units of $k_r$ would be time-1.

Dissociation constant is actually $\dfrac{k_r}{k_f}$; Its units therefore would be conc.


How can omnivores be in more than one trophic level? I'm learning about the ecosystem and its relation to organisms, So organisms in a food chain can be put from producers to tertiary organisms. I just don't get the part where an organism can be labeled into 2 trophic levels ? how is it placed in the pyramid if so ?

I am not sure I fully understand where is your misunderstanding. I think your whole misunderstanding boils down to the representation of food chain. Actually, let's talk about food web as the name gives an intuition of what is happening that is more correct than the term food chain.

The conceptual view of the food web in a pyramid is super misleading. This is not how ecosystem work. But anyway, if one might want to make some ugly approximations and represent food web into a pyramid, then this person is totally free to represent one species twice, at two different levels. It makes sense that a species can eat things at several level in the same time. Just like you. You probably eat vegetables, salads, fruits, rice, corn, bread, etc... but also eventually fish and meat. Note also as indicated by @fileunderwater in the comments, that some species have different relationship with their ecosystem (typically eat different things) at different life stages.

Here are few examples of more or less realistic food webs. As you can see, one can roughly make category of trophic level but it is not all that clear.


Origin of logarithmic sense responses? It's my understanding that most human sensory systems obey an approximately logarithmic stimulus/response curve. This includes the visual system, auditory system, and the smallest perceptible difference on things like weight. Do we know the origin of this pattern? Is it something inherent in how neurons encode information and fire (for example, maybe the refractory period reduces neuron responsiveness to stimulus in just the right way relative to how information is encoded)? Or is it something that specifically evolved to give us the ability to handle a wide range of stimulus amplitudes? If it's the latter, how is the transformation from linear stimulus/response to logarithmic response achieved?

First, the curves are not really logarithmic.

Instead, according to the Stevens' power law, the curves are of the form:

Perceived = k (actual)a

where "a" could be greater, less than, or equal to 1.

When "a" is 1, the curve is linear.

Examples of a=1 (linear), are:

brightness of a "point source briefly flashed"
length perception
cold perception of skin
radiant heat perception

If "a" = 0.5, the curve is a square root curve.  Brightness perception follows the square root (or de Vries-Rose) curve in some intensity regions, and a nearly-linear response in other (Weber's law) regions.

Examples of "a" being positive are perception of electric shock and perception of heaviness of lifted weights.

So, since the perception curves can be linear (a=1), more sensitive than linear (a>1), or less sensitive than linear (a<1), there is no general logarithmic property of neutrons that is responsible for the curves.


Do animals follow tactics? Are animals able to plan hunts, give tasks if they do it in groups and fulfil it adapted to the current situation? Do they use unique tactics for special circumstances (e.g. based on experiences)  or they just act from instincts?

Do some research on wolves hunting. They certainly have tactics that change depending on the prey that they're hunting, the terrain, danger posed by other members of the prey's herd or family (if any), etc. They're very capable of learning, and use fairly complex communications. They run in packs, live with their mother for a number of years, and have a rather involved family structure that allows for the passing on of behaviors learned from previous generations. It would be difficult to tease out exactly which behaviors are instinctual, and which are learned, but you could say the same of humans as well.


Why are skin tactile receptors considered to be phasic receptors? A phasic receptor by definition is one that quickly adapts to change. In terms of neuron firing, this means that it does not trigger another firing because the receptors are used to the stimulus.

But when I place my fingers on my arm, I continuously feel pressure. Does this mean that skin receptors are only phasic in the sense that it will fire as soon as it is touched and does not prolong this touching sensation?

Short answer
Slowly adapting mechanoreceptors in the skin mediate the perception of static pressure stimuli, while rapidly adapting skin receptors mediate swiftly changing (e.g., vibratory) stimuli.

Background
There are various skin receptors. Hairy skin, such as that encountered on the arm, contains at least four specialized mechanoreceptors, namely Pacinian corpuscles, hair follicle receptors, Ruffini endings and tactile discs. They can be roughly distinguished by their adaptation rates, namely fast adapting (Pacinian corpuscles and hair follicle receptors) and slowly adapting (Ruffini endings and tactile discs). Rapidly adapting receptors generate robust responses to vibratory stimuli, but respond weakly to static pressures. The opposite is true for slowly adapting receptors (Kaczmarek et al., 1991).

Hence, the static pressure is faithfully registered by static pressure receptors, while the phasic receptors are specialized in vibratory perceptions.

Static receptors fire a continuous train upon a continuous pressure stimulus, phasic receptors do so only at the start and the end of a static pressure stimulus. Hence, when there is a fast vibrating stimulus (say 200 Hz), then the phasic receptors will also fire action potentials each time at onset and offset of a pressure phase, thereby faithfully representing the stimulus. Here follows a picture of various skin receptors and their responses to a static pressure stimulus. Note that only the slowly adapting receptros show a rocust response:

Source: Michael Mann

Reference
Kaczmareck et al., IEEE Trans Biomed Eng 1991;38:1-16


Macroevolution vs. microevolution Where is the line usually drawn between macroevolution and microevolution?

I thought that, although similar processes govern both, the line was at the species level, with macroevolution being changes at the above-species level and microevolution being changes within a species (something like changes in allele frequencies).  (So it's a question of timescales?)

However, I heard someone talk about microevolution among different species of Drosophila, specifically referring to copy number variation.  Was the choice of "microevolution" to describe this process (more likely) due to the similarity between Drosophila species or the type of change in the gene? Or at this level, is the distinction rather arbitrary?

Let's start with a word of caution: on the internet, the terms macroevolution and microevolution (especially together) are usually used primarily in creationist rhetoric. As such, it is usually best to avoid them, especially when talking to a lay audience. The main mistake creationists perpetuate when thinking about micro-vs-macro evolution, is that the two are somehow different and distinct physical processes. This is simply not the case, they are both just evolution. The scientific distinction between the terms, comes not from the physical world around us, but from how we choose to talk about it. When a biologist says "microevolution" or "macroevolution" they are actually signaling what kind of questions they are interested in asking, or what sort of tools they plan on using.
Verbal and empirical theories
In verbal and empirical theories, the micro-macro distinction is usually one of timescales. A person in the macroevolutionary paradigm, usually asks questions above the level of individual species, as Evolution 101 writes (emphasis mine):

instead of focusing on an individual beetle species, a macroevolutionary lens might require that we zoom out on the tree of life, to assess the diversity of the entire beetle clade and its position on the tree.

