Do common terms for animals such as amphibian or reptile fall somewhere in taxonomy levels? Where in the "ranks" of taxonomy (domain, kingdom, phylum etc.) do common words used to describe animals such as amphibian and reptile fall?

This is all a matter of how we define terms, and which definitions are scientifically useful.

Traditionally (since Linnaean times), organisms were classified based on their outward similarities (phenetic systematics). As such, the traditional definition of reptile, which is the same as any common usage that I've heard, includes organisms like snakes, lizards, turtles and crocodiles but does not include birds. This is the class Reptilia. As evolutionary understanding increased, however, it was found that some reptiles, like crocodiles, are actually more closely related to birds than to other reptiles. This makes the common use of reptile a paraphyletic classification.

In modern phylogenetic systematics, organisms are classified in monophyletic groups, or clades, that include an ancestor and all of its decedents (ie it is based on evolutionary relationships). Thus the class Reptilia, since it is paraphyletic, is essentially meaningless in this system. In order to have consistent nomenclature, you could either say that birds are reptiles (a new, cladistic meaning of the term, but which contradicts traditional/common usage) or come up with a new name that includes all traditional reptiles and birds. Taxonomists taking the latter approach use the term Sauropsida for this clade. Sauropsida does not have a taxonomic rank like class because such ranks are useless in cladistics (and actually quite arbitrary even in the traditional system).

So, to specifically address your question:

In phenetics, both Reptilia and Amphibia have the taxonomic rank of class.

In phylogenetics, what we commonly consider reptiles and birds are grouped in a single clade that can be called Sauropsida or Reptilia (re-defined to include the clade Aves) depending on who you ask or which paper you read. Amphibia form a clade.

Perhaps the most important take-away message is that taxonomy is largely un-standardized.


What species is this colourful caterpillar? What species is this colourful caterpillar found on a road in Central Europe?

Just by its appearance and location, that’s maybe a Pale Tussock (Calliteara pudibunda), a kind of moth found in Central Europe.
You can find some observations of that species on iNaturalist: https://www.inaturalist.org/taxa/205294-Calliteara-pudibunda?locale=en-GB


What determines the number of chromosomes an organism carries? This is an extension of this question about What limits chromosomal length?.

I am wondering what could be the specific reasons behind the number of chromosomes an organism carries. In other words, what drives the number of chromosomes and is there anything "stabilizing" the number of chromosomes.

Of course I am not talking about multiple copies of the same chromosome, i.e. trisomy, but rather the reasons behind the partition of the genetic information into a defined number of chromosomes.

From the question I referred to, chromosomes have an upper length limit which is based on their physical size, i.e basically they must be shorter than half of the spindle arm axis and they probably also have a lower limit. Yet it is unclear to me if any non-random equilibrium exists between chromosome number and length other than just being bound by an upper and lower limit in size.

Also let's restrict this question to diploid organisms to avoid organisms such as the Oxytricha trifallax which has 16,000 chromosomes but is also ampliploid or plants such as wheat which can be tetraploid.

I tried to search in the literature and couldn't find a satisfying answer. Also I had in mind the example of the Hela cells which have completely shuffled chromosomes yet still exactly 46.

Practically, there is an obvious barrier to changes in chromosome number: haploid cells produced by diploids must contain exactly one copy of each chromosome (or chromosome section, or locus). Otherwise over- or under- expression of genes can lead to dosage problems. Across all of diploids some large groups show strong conservation of number of chromosomes but others seem fairly free to change the number.

An example of conservation are the Drosophilids (fruit flies) where for approximately 100 million years they have maintained five or six chromosomes (search for Muller elements). Incidentally, with a huge amount of intra-chromosomal shuffling of genes "Drosophila 12 Genomes Consortium", 2007, Nature.

An extreme example of changes in chromosome number can be seen between similar species of Muntjac deer . Where in a relatively short time period (of the order of a million years or less (?) - my guess), the number of chromosomes has reduced from 46 to six (Wurster, D. H., Benirschke, K., Jun. 1970). Someone may correct me but I think amongst vertebrates, mammals show particularly fast evolution of chromosome number relative to, say, birds (though more birds also have micro-chromosomes...).

The above changes (or lack of change in Drosophilids) appear to be independent of genome size - so that was a long way round to saying "It's not genome size".

It could be repetitive DNA. The centrosomes (where mitotic spindles attach) of mammals are full of repetitive DNA and for this reason have been hard to sequence accurately (Graphodatsky, A. S., Trifonov, V. A., Stanyon, R., 2011. ). These repeats evolve (in sequence and copy number) and may promote more or fewer spindle attachments. Drosophilids (in general) have fewer repeats but I don't know if this is a diploid-wide pattern [Research anyone?].


Can insects metabolize poisons? I am new to this community, and I was wondering if insects could metabolize poisons. I'm not sure if I use the correct concepts, I simply wonder if insects can get rid of non-lethal doses of insecticides, and live as they have never been exposed at them. I know that human liver does this task for us, but I don't know if insects have this mechanism.

Insects absolutely can metabolize poisons. This is because plants are absolutely chock-full of them, precisely to avoid insect predation, and in return many insects have developed immunities to many of these poisons. Or as this paper "DETOXIFICATION OF PLANT TOXINS BY INSECTS", which looks like it would be the answer to your question if it were free to read says:

  It is estimated that all plants
  contain some type of defensive compound (Rhodes
  and Gates, 1976). However, plant defensive compounds
  are not universally toxic to insects (Janzen,
  1979). Since almost all plant species are attacked by
  some insects (Schoonhaven, 1972), it is obvious that
  phytophagous insects have been able to develop
  countermeasures which allow them to feed successfully
  (Jones, 1972).

There are three main ways for an organism to neutralize a toxin: sequestering it where it will not harm the rest of the organism (and conveniently, may make the organism itself toxic to its own predators), excreting it (i.e. getting it out of the body altogether) and metabolizing it, i.e. chemically converting it into safer compounds. Often you will actually get combinations of those.

The first page of the paper sadly does not get into details about the extent to which insects use the third strategy, but it clearly states that they do.

This picture from Wikipedia shows some of the digestive organs that contribute to metabolizing toxins:

Organs that appear to deal with neutralizing toxins include the midgut (13), the fat body (not pictured), the hemolymph (not really an organ, it's the blood-equivalent liquid that all the organs bathe in), and the Malpighian tubes (20), though the latter (the apparent equivalent to our kidneys) probably serve more to physically get rid of the toxins than to metabolize them. From the Wikipedia page :

  In insects which feed on plant material containing noxious allelochemicals, Malpighian tubules also serve to rapidly excrete such compounds from the hemolymph.

And from here:

  Some small organic molecules are also
  actively transported into the tubule
  lumen by the transcellular pathway,
  including alkaloids (plant compounds
  which may be toxic to the insect).

This PLoS One paper (so, free to read) studies the enzymes that insects use to metabolize some toxins and notes among other things that:

  One of the best studied examples is the CYP gene superfamily of Papilio butterflies (Papilionidae), which have adapted to furanocoumarins, the toxic components of their food plants [15], [16]. These toxins are degraded by inducible CYPs that are expressed in the midgut and also in the fat body [17], [18].

and

  For Tyria, senecionine N-oxygenase (SNO), a soluble enzyme located in the hemolymph, has been shown to convert the pro-toxic free base efficiently into its non-toxic N-oxide [22] (Figure 1).

(emphases mine)

Another paper, "Chemical detoxification vs mechanical removal of host plant toxins in Eucalyptus feeding sawfly larvae (Hymenoptera: Pergidae)" describes how some sawfly larvae have special mechanisms for getting rid of and sequestering toxic oils, but also says :

  The oil sequestration is, however, incomplete and chemical gut content analyses by gas-chromatography (GC) revealed that 1,8-cineole does enter the midgut and is metabolised to hydroxycineole.

Another paper studying a class of enzymes generally associated with detoxification (but note the paper itself is about how those enzymes have other roles as well):

  Insect monooxygenases can be detected in a wide range of tissues.
  Highest monooxygenase activities are usually associated with the midgut, fat bodies and Malpighian tubules [9], but again the expression of individual P450s can vary between these tissues [17].

Insofar as insects have an equivalent to our livers it would seem to be the fat body. Like the liver this organ has many functions, including fat storage, energy metabolism and regulation, but also metabolizing toxins. From "INSECT FAT BODY: ENERGY, METABOLISM, AND REGULATION" (free to read):

  Whereas many insect tissues have vertebrate analogs, the fat body is an organ unique to insects (77). The fat body is a relatively large organ distributed throughout the insect body, preferentially underneath the integument and surrounding the gut and reproductive organ (36). Unlike the solid structure of the liver, the insect fat body is a loose tissue.

and

  Most of the insect’s intermediary metabolism takes place in this organ, including lipid and carbohydrate metabolism, protein synthesis, and amino acid and nitrogen metabolism.

and

  In addition to its role related to storage and utilization of nutrients, the fat body is an endocrine organ (65), produces several antimicrobial peptides (44), and participates in detoxification of nitrogen metabolism (74).

And from the other link:

  As in vertebrates, the oxidative metabolism is mediated via the tricarboxylic acid (TCA) cycle and the electron transport enzyme systems. The fat body contains enzymes mediating the gluconeogenesis process as well as enzymatic systems with a detoxification role to manage harmful endogenous metabolites and toxic xenobiotic compounds. Detoxifying enzyme systems include microsomal mixed function oxi-dases, in which the cytochrome P450 is predominant, various hydro-lytic enzymes (esterases, phosphoesterases), and conjugating systems.


What exactly is "lateral septum"? I came across the phrase lateral septum and I can't seem to find the precise definition online. Is it "the areas roughly to the right and the left of the septum pellucidum"? Or is it the parts of the septum pellucidium itsef? I'm confused.
If it is near the septum pellucidum (to the left and right), does it include particular nuclei?

Brain pathways for sexual excitation involve the activation of incertohypothalamic and mesolimbic DA transmission in the mPOA and NAcc that focuses attention on incentive sexual stimuli and engages motor patterns of approach and consummation. Collectively, the behavioral patterns stimulated by those systems and the subjective feelings that accompany them constitute the epiphenomenon referred to as sexual desire or, when mixed with genital and sympathetic arousal, “libido.” The core of this pathway includes the mPOA and its outputs to the VTA, which contain DA cell bodies that project to various limbic and cortical regions, such as the prefrontal cortex, olfactory tubercle, NAcc, ACC, lateral septum, and corticomedial amygdala.

