Is there evidence that some non-human species perform sexual selection based primarily on intelligence? How do they do this?

Very intresting question. The problem is that animal intelligence is hard to measure not only for scientists, but probably also for the potential mate. Paradoxically, that is why selection for intelligence, if it occurred, may be very strong. One has to be smart in order to recognise smart behaviour, so preference and preferred feature are strongly connected. But that's only my opinion.

Boogert et al., 2011 1 reviews the current knowledge about animal preferences for cognition skills. They conclude that there is very little data on this subject. The given examples are:

1) Preference for elaborating birds songs (as songs are not inborn and have to be learned)

2) Spatial abilities:

  In meadow voles (Microtus pennsylvanicus), males with better spatial learning and memory abilities were not only found to have larger home ranges and to locate more females in the field (Spritzer, Solomon, et al. 2005 2) but were also preferred by females in mate-choice tests, even though the females did not observe males’ performance on spatial tests (Spritzer, Meikle, et al. 2005 3).

  In guppies (Poecilia reticulata), males that learned faster to swim through mazes to gain a food reward were found to be more attractive to females (Shohet and Watt 2009 4). However, females were not able to see the males’ performance in the mazes. Although male learning ability was weakly correlated with saturation of the orange patches on his body (a sexually selected trait (...)), orange saturation surprisingly did not correlate with female preferences. Thus, the cues leading female guppies to prefer faster learners are unknown.

It is possible, that females base their choose on some factors that correlates with cognitive skills or on total wellness, what may depend on intelligence.

3) bowerbird's abilities to build bowers (courtship constructions):

  Comparative studies across bowerbird species have shown that relative brain size is larger in species that build bowers than in closely related nonbuilding species (Madden 2001 5). In addition, relative brain size increases with the species-typical complexity of the bower (Madden 2001 5), and a comparative study on the relative size of specific brain regions showed that species with more complex bowers have a relatively larger cerebellum (Day et al. 2005 6).

4) foraging performance

  A recent experiment by Snowberg and Benkman (2009) 7 using red crossbills (Loxia curvirostra) showed that, after observing 2 males extracting seeds from conifer cones, females associated preferentially with the more efficient forager of the 2. The authors were able to exclude female choice for correlated traits by experimentally manipulating foraging efficiency, such that fewer seeds were available in the cones of one of the males. The males were also swapped between treatments (i.e., slow vs. fast forager) so that male identity could not explain the females’ preferences for the most efficient forager.

Another way that intelligence may be favored by sexual selection is "cheating" during courtship. For example most frog species call to attract females. But this signal may also attract aggresive rivals or predators. Some males, especially the weaker ones, do not call  but stay near calling individual.  This allows them to avoid confrontation and wait for approaching females [8]. The successfulness of this strategy may depend on how "smart" the individual is (only my opinion).

[1] Boogert, N. J., Fawcett, T. W., & Lefebvre, L. (2011). Mate choice for cognitive traits: a review of the evidence in nonhuman vertebrates. Behavioral Ecology, 22(3), 447-459.

[2] Spritzer MD, Solomon NG, Meikle DB. 2005. Influence of scramble competition for mates upon the spatial ability of male meadow voles. Anim Behav. 69:375–386.

[3] Spritzer MD, Meikle DB, Solomon NG. 2005. Female choice based on male spatial ability and aggressiveness among meadow voles. Anim Behav. 69:1121–1130.

[4] Shohet AJ, Watt PJ. 2009. Female guppies Poecilia reticulata prefer males that can learn fast. J Fish Biol. 75:1323–1330.

[5] Madden J. 2001. Sex, bowers and brains. Proc R Soc Lond B Biol Sci. 268:833–838.

[6] Day LB, Westcott DA, Olster DH. 2005. Evolution of bower complexity and cerebellum size in bowerbirds. Brain Behav Evol. 66:62–72

[7] Snowberg LK, Benkman CW. 2009. Mate choice based on a key ecological performance trait. J Evol Biol. 22:762–769.