Empirically, macroevolutionary answers to these sort of questions are usually ones that don't have access to detailed evolutionary histories or direct experiment. Instead, the method tends to be ones that use geology, fossils, and back-inferences from broad differences/similarities of existing species. As such, most macroevolutionary theories tend to be descriptive, instead of predictive. Most of paleontology can be classified under the macroevolutionary paradigm.
If someone explicitly says that they are looking at microevolution then this usually refers to a contrasting methodology that tends to be heavy on direct experimental manipulation. Most importantly, microevolutionists tend to have access to rich and detailed evolutionary histories. As such, it is not surprising that you saw a study that identified itself as microevolutionary while looking at different species of Drosophila. The fruit fly is one of the widest used model organisms, and as such the study you are referring to probably experimentally manipulated populations of fruit flies and collected a rich dataset of genetic changes in the generations of fruit flies that they studied.
Of course, most studies are at intermittent levels, and no this isn't called meso-evolution (except by silly people). If you are not clearly using the macroevolutionary nor the microevolutionary paradigm but still looking at evolution, you would just simply say 'evolutionary' without any prefix.
Formal and mathematical models
For formal and mathematical theories, the micro/macro distinction is also one of methods used by the theorist not of the underlying domain they are studying. Mathematical modeling of evolution falls into two broad categories: frequency-dependent and frequency-independent models. Frequency-dependent models almost never make the micro-macro distinction. Although you could argue that dynamic models in evolutionary game theory are micro, and static equilibrium concepts like ESS are macro, but I doubt theorists would endorse this view. As such, I will focus on the frequency-independent models.
For frequency-independent models, they key concept is the fitness landscape -- a way to map each genotype to a fitness. If the model tracks a population (a distribution over vertices in the fitness graph) on a static fitness landscape, then it would typically be just called an evolutionary model (the word microevolutionary is seldom used explicitly in this field). However, if the authors assume that mutations are extremely rare and thus any mutant goes to fixation before a new one arises then they can use Gillespie (1983, 1984) to replace the population by a single "typical individual" occupying one vertex of the fitness graph. At this point, the model becomes macroevolutionary and the underlying rule for calculating fixation probabilities would be the microevolutionary component. This approach is often also coupled with an alternation of change in fitness landscape followed by mutations and a selective sweep. Fundamentally, though, macroevolutionary models are just convenient (or tractable) approximations to a real underlying evolutionary dynamics. This should never be forgotten.
Strange example bridging the gaps
Finally, it is important to stress that the macro- and micro-evolutionary paradigms are not necessarily exclusive and do not have to correspond to a difference in timescales! This is best done with an example of a respected theoretical study that mixes everything together. Kauffman & Weinberger (1989) used their newly developed NK model or rugged fitness landscapes to study maturation of the immune response (Tonegawa, 1983). The developed a macroevolutionary mathematical model because they used Gillespie's trick to replace a population by a typical individual by abstracting away from the underlying microevolutionary calculation of fixation probabilities. However, their model was studying evolutionary dynamics within the human immune system (so timescales of days to weeks) and was tuned by parameters gathered by empirical microevolutionary studies that tracked individual nucleotide changes (Crews et al., 1981; Tonegawa, 1983; Clark et al., 1985). Lastly, the study results can be used to inform a question typical of verbal macroevolutionary theory: Are there any examples of sudden leaps in evolution?.
As such, the above study used a formal macroevolutionary model, informed by empirical microevolutionary work, to help us understand a question typical of verbal macroevolution while looking at a physical process that operated on the incredibly short timescale of days to weeks. No wonder people are so confused by the micro-macro "divide"!

References
Clark, S.H., Huppi, K., Ruezinsky, D., Staudt, L., Gerhard, W., & Weigert, M. (1985). Inter- and intraclonal diversity in the antibody response to influenza hemagglutin. J. Exp. Med. 161, 687.
Crews, S., Griffin, J., Huang, H., Calame, K., & Hood, L. (1981). A single V gene segment encodes the immune response to phosphorylcholine: somatic mutation is correlated with the class of the antibody. Cell 25, 59.
Gillespie, J.H. (1983). A simple stochastic gene substitution model. Theor. Pop. Biol. 23, 202.
Gillespie, J.H. (1984). Molecular evolution over the mutational landscape. Evolution 38, 1116.
Kauffman, S. and Weinberger, E. (1989) The NK Model of rugged fitness landscapes and its application to the maturation of the immune response. Journal of Theoretical Biology, 141(2): 211-245
Tonegawa, S. (1983). Somatic generation of antibody diversity. Nature 302, 575.


Alcohol consumption and central nervous system After alcohol intake, the cerebrum related functions like vision and speech is affected first and later on there's problem with the cerebellar functions like balancing and hand-eye coordination.
My question is- why is it so? Why do they appear in that order?
Like does it have anything to do with differential rate of absorption in cells, or anything else like related to anatomy rather than physiology.

After alcohol intake, the cerebrum related functions like vision and speech is affected first and later on there's problem with the cerebellar functions like balancing and hand-eye coordination. My question is- why is it so? Why do they appear in that order?

It is and it isn't complicated. When you include what each does, it's an interesting question.

We know from experience (and even research, though the ethics of carrying out such research is questionable) that of the noticeable effects on the brain, the first part of the brain (that we can see the effects of) are on the cerebrum. At relatively low doses, the drinker feels more relaxed, more talkative, less inhibited. (there is also a measurable decrease in information processing and reaction time, as well as other less obvious effects.) All these are under the control of the cerebrum.

At this stage, the cerebellum is affected as well, but not grossly (in a manner that we can observe as change in behavior.) The cerebrum is critical to functioning; the cerebellum is critical to survival. Although it's presented as a teleological argument, the simple fact is that effects of alcohol and other sedatives on various parts of the brain are dose-dependent.

  First, dose-dependent functional magnetic resonance imaging (fMRI) changes were revealed in orbitofrontal (OF) and motor (but not cerebellar) regions; visual and medial frontal regions were unaffected. Second, cerebellar regions were significantly associated with driving behavior in a dose-dependent manner. Finally, a global disruptive effect of alcohol on the ICA time courses was observed with highly significant differences in OF and motor regions. Alcohol thus demonstrated some behavioral effects and unique, disruptive, dose-dependent effects on fMRI signal within several brain circuits. The fMRI data also suggest that the deficits observed in alcohol intoxication may be modulated primarily through OF/anterior cingulate, motor and cerebellar regions as opposed to attentional areas in frontoparietal cortex.

If you want to know why different parts of the brain require higher doses to become impaired, that is easy in theory but very complicated in reality. In theory, the brain is no different than any other complex organ in the body: it's made up of different cells. Sure, they're all neurons (excluding glial/etc cells), but not every neuron is the same, just like not every cardiac myocyte is the same. In reality, the answer is unknown.

  Neuronal mechanisms underlying alcohol intoxication are unclear. We find that alcohol impairs motor coordination by enhancing tonic inhibition mediated by a specific subtype of extrasynaptic GABAA receptor (GABAR), α6β3δ, expressed exclusively in cerebellar granule cells. In recombinant studies, we characterize a naturally occurring single-nucleotide polymorphism that causes a single amino acid change (R100Q) in α6 (encoded in rats by the Gabra6 gene). We show that this change selectively increases alcohol sensitivity of α6β3δ GABARs. Behavioral and electrophysiological comparisons of Gabra6100R/100R and Gabra6100Q/100Q rats strongly suggest that alcohol impairs motor coordination by enhancing granule cell tonic inhibition. These findings identify extrasynaptic GABARs as critical targets underlying low-dose alcohol intoxication and demonstrate that subtle changes in tonic inhibition in one class of neurons can alter behavior.

The above sounds like a reason, but it is debated still. I think it's safe to say that like so many cellular reactions, the answer will come down to receptors and their activation or inhibition, be it for GABA/NMDA, combinations or others.

Alcohol impairment of behavior in men and women
Differential effects of ethanol on motor coordination in adolescent and adult rats
Alcohol Intoxication Effects on Simulated Driving: Exploring Alcohol-Dose Effects on Brain Activation Using Functional MRI
Modulation of GABA A receptors in cerebellar granule neurons by ethanol: a review of genetic and electrophysiological studies
Ethanol affects NMDA receptor signaling at climbing fiber-Purkinje cell synapses in mice and impairs cerebellar LTD


Opposite results between Blomberg's K and phylogenetic signal in Phylocom (AOT) I've been trying to test for significant phylogenetic conservatism in some plant traits. So far I used R-package picante (Blomberg's K) and AOT in Phylocom. So far these two methods yield completely opposite results for the same traits, and I'm confused. Is it possible to get such very contrasting outputs from these two methods?

For example, one trait shows Blomberg's K = 0.2892 (P = 0.001), suggesting that the evolution of this trait overall has not been greatly constrained by phylogenetic relatedness. In contrast, for the same trait AOT yields variance of standardized contrasts across tree = 0.006, significance of contrast variance relative to null model (low rank) = 1, and significance of contrast variance relative to null model (high rank) = 1000 (i.e., P = 0.002), suggesting that treewise phylogenetic conservatism is significantly greater than the expectations of random tip swapping.

I've just started looking at these phylogenetic signals, so I may be overlooking something critical. I will greatly appreciate if you could kindly give me directions, thank you very much!