The article is "Pathways of Sexual Desire" by James Pfaus (2009).
I have read the Septal area article in Wikipedia but still cannot get it.

It is confusing.  The septum pellucidium is a thin membrane separating the left and right lateral ventricles.  It contains white matter (nerve fibers), blood vessels and a few neurons.  It has traditionally been thought of as just a separating membrane, but the fibers running through it connect to the hippocampus and hypothalamus and so it is probably a relay to those structures.
Lateral to the septum pellucidium are the septal nuclei. The septal nuclei are NOT considered part of the septum pellucidium (or vice versa).  The septal nuclei are traditionally divided into two major subregions, the medial and lateral septal nuclei.  As you might have guessed, the medial nuclei are immediately adjacent to the septum pellucidium.   As the septum pellucidium is quite thin, the right and left medial nuclei appear to compose a single midline nucleus with the septum pellucidium running through it. The lateral nuclei are the ones a bit further out and it is these that are called the lateral septum. The septal nuclei may be further divided into caudal and ventral regions.  Many neuroanatomists group the most posterior parts of the septal nuclei into a third group, the posterior septal nuclei distinct from the lateral and medial divisions.
This is part of the problem.  Structures in the brain were named based of where they were and what they looked like since their functions were unknown. For example the hippocampus was given this name because it looked like the tail of a seahorse (genus Hippocampus), and the locus ceruleus ('blue place') looks blue. As we have learned more, some neuroanatomists have divided regions into subregions or sometimes lumped regions together based on their models of the proposed physiologic functions or neurochemistry of those regions. The subcortical 'limbic' nuclei, including the septal nuclei are among those most subject to these changing definitions,.  And as you might guess, different neuroscientists often disagree about these divisions.  Being human, they sometimes behave as though their definitions are THE definitions, or gloss over differences between sometimes unclear definitions.  Ideally, people splitting nuclei into proposed subregions try to propose clear definitions, but this is not always the case and these proposed definitions may not be accepted or used.  This can make it difficult for experts to know exactly what regions are being discussed, let alone people not long immersed in the field.  Over time however, fields tend to come to a consensus on terminology though for many brain regions this consensus remains elusive.  I hope this discussion makes the topic of the lateral septum a little more comprehensible, if only by validating your sense that the topic is confusing.
Here is a readable overview about the septal nuclei and septum pellucidium:https://www.neuroscientificallychallenged.com/blog/know-your-brain-septum
Check out the first reference here to discussing the neurochemistry of the medial septal nuclei from a chapter by Risold in the Rat Nervous system https://www.sciencedirect.com/topics/neuroscience/medial-septal-nucleus
In contrast look at the introduction of the following paper regarding the lateral septal nuclei:
https://bio.biologists.org/content/8/7/bio043554
"Whole-brain mapping of projection from mouse lateral septal nucleus"
And if you have access, you may be interested in
https://onlinelibrary.wiley.com/doi/abs/10.1111/ejn.13746
"Differential and complementary roles of medial and lateral septum in the orchestration of limbic oscillations and signal integration"
And here is a paper that describes development of the posterior nuclei as being different from that of the lateral and medial nuclei
https://www.nature.com/articles/s41598-018-30020-9


Does cheese contain cells of animal stomachs? When cheese is made with calf rennet, is it possible that the cheese contains cells of this calf (stomach)?

Dried and cleaned stomachs of young calves are sliced into small pieces and then put into salt water or whey, together with some vinegar or wine to lower the pH of the solution. After some time (overnight or several days), the solution is filtered. The crude rennet that remains in the filtered solution can then be used to coagulate milk.
Does this filtering exclude all stomach cells of the calf?

Yes it is possible, filtering is unlikely to be fine enough to remove all cells (though the presence of intact cells based off of the culturing methods is unlikely), note though that modern methods of rennet extraction from stomachs are different than what you described. There are also non-calf rennet made with everything from fungi and bacteria to vegetables. Source


What is the mechanism behind tinnitus? I seem to have come across two contrasting explanations for tinnitus induced by loud noises- i.e. damage to the hair cells in the cochlea.

On the one hand, I have read that damage to the hair cells results in them releasing excess glutamate, the neurotransmitter that carries the impulse from the hair cells to the neurones in the auditory nerve. This would result in the neurones constantly being excited, which I can understand would lead to constantly perceiving sound.

On the other hand I have read that when the hair cells are damaged, the auditory cortex is no longer receiving electrical impulses from the hair cells that detect those frequencies, and so the neurones start to fire (although I am not sure why no input would lead to neurones going off by themselves! Surely there must be some input to cause the initial depolarisation to cause an action potential?) and so you perceive a constant sound.

These seem to me to be two contrasting explanations. My only other guess on how these explanations overlap is that the excess glutamate being released causes death of the neurone, and therefore the neurones after that one do not receive and input and they start firing spontaneously (although again I would appreciate if someone could explain how lack of input results in neurones firing by themselves).

Thank you in advance!

Short answer

The exact mechanism behind tinnitus (ringing in the ear) is unknown.

Background

Of the two theories you pose here, to the best of my knowledge the second one is the most widely accepted. It is a generally accepted phenomenon that whenever neural systems are being deprived of input, they start seeking new input, or even generate it themselves. For example, blind folks rarely have no visual perceptions at all. In contrast, they often perceive spontaneous visual sensations. For example, many blind folks report perceiving a persistent grayish background hue. In other words, it is never black in the eyes of a blind person. They also often see spontaneous spots of light. The most striking example, however, being Charles Bonnet syndrome, where the blind person may perceive complex scenes with faces and objects (Bhatia et al., 2013).

In the case of tinnitus, the perceived sounds are mostly not complex, but repetitive and simple in nature ('ringing', beeps etc.). It is thought that the deafferented auditory cortex actively starts generating sound perceptions. However, many other explanations have been brought forward, such as spontaneous activity in the hair cells in the cochlea and spontaneous activity in the auditory nerve fibers (Luxon, 1993). I will sum up a list of potential causes mentioned in Han et al. (2009):

Peripheral mechanisms

(1) Spontaneous otoacoustic emissions
Spontaneous otoacoustic emissions (SOAEs) are small acoustic signals generated by the electromotile activity of outer hair cells (OHCs) in the cochlea. While normally inaudible, SOAEs may be perceived as tinnitus. Tinnitus due to SOAEs is mild and is more common in subjects with functional hearing.

(2) Discordant theory
Tinnitus may be induced by the dysfunction of damaged OHCs while inner hair cells (IHCs) are still intact. For example, intense noise and ototoxic agents initially damage OHCs in the basal turn of the cochlea, and subsequently, if continued or repeated, affect IHCs, because IHCs are generally more resistant to such damage. IHCs are the receptor cells for sound transduction. In contrast, OHCs work as mechanical amplifiers, enhancing weak sounds by providing up to 50 dB, which can be evaluated by measuring OAEs. When OHCs die, cells in the dorsal cochlear nuclei (DCNs) show increased spontaneous activity due to the fact that IHC input is relatively normal, but OHCs input is decreased due to damage to the OHCs. This spontaneous activity is perceived as tinnitus.

Spontaneous activity in neurons can occur through a host of mechanisms. Basically, a depolarization beyond a certain thresholds sets the neuron off to fire. In case of the disinhbited DCN neurons, the input from the OHCs is taken away. OHC input to the DCN is inhibitory,m as it is believed OHCs activate inhibitory interneurons. The exact mechanism is unknown, but a central inhibitory neurotransmitter is GABA. GABA can activate GABA-A receptors, that open up a Cl- channel, which in turn leads to Cl- influx into DCN neurons and hyperpolarization. When this input is taken away, you can imagine that DCN neurons depolarize and when this depolarization reaches threshold, the DCN neuron may increase firing Kaltenbach et al. J Neurophys 2002;88:699-714. Hence, as you question whether, in the absence of neurotransmitters, cells can fire action potentials, I say: **yes*. In fact, many neurons have spontaneous spiking activity, often with very regular frequency. These oscillating behaviors are often mediated by cation channels that gradually depolarize the cell up until its spiking threshold.

(3) Crosstalk theory
Nerve compression (e.g., due to a tumor) may cause artificial synapses to be formed between nerve fibers of the cochlear and vestibular nerve  (crosstalk). The breakdown of the myelin insulation of the nerve fibers may further enhance coupling. Hence, spontaneous activity in the auditory nerve may be generated through vestibular activity.

Central mechanisms

Some patients may still perceive tinnitus after the auditory nerve is transected. Hence, tinnitus in this subgroup must be caused by mechanisms located more centrally from the auditory nerve.

(4) Auditory plasticity theory
Damage to the cochlea enhances neural activity in the central auditory pathway, specifically in the temporal lobe in the auditory association cortex and inferior colliculus. This theory was touched upon further above in the first paragraph. Basically, when neural tissue is deafferented, it tends to look for new input or even generate activity de novo.

(5) Somatosensory system
The activity of the DCN is also influenced by stimulation of nonauditory structures and the somatosensory system has been implicated in development of tinnitus. Somatic tinnitus can develop as somtaosensory input may disinhibit the DCN.

(6) Limbic and autonomic nervous systems
The aforementioned theories cannot explain why some people suffer from tinnitus while others do not. More than 80% of those perceiving tinnitus for the first time do not associate the sound with any negative meaning and experience spontaneous habituation. However, if the first perception of tinnitus induces high levels of annoyance or anxiety by association with unpleasant stimuli or with periods of stress and anxiety, tinnitus might develop into a problem.

References
- Bhatia et al. Delhi Psych J 2012;15:423-4
- Han et al. J Clin Neurol 2009;5:11-9
- Kaltenbach et al. J Neurophys 2002;88:699-714
- Luxon, BMJ 1993; 306:1490-1

Further reading
- Action potentials in the absence of neurotransmitters: how-does-optogenetics-work


Does sample buffer require EDTA for protein separation on SDS PAGE? In sample buffer preparation we add EDTA, but if SDS-PAGE is for protein then is it necessary to add EDTA in sample buffer? What is role of EDTA in sample buffer for protein separation for SDS-PAGE.

