Why are many anti-malaria drugs gap junction antagonists? Why are many anti-malaria drugs gap junction antagonists?

My professor recently just mentioned that many of the anti-malaria drugs block gap junctions. i am wondering if this blocking is important for stopping malaria, and how blocking gap junctions is anti-malarial. How does this effect connect to the mechanism of malaria?

I wasn't sure when I first read this, but this is actually a very interesting question.

Right now there seem to be two completely divorced lines of inquiry that researchers are pursuing with respect to the antimalarial drugs.

One group of researchers is working on working out the mechanism by which say, chloroquine and its ilk bind to and  interfere with the formation of hemazoin (a parasite-friendly form of red blood cell proteins) in the vacuoles of the plasmodium (the parasite that causes malaria). Some folks have recently gotten some pretty reasonable crystals of chloroquine interacting directly with hemazoin. This all provides strong evidence for the view that, as regards killing plasmodium, the most significant interaction for an antimalarial is the one between it and hemazoin.

In (probably) unrelated news it was discovered that many of these antimalarials are also potent channel blockers of various kinds. I haven't dug into this too deeply yet, but most antimalarial people seem to view the channel blocking activity as a side effect. There are a number of other studies underway right now evaluating the psychological effect of the channel blocking activity of the antimalarials. There's one out of Iran that says that the blocking activity of Mefloquine can be used to ease the symptoms of morphine withdrawal.

Another thing to keep in mind is that Mefloquine fell out of favor not due to a decrease in efficacy, but was instead mostly taken out of circulation due to it's (justified) reputation for causing psychotic episodes in patients. So maybe this gap junction blocking stuff could be used to explain Mefloquine psychological side-effects. That would be neat!


Speed of effective lymphatic drainage? Lymphatic drainage occurs from many portions of the body:

To venous angle:

head
axillary lymph nodes

hands
abdomen

legs (I think legs' drainage goes through abdomen)

The speed of the lymph drainage is different in each part of the body depending on the situation at hand.

Assume you have tense muscles in the hand (biceps and trieps).
The lymphatic drainage there can be lowered and be the limiting factor in the system.

I think lowered lymphatic drainage in one part of the body causes more lymph goes to other parts of the body.

What are the negative results of too high lymphatic drainage in an organ?
My intuition

edema
hypertrophy in some cases (excess of nutrients)
hypertension

Negative results of too slow lymphatic drainage are the prolonged intoxication times of

biological,
chemical and
physical factors.

I am trying to find any studies about the effective speed of lymphatic drainage.
I have an intuition that the lowest drainage of one section is the limiting factor in the whole system.
Is there any studies about how to quantify the speed of lymphatic drainage from one part of the body?

Heart pumps (blood) and sucks (lymph).
So probably some cardiovascular study relates the pumping to the lymphatic drainage.

Leonardo's answer:

Animal study on sheep - here.

where

  [L]ymphatic flow in sheep, and
  the range being very heterogeneous (virtually no flow at the lower
  bound). I would agree that, in general, this is a very heterogeneous
  effect subject to many chemical (hydration, osmotic balance, blood
  pressure modifying drugs) and physical (cardiovascular tone, posture,
  activity level) factors.


Where can I find SSR and/or SNPs that locate RC1 genes in Soybean? Where should I look to find SSR and/or SNPs that locate RC1 genes in Soybean?

SoyBase has Illumina SoySNP50K iSelect BeadChip and they've identified soy SNVs. You could find them in dbSNP - identifiers starts with 'ss'.


Can the concentration of a kinase be used to identify its substrate? I'm currently working on a dataset were I'm trying to identify substrates of an kinase in silico, I have a dataset which contains the concentrations every 0h 2h,4h,6h,8h,10h,24h for a lot of proteins found in the sample when the kinase was active. However some of these aren't targeted by the kinase but other proteins that got activated or were indirect activated by the kinase. So what I did I used R to plot the concentration of the detected proteins only if they fitted the concentration line of the kinase of interest(with a little devition allowed) this gave me the following graph:

the blue line is the kinase and the other lines are proteins found in the dataset. I know there could be postive or negative feedback which has effect on the concentation of these proteins.So my question is could the lines shown here be a possible substrate?

The concentration of a kinase is completely independent of the concentration of the substrate, and vice versa. In a typical kinase cascade (such as the Ras→Raf→MEK→Erk pathway), signal transduction is generally amplified with each successive step. A relative small population of one kinase (like Raf) phosphorylates orders of magnitude more of its substrates (like MEK1/2), which in turn phosphorylate orders of magnitude more p44/42 MAPK (Erk1/2) molecules. These then phosphorylate transcription factors like c-Myc which translocate to the nucleus and affect the expression of target genes. Over time, protein levels inside the cell are changed, including the levels of the various components of the pathway or their inhibitors (such as phosphatases, components of the protein degradation machinery like ubiquitin ligases, etc.), allowing for regulation of the signal.

Therefore, for any given kinase at any given time post-stimulation, such as with a growth factor, the concentration and phosphorylation state of its substrate(s) can vary tremendously. For example, in the classical NK-κB pathway, activated by TNFα, one of the main substrates of the IKKα/IKKβ kinase complex is the inhibitor IκBα, which upon phosphorylation is rapidly ubiquitinated and degraded by the proteasome. However, one of the first target genes of the activated NF-κB p65/p50 transcription factor dimer is Ikba itself, which negatively regulates activation of the pathway.

I don't know exactly what information your data set contains, so I can't comment too much on your results. However, just graphing substrate concentrations that correspond to kinase concentrations at various time points will only give you one piece of information - that some substrates have grossly similar concentrations to the kinase - which means nothing. All that is is confirmation bias - you've decided on your result, then picked the data that confirm it. I bet if you were to graph the concentrations of direct substrates along with your kinase, you would find no relationship whatsoever, because as I've described above, there is none biologically.


What are some examples of evolving networks in biology? I'm a master student working on networks analysis in general. A network is something that has nodes and there are links between the nodes. Nodes and links could have attributes. An evolving network is one that changes overtime (new nodes and links are added..etc). An example of that is Facebook. Nodes are users and links represent the friendship relationship. Users have attributes (gender, age, etc.). A Facebook network as you know is an example of a social network.

The issue is that so many people studied traditional evolving networks like social networks, the web, or transportation networks. Currently I'm looking for novel examples of evolving networks to study them. So I thought there might be some examples in biology that could represent some kind of an evolving network.

So my question: Can you give me examples in biology for evolving networks? I'm aware of metabolic networks, but that is also heavily studied, I need something else.

Others have nicely summarized to different types of biological networks and how they can evolve. I would like to make a fine distinction between evolution and dynamic adaptation and add some comments about relative evolvabilities of different biological networks.

Given an architecture, a network can respond dynamically to different inputs. The preferred paths may change and the output characteristics can vary. Example cases include the effect of environment on metabolism. Personally, I would not consider this as network evolution because the architecture remains the same. Network evolution refers to rewiring or addition of new connections.

It would be apt to classify the biological networks like this:

molecular networks

Gene regulatory networks (GRN)
Molecular (protein-protein) interaction networks (PPI)
Cell signaling networks

cellular networks

Neural networks
Biofilms (?)

organismal networks

Ecological networks (food webs etc)

There are several ways in which a network can evolve: Edge addition, edge deletion, edge modification, node addition, node deletion and node duplication.

In molecular networks edge modification happens when the chemical interaction is affected. For e.g. in a gene regulatory network a promoter-Transcription Factor (TF) interaction can change if there is a mutation in promoter sequence or in the DNA binding domain of TF. Similar situation exists in the cases of PPI and ligand-receptor interactions (Though concept of mutation doesn't apply to ligands).
Gene (node) duplications are also common mechanism of evolution of GRN. Gene deletions/inactivations also change the network and in some cases result in complex diseases. Metabolic networks evolve if an enzyme mutates and a new pathway is created.
Usually node additions rarely happen; node duplications and edge modifications are more common in molecular networks.

In neural networks the plasticity is higher than molecular networks. There is a basic architecture that is essential to support life but the connections keep changing, nonetheless, in the non-core regions. Since active neurogenesis stops after a certain point, we can assume that number of nodes remains unchanged but edge addition (new synapse), edge deletion (synaptic pruning) and edge modification (long term potentiation/depression) is quite rampant and widespread. In neurodegenerative diseases neurons die and therefore nodes are lost.

Ecological networks are affected by environment and geological barriers. So there are several subnetworks (ecosystems) that are weakly or strongly connected with each other. Introduction of foreign species (node addition) causes immediate perturbation of the local network architecture. Long term effects arise because of extinction (node deletions), speciation (node evolution leading to edge modification i.e feeding habits etc).

It is also to be noted that in all the cases the effect of a change on a network depends on which node/edge is affected; hubs are under tight scrutiny and are protected from perturbations because any dysregulation can lead to network collapse. Some networks also follow the preferential attachment behavior (which appears contradictory to hub preservation as a mechanism). I guess that molecular networks do not employ preferential attachment whereas ecological networks do.


Why do genetic drift generates negative linkage disequilibrium? The very first sentence of the abstract of this article is:

  "In finite populations subject to selection, genetic drift generates negative linkage disequilibrium, on average, even if selection acts independently (i.e., multiplicatively) upon all loci."

Question

Why does genetic drift generate negative linkage disequilibrium?

Genetic drift is the change of allele frequencies in a population due to random sampling during reproduction. This can cause some allele combinations to become more or less common than would be expected without drift, thus creating a disequilibrium. However, it's the combination of genetic drift AND selection that generates negative (instead of positive) disequilibria. From the discussion of the article you linked to:

  Selection eliminates positive disequilibria more efficiently than it eliminates negative disequilibria, because negative disequilibrium reduces the genetic variance upon which selection acts. Consequently, the average disequilibrium over loci ... becomes negative over time.


Mechanism behind negative conductance of ion channels I am struggling to understand negative conductance shown on I-V curves on ion channels. Mechanistically, negative conductance means that inward (or outward) current increases when voltage across membrane decreases. I-V curves of such a channel have both positive and negative slopes. How it is achieved by ion-channels?