I think I figured. Someone told me that the above results are the same. The absolute value of K = 0.29 indicates the magnitude of the signal is less than expected under a Brownian motion process, but it’s still more than random expectation (according to the P-value,P = 0.001). So both methods suggest that treewise phylogenetic conservatism is significantly greater than random expectations.

Actually the meanings of K statistic and P-value were clearly stated in the original paper (Blomberg et al. 2003). I should have looked at it first... but anyway, I think it is solved now.


Microscope parameters for whole blood alalysis I wonder, what are the minimum requirements for a microscope for blood cell analysis. I'm interested in:
-Counting erythrocytes
-Counting and differenciating all typed of leucocytes
-Counting of thrombocytes

What is the minimum magnification of the objective required?
Which type of objective is sufficient?
What is the minimal price-class of such an objective?

As I found out in medical lab-groups, the most lab-workers use 100x Objective (oil or dry Leica objectices) and 10x ocular. This results in 1000x and the images like the below.

My idea was to use 20x objective (as it is much easier to handle) and 14MP camera. The erythrocyte should have the resolution about 60x60 pixels then, which should be enough for the differentiation.


What are some good biological tests you can do to yourself? I would like to do things like study my own blood and DNA. What kind of things can one do at the present time that are fairly simple. Or require minimal equipment like a microscope?

Are there some genetic diseases or predispositions that one can do self tests?

I mean there are a few tests I know of that are very simple, like measure your own heartbeat or eyesight. But these are a bit too easy.

One category of tests that are relatively safe to perform on yourself - are reflex tests. Some of them are actually very fun to test, say Babinski reflex.

No body fluids are used; however, I would still qualify those as "biological" enough.


Is there a website that shows population sizes? I'm looking for a website that shows the population sizes of a species (doesn't matter which) as a function of time at a geographic coordinate. Is there a government website or other free database with such information?

You can access the Imperial College global population dynamics database.  They will have time series data at specific locations.  http://www3.imperial.ac.uk/cpb/databases/gpdd
There is a sister database as well that might be useful. http://lits.bio.ic.ac.uk:8080/litsproject/

These contain several hundred time series, and you can see a paper that used them here:  http://onlinelibrary.wiley.com/doi/10.1111/j.1461-0248.2011.01702.x/abstract


What is causing my problem with very low yields when isolating a 42kb yeast plasmid? I have to isolate a large plasmid from yeast and transform it in E. coli. After transformation, I often get no colonies. One reason for that is the yeast mini prep hasn't worked or the DNA concentration is too low. I tried two different isolation protocols:

Zymoprep I yeast plasmid prep kit

From the doc: "based on the old E.  coli alkaline lysis method with our Zymolyase added in the first  solution."
Phenol chloroform YAC isolation protocol

used by Dan Gibson et. al] for their huge constructs (>100kb)

They use an expensive Qiagen large-construct column at the end, in order to purify and visualize the yeast extract on a gel, but I skip that step because the Qiagen column cost $40 per yeast clone which doesn't scale if we do many of these.

How can I troubleshoot and optimize the above-mentioned protocols? Are there any other protocols that might be more suitable for a large plasmid and don't use too expensive materials?

A dependable protocol for yeast DNA extraction I used to use was broadly similar to the protocols you cite but included an ethanol precipitation before and after the P:C extractions. The only expensive material was time. The general outline was:

Alkaline lysis
Ethanol precipitation
RNase A treatment of resuspended DNA for 15 minutes
Phenol:chloroform extraction (x2)
Ethanol precipitation

You probably know that the ethanol precipitation lore is that the yield is better the longer and colder you do your ethanol precipitations. I only ever did reverse transcriptase reactions a few times, but the template DNA I prepared spent the night in ethanol at -80C to maximize yield. Another place to double-check is that your yeast cultures are sufficiently dense before starting.


Why is there a carbon atom without a greek letter in protein residues? For protein residues I know that $C\alpha$ denotes the first carbon atom attached to a functional group. Each subsequent carbon is given a corresponding greek letter ($\beta, \gamma, \delta$) except for one. For example, each residue in a PDB file has a list of atoms that looks something like this:

ATOM     32  N  AARG
ATOM     33  CA AARG
ATOM     34  C  AARG
ATOM     35  O  AARG
ATOM     36  CB AARG
ATOM     37  CG AARG
ATOM     38  CD AARG

(A,B,G,D are stand-ins for the greek letters). Why is there just a plain C in this list? What is significant about that carbon?

In your context, the "plain-C" labelled carbon is the carbon atom in the carbonyl ($\ce{C=O}$) group.
In organic chemistry, the alpha carbon is the carbon immediately adjacent to a functional group. In general, the greek letters in alphabetical order denote the distance in increasing order from a functional group.  The $\ce{C_\alpha}$ in the case of amino acids is alpha carbon with respect to both the amine and carbonyl.


Wasp? Wicked looking bug Saw this bug this morning in Colorado. Looks like a giant wasp.

That is a horntail, family Siricidae. https://www.insectimages.org/browse/taxthumb.cfm?fam=455
They are a family of sawflies. Not technically wasps, but they are Hymenoptera.


Why don't we bleed interstitial fluid? Interstitial fluid is the fluid between cells in tissues - forming the medium between cells and capillaries. From what I gather, the typical human has 5L of blood and 11L of interstitial fluid. This raises an interesting question. If I get cut, why do I not bleed interstitial fluid?

When humans are cut, generally their capillaries open and blood comes out. But this should also allow the interstitial fluid to come out - so why don't we see it?

For fluid to flow from a wound there needs to be a significant pressure gradient between where it is now and the outside of the body. Your skin generally does not have a strong compressive effect, which is why a deep cut exposing fat will not lead to the fatty tissue being expulsed from the body any more than the interstitial fluid is.

Blood, however, flows. For it to circulate there needs to be a pressure gradient between where it is now and where it is going. Since veins (including the vena cava, which channels blood back into the heart) do not have vascular walls strong enough to create a suction effect (i.e. lower pressure than the surrounding tissue), you can conclude that the pressure of blood vessels is always higher than that of surrounding tissues, and thus higher than the pressure outside of your body. This is why all blood vessels, including veins, will bleed, whereas less pressurized systems such as interstitial fluid will not.


Do there exist T helper memory cells? I'm translating a Russian text touching upon the IL-17 interleukin family, and it has a kind of typo in it. I'm not sure:

  As mentioned above, IL-17 was found to be expressed at the highest levels by CD3+ Th17 cells. However, subsequent studies showed that it may be produced as well by stimulated CD8+ memory T cells, γδ T cells, Th memory cells (?) and NKT cells.

The Russian text says "Th memory", there is no "cells" there. It might be a typo.

I've read a little about T cells and became curious. Are there T helper memory cells, or does being a T helper cell exclude the possibility of being a memory cell as well?

P.S. The original Russian sentence is

  Как уже было сказано выше, наибольшей экспрессией ИЛ-17 характеризуются CD4+ Th17 лимфоциты, однако последующие исследования установили, что стимулированные CD8+ Т-лимфоциты памяти, γδ Т-клетки, Th памяти и популяция NKT также способны к его продукции.

Yes, T cells -- including T helper cells and cytotoxic T cells -- form memory cells.

CD4 memory T cells: what are they and what can they do?
Origins of CD4+ effector and central memory T cells
Immunological memory
Control of innate immunity by memory CD4 T cells


What is the actual chance of sibling incest child suffering from a genetic disorder? This is not a question about the (a)morality of incest or current laws. However, there seems to be a widespread misconception about the impact of sibling incest on the genetic health of the eventual offspring.

What is the average chance that an offspring of a random sibling couple will suffer from a genetic disorder compared to an offspring of any random unrelated couple?

Usually when we talk about genetic disorder risks for closely related pairings, the concern is the high probability of homozygous recessive alleles.

Lazarin et al. 2013 screened ~23,000 individuals for 108 genetic diseases and found 24% were carriers of a known allele for some disease. Including carriers of multiple alleles, the total frequency comes to about 38% (this is a lower bound because only known alleles can be screened; there may be many other variants that are not known to science that cause the same symptoms).