EDTA is a complexing agent for bivalent cations and is usually used to inhibit enzymes (proteases, nucleases) which need these ions in their active center to work. Without it they do not attack the sample.

The presence of EDTA in the sample buffer is interesting, since Laemmli's original paper from 1970 ("Cleavage of structural proteins during the assembly of the head of bacteriophage T4.") doesn't use it and I think it is not necessary.

The reason for this is simple: Protein samples are usually generated in buffers which contain different protease inhibitors, which protects the samples. Additionally the purpose of the sample buffer is to denaturate (at least for the standard SDS gels) the protein sample completely, so it will run uniformly. Both steps ensure that proteases are either inhibited or completely denaturated, which will both protect the sample.

The only reason I can think of for using EDTA is that it can help to destabilize your target protein, when a co-factor which is important for the structure is complexed by EDTA and thus keep it in solution after the denaturation.

There are of course ressources which state that EDTA is necessary for protein integrity, but they only say it is there to inhibit proteases by complexing metal ions (see here for example).

As a 2x sample buffer, I use the following recipe (this can also be made 5x if necessary), which contains EDTA, but can also be done without. If you prefer β-Mercaptoethanol, you can use it in the same concentration as the DTT (which has the advantage of being less smelly):

2x sample buffer:

4% SDS
20% glycerol
2 mM EDTA (ethylene diamine tetraacetic acid) - can be made without
100 mM Tris-Cl, pH 6.8
200 mM DTT (dithiothreitol)
0.1 % (w/v) bromphenol blue dye


Why do athletes see a dip in performance in their thirties? I have noticed a lot of athletes hit their prime when they are in their 20s and that by the time they reach their 30s they are past it and start to decline. Great athletes tend to prolong their careers by adjusting their game strategy, but even so they can't do the things they used to do when they were younger. Examples of this are abundant in the NBA, NFL, MLB, NHL, football, etc.

Why do athletes suddenly have such a drop off in performance? What happens to their bodies,  muscles, etc that prevents them from doing what they once did? Can someone explain the biological/physiological reason for this?

The decline in athletic performance is a result of senescence; the question then becomes "why do we senescence?"

A number of questions on this site have addressed this. These include Why does evolution not make our life longer?, Why do we age?, and any number of others that one can pull up with a search for senescence. It is key to distinguish between proximate (how, physiologically ) and ultimate (why, evolutionarily) explanations. It's not entirely clear to me from your question which of the two you are asking.


How to best conserve a beetle inside a jar? Few days ago a giant beetle appeared on my house. Well, it's dead now. Since it attracted some attention from my little girl, I'd like to preserve it inside some jar. What's the best way to do it? What products should I use?

I've researched a bit in the internet, and it's said not to use formaldehyde because the specimen would become too hard (that's not a problem to me, but I don't like using such strong products considering that a child will probably handle the jar).

The answer to this question depends on how you want to preserve it - as a pinned specimen (also dry preservation, most common) or in a liquid. If you want to pin it, placing it in a jar with a cottonball soaked with ethyl acetate (also used in killing jars) is good because it softens the muscles and makes the insect easier to pin and mount. Beetles are then usually pinned with a needle through the right elytra (wing cover), but there are also other ways to pin them. You can also glue the beetle to a piece of cardboard, which is then pinned. Gluing insects generally helps to protect them (so that legs and antennas dont fall of when handling them), but makes it more difficult to see the ventral side and it can also be cumbersome to have large glued beetles in a collection.

If you want to keep it in a liquid, 70-80% alcohol (ethanol) is a good choice, but not stronger (95% alcohol makes the insect stiff and brittle and might distort smaller insects). As you say, formaldehyde is generally not used since it's very toxic and it can also make the insect stiff.

Here are some more good tips on collecting and conserving insects from the University of Minnesota.


Egypt bug needs identification please Is it possible to identify this bug,,? Found in South Sinai  .in Egypt . Only seen crawling but maybe it can fly ? Black with 6 legs. 2 long black "strings " coming from back end
Thank you

This is a cricket in the family Gryllidae. The two thin "strings" on the left are antennae, and the two sturdier "strings" on the right are cerci (though your image is not clear, and perhaps one of the extensions on the right is actually an ovipositor). See here for a clear image showing cricket anatomy.

An example cricket with wide geographic range that includes Egypt:

Gryllus bimaculatus

 Credit: Vlad Proklov

Without additional info, I'm not sure you'll get an accurate species ID on your specimen.


Are hormone secretion variations the same for a pair of monozygotic twins? I have recently read a paper about how stress affects morning salivary cortisol levels in an individual. I am conducting a study on monozygotic twins and was wondering if cortisol levels would fluctuate similarly in a pair of twins, or whether cortisol and other hormones are unrelated to the genetic makeup of the twins.

Bartels et al. 2003 is a review that reports an estimate of the heritability of the cortisol level of 0.62. In comparison to most traits, it is a relatively high heritability.

So, in short, the answer is "no". Cortisol level variation is lower among twins than among unrelated individuals. If the definition of heritability is a little bit unclear to you, you should have a look at this post.

The reaction norm of cortisol level (and other stress response) with varying stress level also seems to be heritable (Ilsing and Hoelsboer 2006, Volckaert et al. 2012).


Visibility of a cell membrane under microscopic Imaging When we see any cell under a microscope the membrane surrounding the cell is opaque. But then if the cell membrane surrounds the cell in all the three dimensions how come we can see through the cell membrane and have a look at the organelles inside if the membrane is also covering the cell from the top and not just at the boundries on the object plane.

The membrane(and associated proteins) isn't actually opaque, it is just "more opaque" or "less translucent" than the cytosol: when you look through the microscope, you are utilizing this contrast to detect the edges.

In the center of the cell you observe, you see the membrane straight-on, and light is only affected by 1-2 layers of membrane. On the edge, you are viewing through the membrane somewhat "sideways" , so there is effectively more "thickness" of membrane. Maybe not an exact replica of the situation, but one that might be easier to visualize, is earth's atmosphere viewed from space. You can see the "blueness" of the atmosphere at the edges, but when you look straight down at the ground you see clouds, oceans, landmasses not tinted as blue.


Where is ATP used in Phosphorylation? In the section describing the Calvin Cycle, under the subheading "Reduction",  my textbook states that:

  The steps involve utilisation of 2 molecules of ATP for Phosphorylation...

I could not get where is ATP used in Phosphorylation (ATP synthesis by cells)? Please help me to understand.

In biology phosphorylation marks the addition of inorganic phosphate groups to proteins or other organic molecules. The phospho-group usually comes from ATP which is converted into ADP in this process.

In the context of the Calvin Cycle there are two positions where molecules get phosphorylated. The first is the phosphorylation of 3-phosphogylcerate to 1,3-bisphosphoglyerate, the other is the phosphorylation of Ribulose 5-phosphate to Ribulose 1,5-bisphosphate.

See the image (from here):


Why do moths not die when they fly into a window? Sometimes at night when I'm inside with a light on, I can hear (I'm sure) moths fly into the window, and it's so loud I can sometimes hear it over the TV from the other side of the room.

Since they're so small, how do they hit the window hard enough to cause such a big noise and not die?

Simply because their body mass is small. It's the same as if an ant falls off from the roof of a building. It will suffer no harm because the speed of its fall will be very slow, but try the same yourself and you will surely die.

More scientifically, it's a question of kinetic energy: $E_{kinetic}=\frac{1}{2}\times mv^2$
You can see from this formula that if mass is small, then kinetic energy will also be small.

The second reason is that although insects are small in size, the materials they are made of are extremely resistant comparatively to their size. Therefore, the bug will survive when it meets the window pane.

An interesting corollary is that the common saying "if an ant was the size of a human, it could carry a locomotive, because it can carry many times its weight" is totally wrong. If an ant the size of a man tried that, it would break its back just like you and me, because material resistance is not proportional to size.


Fraction of naive T-cells in CD4+ T-cells isolated from whole blood? Many papers isolate CD4+ T-cells from whole blood.
I am wondering approximately what proportion of naive T-cells there will be from such a sample? Are these predominately naive T-cells or are there more memory and effector cells?

Stemcell Technologies has a really good wall poster for this. You can enumerate roughly 80,000 to 760,000 naive CD4+ T cells from peripheral blood per mL. This is 1-10% of leukocytes.

One of the things you need to remember about memory cells is that they do circulate, but it follows that among the circulating subsets of memory cells, they highly express markers for lymph node localization such as CCR7 and CD62L. Their presence in the blood at a given time is influenced by a number of factors including disease state.

Likewise, effector cells are programmed to localize within infected or distressed tissues through the actions of chemokines and chemokine receptors. The presence of effectors will depend on the same sort of factors, and as effector T cells, they are typically either made anergic and die by apoptosis or differentiated into memory cells.


What is the species of these mushrooms? The mushrooms are gilled with a light-brown cap. The stem is widened to the base.

What species is it? Is it considered edible?

They are found in mixed forest in Moscow, Russia. They grow in the ground quite separated from each other.

I had a quick look in my books (for the British Isles and Europe) but although I found a couple of candidates I don't feel confident in either identification.

I suggest that you have a look at Roger Phillips' online identification guide  - this will suggest a few identification criteria that you haven't considered in your question.


Is there an evolutionary basis for why women mature faster than men? Females develop both physically and mentally earlier than males do. For example; females start puberty at an earlier age than males, and females brains mature more quickly than male brains.

  Girls have always developed earlier than boys - on average the onset
  of puberty happens between the age of 8 and 12 years in girls and
  between 9 and 14 years in boys.

Is there an evolutionary basis for this? Are there theories for why females mature earlier in life?

Reproduction is kind of the definition of biological success. Logically, it works because it works because it works. Provided that the mother is responsible and healthy, there's a good chance the offspring will survive and reproduce. And since health and age are like opposing forces, the sooner a female develops and develops responsibility, the more likely they will be to reproduce and supply viable offspring to the population.

Similarly, males remain verile for many years past their prime. Since it doesn't matter (as much) whether the father survives child birth, his health is less important. More important (genetically) is the spread of his DNA. The more time a male has to do that the more his DNA will spread. So why not start earlier? Reproducing for an extra ten or twenty years will cause the spread of a much greater amount of DNA than 1 or 2 years early on, and (plausibly) since the male often has a dangerous occupation, males that develop(ed) later (when their size/strength was greater), probably help(ed) ensure the males' survival.