For example, this is in addition to the example posted in the answer by aandreev.

This is the figure OP talks about:

Negative Conductance Caused by Entry of Sodium and Cesium Ions into the Potassium Channels of Squid Axons, Francisco Bezanill, Clay M. Armstrong (1972).

Short answer is that in non-linear mode of ion channel operation other ions start passing through it (channel loses specificity). Cumulative effect (because of different concentrations of different ions) is negative total conductance, if you don't measure currents of specific ions.


How are epiphytes symbiotic? I understand epiphytes are not parasitic. But how exactly are they helping the tree on which they grow?

It's important to note that not all symbiotic relationships must be expressed in terms of a positive-negative (parasitism) or a positive-positive (mutualism) framework. I would guess that most tree epiphytes exist in a commensal framework with their host trees. That is, the epiphyte has a positive interaction (it gets somewhere to grow), and the host species has neither positive nor negative effects.


Why does the body not recycle red blood cells? This question is out of curiosity.

The life expectancy of a red blood cell (RBC) is approximately 3 months, and then RBCs are disposed of. Why does the body opt to build new red blood cells rather than using the existing ones? Do RBCs lose functionality/efficiency as they get older?

They are recycled, the iron and other components are broken down and then absorbed. Adaptations of the RBC prevent the same RBC being used. They lack a nucleus to make them highly efficient oxygen carriers (pack as much haemoglobin as possible). Without a nucleus and other organelles they're unable to synthesise the stuff they'd need for renewal. There's a lot of wear and tear that occurs as they're constantly flowing in tiny blood vessels and getting damaged or affected by substances in the blood.


T7 promoter leakiness Can a gene be expressed under the T7 promoter in an E. coli strain (e.g. DH5 alpha), which does not have the T7 polymerase gene encoded in its genome? In other words, is T7 promoter leaky?

To be more specific, how is it possible that a regular E. coli strain, which does not encode for the T7 polymerase, can grow on kan selective media if it was transformed with a plasmid that has the kanR gene under T7 promoter?

Apparently not, leakiness can be controlled by tightly regulating the T7 polymerase with a tight promoter (in this case lacUV5).


Difference between "wash" and "rinse" in biotechnological procedure descriptions Is there a difference between "rinse" and "wash" in sentences like this:

  Following the staining, the sections were washed twice with deionized water, then dehydrated using ethanol solutions of incrementally increasing concentration (70%, 80%, 96%), cleared using a xylene substitute, embedded in the mounting medium and coverslipped.

Can we use "rinsed" freely in the place of "wash" here, or are there nuances of meaning?

I know the difference between the two verbs in non-specialized English, but I'd like to know if there's a difference in a biotech procedure context.

Google Ngram search gives the following for "sections were washed, sections were rinsed":

This is a very interesting question and it's kind of strange there doesn't seem to be any literature on it. One would expect those to have been carefully studied by the designers of automated microtechnique equipment such as tissue processors and slide stainers.

I own a fair amount of literature on microtechnique, ranging from the end of the 19th century up to the 1980's. I went trough some of those briefly this morning, but I couldn't find a definition for "dip", "rinse" or "wash" or their German, French, Dutch equivalents (And there are a lot more of those, such as "drain", "agitate", "flood", ...).

The problem is even more complicated than it looks alread, as, very often those terms are acompanied by an adjective adding even more confusion, such as "quick/slow dip", "brief rinse", "thorough wash" etc.

I suppose (but that's only speculation on my part) those therms being undefined has to do with the fact that, in microtechique there are that many variables involved, that it's often next to impossible to achieve reasonable results without esoteric stuff such as "technicians experience" coming into play. That's defenitly the case in the field of for example staining technique, when "the classics", such as Masson, Mallory/Heidenhain's AZAN, Van Gieson etc... need to be used.

But not only in that field: If you do some reading in mailing lists such as the Histonet Listserver, you'll notice that messages, questions etc. on "inadequate processing schedule", "reprocessing inadequatly paraffin infiltrated brain/heart/liver/pancreas/... tissue", "bubelled nuclei and an unidentified artefact", "Feulgen stain doesn't work!" are fairly common occurences. Regardless of how expensive the equipment, regardless of however wel reviewed the protocols, regardless of however strict the quality control.

The only -brief- definition of "dip", "rinse" and "wash" I know of and I can remember, is in the book I have, but I can't find for the moment (you'll always see it...):

Smith, A., Bruton, J.: "A colour Atlas of Histological Staining Technique",
? th edition, 1977, ISBN: 07234 0721 5
Publisher: Wolfe Medical Publications Ltd, UK.

Perhaps you'll get any further, starting from there.

O, and while probably pointing out the obvious: dip is shorter than rinse is shorter than wash.


About embryonic and genetic evidence of evolution? My question here is about evidence for evolution from Embryology and from Genetics.

Mammals do have similar Embryos, but is it the case that for each species there is an embryonic development that occurs in earlier species, has such relationship been observed?
What I mean for example if we generally conceive of having species$Sp_1,Sp_2,...,Sp_n$ where each $ Sp_{i+1}$ being evolved from $Sp_i,$ then is it the case that the embryonic development stages of $ Sp_{i+1}$ contains some of the embryonic development stages of all of its ancestor species.

Similar question to 1 but regarding Genetics, is it the case that every species has a genetic thumbprint of its ancestors that lie there in the non-functional sections of its DNA, i.e. is it the case that all the genetic history of our evolution is recorded in the non-functional section of our DNA. So do human DNA have some portions of the DNA of some dinosaurs for example?

Question 1 asks whether ontogeny recapitulates phylogeny. It is striking that the when observing e.g. human embryo development, the embryo seems to go through stages that its ancestral species would go through, but where those 'lower' species would terminate at a specific stage. In other words, embryonic development seems to recapitulate a species' evolutionary lineage.

This is the recapitulation theory, which is outdated and incorrect, but a great example from the history of science. The most prominent of these was Ernst Haeckel's biogenetic law and the Meckel-Serres Conception. There were many problems with this, especially because they focused on noting similarities rather than differences, and several exceptions exist to the rule. They were not very scientific. It also incorrectly presumes that complex organisms have more predecessors. However, it is a compelling piece of evidence to elegantly show that evolution acts incrementally on existing embryological processes.

Question 2 asks whether there is evidence of ancestral DNA in our genome. The answer is yes. Where to begin? We share almost all of our genes with close relatives (e.g. chimpanzees and bonobos) and progressively fewer with more distant relatives. 50% of a banana’s genes (and indeed most other plants') can be found in the human genome. But remember, logically, that doesn't necessarily mean that 50% of human genes are found in bananas, though, because of the way divergence works. The human genome also contains a record of many viruses that have inserted themselves over tens of millions of years. Though they are not ancestors, they have been added 'horizontally' as opposed to the 'vertically' that ancestor DNA is modified over a species lineage.

It's very possible to answer your questions from many, many different angles, and present countless pieces of evidence in favor, but I think this should suffice.


c4 cycle in photosynthesis occurs in monocots or dicots the biosynthetic  portion of the c4 cycle occurs in the bundle sheath cells and i have studies that bundle sheath cells are present only in dicots and not monocots.
according to this, the c4 cycle shold be occuring in dicots and not monocots (due to the absence of bundle s. cells).
but important examples of pants following the c4 pathway like maize and sorghum are monocots.

i dont understand if there is a confusion on my side regarding presence of bs cells in dicots or if there is somewhere else that im going wrong.the following link is contradicting my answer as to presnce of bs cells in dicots

monocots don't lack bundle sheath cells.  In fact, they are much more likely use c4 respiration than dicots.  There are actually about 10 times more c4 monocot species than c4 dicot species.  the c4 cycle is really primarily a monocot adaptation.  I think that the confusion often comes from the fact that dicots appear to be "more sophisticated" than monocots when you look at them, with their pretty, well organized vascular bundles and branching veins, which makes it intuitive to assume that they would be the ones using the "higher tech" c4 system.


I found this insect in Utah, USA. What is it? I keep seeing this insect around my house. What is it?

Here is another image:

It looks very much like the Indian meal moth, Plodia interpunctella, to me. The size, morphology of the antenna and wing tips, and the pale band of scales are all fairly distinctive. (The proboscis isn't very clear in the photo below but it is in most other images you could find via Google; I just couldn't find a better one with a license allowing me to post it here.)

(Image by Kaldari (Own work) [Public domain], via Wikimedia Commons; URL https://upload.wikimedia.org/wikipedia/commons/5/50/Indianmeal_moth_2009.jpg)


What senses are active while sleeping? During sleep, our body activity decreases. I am wondering on the extent of the lowering of this activity regarding our five senses. Clearly, the sense of touch is still very efficient since shaking a body is the most common way to awake someone, and hearing is also quite unaffacted (most, if not all, alarm clock, rely on this sense). Most deaths due to fire are due to intoxication rather than the burnt of the fire, so it suggests that smell and taste are pretty dimmed during sleep.

My main question: To which extent each sense is dimmed during sleep?

For example,

Can we smell during sleep? I don't remember having been awoken by the smell of something during my life...
Similarly, can we taste? If someone gives me delicious food during my sleep, would I be able to feel its taste and remember this experience?
Can we see? REM are well known but it is a mechanical feature of the sleep. Some people sleep with the eyes opened: what do they see?

Note: This related question tries to explain how senses are dimmed during sleep but not how much they are.

Note 2: I am aware this is person-dependant: any sound would awake my mother (a skill during my nightly escapades) whereas I would not notice a party around me when I am in deep sleep. But there should be some kind of average... It also depends on the phase of sleep; I am mostly interested in deep sleep and REM sleep, but an answer detailing every phase would be awesome.

Note 3: This question is certainly naive in its current form. Please help me to improve it.