That means about a 62% chance that one of an individual's parents carries one of these alleles (1-.62*.62 - note that this 62% has nothing to do with 1-.38, just a mathematical coinicidence with rounding).

If a parent is a carrier, each sibling would have a 50% chance of also becoming a carrier; the probability that both siblings are carriers would be 25%. The probability that an offspring from those siblings would be homozygous recessive would be another 25%. .62*.25*.25=3.9% (note that these are all lower bounds, the chances would be much higher if there were multiple recessive alleles present or if both parents were carriers for the same gene).

However, this is limited to Mendelian mutations just for this subset of known alleles. There are many many more conditions and disorders that have more complicated genetics that we may or may not understand, so that the original question becomes nearly unanswerable. In fact the paper I cited only paid attention to what were considered "major" disorders and even left out the Mendelian alleles known to cause more minor issues (including clotting disorders that can easily lead to death in the right circumstances). There are also many mutations that don't cause a clearly defined disorder but cause some other more limited issues that could predispose the offspring to other illnesses.

Lazarin et al. 2013 refers to estimates that each individual carries about 4-5 lethal recessive mutations. Given that siblings are very likely to be carriers of the same particular recessive mutations, this would significantly impact any offspring well beyond the estimates for the known disease alleles.

References

Lazarin, G. A., Haque, I. S., Nazareth, S., Iori, K., Patterson, A. S., Jacobson, J. L., ... & Srinivasan, B. S. (2012). An empirical estimate of carrier frequencies for 400+ causal Mendelian variants: results from an ethnically diverse clinical sample of 23,453 individuals. Genetics in Medicine, 15(3), 178-186.


How to Extract RNA and perform RT-qPCR from very few cells ( ~5,000)? I am currently conducting an experiment which involves FACS-sorting a specific population of cells using an antibody of interest.

In order to validate the type of cells I have collected using this marker, I want to perform qPCR on their extracted RNA, using certain known cell-type marker primers.

My problem is that in each sorting session, I am only able to collect anywhere from 5,000 - 10,000 cells. Do you know if it is possible to perform RT-qPCR on such a small sample size?

I have collected the cells in 1mL of Trizol.

Would I maybe have to amplify the cDNA after reverse transcription in a general manner ( using random primers)?

Thanks for your help.

You can consider use of single-cell RT-qPCR kits such as this one if you have the budget for them. (Note: I have not personally used this kit, just putting out an idea)

  The Ambion® Single Cell-to-CT™ Kit contains a complete validated
  workflow for gene expression analysis for samples containing 1–10
  cells. Each kit contains reagents for sample preparation, reverse
  transcription, pre-amplification, and qPCR that have been optimized
  together in a simple workflow that can be completed in only 5 steps
  (see figure).


How do viroids propagate to other hosts? As viroids are simply non-encapsidated non-coding RNA molecules, it is difficult to imagine a mechanism for their continual infection, other than horizontal transfer which doesn't seem to be the case.

Is there a working theory on how viroids propagate and continually infect hosts?

Viroids are commonly thought of as remnants from the "RNA world" since they are composed of only RNA and have ribozyme activity.
Viroids can be considered as plant parasites of the transcriptional machinery of the organelles (nucleus or chloroplast), since they are non-coding and they replicate by RNA–RNA transcription (in a rolling cycle mode).

Viroids infect the epidermis of their hosts after mechanical damage of the plant cell wall. After entry to the first cell layers, viroids initiate replication in the nucleus or in the chloroplast and then are transported to neighbouring cells, reaching the vascular tissues and virtually all plant tissues.

The transmission of viroids is both "natural" and human-driven. Viroids are mostly transmitted via mechanical methods by contaminated machinery and tools, pruning, and other mechanic argricultural techniques. Transmission also occurs through infected seed and pollen, they don't have important natural vectors from the animal kingdom. Also contact between adjacent plants can be another (inefficient) way to transmit viriods.

I have found a reference here for further informations. It isn't open access but it is possible to watch an abundant Google preview.


Why don't breast enlargements leave any marks of surgery on breasts? If we get stitches, we get marks left on the skin, but there are no marks for breast enlargements. I saw a YouTube video about a breast enlargement wherein a doctor makes a cut. Where does the cut mark go after surgery?

All cuts that go through the dermis (the full thickness of skin) will leave a scar, no matter what (and no matter what anyone tells you). The visibility of scar tissue has a lot to do with how a person heals, how much stress is put on the incision as it's healing, where the scar is, if it crosses the natural direction of skin (called Langer's lines) or goes along the lines.

Plastic surgeons have many years of training and experience in cosmetic skin surgery, and know how to minimize scar formation by their more fastidious closure methods and wound care, as well as hiding scars in ceases and along Langer's lines. But even the best plastic surgeons cannot prevent scars, only minimize them. If you still don't believe breast augmentation doesn't leave scars, you can look at this page (NSFW).


Why does the liver produce ketone bodies instead of exporting acetyl-CoA from beta-oxidation for use elsewhere? Under conditions of low oxaloacetate in the liver, acetyl-CoA that cannot be oxidised in the TCA cycle is converted to ketone bodies, which can then be exported for use as fuel in non-gluconeogenetic tissues (e.g. heart, brain).

To avoid this pathway, and the additional enzymes it requires, as well as the enzymes in the receptive tissues which are needed to reverse the pathway and re-produce acetyl-CoA, why does the liver not just export acetyl-CoA directly?

One consideration is an inability to transport acetyl-CoA across membranes, but fatty acyl-CoAs deal with this using a carnitine shuttle across the mitochondrial membrane. Would developing a transport system not, evolutionarily, be a more efficient solution?

This is simplified version of a complex situation, but in summary:

A key role of liver is to control the distribution of metabolic fuel
for the other tissues (it always has enough for its own
requirements).
The way it behaves differs in the fed and fasted states (because of control by hormones and the concentration of metabolites).
In the fed state (after storing some sugars as glycogen) the liver will synthesize triglycerides and export them as lipoproteins to the adipose tissue, which will take them up and store them. (Other tissues in the fed state will be able to obtain glucose or fatty acids from the blood.)
In fasting and starvation the triglycerides in the adipose tissue will be broken down to fatty acids and glycerol, much of which will be used by tissues such as muscle.
The priority of the liver in starvation is to provide fuel for the
brain and nervous tissues in the form of glucose, by gluconeogenesis. The substrates for net gluconeogenesis under these conditions include glycerol and some amino acids derived from breakdown of protein.
Other amino acids, produced in protein breakdown lead to acetyl CoA,
which cannot serve as a precursor for gluconeogenesis. However it can
be converted to ketone bodies (acetoacetate and β-hydroxybutyrate)
that the brain can use to replace some of its glucose requirement.

With this in mind, it can be seen that the reason for producing ketone bodies is not to generate a molecule that can cross the cell membrane into the blood, but to generate a molecule with special properties, lacking in fatty acids or acetyl CoA, that allows its use by the brain in life-threatening circumstances.

Of less importance, but worth mentioning, is the fact that citrate is used as an export form of acetyl CoA (when there is sufficient oxaloacetate available), a surrogate role it plays in any case in the transfer of acetyl CoA across the mitochondrial membrane for fatty acid synthesis. So it is not necessary to export acetyl CoA, and perhaps preferable to it keep intracellular.

A more detailed account of this is available at NCBI bookshelf online in Berg et al. sections 30.2 and 30.3


Is there any genetic similarity that defy evolution theory? For example,

say species A is common ancestor of B, and C. Species B is a common ancestor of D and E.

We would expect that there will be more genetic similarity between D and E than D and C. And those genetic similarity must exist in B.

In other word, we won't expect genetic similarity that don't "cross" the common ancestor or the evolutionary tree.

The exception is probably genetically engineered bacteria.

That being said, am I correct?

Some people say that we have similarity with pigs and chimps even though our common ancestors may be to far off. That won't happen right?