And there is something to say about sexual preference. It is likely that the males' disposition toward healthy females and a females' dispositon toward successful males is genetic... much like a bird who sings the best song. Why? Because it is/was a successful cascade of events.


Why are fertilizers with polonium 210 used when growing tobacco? Why are fertilizers with polonium 210 used when growing tobacco?

I'm thinking of pursuing a science fair in which I create my own fertilizer for tobacco that doesn't contain polonium or lead. However, I need more background research. Does anyone know why these fertilizers are used?

According to RADIOACTIVITY IN CHEMICAL FERTILIZERS by Milica M. Rajačić, Nataša B. Sarap, Marija M. Janković, Jelena D. Nikolić, Dragana J. Todorović and Gordana K. Pantelić at the Institute for Nuclear Sciences "Vinča", University of Belgrade, Belgrade, Serbia, and the relatively short half-life of polonium, it appears that primordial metals are the only hazard in fertilizers:

  Natural radioactivity results mainly from primordial radionuclides,
  such as 40K and the radionuclides from the 232Th, 238U and 235U series
  and their decay products. Terrestrial radioactivity and exposure due
  to gamma radiation depend primarily on the geological conditions and
  appear in different quantities in the soils of each region in the
  world. 1 [...]

  Fertilizers usually employed in the agriculture contain traces of
  heavy metals and relatively high concentrations of naturally occurring
  radionuclides. Phosphate containing fertilizers have been used
  worldwide to increase the quantities of the micronutrients, which are
  being continuously taken off from the soil due to farming activities.
  At the same time, the use of such fertilizers is the main
  anthropogenic source of the uranium input in the environment (about 73
  % of the total input of uranium) 2. [...]

  A total of 140 samples of different types of fertilizers were measured
  for their radioactivity content using gamma spectrometry technique in
  order to assess the implications of extended use of fertilizers on the
  concentrations of natural radionuclides in cultivated soil. The
  obtained data show that the activity concentration of naturally
  occurring radionuclides in fertilizer samples were 87 Bq/kg, 4860
  Bq/kg and 220 Bq/kg for 226Ra, 40K and 238U, respectively, which
  exceeds the activity concentration in soil by an order of magnitude.
  As it was shown in the paper, the use of fertilizers has a negligible
  effect on Raeq and D in soil due to dilution of fertilizer used on the
  large amounts of cultivated soil. However, the long term application
  of these fertilizers can have the effect of an accumulation of
  radioactivity in soils that can be harmful for the health of farmers
  and consumers of the products. [...]

  1: Akhtar N. Radionuclide pollution due to fertilizer use in some
  saline soils of the Punjab and their potential risk assessment on
  human health. Department of Physics Bahauddin Zakariya University
  Multan, Pakistan, 2006. 2: Stojanović M, Stevanović D, Milojković J,
  Mihajlović M, Lopičić Z, Šoštarić T. Influence of soil type and
  physical–chemical properties on uranium sorption and bioavailability.
  Water Air Soil Pollut 2012;223:135-
  144.

Artificial fertilizer is cheaper than regular fertilizer that also contains long-term nutrients, but also contains Po-210:

  Among all carcinogenic substances contained in tobacco smoke, Polonium
  210 (Po-210), with a half-life of 138 days, is one of the most
  dangerous, by exerting a devastating, chronic, slow and progressive
  carcinogenesis activity. The main source of Po-210 in tobacco is
  represented by fertilizers (polyphosphates) containing radium-226
  (Ra-222) which decades to plumb 210 (Pb-210). Through the thricomes
  Pb-210 is concentrated in the tobacco leaves, where it turns to
  Po-210, which at the cigarette combustion temperature (800-900 degrees
  C) reaches the gaseous state and it is absorbed by the micro particles
  released into tobacco smoke. Thus, smoke becomes radioactive in both
  its gaseous and corpuscular components and reaches the airways, where,
  particularly at the branches level and together with other substances,
  it exerts its carcinogenic activity, especially in those subjects with
  impaired respiratory mucosal clearance. The carcinogenic risk/one year
  lifetime of a smoker of 20 cigarettes per day is equivalent to that of
  undertaking 300 chest x-rays. It is calculated that Po-210 may be
  independently responsible of 4 lung cancers every 10,000 smokers.
  During cigarette's combustion, tobacco smoke is also released in the
  air, contributing to serious health risks for those exposed to passive
  smoke.


Question on thick filaments In this photo, I know that the arrows pointing towards the M-line of sarcomere on actin filaments are due to the power strokes of myosin heads. However, what I don't understand are the arrows on the myosin filaments pointing away from the M-line.
Are they the reaction forces (action-reaction pair, where the action force is power stroke)? Also, will this force (pointing away from M-line) 'tear apart' the myosin filaments on M-line? If not, how can the filament withstand this force?

Yes, they are action-reaction pair.( Newton’s third law).
No, it won’t tear under normal circumstances. The filament withstands all that force because the attractive force between its constituents is far more than the force generated by myosin actin cycle.


Sexual reproduction in organisms with 1 parent An organism that carries out sexual reproduction with itself,  for example a flower with both the anther and stigma,  does it actually contain 2 sets of genes in order to produce genetically dissimilar organisms or do it just leave the offspring to become genetically dissimilar through random crossing over during miosis?

Your second piece is correct: dissimilarity is produced through meiosis.

from The evolution of meiotic sex and its alternatives

  Strikingly, almost all forms of uniparental reproduction do maintain
  meiosis, but abandon just outcrossing. Hence, the paradox of sex in
  eukaryotes must focus on the purpose of meiosis.


How does non-homologous end joining (NHEJ) work? I was reading about non-homologous end joining (NHEJ) in my molecular biology of the gene textbook but the explanation provided in the text was rather vague to me, and I was not able to understand it completely. I understood that NHEJ can be used as a repair mechanism when double-strand breaks in DNA occur. The two broken ends are then joined together. What I didn't understand is how this is done. The two broken ends won't always have complementary bases so, won't this lead to mismatched bases? How is this problem fixed? I really need a detailed explanation of how NHEJ occurs please.

Non-homologous end joining indeed induces errors in the affected sequence. But you have to keep in mind, that NHEJ is an emergency repair mechanism which involves a "repair or die" chance. If the chromosomal break is not repaired it is not unlikely that the cell will get into apoptosis, or, even worse, develops into a cancer cell. Introducing small errors is a relatively small price compared to this, although this can still disrupt genes or regulatory sequences. For the mechanism have a look onto the figure (from the first reference):

For further reading have a look onto the Wikipedia article on NHEJ and/or the following references:

The mechanism of human nonhomologous DNA end joining.
The mechanism of double-strand DNA break repair by the nonhomologous
DNA end-joining pathway.


Probability of Extinction under Genetic Drift Here is the Wright-Fisher model of genetic drift:

$$\frac{(2N)!}{k!(2N-k)!}p^kq^{2N-k} \Leftrightarrow \binom{2N}{k}p^kq^{2N-k}$$

where $\binom{2N}{k}$ is the binomial coefficient.

This formula gives the probability of obtaining $k$ copies of an allele at generation $t+1$ given that there are $p$ copies of this allele at generation $t$. $N$ is the population size and $2N$ is the number of copies of each gene (this model applies to diploid population only).

From this formula, how can we calculate the probability of extinction of an allele in say 120 generations starting at a given frequency, let's say 0.2?

and

How can we calculate the probability of extinction rather than fixation of an allele present at frequency $p$ if we wait an infinite amount of time?

update

The answer is here!

Original comment/answer

Kimura and Ohta (1969) showed that assuming an initial frequency of $p$, the mean time to fixation $\bar t_1(p)$ is:

$$\bar t_1(p)=-4N\left(\frac{1-p}{p}\right)ln(1-p)$$

similarly they showed that the mean time to loss $\bar t_0(p)$ is

$$\bar t_0(p)=-4N\left(\frac{p}{1-p}\right)ln(p)$$

Combining the two, they found that the mean persistence time of an allele $\bar t(p)$ is given by $\bar t(p) = (1-p)\bar t_0(p) + p\bar t_1(p)$ which equals

$$\bar t(p)=-4N\cdot \left((1-p)\cdot ln(1-p)+p\cdot ln(p)\right)$$

This does not answer any of the two questions!

This answer gives...

the average persistence time

but not...

the probability of fixation rather than extinction if we wait an infinite amount of time

neither...

the probability that the allele get extinct over a period of say 120 generations.

Can someone improve this answer?


What insect is this with 'horn' at the side? Found this interesting insect hiding behind the thin branch of flower (the diameter of the branch is 3-4mm) in my garden in Kuching, Sarawak, Malaysia

That is a treehopper. Order Hemptera, family Membracidae. I looked on a site for membracids of Malaysia, and could not bring it to species-level. But I am confident that it is a membracid. This family is characterized by sometimes bizarre protrusions of the pronotum.
https://en.wikipedia.org/wiki/Treehopper


How to distinguish the Ct of the target gene from the Ct of the housekeeping gene? (very basic qPCR question) I will do a qPCR experiment for the first time, and I have a bottom-level question to ask. I know that for normalizing the quantity of your target gene you have to add an endogenous control, like a housekeeping gene, in your qPCR sample, and then you subtract the Ct of the housekeeping gene from the Ct of your target gene. However, since the same SYBR green fluorophore is used to quantify both the target gene and the housekeeping gene in the same sample, how do you know which Ct is from the target gene and which one is from the housekeeping gene?

You do not take readings from the same reaction, you split the sample. You would run each primer pair in their own reaction. You also want to run each reaction in triplicate so you can get some idea of the error.
So, a general plate set up might look something like this:

A1: Control sample, housekeeping primers; A2: Control sample, target gene primers
B1: Control sample, housekeeping primers; B2: Control sample, target gene primers
C1: Control sample, housekeeping primers; C2: Control sample, target gene primers

D1: Treatment sample, housekeeping primers; D2: Treatment sample, target gene primers
E1: Treatment sample, housekeeping primers; E2: Treatment sample, target gene primers
F1: Treatment sample, housekeeping primers; F2: Treatment sample, target gene primers

So in this scenario, the delta-delta Ct value comes from the following:

delta-delta Ct = ( Ct(treatment, target) - Ct(treatment, housekeeping) ) - ( (Ct(ctrl, target) - Ct(ctrl, housekeeping) )

If the PCR machine does not offer to do the delta-delta Ct analysis for you I recommend this blog which both explains it well and provides and excel spreadsheet so you can just drop you Ct values in.
HTH.