The answer is of interest not only in sleep but also the perceptions of patients under anesthesia, comatose states, etc.
Our senses aren't 'dimmed' in sleep. There is no effective way to turn off our senses. The best way to explain what happens in sleep is that at some point (the last point, actually), our cognitive processing of sensations changes. That is, our higher brain functions allow us to ignore certain sensory input. This effect has been most studied in sound perception.
In a sleep study involving sound and EEG/fMRI during all phases of (drug-free) sleep,

The first significant result of this study is that the pattern of brain activation associated with auditory stimulation was strikingly similar in wakefulness and sleep, suggesting that sensory processing occurred in both conditions. However, we found qualitative differences in brain activation associated with auditory processing during sleep compared to wakefulness. The reduced regional activity during sleep, compared to wakefulness, in the left parietal and, bilaterally, in the prefrontal cortex, thalamus, and cingulate gyrus (part of the limbic system) suggests that these areas may be involved in the further processing and perceptual integration of sensory inputs likely to occur during wakefulness only.[1]

Supporting this is evidence that some sounds awaken someone no matter at what stage they are in sleep, for example, young mothers are woken up by their infants' lightest movements[2], and the fact that we respond to our own names in a similar fashion in sleep and in wakefulness, but such responses are not shown for presentation of other first names.[3]

These results suggest that the sleeping brain, during SII and PS, elicits a differential cognitive response to the presentation of the subject's own name, comparable to that occurring during wakefulness, and therefore that the sleeping brain is able to detect and categorize some particular aspects of stimulus significance.[3]
Thus, the results suggest that when subjects were listening to their own name during sleep some brain regions were selectively more responsive than in any other condition. ...we have demonstrated that the sleeping brain is able to process auditory stimuli. In addition, we postulate the existence of a functional network capable of detecting and facilitating processing of emotionally relevant inputs during sleep.[1]
Our results support the view that PS is not a state of "sensory isolation"; failure to respond to external stimuli during this stage may depend upon mechanisms occurring only after the sensory input has undergone cognitive analysis.[4]

However, as you noted, odors are not good at waking people up.

Some suggest that the human olfactory system during sleep is sufficiently well tuned to ensure arousal to such threatening stimuli as odors associated with smoke from fire. Our results strongly suggest otherwise. The intensity, strength, and noxiousness of the pyridine stimulus elicited behavioral arousal or EEG activation on fewer than half of stage 2 trials, less than one third of REM-sleep trials, and virtually no stage-4- sleep trials. This is a nontrivial lack of response, since pyridine is a component of coal tar and is also used as a herbicide for firewood, and thus is a likely by-product of many real fires. In practical terms, therefore, olfactory awareness in humans is low to absent during sleep, and human olfaction appears insufficiently sensitive and reliable to act as a sentinel system. We further note that auditory arousal threshold is highest in young and sleep-deprived individuals, increasing the likelihood that olfactory processing is even worse for children and sleep-deprived adults.[5]

The methodology in the olfactory study varies quite significantly from the auditory study. Better studies may shed more evidence on why olfactory stimuli are processed differently from other stimuli.
As to what percent? That probably differs from person to person, and I did not search the literature for that.
[1] Auditory Processing across the Sleep-Wake Cycle: Simultaneous EEG and fMRI Monitoring in Humans
[2] Changes in sleep patterns of young women from late pregnancy to postpartum: relationships to their infants' movements
[3] A differential brain response to the subject's own name persist during sleep
[4] Brain Processing of Stimulus Deviance During Slow-Wave and Paradoxical Sleep: A Study of Human Auditory Evoked Responses Using the Oddball Paradigm.
[5] Minimal Olfactory Perception During Sleep: Why Odor Alarms Will Not Work for Humans


Why do antidepressants have a delayed onset of action? Why do antidepressants take so long to reach efficacy? I've read of theories about it perhaps being due to the strength of negative feedback via serotonergic and adrenergic autoreceptors during the first few weeks of treatment. What I'm looking for in an answer is the following:

The current theories regarding why currently-in-practise antidepressant regimens have a delayed onset of action.
The evidence for these theories.
How these theories fit in with the monoamine hypothesis or whether it is inconsistent with the monoamine hypothesis and how.
Possible solutions to this problem of delayed responses to antidepressant therapy.

All of this is strictly theoretical, there are no actual people involved here, this is simply a scientific inquiry.

Short answer
The mechanism of action of serotonin-specific reuptake inhibitors, a commonly-prescribed class of antidepressants, is a downregulation of 5HT1A receptors through negative feedback. This downregulation of receptors takes time.

Background
Serotonin-specific reuptake inhibitors (SSRIs) are a class of antidepressants commonly prescribed to treat depression. Their therapeuric effects may need weeks of treatment (Celada, 2004), which can be explained by their action on 5HT1A receptors in the dendritic region of the serotoninergic neurons in the raphe nucleus. By blocking serotonin (5HT) reuptake, negative feedback mechanisms cause the 5HT1A receptors to downregulate. This downregulation of the presynaptic modulatory 5HT1A receptors changes the firing pattern of the serotonergic neuron into a more fluttering mode, so that it releases more 5HT (Duman, 2007). More 5HT makes you feel better. That is how it fits into the monoaminergic hypothesis. To have the 5HT1A receptors respond this way takes time, as it is an adaptive response that downregulates of 5HT1A receptors, i.e., less receptors are present on the cell's membrane.

This is only an expanation of delayed action of SSRIs, a specific subclass of antidepressants. For example, there are newer classes of antidepressants that seem to work faster (5HT4 action) (Duman, 2007).

References
- Celada et al., J Psychiatry Neurosci (2004); 29(4): 252–65
- Duman, Neuron (2007); 55(5): 712-25


Why does our body regulate metabolic processes using the thyroid hormone? People with hypothyroidism do fine when taking medication containing their daily dose of thyroid hormone. This means that the signaling function of the thyroid hormones is, in principle, unnecessary. If a constant signal would do, then there is no need for that signal in the first place, as you could just by default switch on whatever process is now switched on by the thyroid hormone. So, what's the whole point of regulating metabolism via the thyroid hormone, especially considering that it predisposes us to thyroid disease?

The answer is in special situations, where a trade-off has to be done between thermogenesis and energy saving. This applies to hibernation of animals as well as to critical illness in humans.

This kind of adaptation is referred to as TACITUS syndrome (thyroid allostasis in critical illness, tumours, uraemia and starvation), NTIS (non-thyroidal illness syndrome) or ESS (euthyroid sick syndrome). In this situation, total and free T3 are downregulated, and, in special cases, TSH and T4, too. See an open review article by Wajner and Maja, which is available from http://dx.doi.org/10.3389/fendo.2012.00008 , for details.


List of all reported bacteria I would like to know were to download a table file with all reported bacteria and its corresponding PHYLUM, CLASS, ORDER and FAMILY.

Basically, its the same table than this one from GOLD genomes but containing the non-sequenced bacteria too:

Thanks for you help, Bernardo

I am not sure if such a complete list exists. There are some lists available, which look pretty complete. Have a look at Labrat and Microbexpert. There is also a book available, which contains an approved list of bacterial names, see here. Otherwise you can of course search your way through PubMed and see, what comes out.


How do single-celled predators chase other cells? From my understanding, single celled organisms have been seen avoiding, and chasing, potential food or other organisms.

How do they accomplish this? They do not have eyes or ears or a nervous system. My understanding is that chemical reactions are involved somehow.

How do single-celled predators chase other cells? What happens on a chemical level?

Edit:To help keep a more constrained question, the single-celled organism I am considering is Paramecium

Detection of and movement according to a gradient of a chemical species is a strategy that single cells use to track a target across space. There are very many strategies of movement depending on the cell and its environment, but a common problem that while cells can sense the concentration of chemicals, they cannot sense its gradient (the direction in which it increases) because they are of too small a size to rely on the difference of concentration on one side and the other. Howard Berg and his co-workers have discovered a mechanism that allows single cells to move toward increasing concentration zones by a combination of concentration sampling and movement. See his webpage, http://www.rowland.harvard.edu/labs/bacteria/projects/track.php


Alternatives to TBE buffer for denaturing polyacrylamide gel electrophoresis of DNA and RNA? I just stumbled upon an article promoting 10 mM sodium borate as an alternative to the well-known TAE and TBE buffers for agarose gel electrophoresis of DNA (Brody & Kern, 2004). They claim that sodium borate outperforms TBE and TAE at high-voltage conditions due to the significantly lower heat development.

I'm currently using TBE buffer and gels with 7M urea for my denaturing PAA gels, and I'm wondering if there are similar alternative conditions for those denaturing PAA gels of nucleic acids?

I couldn't find anything on using sodium borate for denaturing PAA gels, so I'm wondering if it should work the same as for the agarose gels or if it just isn't a good buffer for that kind of gel.

Brody, J. R. & Kern, S. E. Sodium boric acid: a Tris-free, cooler conductive medium for DNA electrophoresis. BioTechniques 36, 214–216 (2004).

You can try SB (sodium boric acid), LA (lithum acetate) or LB (lithium boric acid) buffers. Thex generate must less heat then TAE or TBE buffers and can be run on much higher voltages and are much cheaper than TAE or TBE. Also they do not interfere with standard applications such as band excision and they last longer.

For more info try this sites:

http://www.fasterbettermedia.com/products.html
http://ddgehelp.blogspot.com/2008/01/alternative-electrophoresis-buffer-to.html


Is studying complete mitochondrial genome need biological lab work? The research complete mitochondrial genome study done on species:

Juema pig Sus scrofa (Suina: Suidae) from southern Gansu
red rainbowfish
speckled dace, Rhinichthys osculus
white char Salvelinus albus (Salmoniformes, Salmonidae)
Himalayan honey bee, Apis laboriosa

Did they need to do any work in biological laboratory?

More specifically, Are they related to bioinformatics completely?

Most of them just wrote length in bp (base pair), percentage of ATGC and several combinations of them and some special behavior. These seemed to me as expressing some statistics.

So, how could it be a research work?

All papers you mentioned have involved biological lab work. They all have sequences specific mitochondrial genome and then have analyzed it with the help of bioinformatics. Sequencing genome requires lot of bench work (wet work or "biological lab work"). Even one of them have mentioned it in abstract itself.