To summarize

I expect that evolutionary tree will form a well, tree. Genetic similarity would infect "nearby" trees and can't jump between trees without connectors, such as common ancestors.

Is that what we observe for ALL species?

Your question seems rather confused to me, I don't quite understand it. Below I try to explain some stuff, I am not quite sure it would help you finding the answer to your question. Let me know if it helps you and how I can improve this answer.

While natural selection selects for a given allele (gene variant), mutations create new variation. And because of this process of mutation there is genetic pattern in species D that would cannot be found in species B (assuming that we have the DNA of species D). But what is similar between B and D were probably also present in their common ancestor B. The exceptions are molecular convergent evolution and horizontal gene transfer (natural of artificial).

Because of common ancestry …

Humans have similarities with pigs

Example: endothermic amniotes

Humans have similarities with a bug

Example: bilaterial symmetry

Humans have similarities with jellyfish

Example: Heterotrophy

Humans have similarities with an oak tree

Example: We have mitochondrias

Humans have similarites with any living things on earth!

Example: Genetic information is hold into a DNA/RNA molecule.

If you might observe that D is genetically speaking more similar to C than to E… This can be due to:

Horizontal gene transfer (artifical or natural)
The mutation rate (or ability to fix mutations) in one lineage might be greater than in another lineage.

For example, if lineage E underwent many mutations, they might be genetically speaking have accumulated many difference compare to D, way more than the number of difference that D has with C.

The phylogeny might be wrong
There might have had some convergent evolution.

Think about fishes which opsins in the eyes need to be adapted to the amount of light which depends on the turbidity of the water. After the three lineages splitted, the change of envirronment might have occured the sequence AATGATCCT suddenly became beneficial. Only two lineages had the chance to produce the right mutation. Or maybe lineage E live at low depth and therefore it doesn't need this mutation because there is enough light at low depth anyway.

Therefore, one should not expect a common ancestor to be the arithmetic mean (supposing it means something) of the current species. And one should not expect that two closely related species on the tree of life should necessarily be more genetically similar to each other than any of the two to a third species.

Note that the phylogeny is constructed mostly based on genetic data. Which makes that two closely related species (on our tree which is not necessary the absolute tree of life) are (almost) necessarily more genetically similar (it is kind of a definition then).


How do aerobic Rhizobium bacteria survive in root nodules while fixing atmospheric nitrogen? I read that rhizobium carry the enzyme nitrogenase, which is irreversibly damaged upon the exposure of oxygen. Inside the root nodule of legumes leg-haemoglobin keeps a microaerophilic environment where nitrogenase enzyme can function and molecular nitrogen can be fixed (source: Brock's Biology of Microorganisms).

Shouldn't therefore Rhizobium bacteria die in such microaerophilic condition inside the root nodules?

TLDR
One hypothesis for survival is nitrate respiration.

Long Answer
Ampount of oxygen available in root nodules is controlled by the host plant by two ways:

By presence of leghemoglobin
By the diffusion resistance
Under anaerobic condition the bacteria survives by making use of denitrification process which could be used to produce ATP under anaerobic conditions.

It is known for a while that, beside nitrogenase activity, in many symbiotic associations between legumes and Rhizobium the activity of nitrate reductase also exists 12. Most of the nitrate reductase ativity has been found to be concentrated in infected bacterial body i.e., bacteriod3. The bacteriod uses the process of conversion of nitrate into nitrite for creating a proton gradient which is inturn used for generation of ATP.
Reference.


Are inflammation and anxiety connected? I've been reading a curious paper about the use of cannabis, and one of the passages piqued my interest:

  There’s also been a lot of work done on another constituent of
  marijuana, cannabinoid, which is not psychoactive by itself. A lot of
  research has shown that it’s a great anti-inflammatory, it’s a
  neuro-protectant, and it may be what gives medical marijuana patients
  relief from things like epilepsy and anxiety

Has there been any scientific evidence that links inflammation and anxiety?

Source:
Cannabis, Forgetting, and the
The Botany of Desire

See this paper on link between inflammation and anxiety.

Also, quoting one of the paragraphs of this paper

  Clinical
  studies have shown increased serum inﬂammatory markers in patients with depression as well as a correlation
  between plasma cytokine levels and the severity of depression, and have described improvement in depression
  after anti-inﬂammatory treatment.

Even if you do a simple google search, you will get thousands of results on this.


Why did women historically have such a high mortality rate during birth? Historically women had a relatively high chance of dying while giving birth.

At first thought it seems to me that this would be a disadvantage for the species for the obvious reason that a dead person can no longer give birth (and can't care for her offspring).

Is this outweighed by some advantages? I can imagine that there would be some evolutionary advantage to have the "weaker" women die during child birth and let the "stronger" ones live to produce more children with "stronger" genes.

Or is the high mortality rate in humans during child birth a result of civilization (pre-moderne civilization of course, with the general lack of hygiene/medical knowledge)?

What is it like for the relatively un-civilized tribes around the world?

How is it compared to other closely related mammals?

That's an interesting question. And it is also a common misunderstanding of evolutionary processes.

Thanks to @Chris comment, we know/can assume that high mortality rate is not a consequence of industrialization but has ever been before the era of modern medicine.

Women don't let themselves die in order to improve the species. Those women that carry a gene forcing them to commit suicide in order to improve the species won't pass on their genes, and in consequence no women will ever suicide in order to improve the species. In other words, altruistic behavior cannot appear and spread over time. This is the standard view of selection (and probably the good explanation in our case).

Now, I have to say that I lied in the previous paragraph! There is a field of study called social evolution which aims to study social traits. Social traits are those traits which influence not only the fitness of the individual carrying the trait but also the fitness of other individuals in the population. Theoretically all traits are somehow social traits! Typically altruistic behavior is among those social traits that cause a decrease (a cost) in the carrier fitness for an advantage (a benefit) for one or several other individuals in the population. There are several models (which are still debated in particular concerning the assumptions of these models) to explain the evolution of such traits. The most famous, most commonly used and most theoretically studied one is Kin selection/Hamilton's rule. You'll find some explanations about this rule on this post. The concept of population structure is key in the understanding of Hamilton's rule. Also important are the concept of levels of selection, which gives a possible explanation for the evolution of altruism, the concept of lineage selection, and finally the concept of reciprocity (but that doesn't make much sense in the current context!). Some people would not classify these models as I did, some would add other models, some would melt two models into one…

For one of these models to be correct we would need high lineage split and extinctions in human history which I don't think is really the case. Or we'd need that the death of a woman is particularly benefit to her family. I don't think first human were cannibals. Women were probably very often pregnant and males had to fight to be the father. So dying would probably not free much opportunities for the sisters and brothers…. One would need to write some equations and gather more information than what I have but intuitively I don't think that high mortality rate in women while giving birth is an altruistic behavior.


Can I dry digested protein sample over weekend in a vacuum concentrator? I have digested with trypsin the tissue protein extract for mass spectrometry, and forgot to transfer the sample from the SpeedVac to the -80C freezer. As I did this on Friday, I can transfer the samples only on Monday. Will this temper with my sample and subsequent protein identification?

If your sample dried in the speed-vac then it should not cause to much damage to the sample. But if Speed Vac stopped and there was some liquid left, then incubation at room temperature would result in hydrolysis and sample degradation ( also depends on the pH, neutral would be slower). Also you would have modifications to the amino acid side chains like oxidation and deamidation


How are new staining protocols designed for microscopy? How are new staining protocols designed for microscopy? Is it manual work or does it rely on computer simulations?

Say for example I thought the H&E staining does not bring enough contrast. How would I go about producing The Superb H&E Staining Protocol (not necessarily using just hemalum and eosin Y)?

Looking this from a mathematical point of view, the staining is some operator O applied on image I to produce enhanced image E. While clearly the operator O depends on the particular type of specimen, what I want to see, etc., there are surely some general principles guiding the search for finding an appropriate operator O? What are they?