Why do flowers naturally reproduce with their own species? I have always wondered why flowers reproduce with the same species naturally. Why can't the pollen grains get to a different species flower through via the wind, water, or insects?

The pollen from a given species of flower does get transmitted to other flowers of different species (like you said, through air, insects, etc.)..the problem though is that those two species of flowers are just that!: they are two different species, and by definition, aren't able to reproduce amongst one another.

I would recommend looking into the definition of a species. There isn't a single, blindly-conformed-to definition, however, its most commonly accepted that a species can be defined by the "boundaries" in which that species can or can't produce offspring with other organisms. Organisms that can produce offspring together are generally considered to be of the same species.

There are odd cases though where some interspecies reproduction occurs, such as a donkey and a horse producing a mule. Yet, if two mules were to attempt sexual reproduction, they wouldn't be successful in producing offspring (mules are sterile). So, this is a tricky situation to define, in terms of if the donkey and horse are the same species or not, since they can produce offspring, yet that offspring is a dead-end, so to speak.

A different example.. if (somehow) a chicken attempted sexual reproduction with a pigeon, the sperm would reach the females egg, however, no offspring would occur.

A major impedence of offspring occurring for interspecies reproduction comes down to the mechanics of meiosis, and how chromosomes match up with each other throughout the process. Chromosomes need to be of similar size, shape, etc., in order to properly pair with their complement during meiosis. Also, the correct number of chromosomes need to be present. These dynamics, as well as many others, get messed up when interspecies reproduction is attempted.

I hope this addresses your curiousity.. All the best!


Do animals exhibit handedness (paw-ness?) preference? I have been observing my cat and found that when confronted with an unknown item, she will always use her front left paw to touch it.

This has me wondering if animals exhibit handedness like humans do? (and do I have a left handed cat?)

One note of importance is that with an unknown item, her approach is always identical, so possibly using the left paw means allowing a fast possible exit based on how she positions her body.

This question is related to Are there dextral/sinistral higher animals?. However, I question the "paw-ness" as a consequence of how the cat is approaching new items (to be ready to flee), whereas the other question remarks about the high number of "right-pawed" dogs and questions the influence of people for this preference.

Short Answer
Yes. handedness (or Behavioral Lateralization) has been documented in numerous vertebrates (mammals, reptiles and birds) as well as invertebrates.

This includes domestic cats (see Wells & Millsopp 2009).

 Long Answer
There have been numerous studies that have documented behavioral lateralization in many groups of animals including lower vertebrates (fish and amphibians), reptiles (even snakes!), birds and mammals. More recent work (e.g., Frasnelli 2013) has also shown that lateralization can also occur in invertebrates. In other words, "handedness" (or pawedness, footedness, eyedness, earedness, nostriledness,
toothedness, breastedness, gonadedness, etc.) occurs rather extensively across the animal kingdom.

These studies suggest that the evolution of brain lateralization, often linked to lateralized behaviors, may have occurred early in evolutionary history and may not have been the result of multiple independent evolutionary events as once thought.

Although this view of brain lateralization as a highly conserved trait throughout evolutionary history has gained popularity, it's still contested (reviewed by Bisazza et al. 1998; Vallortigara et al. 1999).

Note: Laterality of function may manifest in terms of preference (frequency) or performance (proficiency), with the former being far more often investigated.
And no, right-handedness is not always dominant.
But Why?

One hypothesis is that brain lateralization was the evolutionary result of the need to break up complex tasks and perform them with highly specialized neuronal units to avoid functional overlap (i.e., to account for "functional incompatibility").

In humans, many hypotheses have been developed including: division of labor, genetics, epigenetic factors, prenatal hormone exposure, prenatal vestibular asymmetry, and even ultrasound exposure in the womb.

Snake studies (see below) have suggested lateralization behavior can be dictated by environmental conditions (specifically, temperature).

Other work (Hoso et al. 2007) suggest that lateralization could be the result of convergent evolution. In this case, snakes developed feeding aparati that allow them to better consume more-common dextral species of snails.

Note: dextral (meaning "clockwise") is a type of chirality -- another form of "handedness"

Reviews:

Lateralization in non-human primates: McGrew & Marchant 1997.

Lateralized behaviors in mammals and birds:
Bradshaw & Rogers 1993; Rogers & Andrew 2002.

Lateralized behaviors in lower vertebrates: Bisazza et al. 1998; Vallortigara et al. 1999.

Some Examples:
Invertebrates

Some spiders appear to favor certain appendages for prey handling and protection (Ades & Novaes Ramires 2002).

Octopi (or octopodes) preferably use one eye over the other (Byrne et al. 2002; with seemingly no preference for right/left at the population level: Byrne et al. 2004) and also apparently have a preferred arm (Byrne et al. 2006).

Fish

Preferential ventral fin use in the gourami (Trichogaster trichopterus). [Bisazza et al. 2001].

Preferential eye use in a variety of fish species [Sovrano et al. 1999, 2001].

Amphibians

Lateralization of neural control for vocalization in frogs (Rana pipiens). [Bauer 1993].

Preferential use of hindlimbs (Robins et al. 1998), forelimbs (Bisazza et al. 1996) and eyes (Vallortigara et al. 1998) in adult anurans.

Snakes

Preferential use of right hemipenis over left under warm conditions. [Shine et al. 2000].

Coiling asymmetries were found at both the individual and population levels. [Roth 2003].

Birds

Tendency for parrots to use left-feet when feeding. [Friedmann & Davis 1938].

Mammals

Pawdness in mice. [Collins 1975].

left forelimb bias in a species of bat when using hands for climbing/grasping. [Zucca et al. 2010]

Behavior experiments show domesticated cats show strong preference to consistently use either left or right paw and that the lateralized behavior was strongly sex related (in their population: ♂ = left / ♀ = right). [Wells & Millsopp 2009].

Non-human Primates

Posture, reaching preference, tool use, gathering food, carrying, and many other tasks. See McGrew & Marchant (1997) for review.

Citations

Ades, C., and Novaes Ramires, E. (2002). Asymmetry of leg use during prey handling in the spider Scytodes globula (Scytodidae). Journal of Insect Behavior 15: 563–570.

Bauer, R. H. (1993). Lateralization of neural control for vocalization by the frog (Rana pipiens). Psychobiology, 21, 243–248.

Bisazza, A., Cantalupo, C., Robins, A., Rogers, L. J. & Vallortigara, G. (1996). Right-pawedness in toads. Nature, 379, 408.

Bisazza, A., Rogers, L. J. & Vallortigara, G. (1998). The origins of cerebral asymmetry: a review of evidence of behavioural and brain lateralization in fishes, reptiles and amphibians. Neuroscience and Biobehavioral Reviews, 22, 411–426.

Bisazza, A., Lippolis, G. & Vallortigara, G. (2001). Lateralization of ventral fins use during object exploration in the blue gourami (Trichogaster trichopterus). Physiology & Behavior, 72, 575–578.

Bradshaw, J. L. & Rogers, L. J. (1993). The Evolution of Lateral Asymmetries, Language, Tool Use and Intellect. San Diego: Academic Press.

Byrne, R.A., Kuba, M. and Griebel, U. (2002). Lateral asymmetry of eye use in Octopus vulgaris. Animal Behaviour, 64(3):461-468.

Byrne, R.A., Kuba, M.J. and Meisel, D.V. (2004). Lateralized eye use in Octopus vulgaris shows antisymmetrical distribution. Animal Behaviour, 68(5):1107-1114.

Byrne, R.A., Kuba, M.J., Meisel, D.V., Griebel, U. and Mather, J.A. (2006). Does Octopus vulgaris have preferred arms?. Journal of Comparative Psychology 120(3):198.

Collins RL (1975) When left-handed mice live in righthanded worlds. Science 187:181–184.

Friedmann, H., & Davis, M. (1938). " Left-Handedness" in Parrots. The Auk, 55(3), 478-480.

Hoso, M., Asami, T., & Hori, M. (2007). Right-handed snakes: convergent evolution of asymmetry for functional specialization. Biology Letters, 3(2), 169-173.

McGrew, W. C., & Marchant, L. F. (1997). On the other hand: current issues in and meta‐analysis of the behavioral laterality of hand function in nonhuman primates. American Journal of Physical Anthropology, 104(S25), 201-232.

Robins, A., Lippolis, G., Bisazza, A., Vallortigara, G. & Rogers, L. J. (1998). Lateralized agonistic responses and hindlimb use in toads. Animal Behaviour, 56, 875–881.

Rogers, L. J. & Andrew, R. J. (Eds) (2002). Comparative Vertebrate Lateralization. Cambridge: Cambridge University Press.

Roth, E. D. (2003). ‘Handedness’ in snakes? Lateralization of coiling behaviour in a cottonmouth, Agkistrodon piscivorus leucostoma, population. Animal behaviour, 66(2), 337-341.

Shine, R., Olsson, M. M., LeMaster, M. P., Moore, I. T., & Mason, R. T. (2000). Are snakes right-handed? Asymmetry in hemipenis size and usage in gartersnakes (Thamnophis sirtalis). Behavioral Ecology, 11(4), 411-415.

Sovrano, V. A., Rainoldi, C., Bisazza, A. & Vallortigara, G. (1999). Roots of brain specializations: preferential left-eye use during mirror-image inspection in six species of teleost fish. Behavioural Brain Research, 106, 175–180.

Sovrano, V. A., Bisazza, A. & Vallortigara, G. (2001). Lateralization of response to social stimuli in fishes: a comparison between different methods and species. Physiology & Behavior, 74, 237– 244.

Vallortigara, G., Rogers, L. J., Bisazza, A., Lippolis, G. & Robins, A. (1998). Complementary right and left hemifield use for predatory and agonistic behaviour in toads. NeuroReport, 9, 3341–3344.

Vallortigara, G., Rogers, L. J. & Bisazza, A. (1999). Possible evolutionary origins of cognitive brain lateralization. Brain Research Reviews, 30, 164–175.