  The complete mitochondrial genome of Himalayan bee Apis laboriosa, from Mizoram, India, has been sequenced using Illumina NextSeq500 platform and analysed.


Do mosquitos excrete blood? Since insects like mosquitos ingest only blood, and insects generally excrete their solid and liquid waste at the same time as frass, I was wondering: is mosquito defecation more like iron pellets or droplets of blood?

I've never seen a mosquito defecate, so I have no evidence. Do they defecate during flight? If so, are tiny little droplets of digested-blood falling from the sky?

When mosquitos feed on blood they release water droplets, this is so they can condense the amount of nutrients from the blood but dispose of the unnecessary water weight. This act of releasing excess water is often mistaken as 'pooping', a clearer view of the process here. Actual footage of fecal excretion however, is harder to come across.

Mosquito defecation is more like iron pellets, to maximize their meals they excrete water during or after feeding (in case they need to make a quick get away). Iron is toxic in high doses, so the mosquito excretes it after absorbing the nutrients in the blood, resulting in dark pellets, containing iron and uric acid.


Why do we feel cold on having fever? Why do we feel terribly cold on catching fever of any sort, however our body becomes hotter?
Why is it that a rise in temperature makes the sufferer feel colder? Also, sweating symbolises betterment of the conditions. Why?
{This question has been asked with reference to personal experiences}

Body temperature results from a balance between the heat generated by our cells and the heat “lost” to the environment. Heat created by our cells comes from the energy used to keep us alive. Heat is lost through our skin and the air we breathe out. Human beings have an average temperature of 98.6 degrees Fahrenheit. The brain monitors body temperature and controls our bodies to keep our temperature within the normal range.

If you get a fever when you’re sick, it’s because your brain has told your body to get hotter. It directs the body to make a number of changes to correct the imbalance. Those changes include increasing heat production within the body (by shivering, for example) and reducing heat loss to the environment. Heat loss is reduced by decreasing blood flow to the skin.


Does AMP/ATP ratio affect lifespan in vertebrates? The reference below says that a higher AMP/ATP ratio is associated with lower lifespan in C. elegans.

Is this finding also generalizable to vertebrates as well?

Reference:
Apfeld, J., O’Connor, G., McDonagh, T., DiStefano, P. S. & Curtis, R. The AMP-activated
protein kinase AAK-2 links energy levels and insulin-like signals to lifespan in C. elegans.
Genes Dev. 18, 3004–3009 (2004). PMCID: PMC535911.

There are many papers suggesting a link between AMPK (the major cellular sensor of the AMP/ATP ratio) and lifespan.  As with most of these sorts of experiments, I think it is currently unclear precisely what the mechanism for this is, but AMPK regulates TORC1 and autophagy, both of which are also important for lifespan regulation.  Here is a PubMed link to search results.


What is neutral theory of evolution? The question is not about the very basics, but more about where the line separating the neutral theory from the rest of population genetics lies.
One often reads/hears claims that "the findings of the neutral theory are still disputed" or that "there's no experimental proof for its validity". It is hard to accept these claims wholesale, since:.

It is hardly in doubt that some mutations are neutral
It is hardly in doubt that neutral or even slightly deleterious mutations may fix in the population due to genetic drift, or that beneficial mutations may fail to fix for the same reason.

I therefore interpret such statements as attacks on specific points of the neutral theory, or its most sweeping claims (e.g., that most mutations are neutral), or perhaps as attacks on specific meaning of the term. Moreover, such wholesale rejection seems to ignore that the theory may have very different degrees of validity for different organisms (say, more likely to be true for RNA viruses than for mammals).
I will appreciate clarifications of these points.
Update
Here is an article that raises several issues regarding the applicability of the neutral theory framework to bacteria: Neutral theory, macrobial practice: challenges in bacterial population genetics

Your question would deserve a long essay. R.C. Lewontin wrote a book ("The genetic basis of evolutionary change" - Columbia U.P) on this subject in 1974, right after the neutral theory had been explicitly formulated in the previous few years. The reasons for the controversy over this theory are still alive some 50 years later, despite the enormous advancements in DNA technology. For example the not so hidden polemical tone of this recent paper would not be understandable if some profound ideological issues were not involved; these issues involve something more than "attacks on specific points of neutral theory, (...) or perhaps as attacks on the specific meaning of the term".
In essence, Lewontin argues that the neutral theory has its philosophical roots in the Platonic notion of "ideal" or "type", for which real objects (the genes, in the present case) are only imperfect approximations. This view, applied to the genetic variation in animal species, implies that the role of natural selection is mainly “purifying”, that is, it acts by removing the slightly deleterious mutations that happens continuously and degrade all genomes (when mutations are perfectly neutral, selection does not act at all). As Kimura and Ohta have said, quoting Muller, “the gene through the long course of evolution has finally found itself in man” (quoted in Lewontin, above, p. 30).
The opposite view (can we refer to it as Democritean?) sees all natural populations, man included, as being continuously modeled by unstable and ever-changing environments, so that any attempt to define an “optimum” is intrinsically meaningless. Genomes are highly integrated pieces of firmware, but they are much more fluid, over the generations, than once thought. This means that all genetic variation may have or may acquire meaning, as their molecular or ecological context changes.
Consider an applied consequence of the two views. One of the claims of most anti-racist geneticists is that the variance component among populations of gene frequencies is much higher than the component within populations; this allegedly falsifies the racist argument according to which the differences observed among human population (races) are mostly genetically determined. But if you claim that most of that genetic variation is irrelevant (“neutral”), what remains are the genes responsible for the differences in phenotypic traits, and it becomes obvious that the variance component among populations in the frequency of these genes is lower with respect to the component within populations; and this may be interpreted as supporting a racist view.
It is not automatic that scientists who prefer one theory to the other also support the philosophical implications of that theory. However, the dispute about the neutral theory of evolution cannot be understood without reference to the above conceptual basis.


Why are ammonium ions reabsorbed in the thick ascending limb during acid secretion? In order to produce HCO3- from glutamine and to subsequently reabsorb it,
H+ ions need to be secreted. The kidney does this by via ammonium ions
in the PCT. But why are the ammonium ions then reabsorbed in the TAL before
being put back into the collecting duct? Wouldn't it be more efficient if
they were just left in the tubule fluid where they would reach the
collecting duct eventually? The first method seems to be a longer way of
achieving the same result.

Isn't it all to do with the reabsorption of water, i.e. everything gets flushed out in the Bowman's capsule and then some stuff is reabsorbed to lower the water potential of blood, so water is reabsorbed as well.

I guess I figured it was easier to have a leakier sieve at the Bowman's capsule than try to only release the waste products via facilitated diffusion.


What happens to intrinsic factor exactly at the terminal ileum, where B12 is absorbed? IF is very important for IF-dependent B12 absorption in the terminal ileum, the mechanism by which most of dietary B12 is absorbed. The B12-IF complex bind to IF receptors on enterocytes, but does the complex in its entirety get absorbed, or does B12 alone get absorbed and the IF is left outside?

The latter mechanism I came across in source 1 (see below), which stated the following:

  IF-B12 complex binds to specific receptors. Following this, the vitamin B12 is absorbed into the cytosol of the enterocyte by endocytosis, leaving behind the IF at the brush border.

However, several other books and articles (like 2-4) rather vaguely state that the IF-B12 complex is absorbed into the enterocyte. I've found two articles that discuss the existence of these two viewpoints, (5 and 6), but they are kind of old (from 1965 and 1989 respectively) and I don't know if the "mystery's been solved" as it were.

Sources:

Concise Textbook of Human Physiology (this specific page)
The Mechanism of Absorption of Vitamin B12 (cobalamin) in the GI Tract
Marks' Essential Medical Biochemistry (this specific page)
Textbook of Pharmacology (this page)
Intrinsic Factor
Vitamin B12 absorption and malabsorption

After reversible attachment of intrinsic factor-cobalamin complex to its ileal surface receptor, an energy-dependent
process prevents removal of the complex from the cell surface by EDTA or acid; cobalamin dissociates
from intrinsic factor and, as suggested by previous
workers, binds to a molecule antigenically similar to
transcobalamin II; and  intrinsic factor is slowly(after some hours)degraded and forms breakdown products that are detectable in ileal extracts.

References
Textbook of Pathology Page 318

One article
Intrinsic factor mediated absorption of cobalamin

Recent articles-
Physiology of absorption of vitamin b12


What type of Interspecific relationship does this graph depict? The other day in class, our AP Biology teacher presented us with the following graph and asked us to determine which of the following interspecific relationships it represents:

(A) commensalism
(B) predation
(C) mutualism
(D) competition
(E) parasitism.

She explained to us that since there is not enough information in the graph to explain why species A suddenly drops off after time "x" and species B suddenly rises after time "x", the best answer out of the choices is (A) commensalism.
But to me, that seems to be a faulty line of thinking. After all, my teacher arrived at that answer only under the assumption that the graph/question itself is good to begin with. I tried finding graphs of commensalism using Google Images, and I actually found the original source of the graph that our teacher presented us.
Now, the question on Regentsprep actually gives us a point of reference and states that we are considering two herbivores in a grassland environment, so in my opinion it's reasonable to conclude that the relationship between species A and B is competition.
The problem is that my teacher never gave us a frame of reference: she just told us to identify the relationship in this graph without any "backstory". So what are your thoughts: is it possible to conclude that "A" is the best answer choice if we are not given any information aside from the graph?

Competition makes the most sense, IMO.

For every other type of relationship, A and B should be dependent and roughly proportional: If parasites kill their host, they die in proportion. If predators eat all their prey, they drop in numbers due to food scarcity until food repopulates, the graph would almost look like a double helix. Mutual/commensals also share a dependent and proportional graph. The inverse proportionality of the sample chart, to me, gives away competition: one organism is flat out winning against another through some method.


What is the definition of an opioid, beyond that it's something that stimulates opioid receptors? At first glance, this looks like a circular definition.