Since the question is on hold, maybe I can try to put it even more clearly. How was the H&E staining invented? What was the process for its invention? I don't see why it would be unclear what I am asking. Dear biologists please take a more interdisciplinary approach.. If the question really is not answerable as such, please explain why. There's probably an answer in that.

This answer addresses the question of how stains were developed historically, which may bring into perspective your overly modern assumptions.

Most of these older (but stil very usefull!) staining techniques, such as haematoxylin (or rather haematein), cochenial/carmine etc. were inspired by the work of textile dyers of that era, starting somewhere in the middle of the 19th century.

It was more a question of trial and error, coïncidence and luck, rather than it being a case of systematic, structured research, starting from the well known molecular structure of the dye and the sample to be stained... Most of the time those were still -at least partial- mysteries.

You should keep in mind, that many of the protocols still in use, were developed in an era when the dye industry as well was still in its infancy, so to speak. Standardization of dyes, Biological Stain Commission and all that, came later. Biologists, histologists etc. used what worked for them. At that time, at that place, with that lot of dry dye powder. Much inspiration, the right idea at the right time and a fair amount of luck. Up to well into the 20th century.

As an illustration: in 1917-1918 there was a shortage on haematoxylin in the German histopathological labs, due to the allied blockade. A lab worker, Fraulein Wilhelmina Schmidt, inspired by the impossibillity to remove elderberry stains from her hands, wondered if it would be possible to use elderbery juice as a substitute for haematoxylin. As there wasn't really an alternative, it was tried. Elderbery juice was concentrated by boiling, diluted with an alum solution and tried. It turned out to work very well.

The story went unnoticed until 1949, when an article on it was published in the German “Zeitschrift für die Wissenshaftliche Mikroskopie”. In the article, the author, Grüber, pointed out that, even after more than 20 years of storage, the slides were still vividly stained, not showing any trace of fading.


Are there any 6 limbed reptile fossils? Were any 6 armed "tetrapod" fossils ever found? I've seen some lobe finned fish with two sets of shoulders in an evolutionary bio book... I'm curious because I'd like 4 limbed and 2 winged dragons to have existed :)

I think, you misidentified the unpaired anal fin of coelacanth as an extra pair of limbs.

I personally haven't ever heard of six-legged vertebrates, although the phenomenon of supernumerary legs is well known as an anomaly. Such anomalies can be easily induced in different vertebrates (including mice: Rutledge et al), if you treat their embrya with retinoid acid (which normally defines embryonic polarity) or fibroblast growth factor. In nature, different factors can lead to development of extra legs, and the most well-known and wide-spread cases are limb abnormalities in amphibians, induced by trematodes and pollution (including retinoid acid mimics?) (Blaustein & Johnson).

That said, I would not be surprised by a discovery of a fossil amphibian with extra limbs. But such a find then should be interpreted as an abnormality, if not proved otherwise. It's true that the fore and the hind limbs are serial homologues, but their number seems to have been fixed very early (in contrast to the number of the fingers).


Are there any known health benefits / risks from milliampere current (0.1-2 mA) on forehead? This is about devices like that sold by foc.us that allows user to apply a small current on a specific part of the forehead.

For the sake of this question I use the foc.us "gamer" model as example. This device has:

a headset with two (moist)electrodes that are positioned on the forehead
a controller unit that is used to apply a (selectable) current between 0.1mA - 2.0mA through the electrodes

[Update:] the electrodes have a surface area of 35mm x 35mm (they are 12mm thick).

According to information received from the company this device is a "micro current signal generator" and can be operated in "tDCS" mode (I am not sure what "tDCS" means). The device has a timer so that it can be set to provide this current between 1 - 40 minutes.

They sell this device with an (explicit or implicit) claim that is helps the wearer improve their ability to focus (on, for example, a game that the wearer is playing).

Are there any known health benefits (such as improved ability to focus) or dangers (damage on the nerve system?) from applying a current on the forehead?

Interesting question!

You ask 3 questions if I am correct:

What is tDCS;
What are the adverse effects of tDCS (at 0.1 - 2 mA);
What are the health benefits (enhanced focus);

I will answer your questions one by one:

(1) What is tDCS: tDCS devices are TransCranial Direct Current Stimulation (tDCS) devices. They send direct current through (trans) the skin and skull (cranial) to the brain.

(2) Adverse effects: EDITED: A review by one of the leaders in the field (Nitsche et al. Transcranial direct current stimulation: State of the art 2008; Brain Stim. (1) 206-23) mentions that current densities between 0.029 and 0.08 mA/cm2 are regularly applied in humans, with session durations of up to 40 min. Side effects are summarized in Table 1 in the cited review. Side effects are mostly nonexistent, though quite a few studies report some itching or tingling sensations under the electrode surface. Very rarely headaches or more serious side effects are reported. The authors predict that the limits will probably increase in the coming years (i.e., after 2008).

A more recent review, however, mentions a slightly lower upper limit of regularly applied current densities, namely 0.066 mA/cm2 in humans, using stimulation times of up to 20 min.

The highest upper safe current limit I could find is mentioned in a 2009 paper by Bikson et al. that mentions 0.14 mA/cm2 based on animal data.

Note that it is not current level per se that determines safety, it is the density of the current that matters. Moreover, the duration of stimulation will be an important factor to take into account.

To go back to your device: in case of 3.5 x 3.5 cm square electrodes (i.e., 12 cm2) as mentioned in the question, the current level range (0.1 - 2 mA) represents a current density range of 0.008 - 0.16 mA/cm2. However, I skimmed the website and they mention 3 cm square sponges or 3.5 cm diameter circular sponges, which brings the upper limit to 0.22 and 0.28 mA/cm2, respectively. The website says the device can be used up to 40 min.

In all, based on this literature review on tDCS and despite the company claiming their device is safe, I would conclude the upper limit of 2 mA not advisable, as its assciated current density exceeds the upper limits that I was able to find (Note, my answer is by no means a comprehensive review on safety of tDCS !). Dependent on the exact electrode surface you could calculate your own safety limit based upon the references cited.

(3) tDCS and enhanced focus: Health benefits in terms of ability to focus: I searched Google Scholar using the search term "TransCranial Direct Current Stimulation attention", which yielded no useful hits.

Another way to go for your focus question is to look at what cortex is situated underneath the 'forehead' that is stimulated by this device. Basically it is the prefrontal cortex:

Stimulating the prefrontal cortex reportedly increases working memory (Fregni et al., 2005) and motor learning (Nitsche et al., 2003). Working memory basically allows a person to use acquired information (let's say seconds or perhaps minutes ago) in subsequent tasks. Motor learning is essentially training of motor skills. Both motor learning and working memory are essential in gaming(!). However, one should carefully read the cited articles (and perhaps related ones, I gave just a few) in terms of effect size, electrode placement and stimulus conditions (including, but not limited to: current level, stimulus duration, stimulus waveforms, stimulus frequency, session duration etc.) to extrapolate their findings onto your device.


Why does Edema occur in Kwashiorkor? Edema in lower leg and face is a symptom of Kwashiorkor. It is the most distinguishing feature of it which distinguishes it from Marasmus. Why would decrease in amount of proteins cause Edema? Why doesn't it occur in Marasmus (which is both protein and energy deficiency)?

Why would decrease in amount of proteins cause Edema?

Proteins in the blood (esp. albumin, because it's the most abundant one there) cause fluid to come from the interstitial space into the capillary. This phenomenon is called oncotic pressure. On the other side there is hydrostatic pressure on the vessel wall, which causes fluid to exit the capillaries. This hydrostatic pressure gets lower as the blood passes through the capillary, while the oncotic pressure stays the same, because under normal conditions, proteins don't exit the capillary very much compared to their amount in blood.

In the first part (closer to the arteriole), hydrostatic pressure is bigger, so the fluid exits the capillary site, while as you get closer to the venous site, the hydrostatic pressure gets lower than the oncotic pressure and the fluid flow is reversed. (see picture)

If you lower the amount of proteins in the blood drastically (as in Kwashiorkor) the oncotic pressure is lower and therefore less fluid is reabsorbed from the tissue, which leads to its accumulation there - this results in edema.