Wells, D. L., & Millsopp, S. (2009). Lateralized behaviour in the domestic cat, Felis silvestris catus. Animal Behaviour, 78(2), 537-541.

Zucca, P., Palladini, A., Baciadonna, L. and Scaravelli, D. (2010). Handedness in the echolocating Schreiber's long-fingered bat (Miniopterus schreibersii). Behavioural processes, 84(3): 693-695.


Are there any strictly chloroplast/mitochondrion-residing ribozymes? A simple question that had occurred to me. Considering the small doubt of transcribed genes in both organelles, I would doubt it, but are there any known ribozymes strictly found in either mitochondria or chloroplasts?

UPDATE: Actually, I just thought of rRNA acting as a peptidyl transferase in mitochondrial ribosomes... Any other ideas?

You've already mentioned rRNA. An interesting review (Tanner, 2006), outlines some more:

Group I Introns - self-splicing; "They are abundant in fungal and plant mitochondria..."
Group II Introns - some have been shown to self-splice; "...they are found in fungal and plant mitochondria, in chloroplasts of plants ... and especially in the chloroplasts of the protist Euglena gracilis."
RNase P - involved in tRNA processing, found in mitochondria

None of these are strictly found in mitochondria or chloroplasts. However, the paper goes on to describe VS RNA ribozyme:

The mitochondria of certain strains of Neurospora contain the Varkud plasmid (a retroplasmid), which encodes a reverse transcriptase, and a small, unrelated, RNA (VS RNA). The VS RNA is transcribed from circular or multimeric VS plasmid DNA by a mitochondrial RNA polymerase, and the resulting transcripts are subsequently site-specifically cleaved and ligated to form circular, 881 nucleotides long, RNA monomers. These monomers are then reverse transcribed and made double stranded to form the mature VS plasmid.
In vitro transcribed VS RNA precursors are cleaved and ligated by the RNA itself and this is presumed to occur in vivo as well. Of all the self-cleaving RNAs, the catalytic properties of VS RNA are the most poorly understood.

References

Tanner NK. 2006. Ribozymes: the characteristics and properties of catalytic RNAs. FEMS Microbiol Rev. 23(3):257-275.


What is this small tissue structure found in kidney? It's covered with white adipose tissue and it is smooth with reddish brown colour. HE dyed with dimensions 3 cm long and 1 cm wide. I'm guessing that this is a rare thing because I already checked pubmed etc. On the right is a closer picture of the tissue.

This is a slice of an adrenal gland:

Source (Creative Commons Attribution-Noncommercial-Share Alike 3.0 License): http://histology.medicine.umich.edu/resources/endocrine-system

These glands sit on top of the kidneys, typically under adipose tissue (which can also be seen in both your image and the image I included here). The most identifying feature of the adrenal gland is its clear separation into two parts: the outer "cortex" and inner "medulla", as labeled on the image.

The two parts have different endocrine functions: the cortex primarily produces steroid hormones, like aldosterone and cortisol, whereas the medulla makes catecholamines epinephrine and norepinephrine (also called adrenaline and noradrenaline). I believe the inset in your image is of the medulla.


Stabilizing forces between the protein sequences? we know that Protein structures from secondary to Quaternary are maintained by noncovalent or weak interactions including electrostatic interactions,van der Waals forces & hydrogen bonding. What is the significance of these weak interactions why they are preferred by nature rather then strong covalent interactions?

Proteins often undergo conformational changes. The activation energy required to undergo a conformational change in a protein with only covalent interactions would be much higher compared to that of a protein with weaker bonding forces. An example of a conformational change seen in enzymes is the change in conformation during allosteric regulation, in which an effector molecule binds a site on the enzyme distant from the enzymes active site. The binding of the effector molecule induces a conformational change that exposes the active site of the enzyme. Another example of conformational change is the change in conformation seen in Toll-Like-Receptors (TLRs). Additionally, many proteins change their conformation in response to pH. These changes would likely not occur if the protein only contained covalent bonds, and the ability of proteins to undergo such changes makes them responsive to the environment, as well as allowing them to carry out their enzymatic actions, if such actions exist for that particular protein.

Here is the wiki on allosteric regulation https://en.wikipedia.org/wiki/Allosteric_regulation

Here is a figure on conformational changes in TLRs http://www.nature.com/ni/journal/v8/n7/fig_tab/ni0707-675_F1.html

And here is the wiki on activation energy, a concept used in chemistry (see section on catalysis and Gibbs free energy) https://en.wikipedia.org/wiki/Activation_energy


Microarray data and analysis tools Microarray has various uses, and to analyse the data a main function classification is used. There are many methods used to classify the data but what are the best and most frequently used methods? Are there any well-known, web-based tools for microarray analysis?  Where can I find datasets of gene expression profiles, where I can find and understand the matrix of the dataset?

This is a fairly broad question and a book or two will give a more complete answer.  I'm assuming you are interested in expression microarrays.  Genotyping microarrays are also very popular these days and are quite different though.

Where can I understand the matrix of the dataset ?
This is a little unclear as a question, but I'll start with a numerical description.  Microarray data is reducible to a one dimensional array of intensities.  As a vector of numbers, each representing the amount of a given species of RNA in a sample, it has many interpretations.  Most of what is said here applies to RNASeq data too.

These numbers are sequence dependent - that is, they should not be interpreted as an absolute count of a specific mRNA in the sample, so comparing two entries in the vector (e.g. "gene A has 10% more RNA than gene B") will probably not be useful.

For this reason, microarray experiments are typically done as difference experiments, where two or more conditions are compared, producing a matrix of numbers, where N rows represent N experiments, and the M columns each represent a probe set / gene.  The transpose of this matrix is also common.

**Methods to classify microarray results. **
Taking the matrix of data, there are many ways of interpreting data in matrix form and most of them have been tried credibly with microarray data.

The most common are to take a set of probe sets whose biological action are related (e.g. all in a metabolic pathway and display them as a heat map where the columns have been clustered by a distance based algorithm to produce a tree, where neighbors have the greatest numerical similarity.

For purely numerical methods, Principal Component Analysis is often used (despite the fact that this is not a great method), but Self Organizing Maps, neural nets and just about any machine learning algorithm have been used.

Most common method by far though, is Analysis of Variants (ANOVA), where the probe sets/ genes have been scored by their greatest to smallest variance.  The most common case of this is a two condition difference experiment where the largest differences are taken as results.  This is not a great experiment, but the data is not super cheap to produce.

**Microarray data repositories **
Gene Expression Omnibus (GEO) is a highly regarded repository for microarray data, with over a million sets of data. They also have some tools, see below.

EMBL ArrayExpress claims to have slightly more data than GEO (1.2 M assays).

There are many many specialized microarray websites, mostly focusing on a particular organism (E coli for instance) or problem (like cancer).  Google is pretty helpful for this sort of thing once you have the right keywords.

**Web based tools for microarray analysis **
There are several tools you will use for microarray analysis and there are lots of websites for different aspects of this data.  I'm going to cite a couple, but the most commonly used tools are command line tools like R/bioconductor or the software that comes from the array manufacturer.

GEO2R is a great tool to browse expression data experiments.  It does a simple version of ANOVA and will really help you find some cool biology quickly.

VAMPIRE is a web analysis suite for microarray analysis.  Scaling the data into numbers from images to intensities to data analysis to compare several arrays.  Its probably one of the most comprehensive analysis sites out there.


Why does polyploidy give an evolutionary advantage? I would like to know what advantages polyploidy holds. I have come across a few examples during my research of polyploidy, for example human adults' hearts contain 27% diploid, 71% tetraploid and 2% octaploid nuclei, Deinococcus radiodurans can have up to 10 copies of genome, and most of the plants consumed by humans have more than 2 copies.

I have no source of any sort for these, but I think they could be advantages:

One of the most obvious one would be resistance to more physical effects.
In the case of plants it might be the increased need for protein construction during the development of the seed.

What I would like to ask is whether the ones I wrote are correct, and if there are any other possible advantage.

I have read similar questions but could not find what I was looking for.

First of all I am not sure if your examples are per se correct. But they might also be an additional bonus. Secondly, I would like to refer to two articles: "Polyploidy" and "The advantages and disadvantages of being polyploid".

One of the main benefits could be allowing organisms long-term evolutionary flexibility. Often adapted polyploids can undergo a proces that is called diploidization, during which genomic redundancy is removed. This means extra copies of genes will undergo less negative selection. Meaning alleles containing deleterious mutations at functionally important nucleotides are selected against. This allows more mutational freedom, leading to what is called subfunctionalization and neofunctionalization: new genes are created with slightly different or new functions. Other redundant genes are lost or become inactivated (pseudogenes).

Another example of benefits from polyploidy, this time not in an evolutionary, but in a more individual context, is the fenomenon called hybrid vigor or heterosis. Heterosis is a phenomenon in which a polyploid offspring of two diploid parents is more healthy and vigorous than its progenitors. One of the factors explaining this could be due to a protection against recessive characters, as being homozygous as a polyploid is even more 'uncommon'.


What are multicell spheroids? I'm from a maths background and I'm doing some research on mathematical models of cancer. I've come across alot of literature mentioning "multicell spheroids" in the context of avascular tumours. I know that avascular means a lack of blood vessels but I am having trouble finding an explanation for multicell spheroids. Are these some kind of model/approximation of a certain types of tumours, or are they actually a real-phenomenon in and of themselves? It would be great if someone could fill me in on what they multicell spheroids actually are!

They are tridimensional cell cultures according to H Ma et al. 2012.

  Multicellular tumor spheroids are one of the classic 3D culture models that can be applied to the development of anticancer drugs and treatments. By mimicking the 3D network of the cellular–matrix and cell–cell interactions, tumor spheroids resemble many aspects of the pathophysiologic environment within human tumor tissue.

Classical cell cultures are usually monolayer. Many of the differene between these cultures and real life tissues has been overcome by 3D cultures according to Carver et al. 2014.

  The multicellular tumor spheroid (MCTS), a three-dimensional model that closely resembles small avascular tumors and micrometastases, has been utilized as an intermediate between monolayer culture and in vivo studies for the screening of small-molecule drugs.