Is there some way to definitively determine if a given molecule is or is not an opioid? (Medically or scientifically, not legally).

I'm hoping for something more scientific than "if it's on this list, it is; and if it's not, it isn't."

Wikipedia's article Opioid receptor:

  Opioid receptors are a group of inhibitory G protein-coupled receptors with opioids as ligands. The endogenous opioids are dynorphins, enkephalins, endorphins, endomorphins and nociceptin. The opioid receptors are ~40% identical to somatostatin receptors (SSTRs). Opioid receptors are distributed widely in the brain, and are also found in the spinal cord and digestive tract. (emphasis added)

Wikipedia's article on Opioid:

  Opioids are substances that act on opioid receptors to produce morphine-like effects. Medically they are primarily used for pain relief, including anesthesia. Other medical uses include suppression of diarrhea, treating addiction, reversing opioid overdose, suppressing cough, and suppressing opioid induced constipation. Extremely strong opioids are approved only for veterinary use such as immobilizing large mammals. Opioids are also frequently used non-medically for their euphoric effects or to prevent withdrawal. (emphasis added)

First there was opium. Then the active components of opium (morphine etc.) were defined and called opiates. Then the receptors for opiates were discovered, along with their endogenous ligands (enkephalins etc.), and since those endogenous ligands were not derived from opium and indeed (being peptides) were not chemically related to opiates, a new term was needed. This term was opioid, and yes, the definition of an opioid is that it is something which binds to an opioid receptor.

The perceived circularity lies in the shift of emphasis from the drug to the receptor as the central player - when the first binding studies were being done in the early 1970s the search was for opiate receptors, not opioid receptors.


What is meant by "heads" and "tails" in the context of gene orientation? I have a hard time understanding what this paper is talking about when it says:

  We observed maximal cleavage at sites oriented tail-to-tail and separated by -10 bp to +30 bp (Fig. 2d). Finally, adjacent sites on the same DNA strand (head-to-tail orientation) did not show damage by NHEJ

Then it shows a figure/chart that I don't understand. I don't know the head and tail or the gene is, in terms of what it is relative or with respect to.

Any help would be appreciated.
Thanks.

The heads and tails, in this paper, refer to the orientation of sgRNA binding sites. If there are two tandem sites in the same orientation then they are referred to as head-to-tail (end of the first site followed by the beginning of the second site). It is also apparent from the excerpt that you have included in your question.

Head-to-head and tail-to-tail refer to the site pairs that are placed in the opposite strands; the former (H2H) refers to a configuration in which the beginnings of the two sites are closer whereas the latter (T2T) refers to the case where the ends of the two sites are closer.

Regarding your question about the placement of sites within -10 to +30 bp of each other:

I think the point of the paper is that the two cuts by the nickases should be close enough and in the T2T orientation for a maximally disruptive double strand break. If the distance between the single stranded cuts (nicks) is increased then they effectively are just two single strand breaks which are repaired efficiently. The authors also conclude that using two nickases in this fashion produces has lower chances of mistargeting compared to that of a normal Cas9 (that makes double strand cuts).


How long does it take for dopamine to reach normal levels after a significant drop? The building block sequence for is: Phenylalanine << Tyrosine << L-Dopa << Dopamine. It’s produced in only a few, very specific regions: Substantia Nigra and the Ventral Tegmental Area. Although, on average does this take minutes, hours, days, weeks? And does releasing it between synapses or something else for normal activity affect the time?

Ultimately, I am trying to find a graph of the average anergia level after sex. Or similarly, dopamine levels after orgasm. Most of the research I have come across is about disorders or is too general. Also, there are informal articles and graphs of dopamine levels, but they very widely and are not sourced.

I can see a couple of problems in the question:

First problem, you assume that anergia (not sure that's how you call being tired) after sex is caused by dopamine depletion, I'm not sure this is the case or that lack of dopamine has been related to anergia at all. We know from Parkinson patients that Dopamine is related with action initiation (http://www.nature.com/nature/journal/v466/n7305/abs/nature09263.html) not necessarily with lack of energy or motivation.

Second problem, depletion (the term you originally used) means no more dopamine is system, either because you block it somehow (antagonist), you block its receptors (receptor antagonist) or you block one of the precusors involved in synthesizing it eventually depleting your reserves. "Significant drop" needs to be quantified.

Dopamine (DA) synthesis is an ongoing process, and DA is an essential neurotransmitter / neuromodulator in the brain just like Serotonin (more on that later). This means that it probably has different roles. One phasic referring to its neurotransmitter properties and one tonic referring to its global levels in the brain and how it modulates ongoing synaptic activity.

Normal activity does not deplete DA, and yes, no matter how crazy you think you are, sex is considered normal activity. You can obviously have variations of basal levels of DA depending on your activity but they are way removed from the depletion criteria.

Furthermore, the brain is very parsimonious in its synthesis efforts, it has specialized molecules that recover neurotransmitters that where unused from the synaptic cleft, these molecules are appropriately called reuptakers.

Now to attempt to answer your question considering the problems:

I don't know about DA but I do have some experience with serotonin depletion.
Serotonin (5-hydroxytryptamine, 5-HT) is synthesized from tryptophan that you cannot produce endogenously. Lucky for us that tryptophan is in almost every food we eat which means that there is no lack of it.

You can, in experimental conditions, ask people to drink a glass of a very disgusting liquid that will bind to your tryptophan preventing it from being used in new 5-HT synthesis. It takes approximately 4-6 hours for it to work (e.g. http://web.stanford.edu/~knutson/ans/bjork99.pdf methods section), which means that in 5 hours you used up all your reserves of 5-HT. This meansthat your "refilling" process would be about the same time  in order to get to pre-depletion levels (you might be able to be in a functional regime before that if you ignore the reserves part).

So from this 5-HT example I would say that unless something is very different in the case of DA to recover from depletion it would have to be in the hours time frame.

Another way of looking at it can be looking at the half-life of the molecule which gives you an idea of how much time it lives. This can be used to calculate how much production there has to be to maintain a level of X. The turnover is the amount of time that it takes to, well, turn over, so replace DA in the system that should be in the same order of magnitude as coming back from a depletion experiment.


During non-cyclic photophosphorylation, how does NADP+ become NADPH? I know that NADP+ gets reduced to form NADPH, but what exactly is being donated? Is it two individual electrons (from photolysis or the chlorophyll molecules) and a hydrogen ion (proton)? If this is the case, during the Calvin Cycle, do the NADPH molecules donate the same two individual electrons and hydrogen proton from the light-dependent reactions to become NADP+ again? Thanks.

Specifically during non-cyclic photophosphorylation, I know that the chlorophyll already has preexisting NADP+ molecules, water is broken to release 2 hydrogen atoms and 1 oxygen atom (two water molecules break down to form gaseous oxygen that we breath), those 2 hydrogen atoms get sent down and along the Electron Transport Chain via solar energy and then I believe one goes to a protein called ATP synthase and the other goes to photostem 1. After photostem 1 that hydrogen binds to free floating NADP+ molecules to from charged NADPH. This should be the gist of it all but I would also recommend listening to someone else's input as well.


How do I deal with sticky and viscous samples from cell lysates? To check a protein expression I pelleted a small amount of E. coli before and after induction and lysed them by redissolving them in SDS-PAGE loading buffer and heating them to 95 °C for 1 minute.

This lead to a solution with some very sticky and viscous parts in it, that make pipetting the sample into the gel wells extremely annoying. As far as I heard, this is probably genomic DNA, and my usual way to deal with this is to centrifuge the samples and only pipet a small part out from the top. This does seem to help sometimes, but not always.

How can I avoid the formation of that sticky and viscious stuff or how can I avoid pipetting that stuff into my wells?

Yes, it is the genomic DNA that is causing you trouble. Although a brief 1000g spin should bring it all down, the pellet is never tight and you almost always are going to pull up some gunk with the clear supernatant. A better solution is to include a quick sonication step (5-10s) before the 1000g spin. That way, the DNA is sheared and it should pellet better. It has worked for me most times. Also, remember to use a reasonable volume of SDS buffer when you lyse the cells. Too little buffer and its always going to be hard. For comparison, I use about 200ul per 1ml culture pellet and this volume works well for both pre- and post-induced cells.


At what point during an organism’s lifespan do mutations occur? I’m a software developer and I’m implementing something called a Genetic Algorithm. I would like some input on when during an organism’s lifespan mutations occur.
Genes mutate throughout the lifetime of an organism. When do the bulk of mutations, which would effect the offspring of an individual, occur? Do most mutations happen at conception and early adolescence, or do a significant number happen between adolescence and parenthood?

I'm assuming this question is primarily interested in heritable mutations, given the evolutionary nature of the link you shared. Only mutations in germ cells are heritable, so it will vary between males and females.
Female germ cells are formed in utero. Oogenesis in humans and is pretty much finished by 20 weeks gestational age (there's some debate about this, but it seems to be the current consensus view). So any heritable mutations would need to happen during gestational period. Note that that gestational age number probably varies quite a bit for different animals, but I think it's generally completed before gestation is completed (in mammals at least).
Males produce gametes via spermatogenesis continuously throughout life. So, for modeling purposes, you could probably use the age at which they conceive (though the sperm actually take a couple of months to mature).
One thing I'm unsure about is whether or not aging in the male affects the mutation rates in sperm, but might be something for the OP to look into.


Does an allergic reaction kill body cells? I have wondered what actually happens in an allergic reaction that causes the symptoms such as pain, rash etc.

Is it possible that the human body actually kills its own cells in the process?

Is it possible that the human body actually kills its own cells in the
  process?

Yes it is. It is happens not only as a result of allergic reactions (see comment of @terdon). But in case of allergy our body have 3 methods for killing own cells.