  Why doesn't it occur in Marasmus (which is both protein and energy deficiency)?

Sometimes, both features of kwashiorkor and marasmus are present in the patient, which is called marasmic kwashiorkor and the distinction between these two conditions isn't that easy.

However, normally in marasmus, there is also dehydratation present, which balances the effects of decreased oncotic pressure. Cardiac output is usually decreased too, which leads to decrease of hydrostatic pressure, so again, this can counterbalances the decrease of oncotic pressure.


Evidence that Attention Deficit Hyperactivity Disorder (ADHD) is caused by too much cellular ATP? The question is pretty simple — it's just a theory that I remember my biology teacher mentioned long ago and for years now I've wondered about it without ever asking.

Some people with attention deficit hyperactivity disorder (ADHD) report "energy bursts" with the feeling of needing to explode while sitting still. Further, they report that movement, like vibrating the legs, can help suppress this feeling.

Is there any reason to think that symptoms like these might come from too much ATP inside cells?

That's an interesting hypothesis - however, I am not aware of any evidence that this is the case. Importantly, there can be a lot of difference between cellular access to energy, like ATP, and the perception of "energy" or liveliness.

Here is a paper that actually suggests the opposite: that ADHD could be caused by a neuronal energy deficiency because of differences in astrocyte responses to catecholamines (astrocytes are non-neuronal cells in the brain that, among other functions, regulate metabolism in the brain including access to glucose). Importantly, though, this remains just a hypothesis, not a well-established theory.

ADHD is thought to impact the parts of the brain that are important for attentional control, inhibiting responses, and motivation. Based on that perspective, an alternative explanation for the symptoms you describe is that a sensation occurs that doesn't really require a behavorial response, and for a neurotypical individual this sensation is quickly suppressed (attentional control by not focusing on this sensation, inhibiting your response to shake your leg) without any real conscious effort. Instead, with ADHD, it is difficult to direct focus away from that sensation and mental resources need to be directed towards trying to hold still. The relief from moving around comes from letting the activity progress and not trying to suppress it any more, not because there was a literal excess of energy in the sense of ATP.

References:

Barkley, R. A. (1997). Behavioral inhibition, sustained attention, and executive functions: constructing a unifying theory of ADHD. Psychological bulletin, 121(1), 65.

Todd, R. D., & Botteron, K. N. (2001). Is attention-deficit/hyperactivity disorder an energy deficiency syndrome?. Biological Psychiatry, 50(3), 151-158.


Can the dead be brought back to life by viruses? Zombies have been a part of popular culture for decades. The living dead rising up to take over the world is a terrifying concept, worthy of Hollywood blockbusters and television hits. Some of those zombie fiction stories are based on infection by viruses or other organisms.

Is it possible to bring dead tissues back to life by virus infection?

You must tell facts from fiction; viruses need living cells to replicate because they do not have the molecular machinery at hand to generate energy and construct building blocks essential to life. So no, viruses cannot bring back the dead or revitalize dead cells.

One thing that comes close to it are the so-called zombie ants. These ants have been infected by a parasitic fungus that can take over the ant's nervous system (Fig. 1).

Fig. 1. Zombie ant found in Brazil, infested with the fungus Ophyocordiceps. Source: National Geopgrahic.

These fungi eventually kill their hosts, but before doing so they temporarily take over their nervous system. In the case of Ophyocordiceps unilateralis (Evans, 2011), the spores lodge themselves into the ant's head through an exposed part of the ant’s exoskeleton. The fungus then infiltrates and targets the ant’s brain, taking control of the ant. Then it makes the ant leave its colony and head for a leaf that provides the ideal conditions for the fungus to grow. The ant crawls under the leaf and goes into a “death grip”—biting down hard on the leaf's major veins. This allows the fungus to slowly feed on it. When the fungus finishes growing, it eventually kills the ant and releases its spores (Source: Smithsonian).

The interesting thing is that the zombie ant not only provides shade and humidity when hanging under the leaf, it is also positioned directly on top of the ant’s colony, so when the spores burst out they fall on other ants and begin the cycle all over again. There are hundreds of mind-controlling fungi like this one, but the chances of this type of parasitoid fungus evolving to target humans as hosts are unlikely (Source: Smithsonian).

Reference
- Evans, Commun Integr Biol (2011); 4(5): 598–602


Do Noroviruses include many families? Wikipedia says Caliciviridae Family.
My notes say that Norovirus includes the following

Noroviruses

Norwalk-like viruses
Caliciviruses
Astroviruses and some small gastroenteroviruses

which is a larger definition including at least two families than the Wikipedia definition.
I think

Caliciviruses $\subset$ Caliciviridae
Astroviruses and some small gastroenteroviruses $\subset$ astroviridae

so the note is taking subsets among different families and classifying them into abstract class called Noroviruses.

Extension based by Chris' excellent answer.

Criteria of Noroviruses

(+)sense ssRNA viruses
Structure and replication:

1) only (+)sense ssRNA,
2) simple nucleocapsid viruses,
3) only viruses transmitted by fecal-oral route,
4) size about 30 nm in diameter.

and then final classification of Noroviruses by these criteria

Noroviruses

Noroviruses $\subset$ Norwalk-like viruses ($\subset$ F. Caliciviruses)
Some Astroviruses ($\subset$ F. astroviridae) and some small gastroenteroviruses (what?)

which, however, does not make sense since Caliciviridae $\not\subset$ Astroviridae.
I do not understand what is the point of referring to the viruses by the sentence

  Astroviruses and some other round/small gastroenteris viruses

which are not part of Astroviridae.

Which viruses of Caliciviridae are similar to Astroviruses that are apparently round and small gastroenteritis viruses?

You are mixing different things here: Virus are grouped based on their genetic material (dsDNA, ssDNA ssRNA and so on) into several groups (see here for details), then grouped into families, subgrouped into a genus and then into species.

So it is: Group > Family > Genus > Species.

What you have here are are different positions in this classification.
The names you mention belong all to the same tree:

Group: IV ((+)ssRNA-Viruses) > Family (Caliciviridae) > Genus (Norovirus) > Species (Norwalk Virus).

The Astrovirus belongs into the same group, but then form an own family.
To answer your question: No, since the Norovirus forms its own genus in the caliciviridae family.


Why do I see different hues of colors between each of my eyes? Frequently, I see colors with a slightly different hue when looking through my eyes individually. The right eye is more red-tinted ('warmer' hued) and the left is typically more blue-tinted ('cooler' hued). However, sometimes I can't notice any difference in hue between the eyes (even when closing the other) and on a very rare occasion the warm/cool differentiation is switched (left is warm hued, right is cool hued). Numerous others have confirmed they've experienced similar patterns.
My questions:

What causes this differentiation between eyes?
What would cause the hues from being sometimes clearly noticeable and other times non-existent? Is the cause potentially environmental, behavioral, physiological, chemical, etc?
I wonder if this is occurring at the eyeball level (e.g., cone physiology) or somewhere in my brain (e.g., PVC in the occipital lobe)?

This is an interesting phenomenon which I have been aware of for several years, but I haven't yet come across any official description of it or explanation for it.

Nonetheless, the phenomenon is easy to explain. It is a result of light adaptation in your retina responding to different levels of light being received by each eye.

Background

The level of ambient light present over the course of the day varies by as much as 10 orders of magnitude, and our visual systems have evolved to account for this. The human retina and later visual processing centers have a number of ways to adapt to the light level present in the environment. They are constantly doing this, but these adaptation mechanisms take a little bit of time to adjust to a different light level, usually on the order of fifteen seconds to a few minutes. This is why when you step out of a dark room into the sunshine, you are momentarily blinded by the (relatively) bright light.

Some of these adaptation mechanisms are color-specific, such as those that occur in the cone cells themselves.