So is it a 'real life' entity or is it something that is computer generated? It is real life. Let's think of an organ. It's made up of a specific tissue(s) and a stroma that contains vascular, nervous and other components that supply nutrients and limit the organ's specific tissue. This structure develops in vivo in 3D. The blood vessels will follow tissue development in a tree-like 3D structure in order to reach to all cells. But what you do with lab cell cultures? There are no blood vessels there. How do you supply nutrients to all cells? That is why most in vitro cell cultures are developed in monolayer structure. Yet cells are 3D structures. They are joined together in a tissue by intercellular junctions. Monolayer limits this joining to a single plane. Moreover, when it comes to cancer cells which have specific properties (they lose junctions and start to move) the monolayer model becomes limited. This is how spheroids have become a better model for studying in vivo processes using in vitro cell cultures.


Separating DNA Fragments by Gel Electrophoresis. Are all the strands for one size the same? My apologies if my question is too basic, and please point me to a more appropriate forum.  I am reading the textbook "Essential Cell Biology" by Alberts et al, and am consulting other sources as well.  I am reading Chapter 10 about DNA technology and have read how DNA is separated into strands of different lengths by restriction enzymes.  The different size strands can then by separated by Gel Electrophoresis.  I believe I understand these basics. My question is:

Do all strands of the same length have the same sequence of base pairs?  I wouldn't think      so, and this would be a problem in the next step, determining the sequence of one size fragment by  using special base pairs that are lacking a hydroxyl group. Isn't it possible I could have two strands that are 50 base pairs long (for example) that have the same beginning and same end and are thus cut by the restriction enzymes to a length of 50, but are most assuredly not the same within their sequence

The text says that once the different size strands are separated by electrophoresis, you can just cut out one of the bands and work with that.  That makes sense if you are guaranteed to only have 1 strand at that level of the gel agar or if the multiple strands are all the same exact sequence.

If you read this far, thank you.  I think more generally I need to know how many of these segments are produced when you use restriction enzymes and how long the average one is. And is there any guarantee for one chromosone (or all 46 chrmosones) having all the segments be unique sizes (I wouldn't think so)?

And even more generally :), I need additional sources that explain DNA sequencing in simple to understand terms.

Thanks,

Dave

The answer to the part of your question concerned with average lengths of restriction fragments is: if the DNA molecule being digested is of random sequence, and is 50% GC/ 50% AT, then the probability of finding any given short sequence at any position is 1/4N where N is the length of the short sequence. So, for example for a restriction enzyme with a 4-base recognition sequence such as AluI (AGCT) the probability is 1/256 and so the average length of an AluI fragment would be 256 bp. For an enzyme with a 6-base recognition sequence such as HindIII (AAGCTT) the corresponding number is 4096 bp. Please note that this is the average length, and is not an 'expected' length.

The answer to the part of your question about fragments of the same size co-migrating, how would you purify them on a gel for further analysis is trickier. I think the first thing to say is that you wouldn't do this for sequencing, and this is reflected in the various answers you have already received - sequencing no longer requires this sort of approach.

If you were forced into this position for some reason then I can think of two things that could help: the first option would be to run the analysis on an acrylamide gel when you can get much better resolution of different fragments (all 50 bp fragments are not the same molecular weight), but this is really only useful for small fragments (100 bp or less). However the most likely way out of the co-migration problem would be to purify the two comigrating fragments as a mixture and then ligate them into a vector whereupon each recombinant would carry one or other of the two fragments. This is really going back to the original reason why molecular cloning revolutionised things - it allows the 'biological' purification of DNA fragments followed by production of these fragments in large amounts.

You mention "special base pairs that are lacking a hydroxyl group" so clearly you are thinking in terms of Sanger (dideoxy-) sequencing, in which case you could clone directly into an M13 phage vector so that you could make ssDNA for direct sequencing. By sequencing a number of clones you would find two sequences, one for each fragment. You would still have to find a way to decide which one was the fragment that you were actually interested in, however.

Like I say, things just aren't done in this way anymore.


How dirty are bugs? And is it okay if they touch food? Sometimes I see people throw out an entire drink or bowl of food because a small bug was in it. Are they justified in doing this? Is there enough bacteria on common species of bugs (like ants, flies, beetles, dragonflies, caterpillars, moths, etc) to warrant any kind of health concern for a larger amount of food than what the bug was in contact with, or at all?

Well, first of all you should consider that insects and generally animals don't have so much hygiene, like us humans. Some of them, let's say the ants, yes some kind of hygiene is present, but not in the human degree. In fact, most insects are responsible for the most dangerous deseases in the world such as malaria , yellow fiver, sleeping sickness (espacially found in Africa because of the tsetse fly) and many kinds of encephalitis. This article claims that most of insects are carriers of deadly deseases. Also, about the second part of your question, you mentioned " If it is okay for bugs to touch food"... Well the answer is ofcourse no, because you don't know:

1. what the insect was touching before it "lands" to your food

2. If it has dropped any fecesto your food

3. And last but not least if the insect layed any kind of eggs to your food.

4. Some insects carry fungi that if a human being consumes them he might have serious problems, because some fungi are responsible for poisoning or infection.

The third one that I mentioned is responsible for the most cases of Tapeworm infection. This means that the eggs and larvae pass straight to your digestive system and create the infection. To sum up, unknown factors (like bugs) must not touch our food, because there is a chance of infection. To help you here's a wikipedia list that shows the most easily transmitted diseases to humans fron insects: List of diseases caused by insects.


How are fluorochromes conjugated to proteins such as antibody? How are fluorochromes like FITC conjugated to antibodies? Are they covalently bonded? If they are covalently bonded, will low temperature (-20 Celsius or lower) break the covalent bonds and detach the fluorochrome label from the protein?

Fluorochromes are covalently bound to the antibodies to form stably labelled molecules. This paper describes it in great detail, from the abstract:

  Fluorochromes can be covalently conjugated to antibodies through
  reactions with thiol or amine groups. Typically, fluorochromes
  containing isothiocyanate, succinimidyl ester, or sulfonyl chloride
  reactive groups are conjugated to amines on the antibody molecules.

These covalent bonds are stable at room temperature and are also at -20°C. It's more likely that repeated freeze-thaw cycles damage the antibody.


Function and process of TCTE-1 receptor I was wondering if anybody knew of the function and process of the TCTE-1 receptor during the binding of a sperm with an egg. The only think I know of TCTE-1 is that it is a species-specific receptor.
I also know that it's removal will render homozygous males infertile. I know that researchers are experimenting with mice to study TCTE-1.

This is by far too long for a comment, so as an answer: I spend now quite a while using Pubmed and other search tools, to find more information. The most recent article I found over and over again was the one from Juneja and colleagues: "Sequence divergence within the sperm-specific polypeptide TCTE1 is correlated with species-specific differences in sperm binding to zona-intact eggs." (which you probably also found). This article has only been cited two times, which is a bad sign for an article making so important connections. My guess is that no further research in this area either happened or has at least not been published. So beyond this I am afraid that there is no other information available (I am happy to change this, if there is any other information available).


How to do research in bioinformatics without wet lab experiments? I graduated in physics from Bangladesh and keen to work in the field of biology. Like, systems biology, computational biology, bioinformatics or systems medicine. I have not produced any research work in such fields as of now. I am studying sequence alignment and RNAseq and later plan to study flow cytometry bioinformatics. I have no affiliation with any institute now in my country as they don't accept students from other disciplines. Is it possible for me to do research on my own by using databases available? If so, I would be really grateful if anyone can suggest how to approach my research topic/work.

Doing actually valuable bioinformatics research completely on your own after graduating from university (I am assuming that this corresponds to a master's degree) is somewhere between impossible and very unlikely - even for someone who actually studied bioinformatics.

In order to really do research (in almost any field) you will have to become a PhD student first - and for that studying the relevant topics on your own, like you are already doing, is probably the best preparation.

If there are truly no 'cross discipline' applications possible where you are from, you'll probably have to apply for programs or positions abroad. It is, however, becoming increasingly common for bioinformatic research groups to hire people from various different backgrounds - ranging from wet lab biology to physics. I would advise you to actively look for such interdisciplinary research groups (ideally purely computational groups as a physics background will be more valuable there than in a mixed dry/wet-lab group) and potentially directly contact the group leader if the university/institutes don't offer any programs that would allow you to apply.


What is the name of this bush with red fruits? I have seen this on Corsica (Island of France):

It is Arbutus unedo, called "strawberry tree" in English, "arbousier" in French and "medronheiro" in Portuguese. The fruits are ripe around October or November. They are full of little seeds, but if you bear the annoyance, they can be quite tasty. They are used to distill an alcohol in Portugal.


Is it possible to identify a particular gene sequence from next gen sequencing techniques (especially RNA-seq )? I have to check the expression of a gene in a fish whose sequence is not known in the fish in question. Sequence is known in an another fish (zebrafish) but the gene has 10 isoforms. The genome of fish in question is not sequenced, however RNA-seq data is available. I have no knowledge of RNA seq data analysis. Is it possible to know the sequence of gene of interest from this RNA-seq information?

Okay, so you have RNASeq, but no reference genome for your fish?  Just transcript sequence from zebrafish?  Are you just trying to see if this gene is expressed, or you need to a more global view to compare it to?

If you just want to see if the gene is expressed, easy thing to do is to make a reference just made up of zebrafish transcripts, align to that.  If there are too many differences between your fish and zebrafish, that won't work.

In which case, the next thing you could try is de novo assembly of your RNAseq data, then use blast to compare the zebrafish trasncripts to your assembled transcripts.  Blast will make alignments where a short read aligner might not.


Why do lips heal fast Whenever I have any cut in my lips ,it gets healed in 2-3 days so why do lips get healed faster as compared to other body parts?

According to this article:

  Wet or moist wound treatment significantly reduces the time required for re-epithelialization

Since the lips are (normally) constantly being moistened by saliva, this could be the reason you experience accelerated cut healing.


Melting point of a fatty acid? What factors determine the melting point of a fatty acid?

Chain length
The number of methylene group
The ionized state of the fatty acid
Its degree of saponification
Its ability to alter the entropy of water

(1) Chain Length

Will definitely affect melting point, as this website explains pretty well:

"Melting point principle: as the molecular weight increases, the melting point increases."

  (2) Number of Methylene groups.