Cytotoxic, antibody-dependent (Type 2 hypersensitivity) The antibodies produced by the immune response bind to antigens on the patient's own cell surfaces.These cells are recognized by macrophages or dendritic cells, which act as antigen-presenting cells. This causes a B cell response, wherein antibodies are produced against the foreign antigen.
Immune complex (Type 3 hypersensitivity) Occurs when antigen-antibody complexes that are not adequately cleared by innate immune cells accumulate, giving rise to an inflammatory response and attraction of leukocytes
Cell-mediated immune memory response (Type 4 hypersensitivity) is an immune response that does not involve antibodies, but rather involves the activation of phagocytes, natural killer cells (NK), antigen-specific cytotoxic T-lymphocytes, and the release of various cytokines in response to an antigen.

See Wiki about types and diseases and about Hypersensitivity


What is the mechanism behind the F-Wave? Can someone explain the actual mechanism behind the F-wave? Is it really different from a H-reflex response or does it just have another name for historical reasons?
The H-reflex (Hoffmann's reflex) is a reflex motor response triggered by a afferent sensory nerve signals.
As far as I could find, the literature describes the F-Wave as a motor response elicited by "backfiring" motor fibres that were antidromically activated by stimulation. It is unclear to me how such backfiring is coherent with the concepts of refractory periods and normal axonal signal transmission.

This is a great question, and I've had trouble finding any authoritative study; since F-waves are mostly used as a diagnostic tool it doesn't seem like they've been studied much at the mechanistic level. The only non-clinical usages seem to be in pharmacology experiments in intact organisms (in particular people) where people aren't going to be going in and doing whole-cell patch clamp in the spinal cord.

This paper:

Balbi, P., Martinoia, S., & Massobrio, P. (2015). Axon-somatic back-propagation in detailed models of spinal alpha motoneurons. Frontiers in computational neuroscience, 9, 15.

has some relevant simulations, though they don't entire answer your question. However, I think their results are sufficient to make some good guesses. Without developing my own simulations, though, I'll have to mostly hand-wave after establishing some key facts.

Axons are small, so it doesn't take that many ions to depolarize a stretch of axon to threshold. The axon hillock has a lot of sodium channels to sort of 'jump-start' the action potential down the axon, but that's in a context where the rest of the soma is already depolarized.
In a back-propagating action potential, the ions flowing into small compartments eventually meet the soma: the soma is big, and so the number of ions needed to depolarize the soma to threshold is large (lots of capacitance in the membrane to charge): the axon hillock may not immediately bring the soma to threshold. This is called "impedance mismatch" and is also important at synapses (where axon terminals are bigger than the axons).

And so now for the hand-waving component... I can't say for certain which channels are involved, but it's possible that the antidromic action potential depolarizes the soma just a little bit, enough to open some voltage-gated channels but few enough that it takes some time for the rising phase to occur. Could involve other ions that aren't sodium, like calcium; could involve the proximal dendrites as well. Because of the different voltage sensitivities of different channels in different compartments, by the time the whole soma depolarizes sufficiently, the proximal part of the axon has had time to recover enough that it can spike again.

One other piece of evidence in support of this mechanism is that the number of cells that fire an orthodromic spike in the F-wave after the antidromic spike is few and variable - that is, it's a small fraction and that fraction varies from pulse to pulse. That seems to suggest that the specific conditions of the soma and nearby processes matters, so there must be a fairly narrow range of parameters that allows an orthodromic spike to follow.


How to increase the rate of absorption and assimilation of food? i was reading this
and want to know

excerpt from the above linkThus, the time for food to travel from one end to the other probably ranges from about 20 to 30 hours
I believe it's 24 hours for a normal person going for poop every morning, But I was curoius if anybody could increase the rate of absorption making my digestive and defacaeting system better performing.

The rate of absorption is controlled by two essential physical factors:

Contact surface between intestinal content and intestinal mucosa.
Time of contact.

There are many other factors including intestinal peristalsis, gastric, pancreatic and bile secretions that stimulate/help absorption.

So increasing or accelerating intestinal passage of food won't do any good (see diarrhea). Water will not be absorbed into the blood flow thus leading to dehydration and hypovolemia. Also the alimentary principles, vitamins, essential aminoacids won't be absorbed.

On the other hand, slowing down the passage has negative effects. It allows bacterial saprophytic flora to multiply so much that those microorganisms become pathogenic by producing toxins. And increased contact time equals increased absorption both of toxins and food principles.


Why do beta-1 and beta-2 adrenergic receptors result in two completely different effects (though both use Gs pathway)? $\beta_2$ adrenergic Receptors are $G_s$-coupled 7-TM proteins. Considering that $G_s$ , by activation increases $[\text{cAMP}]_\text{cytosol}$ which inhibits MLCK of smooth muscles (and causes relaxation as in bronchial smooth muscles).
But at the same time, in cardiac myocytes ($\beta_1$), $G_s$ activation activates PK-A (through cAMP) which in-turn activates L-type $\ce{Ca^{2+}}$ channels. Thus there is prolonged plateau phase and positive inotropic and chronotropic effect.
I think these two results are contradictory. Why and how are these two seemingly completely opposite effects mediated through similar signal transduction pathways?

Madamanchi A. Beta-adrenergic receptor signaling in cardiac function
and heart failure. Mcgill J Med. 2007;10(2):99-104.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2323471/

The autonomic nervous system is composed of the parasympathetic and sympathetic nervous systems. The sympathetic nervous system is stimulated via adrenergic receptors.
Adrenergic receptors are G protein-coupled receptors stimulated by norepinephrine (noradrenaline) and epinephrine (adrenaline).
There are 4 sub-types of adrenergic receptors:

Beta1-adrenergic receptors
Beta2-adrenergic receptors
Beta3-adrenergic receptors
Beta4-adrenergic receptors

Yes, Beta2-adrenergic agonists reduce bronchial Smooth muscle contraction.
Yes, Beta1-adrenergic agonists increase heart rate.
Here we can see activation of different tissues from different receptors, that activate the same pathway. Thus, despite the example explained - the activation of the same path-way - different responses ensue.

In the human airway - Smooth muscle cells express Beta2-adrenergic receptors the most (100%).

In human heart tissue (Cardiomyocytes/Cardiac muscle cells), of Beta-adrenergic receptors - Beta1-adrenergic receptors are expressed the most (75–80%).

"...the cAMP pathway generally promotes contraction in cardiac muscle; however, in Smooth muscle, activation of cAMP causes relaxation."

Source
cAMP inhibits myosin light chain kinase, the enzyme that is responsible for phosphorylating Smooth muscle myosin and causing contraction. Thus no contraction takes place in smooth muscles cells.
Inhibition of myosin light chain kinase increases intracellular cAMP, which further inhibits myosin light chain kinase thereby producing a lower contractile force (E.g. promoting relaxation).
Source


What is difference between breed, variant, subspecies and species? What is the difference between breed, variant, sub-species and species? Are there any similarities between sub-species and sub-population of a region?

A species is commonly defined as the largest group within which interbreeding produces viable offspring.

A sub-species is a subgroup below the level of a species.  One definition is a group which can interbreed successfully with other subspecies, but does not do so in practice (e.g. due to geographical isolation).  Other terms like variety, form, etc., may be used in some domains to indicate various groupings below the species level.

A breed usually refers to a population of a domestic animal that has been selectively bred for specific characteristics.

A population is a set of individuals within a species that live in the same geographical region.  Depending on rates of gene flow, different populations within a species may eventually differentiate into subspecies or distinct species — this is known as allopatric speciation.


What are the benefits of statins in terms of prolonging life? Recently the UK government suggested that all adults over the age of 50, without exception, would benefit from taking statins.

I have an elderly female relative who may, or may not have had a minor cardiac event (the diagnosis is still out) and low blood pressure. It has been suggested to them that they would benefit from statins and have asked me (a former biologist) to find out more.

I've had a look at the mechanisms of action, which seem clear. But the clinical data is somewhat confusing.

It seems we can state with certainty that a small but significant number of users report relatively minor side effects, and a very tiny minority have serious ones.

In term of the benefits, however, the picture is much less clear. I have found a variety of statistics about how they reduce cardiac events but what this translates to in terms of length of life and quality of life is not stated.

One article I looked at suggested that on average, someone at high risk of heart disease taking statins for 30 years would only live an extra 9 months.

The author of that site has a book to sell, and may have an axe to grind. But there are several other articles out there - such as this, and this and this - which make worrying claims about statins being both more unsafe and less beneficial than clinical trials suggest. In particular there seems very limited evidence of any benefits to women.

I am inclined to treat these as alarmist nonsense - they have that sense of hysteria about them. But given that the authors look legitimate, that clinical trials data do not appear to agree with one another (widely varying in the percentage of users reporting side effects, for example), and that this is a relative, I wanted to get a second opinion.

So - can someone please crunch the numbers and tell me what the benefits of statin use are in terms of life years and quality of life? Is there any benefit for women with or without heart disease? And is there any basis to some of the alarmism around their use?

I suspect I won't be crunching as much numbers as you'd want me to, however here are some basic points:

Statins have shown a clear ability to improve the blood llipid profile.
Their use in primary/secondary prevention for cardiac events is justified by the belief that less blood lipid will leave less lipids to clog the arteries with. This is an old paradigm, and it is debated, even if we nowadays indeed give statins to all (potential) cardiac patients. There is evidence for a positive effect of those drugs, but it is not undisputable.
An enormous amount of money is made from statins, and the pharma pushes very hard for their use.
They do have undesirable effects, but those appear mostly early, so patients are usually well monitored for them and they mostly pose no real threat.

On the subject of women: women before menopause are protected from cardiac events by their hormone profile, and would therefore likely benefit very little from statins at that time. After menopause, women present the same cardiac risk as men do. I do not know if studies have shown a difference in outcome for statins in postmenopausal women. If you want to know more, I advise you to go searching for it on Pubmed

DISCLAIMER: The above does not represent professional medical advice, and is subject to debate.


Is the resting state of the forearm in the pronated or supinated position? It seems to me that my forearm is naturally in a more pronated position than the anatomic (supinated) position and that it actually takes work to make it hold the supinated position. Anyone an expert in human anatomy/physiology here or know of any sources that could point towards a more scientific answer?