Explanation

TL;DR-ers, just read this section

Most of the time, both of your eyes experience roughly the same levels of light intensity, both in general and for each color of light. But this is not always the case.

If you have one eye covered for a period of time, such as when you've been laying down, then your two eyes will be adapted to two different sources of light. If you then uncover that eye, then for a short period of time that eye will perceive the world to be brighter than the other eye. If the light level present in the environment has a tint to it as well, then the just-uncovered eye will perceive that tint more strongly than the other eye.

DIY Science Time

You can verify this yourself, like I have been doing over the past hour, with nothing more than a makeshift eyepatch and nothing better to do.

First, check your initial state by closing one eye and then the other and switching back and forth rapidly while looking at something white. If you've been awake and active, the images from each eye should appear to have roughly the same hue and intensity.
Cover one eye completely (without pressing on it) for a period of about five minutes, while leaving the other eye open.
Then, remove the eyepatch and alternate closing each of your eyes again.

If my hypothesis and explanation is correct, the previously-covered eye should see the world as slightly brighter and more strongly tinted than the uncovered eye does (the hue of this tint should depend on your light source).

If you guys actually do this, you should report your results in the comments, especially if your results demonstrate a flaw with my hypothesis. Let's do some science, people.


Help in identifying an insect My cat has been messing with that insects. It looks quite unusual.

Anybody here can help me identify it, so I can make sure it's not dangerous?

Location: Israel

Once again, this is a  longhorn beetle (Cerambycidae).

The overall appearance fits well with the subfamily Lamiinae (flat-faced longhorns). I would also guess it's in the Batocerini tribe. Though I don't think this is your species, per se, here is an image of a female Batocera rufomaculata with white stripe for comparison:

Once you provide more information about location I can give you a more precise answer.

Monochamus scutellatus is almost certainly incorrect. Notice the lighter coloration , wider body shape, and presence of a lateral white stripe along the side of the OP's insect vs that of M. scutellatus.


Terminology for parts of the leg Going out on a limb here (pun intended)...I'm writing a paper in which I need to refer to various sections of the human leg from upper thigh to knee to calf and ankle. However, "calf" covers a fairly large area. Without having to go into specific leg muscle identification (semitendinosus, biceps femoris, etc.) which could be confusing as they overlap and can be found with Google.

Is there a (standard) anatomical way to describe (cylindrical) sections of the leg from top to bottom?

The lower leg is anatomically called the crus1 and you can refer to the area above the knee as the thigh.

Sural refers to the calf region of the crus, while Peroneal refers to the side of the leg2.
The front (anterior) side of the crus is called the shin.

Patellar and Popliteal refer to areas associated with the front and back of the knee, respectively2.

You can see a summary of regional leg and other body terms here. (Below is a chart from the site):

Alternatively, you can refer to the regions of the leg using relative anatomical directional terms:

 Sources:
 1. Wikipedia;
 2. Rutgers


Meta-analysis of fruits in blocking Cytochrome family My professor says that some drugs cannot be used with grapefruit.
I am trying to search a list of cytochromes and their effect to block members in the cytochrome family. Some in Cyt P450.

What is the main meta-analysis of fruits in blocking cytochrome family?

While I haven't found a list which is restricted to fruits, I found this page: P450 Drug interaction table. They list quite a number of substances which inhibit different isoforms of the P450 protein and also give the original references.

This list gives a large number of herbals which inhibit different P450 isoenzymes. The disadvantage is that they do not give further references so if you want to have a closer look you will probably have to spend some time with Pubmed.


Was the Okazaki fragment experiment ever replicated? Prof said that the experiment "proving" the existence of Okazaki fragments was never replicated.

Is this true? I tried looking on Google Scholar and I cannot find any experiments talking specifically about the existence of such fragments. Wikipedia also doesn't list any other researchers "finding" Okazaki fragments.

Formation of Okazaki fragments in polyoma DNA synthesis caused by misincorporation of uracil - Brynoff, et.al. Cell; Volume 13, Issue 3, p573–580, March 1978 one of many, but you only need one to disprove your professor.

You do not always need to replicate the exact same assays in order to validate a model. Replicate means reproduce the same experimental results in which to draw the same conclusion. Another person need not reproduce your work exactly, so long as your results were the results of experiments that you were able to reproduce on your own. Standards for Replication in Science


Identification of an alpine blueberry type I'm trying to figure out what kind of berry this is. It can be found all over the Swiss, French, and Italian alps, generally right where ordinary blueberries are (the ones one would eat). However, they are distinctly different:

The flower attachment spot (sorry, non-botanist here) at the tip is square shaped (see photo)
Their leaves turn red much later during the season
The berry is more elongated when compared to ordinary blueberries, a bit of an ellipsoid

Possibly Vaccinium gaultherioides (sometimes considered a subspecies of Vaccinium uliginosum), which are present throughout the Alps.

For example, see InfoFlora*:

 Vaccinium gaultherioides Bigelow, © Konrad Lauber – Flora Helvetica – 2012 Haupt Bern

You can see the prevelance of this species throughout the Swiss alps in the below range map (also from InfoFlora):

______________________________________enter preformatted text here
* the national data center for the Swiss flora

I don't know the flora of the Alps personally and I feel you post lacks enough detail for me to confidently pick and choose among many Vaccinium candidates. From those I've examined, this species seems most visually similar to yours.


Is the regulation of lactose operon different between Gram + and Gram -? I know that in E. coli the lactose operon is shut down by CAP protein when binding cAMP. Is this true also for Gram positive bacteria?

I know it's stupid but I answer my own question, for those who are interested.
It is different.  CAP protein regulates lactose operon only in Gram -. In Gram + the presence of glucose shuts down the operon with another mechanism: the TCRS that relies to concentration of fructose 1,6 phosphate.


Bug Identification: Tiny Bugs in Fairport NY We have been finding a ton of these tiny bugs (pin head size or smaller) outside on our patios, outdoor tables, on the grill, etc.

What are they and how do we get rid of them?

These bugs are a type of hexapod called springtails (subclass Collembola). Springtails are often very tiny and hard to see without a lens, so I have to say you did a good job grabbing a fairly detailed picture of this one. Specifically, your specimen appears to be some species in the order Entomobryomorpha.

According to Wikipedia:

  They can be best distinguished from the other springtail groups by their body shape...The Entomobryomorpha...contain the slimmest springtails [with]...long bodies. [They also have] well-developed furculae

Specific species:

Usually, IDing springtails is very difficult, but I believe your specimen matches a fairly widespread species called Entomobrya nivalis (aptly named the cosmopolitan springtail).

 Source: Wikipedia; photo credit: James Keith Lindsey

The description of this species matches yours fairly well. From Wikipedia:

  The cosmopolitan springtail measures about 2 mm in length. Its color consists of a yellow or white background with dark pigment forming transversal bands along the third segment of the thorax and the segments 2 to 6 of the abdomen. The fourth segment of the abdomen has a U- or 11-shaped pattern that easily distinguishes this species from others in the genus Entomobrya+

Somewhat true to its name, this somewhat cosmopolitan species is found in temperate and polar regions across North America and Europe+. Adults typically live among lichens and trees (whereas young live in leaf litter), however, according to NC State Extension:

  Rarely springtails may become exceedingly abundant and may congregate in heaps several inches high on driveways, sidewalks and poolsides.

So what exactly is a springtail??

In general, springtails usually feed on decaying matter, and -- you guessed it -- they're known for their ability to jump!

  Springtails are so-called because they have a unique structure, the furcula, that allows them to jump for considerable distance relative to their tiny size. [source].

 Springing mechanism of a generalized springtail. Credit: Marianne Alleyne [Source]

+ Wikipedia cites Katz, A.D.; Giordano, R.; Soto-Adames, F. (2015). "Taxonomic review and phylogenetic analysis of fifteen North American Entomobrya (Collembola, Entomobryidae), including four new species". ZooKeys. 525. doi:10.3897/zookeys.525.6020