This is another way of describing unsaturated from saturated fats. The more saturated a fat is, the straighter it is. Methylene groups cause kinks, which disrupts the Van der Waals forces along the rest of the carbon chain.

As such, from the link above again:

"On the other hand, the introduction of one or more double bonds in the hydrocarbon chain in unsaturated fatty acids results in one or more "bends" in the molecule. The geometry of the double bond is almost always a cis configuration in natural fatty acids. These molecules do not "stack" very well. The intermolecular interactions are much weaker than saturated molecules. As a result, the melting points are much lower for unsaturated fatty acids."

  (3) Ionized state of the fatty acid.

This will have a very minor affect. The fatty acid generally has an unpaired ester (-ate at the end) which can have a negative charge. However, from the link above again:

"However, in fatty acids, the non-polar hydrocarbon chain gives the molecule a non- polar character."

So even if the ester had a charge, the negative character is miniscule compared to the intermolecular forces exerted by the non-polar tail. Particularly since the charge can distribute amongst the two oxygen molecules which are conjugated, reducing the reactivity further.

  (4) Degree of saponification.

I'm not super-familiar with the degree of saponification, but from a quick overview of the process I'd say this wouldn't affect melting point - counter to my comment. The process of making soap involves only the acidic portion of the fatty-acid triglycerides. That portion of the macromolecule is going to be pretty much the same regardless of the fatty acid, so it will have nearly the same reactivity regardless of its chain length and conjugation.

What will not saponify are usually waxes - which are pretty much fully-saturated hydrocarbon chains with very few (if any) acidic sites. Parafin Wax, for instance, does not saponify, and has the formula ${C_{31}H_{64}}$.

  (5) Ability to alter entropy of water.

Like the degree of saponification option above, the ability of a fatty acid to alter the entropy of water correlates to the number of reactive sites throughout the molecule. As-such, unsaturated fats (those with methylene groups) are going to be slightly more reactive as pi-bonds are more reactive than sigma bonds.

So, given that this answer relies on a previous option, it's probably better to go with the previous option.

Ultimately, if I were answering the question I'd choose 1, 2 since the rest either depend on those two or are miniscule. However, beware that it's your question to answer and not mine.


Why does DNA have its name? Why is DNA called deoxyribonucleic acid and not something else? I get the nucleic acid part (because that's what DNA is made of) but what about the deoxyribo- part, especially the ribo- part. Maybe because DNA doesn't have oxygen, hence the "deoxy-"?

(Also, please tell me what is wrong with my question or whether there was a duplicate I didn't find so I can fix this question or delete it.)

The name is derived from the sugar which is bound to the base. For RNA it is Ribose (that why it is called ribonucleic acid) and for DNA it is Deoxyribose (hence the name deoxynucleic acid). The deoxyribose is missing an OH-group at positition 2 of the sugar ring, the name literally means "without oxygen". See the image below (from here) for further clarification:


What is this beautiful bush? Found this gorgeous bush at Port Orleans resort in Walt Disney World, but none of the employees knew what it was. Can anyone identify it for me?

It's a Queen's Wreath Vine, aka:  Purple Wreath, Bluebird Vine, Sandpiper Vine

  This native Central American flower, which blooms in the dry season, is striking in its unusual blue violet color.  Gracefully arched sprays of delicate flowers contrast with the crisp, sandpaper-like leaves.  The flowers are five deep purple petals about 2 cm across in the middle of five slender, blue or lavender sepals that create a distinctive star shape.  Although the flowers last only a few days, the star-like sepals in the cascading clusters persist for many days, gradually becoming lighter.  They are very attractive to butterflies.


Why does a Urinary Tract Infection cause a strong, persistent urge to urinate? There are plenty of articles on the fact the a urinary tract infection (UTI) causes frequent and urgent urination. For example; on this National Institutes of Health webpage.

My question is:

Why does a urinary tract infection cause an increased desire and hence, a greater urgency to urinate?

Nerve endings exist in a more or less homeostatic interstitial fluid medium which when disturbed in certain ways result in depolarization. This is a very simple explanation, but basically correct. Depending on the nerves being discussed, a change in the medium can be the presence/absence of neurotransmitters (serotonin, GABA, etc.), chemicals released from damaged tissue, pH differences, etc. etc.

Very simply put, anything causing irritation of the bladder or urethral mucosa will cause some of the nerve endings to depolarize; these are some of the same nerves that depolarize when the bladder is full, and therefore the sensation is of urgency (the feeling that one needs to urinate). The substances can be substances excreted by bacteria, released by neutrophils, or some other.

Simply administering a topical anesthetic - something that decreases the depolarization of nerve endings by reversibly binding to/inactivating sodium channels - (lidocaine, for example) will instantly alleviate this sensation. In the case of UTIs, a commonly given medication is the bladder anesthetic phenazopyridine hydrochloride.

The more complex answer is that no one exactly knows. The complexity is more important in the treatment of non-infectious causes of urinary urgency and in the investigation of why catheter-related UTI are often asymptomatic.

Edited to add: If you're looking for a more teleological reason (such as, it hurts so that you'll get flush out the bacteria faster, that's not actually what happens. When it hurts to urinate, very many women intuitively stop drinking fluids in an attempt to avoid the pain of urination, allowing the infection to get much worse. The counterintuitive measure is to drink more, not less, to flush out bacteria.


SARS-CoV - relative size of the spike protein I was given the task of determining the percentage of the S-protein of the SARS-CoV relative to the total of its proteins from the attached image. However, I have been given no explanation of the image, and with a physics background, I simply do not understand it. Can someone please explain to me how it would be possible to solve the task from the given image (i.e., explain the image).

I'm not going to give you the final answer, because this is still a class assignment, after all, but I'll give you some tips. What you are looking at is a Western blot of whole-cell extracts from a cell line called Vero, either on its own (vertical ane 9, from numbering across the bottom) or infected with various viruses carrying specific genes, as indicated. Lanes 1-7 are from Vero cells infected with the BHPIV3 viral vector (a live-attenuated virus that can carry genes from another organism). Lane 1 is just the viral vector itself, with its own proteins. Lanes 2-7 are from cells infected with the viral vector carry certain genes from the SARS coronavirus. Lane 8 is from cells infected with SARS-CoV itself (so it carries all the previous genes). The numbers along the far right side are molecular weights, in kilodaltons.
A Western blot is performed in three parts - 1) separating the protein samples (whole-cell extracts) by molecular weight (size) in an SDS-PAGE gel by using an electric field, 2) transferring the separated proteins to a membrane, also using an electric field, and 3) using some sort of probe (usually a specific antibody) to determine what is present and in what amount. In this case, two antibodies were used. The lower, narrow image shows the samples probed with an antibody that recognizes the HPIV3 F protein, which is present in all the BHPIV3-infected lanes, in relatively equal amounts. This can be determined because the size/intensity of the different bands in each vertical lane is directly proportional to the amount of that protein present in the original sample.
The upper part of the image shows the extracts probed with an antibody that evidently recognizes the SARS S, M, and N proteins, but apparently not the E protein (as Lane 6, with the SARS-E virus, is blank). Using this information, you can now determine which bands correspond to which protein.
Keeping in mind that Lane 8 contains all the proteins from the SARS-CoV virus, while the previous lanes just contain certain ones as labeled along the top, you should now be able to use ImageJ to answer the question. I will give you one hint - there is much more information present than you need to answer the question. You actually only need 4 (well, maybe 5) of the lanes. I'll leave it to you to figure out which ones.


Is it possible that by mutation a human could see infrared or other 'colours'? Incoming light reacts with the several types of cone cells in the eye. In humans, there are three types of cones sensitive to three different spectra, resulting in trichromatic color vision. Each individual cone contains pigments composed of opsin apoprotein, which is covalently linked to either 11-cis-hydroretinal or more rarely 11-cis-dehydroretina.

The opsins (photopigments) present in the L and M cones are encoded on the X chromosome.  A very small percentage of women may have an extra type of color receptor because they have different alleles for the gene for the L opsin on each X chromosome. X chromosome inactivation means that only one opsin is expressed in each cone cell, and some women may therefore show a degree of tetrachromatic color vision. Tetrachromacy is also demonstrated among several species of birds, fish, amphibians, reptiles and insects.

Humans cannot see ultraviolet light directly because the lens of the eye blocks most light in the wavelength range of 300–400 nm.

So, besides above mentioned exceptions, is it possible due to mutations or genetic engineering to see UV or infrared. What kind of mutations should be made or are the changes to be made in the opsines to big to create 'alien' eyes?

Yes.

Far-red vision (>700nm)

The ability for retinal-binding proteins to absorb far-red (between 700nm-850nm) light has been experimentally confirmed in this paper. While the authors did not attempt this in vivo in an animal model, they managed to use directed mutagenesis to induce a significant shift in the absorption peak of the chromophore of the retinal binding protein.

The authors show the shifts induced by these mutant proteins in the figure below. The mutants have significantly different absorption peaks, and assuming that the proteins do not lose their ability to transduce signals via optic nerves, they would allow vision in different wavelengths.

Ultraviolet vision (300-400nm)

It is known that humans lacking a lens (aphakia) are able to see ultraviolet light. As noted in the question, the lens blocks out long-wave UV, and its removal or absence results in ultraviolet vision (although with low sharpness due to the lack of a lens).

  However, aphakic patients report that the process has an unusual side effect: they can see ultraviolet light. It is not normally visible because the lens blocks it. Some artificial lenses are also transparent to UV with the same effect. The receptors in the eye for blue light can actually see ultraviolet better than blue. Military intelligence is said to have used this talent in the second world war, recruiting aphakic observers to watch the coastline for German U-boats signalling to agents on the shore with UV lamps.


What is these mushrooms in my indoor pot? I am living in Japan and in summer, it's very hot and humid even inside my room.
Today, I've found two mushrooms in the pot of a plant.

What is this species? It's very surprising than within one day they grew like this.

They do look a lot like a common mushroom called "shaggy mane" mushroom (Coprinus comatus). This may not be a correct identification though, so do not eat them.  They are widespread around the world, but usually grow outside.

Yes it is amazing how rapidly the fruiting body of many fungi can grow. I am providing an interesting Wikipedia link with more information. You can also search to find other images using Google images online.

https://en.wikipedia.org/wiki/Coprinus_comatus