The main reason why the anatomic position is supinated is because the radius and ulna are crossed when the arm is pronated and parallel when the arm is supinated. It doesn't have anything to do with the resting state of the arm, it's just the easiest way to arrange the bones neatly for description and analysis.


What is the Attributable Risk of birth defects in Zika infected pregnancies? Vital Signs: Update on Zika Virus–Associated Birth Defects and Evaluation of All U.S. Infants with Congenital Zika Virus Exposure — U.S. Zika Pregnancy Registry, 2016

A recent CDC report shows that 10% of laboratory confirmed Zika pregnancies in the US had "birth defect reported."  However, I cannot seem to find an attempt to compare this to a base rate in the US of a similar population.  Is there existing information or a way to determine the Attributable Risk (difference in rate of a condition between an exposed population and an unexposed population).

10% sounds scary, but without a base rate, it's not very meaningful in the context of determining how dangerous the Zika virus is.

EDIT (for clarification):

I'm primarily concerned with the method in which birth defects were collected. 'Clinical experts reviewed reported information to ensure that each fetus or infant with birth defects met the criteria of the USZPR case definition.', but this seems to have been done only with the Zika-positive groups and not with a Zika-negative group. They compare it to a pre-Zika baseline, in which inclusion to the surveillance was different and determination/clinical review of each case was different. Did they (or another research group) perform clinical evaluation of birth defects during the surveillance period on Zika-nagative pregnancies using the same methodology?

The article cited in the question (Vital Signs: Update on Zika Virus–Associated Birth Defects and Evaluation of All U.S. Infants with Congenital Zika Virus Exposure — U.S. Zika Pregnancy Registry, 2016) gives the base rate for the definition of "birth defect" that they use:

  The baseline prevalence of defects consistent with those that have been observed with congenital Zika virus infection was approximately 2.9 per 1,000 live births in the pre-Zika years (4). The initial findings from the USZPR represent an approximate twentyfold increase in Zika virus–associated birth defects among pregnant women with laboratory evidence of possible recent Zika virus infection, with an approximate thirtyfold increase in brain abnormalities and/or microcephaly.

The reference for that background is Baseline Prevalence of Birth Defects Associated with Congenital Zika Virus Infection - Massachusetts, North Carolina, and Atlanta, Georgia, 2013-2014.:

  These data, from Massachusetts (2013), North Carolina (2013), and Atlanta, Georgia (2013–2014), included 747 infants and fetuses with one or more of the birth defects meeting the case definition (pre-Zika prevalence = 2.86 per 1,000 live births). Brain abnormalities or microcephaly were the most frequently recorded (1.50 per 1,000), followed by neural tube defects and other early brain malformations† (0.88), eye abnormalities without mention of a brain abnormality (0.31), and other consequences of central nervous system (CNS) dysfunction without mention of brain or eye abnormalities (0.17). During January 15–September 22, 2016, the U.S. Zika Pregnancy Registry (USZPR) reported 26 infants and fetuses with these same defects among 442 completed pregnancies (58.8 per 1,000) born to mothers with laboratory evidence of possible Zika virus infection during pregnancy (2). Although the ascertainment methods differed, this finding was approximately 20 times higher than the proportion of one or more of the same birth defects among pregnancies during the pre-Zika years.

According to Estimating the Number of Pregnant Women Infected With Zika Virus and Expected Infants With Microcephaly Following the Zika Virus Outbreak in Puerto Rico, 2016. the background of microcephaly in Puerto Rico was around 12 cases per year, while they estimated 180 cases would occur in the presence of Zika.

  We estimated an IQR of 5900 to 10 300 pregnant women (median, 7800) might be infected during the initial ZIKV outbreak in Puerto Rico. Of these, an IQR of 100 to 270 infants (median, 180) may be born with microcephaly due to congenital ZIKV infection from mid-2016 to mid-2017. In the absence of a ZIKV outbreak, an IQR of 9 to 16 cases (median, 12) of congenital microcephaly are expected in Puerto Rico per year.

This is modeling, not pure observation, but was based on observed risk. The paper is online full-text (I think) so you can follow through the assumptions if you want.


Why is it sometimes difficult to resuspend E. coli in P1? It's a curiosity question. When I'm doing minipreps after pelleting the bacteria sometimes it's very easy to resuspend them in P1 (Qiagen kit), but sometimes they form a rubbery clump that is very hard to break up with a pipette and I have to vortex the tubes. It interests me because it adds more time to my lab work and I wish I could avoid it.

This is particularly an issue when you do maxipreps and the pellet is 200x the size of the pellet from a miniprep. The reasons why? Maybe you're pelleting at too high of a g-force (pure speculation). Alternatively, you could be growing the cells too long. I typically miniprep after a 12 hr culture. If you're seeing any darker colors in your pellet, you have a significant amount of dead cells. Those dead lysed cells will spill out their genomic DNA which is very viscous.

For maxipreps, you can't break up the pellet merely by pipetting up and down a few times and calling it a day. What you can do is swirl the side where the pellet is and breakup the clumps. Alternatively you can use a different pipet tip (for an extensive discussion on this very topic see Pipetting damage to cells). I change to a P200 for my minipreps and pipetting only the area around the pellet seems to do the trick for me. For maxipreps I use a P1000 which is better than using a 5mL syringe.


What is the carbohydrate found in almonds, cashews, pecans, hazlenuts and pistachios? So for a school assignment I need to figure out which carbohydrates those nuts have. I first though they probably have starch but I am not sure. Can someone verify this for me, and/or send a link where I could find this information? Thanks.

Firstly you must realize that all the above mentioned nuts are actually the seeds of plants.

So the question now is which carbohydrate is mainly found in seeds of plants.

During the double fertilization of angiosperms, one sperm fertilizes the egg to form the embryo while the other fertilizes the endosperm nucleus to form the endosperm which acts as the nutrient storage for seeds.

The major carbohydrate for seed endosperm is Starch, often stored as granules for their property as being insoluble and compact.

However there are other carbohydrates such as free sugars, glucofructans and hemicelluoses present.

Hope this helped.

References
https://link.springer.com/chapter/10.1007/978-1-4615-2672-8_8


Binding kinetics of 6xHis-Tag For the planning of an experiment I would like to know the binding kinetics (kon and koff) of a 6x-His-tag to a Ni-NTA surface.

I know they should differ due to surface quality and position of the His-tag in the protein. But maybe there is some literature out there (that someone of you knows) from which one could get at least a rough estimate of the kinetics.

Some more hours of literature research finally produced a result:

As published by Khan et al. 2006 6x-His-tag has two distinct dissociation constants of koff1 = 6.3 10-3 and koff2 = 1.8 10-3.


Can an animal evolve after birth? I am wondering if animals do evolve even after birth and gain DNA changes that give them advantages and make them more suitable to the environment while they are alive, then pass these "enhancements" to their children

UPDATE

After all, cell do split and multiply when the animal is alive, and it could end up with a totally different cells than the one born with, so if a mutation happened during this period that led for it to be the dominant "property", what stops it from being passed on?
Is there a research on this?

No.  Certainly not.  There is only a very limited number of cells in the body of any creature which pass on genetic material to the offspring generation; these are referred to as gametes.  Mutations to these cells, however, do not affect the parent in the least, as their sole function is to produce offspring.

One gamete from the father & one gamete from the mother fuse to produce a child with a combination of genetic code, which means that mutations in those gametes (which did not affect the parent) will be present in every cell of the child's body, and affect the child.

Furthermore, do remember that most mutations are not "enhancements"; rather the vast majority of mutations are harmful.

After birth (and really, long before birth) mutations acquired in the organism are unable to be passed on to the offspring, unless they happen in the gametes, in which case they do not affect the parent carrying those mutations.


Term of the type xxx-troph for a compound not used by an organism A prototroph for compound X can make it
A bradytroph grows faster if X is scavenged
An auxotroph needs to scavenge X
A hyperauxotroph lacks both the biosynthetic pathway and the transporters for X

However, I cannot find the term for when the metabolism is rerouted to not need that compound. A term exists and it isn't with an obvious prefix like para, exo, ecto, juxta or similar, but that is as much as I recall: I cannot recall it or where I read it. Has anyone ever encountered said term?

Perhaps you're looking for the word mixotroph?

A mixotroph is an organism that can use a mix of different sources of energy and carbon.

In other words, as stated by Schoonhoven (2010):

The capability of one organism to be autotrophic and heterotrophic at the
same time.


What kind of spider is this (reddish spider)? I just saw this spider on my door and was wondering what kind of spider this is.
information

Country: The Netherlands (Europe)
Color: quite reddish (maybe an idea why this one is reddish?)

pictures

This most likely is Microlinyphia pusilla. Note that this is a male, females look quite different. A picture that closely resembles yours can be found here

https://www.ispotnature.org/node/402405

And in case you want to know, the Dutch name is 'kleine heidehangmatspin'


I want to extract genes from genomes I m a student at computer science and I'm working in a project called Plant Breeding and for moment I need to extract genes from a file with genomes.
I know that the start sequence of a gene is ATG and the stop sequences of a gene is TAA,TGA or TAG.Should I know about inside more apart of the fact that inside I will find only A,T,G,C and inside are exons and introns?

I would highly recommend you to look into the detailed descriptions (or even papers) of how gene prediction and genome annotation is done.
This is a very complicated problem and you seem to missing knowledge of many details that need to be considered, but also there is a lot known about how to do this right, so you don't have to solve this by yourself.

A few very important details, that you either haven't stated or are misunderstanding:

The the ATG codon is the start site of translation, but not the start of a gene. A gene encompasses a promoter (which are very hard to define/predict), 5' & 3' UTRs (untranslated regions) in addition to the open reading frame, which is marked by start & stop codons.
In addition the genomic (i.e. DNA) sequence will contain introns, which are usually much larger than the exons coding for the proteins, and may contain any sequences, so you can not look for codons there.
If you are working with species for which the genome sequence is already known (which is a big number of species), at least a 'rudimentary' gene prediction has very likely already been done. You can find the annotation of all identified features (like genes) in the genome annotation files corresponding to the genome, however this gets very detailed and complicated very fast.
If you are working with a newly sequenced species, where this has not yet been done you need to be aware whether you have genome and/or transcriptome sequences (the latter are important to find gene locations with high quality).


Enzyme kinetics types? In lectures, we have discussed Michaelis Menten enzyme kinetics, but from lectures it was clear that this was not the only type of kinetics.

After looking into this, I have found enzymes that give a sigmoid curve relating initial rate of reaction to substrate concentration.

So so far I have:

Michaelis Menten Kinetics

For which I think the only conditions are that the enzyme reaction follows

and the enzyme does not bind more than one substrate molecule (isn't allosterically binding)

'sigmoidal' kinetics

Where the enzyme is an allosteric enzyme and binding of more substrate to the enzyme increases the enzyme's affinity for the substrate.

Are these the only two main types of enzyme kinetics?

The issue with Michaelis menten curves, is that they presume only one pathway the enzyme can act by. Therefore if an enzyme has multiple pathways the presumptions fail. An example of this is monoamine oxidase, (Ramsay, R. R., Olivieri, A. & Holt, A. An improved approach to steady-state analysis of monoamine oxidases. J. Neural Transm. 118, 1003–1019 (2011).) This paper has the enzyme specific kinetics for monoamine oxidase - the development of the models is incredibly complicated but if you look at the equations you can see how there are multiple pathways.

They also presume only one substrate, so multi-susbtrate reactions need to have the kinetics modified as such. For that the mechanism are: Ping-pong, ternary- ordered and random, all of which impact on the kinetics.If the concentration of the intermediate complex is presumed not to change with time, then another model is the Briggs-Haldane model, known as quasi-steady state kinetics.

Then there are the kinetic models for inhibition. Of which the michaelis menten, where the kinetics vary according to how the inhibitors binds. But as is seen with the above MAO paper, can vary depending on the pathways and binding affinities.  If an enzyme is irreversible then the kinetics also differ (Mcdonald, A. G. & Dublin, T. C. Enzymes : Irreversible Inhibition. 1–17 (2012). doi:10.1002/9780470015902.a0000601.pub2).

It is also worth noting, it is better to use non-linear regression to analyze kinetics as linearizing the data can lead to calculation errors (despite admittedly being the easier and clearer option).


DNA Inheritance- Math vs. Biology After doing some statistical analysis of the raw math involved in DNA contributions, I would like to understand the scale of the biological factors.  I know that 99% of the human genome is identical in all human beings, so genetic recombination and gene conversion should be irrelevant in those areas.  I know that recombination occurs at different rates depending on the chromosomes and loci.  But what is the average order of magnitude?  That is, if I know that a chromosome mainly came from Grandma, how much of it is likely to be from Grandpa?  .1%, 1%, 10% ?  And, does the age of the male affect the rate of recombination to a measurable degree (in spermatozoa only, as body cells would not affect inheritance).

So, at core (it seems) you are interested in the rate of recombination events and the magnitud of their occurrences. This would be the only source I can think of that would give you information about the 'composition' of one chromosome (other than brute-force sequencing).

As you seem to know, recombination is an important factor that 'shuffles' some specific areas of the chromosomal DNA during meiosis (process needed to produce gametes). There is a technique developed by T. H. Morgan almost a century ago, that measures the rate of this 'recombination' events by comparing how two (or/and more) particular loci co-ocurr across generations (when recombination occurs, it is more likely to break co-occurrences of distant loci, as opposed to close loci). Thus, we can use this distance measure as a measure of recombination. In fact, in honor of Morgan, the units used to measure recombination rates are called 'centiMorgans', and abbreviated cM. A cM is the probability for a particular loci (it can be a gene or a smaller sequence) to co-occurr with another loci (to be 'linked' to). Thus, is a relational measure: every particular sequence is related to another, and by transitivity (if A and B are close, and B and C are also close, then A and C will probably be close -this is a generalization-). When done in chromosomal or genomic scale, we can build linkage maps.

In modern times, there's quite more resolution, from whole genome studies at gene/chromosome resolution, and even higher resolutions (remember that a 'loci' can be any unit of your interest in the DNA).

Being all that said, recombination rates, and thus the probability of inheriting certain DNA features from parents/ancestors based on recombination, vary quite a lot. There are many 'hot-spots' and other regions seem to be 'protected' from recombination (for instance, regulatory DNA). According to the work I cite here, the probabilities of recombination can vary within about an order of magnitude (the most likely recombination occurring at 10 times higher probability than the less likely), but this varies a lot.

I hope this helps a bit. I am still not sure what do you mean by "biological factors", but for sure recombination is one of the important factors influencing the identity of each chromosome across generations (others are, of course, point and chromosomal mutations).


Insect ID, Maharashtra, India could someone please identify this insect? This photograph was taken in the Western Ghats of Maharashtra, India, near the town of Mahabaleshwar. Hemiptera was about as far as I could get using other online guides.

Thanks!

Due to its coloration, shape and tarsal formula (5-5-4) I think that a Meloidae(Blister beetle) of the Pyrota genus is likely. You can see several examples of species in this genus from a basic google search. Meloidae has about 2500 species world-wide though, and there might be similar species in other genera. Here is an example of Pyrota bilineata, just for comparison.

(picture from http://bugguide.net/node/view/918423/bgpage)

You probably need somebody more knowledgeable on Indian beetles for a proper species determination though, but hopefully my suggestions can serve as a starting point.


What does the word "refractory" in "refractory period" refer to? What does the word "refractory" in "refractory period" refer to?

I know what it means "refractory period" (both, absolute and relative) in the action potential graph, but I don't understand what the meaning of "refractory" in this context is. What is it refractory for?

From encyclopedia Britannica:

  "After repolarization there is a period during which a second action
  potential cannot be initiated, no matter how large a stimulus current
  is applied to the neuron. This is called the absolute refractory
  period, and it is followed by a relative refractory period, during
  which another action potential can be generated, but only by a greater
  stimulus current than that originally needed. This period is followed
  by the return of the neuronal properties to the threshold levels
  originally required for the initiation of action potentials."

Absolute refractory period = initiation impossible absolutely

Relative refractory period = initiation possible but in greater energy relative to the original required.


Effect of recombination on the rate of loss of genetic variation Following up from this question: Does recombination increase the additive genetic variance for fitness?

(I'm thinking about the evolution of additive genetic variance and differences between the sex chromosomes and autosomes. Assume males are heterogametic (XY) and females XX, recombination occurs on the X in females, but not between X and Y in males. This means X chromosomes recombine at 2/3rds the rate of autosomes. Answers need not necessarily relate to sex chromosomes as many other factors should be affecting their evolution and additive genetic variance)

As far as I can tell, recombination should improve the efficiency of selection as variance in fitness of the population of chromosomes increases (because favourable mutations can combine more easily and deleterious ones do too) which should in turn reduce additive genetic variance (right?). But then recombination means many more combinations occurs which means additive genetic variance might be higher.

So, if I sample the additive genetic variance in a trait in a population where chromosomes that do recombine and a population where chromosomes do not recombine, where should we see the most variance (the recombiners or non-recombiners)?

I found a key paper for myself from an issue of Nature Reviews Genetics last year. It discusses and reviews how recombination affects the rate of genetic variation at the sequence level.

A key concept is that of selective interference, which is what I had stumbled across in the question, this is when the efficacy of selection is reduced because "recombination fails to break down linkage disequilibrium at selected loci." Simply, a beneficial mutation in a system of no recombination is only as fit as the background it is in, if recombination is extremely high (no LD whatsover) then the fitness is defined only by it's own effects. This means that recombination can reduce polymorphism because selective interference will reduce the speed at which non-neutral alleles are fixed or lost.

However, recombination maintains polymorphism, because without it there is a greater potential for hard sweeps, soft sweeps, partial sweeps, and background selection to all remove genetic variance. For sweeps a beneficial mutation will drag any mutations it is linked with to fixation, the further from the allele the weaker that effect is.

It seems that over riding effect of recombination is to maintain genetic variance despite the increased rate at which an mutation can fix when there is no selective interference because it reduces the polymorphism reducing effects of sweeps and background selection.

  "It is expected that neutral genetic variation will be systematically
  depleted in genomic regions with little recombination."


Can a hinge joint technically allow rotatory motion? Let's use a hinge joint and pivot joint as examples.
When talking about the difference between them in terms of movements permitted, I see that on any websites and textbooks, the term 'rotation' is applied to pivot joint only rather than hinge joint.
For example, according to Moore Clinically Oriented Anatomy 10th edition.

Hinge joints permit flexion and extension only, movements that occur in one plane
(sagittal) around a single axis that runs transversely; thus, hinge
joints are uniaxial joints.
Pivot joints permit rotation around a central axis; thus, they are
uniaxial. In these joints, a rounded process of bone rotates within a
sleeve or ring.

I never see the word 'rotation' being used to describe hinge joints' motion, however, doesn't hinge joint technically allow rotation, just that the rotation for hinge and for pivot joints are over a different axis? For example, at the anatomical position, flexion in the elbow's hinge joint involves rotating the joint along the tranverse axis.
So my question is, can a hinge joint technically allow rotatory motion? If not, am I misunderstanding what is meant by 'rotation'/'rotatory motion'?

It is about the movement of the bone along its major axis of movement. A hinge joint moves like a lever while a pivot joint involves rotation side to side like an axle.
It helps if you look at a example of a bone that has both types of joints. The radial head is part of both a pivot and hinge joint, with the ulna it rotates allowing the hand to pronate and is a pivot joint, while with the humerus it is a hinge allowing the arm to swing through an arc.
Keep in mind these are biological terms and not strict engineering descriptions, biology is more interested in how tissues move relative to each other. Biological terms are not interchangeable with geometry and engineering, nor are they designed to be perfectly rigorous, they are descriptive in nature. In biology rotation is a term reserved for more wheel and axle type motion where a bone is revolving around its own axis.

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