[8] Bateson P. 1985. Mate choice. Cambridge University Press. 181-210


It's one of the more unusual Jumping Spiders - similar, as Charles said above, to the North American spider Marpissa pikei, the Slender Jumping Spider (see second link below).  Yours is even thinner and more stretched out, but still clearly a Jumping Spider, from the long, heavy front legs and the big eyes on the front of its head.
Your species appears to be a spider called Mantisatta logicauda (first link below)

http://www.peckhamia.com/salticidae/diagnost/mantisat/longi-ph.htm

http://bugeric.blogspot.com/2012/07/spider-sunday-pike-slender-jumper.html


Specialist evaluation for people aged under 40 years with stage 1 hypertension

Alongside full guidance released by NICE they also produce treatment pathways which give further advice - here is the treatment pathway for hypertension.  You've listed most of the investigations that would be considered in your original question.

Investigations that may be considered as appropriate include:

Urine dipping for proteinuria or haematuria indicative of renal damage
Measuring of plasma urea and electrolytes and estimation of glomerular filtration rate, again as an indicator of renal damage
Measuring of plasma glucose, total cholesterol and LDL/HDL cholesterol to rule out additional risk factors as part of cardiovascular risk assessment - e.g. diabetes, hypercholestrolaemia
Fundoscopy to examine the retina for damage resulting from hypertension
12 lead ECG to show any changes compatible with left ventricular hypertrophy
Scanning for the presence of a phaeochromocytoma if clinically suspected

You may also find the professional reference page on hypertension from patient.co.uk useful.


Evolution of the energy generating system in mitochondria

ANSWER SUMMARY

The criterion of efficiency of mitochondria is taken as the yield of ATP per carbohydrate molecule oxidized using the electron transport chain and oxidative phosphorylation. Experimental values for this are similar for yeast and humans, whereas theoretical values derived from differences in the structures of the ATP synthases actually imply a higher yield for mammalian mitochondria.

It is argued that it is not surprising that the difference in generation times did not produce the result expected by the poster. First, the period after the separation of eukaryotes from prokaryotes is no longer than the period between the origin of eukaryotes and that of the aerobic bacteria from which their mitochondria arose. Second, the stage would have been reached when there were mechanistic limitations on further increases in efficiency of this complex system. If the differences between mammalian and yeast bacterial ATP synthases is real (and an even ‘worse’ yield for bacteria, that have an even shorter generation time), this suggests that the main evolutionary pressure on this system varies between organisms, rather than being simply to maximize the yield of ATP.

ANSWER ELABORATION

Criterion of efficiency

The main function of mitochondria is to use molecular oxygen to oxidize NADH and FADH2 via the electron transport chain and oxidative phosphorylation to produce ATP. A suitable and generally accepted measure of efficiency — reminiscent of that applied to man-made mechanical devices — would be the percentage of the energy of this oxidation that is converted to ATP (rather than being released as heat). Any reader not familiar with the biochemistry of this system is advised to read the footnote* before proceeding further.

Is there any difference?

The traditional way in which the yield of ATP in oxidative phosphorylation has been measured is by the P/O ratio (the ratio of ATP produced to oxygen consumed). Results obtained over the years have varied becauase of technical problems — see review by Hinkle (2005). As summarized more recently (2010) by SJ Ferguson,  the historical controversy was not about differences between species — they were no indications of differences even between bacteria (the precursors of mitochondria, performing oxidative phosphorylation in their intermembrane space) — but merely about the true value of the P/O ratio.

As Ferguson goes on to say, the gradual elucidation of the structure of the ATP synthase and the elucidation of its mechanism led to a believe that deductions from this were a more reliable indication of the stoichiometry than the experimental measurements. Specifically, a 360˚ rotation of the F0 component of the ATP synthase could be seen to result in the synthesis of one molecule of ATP, and that this required on hydrogen ion bound to each of its c subunits (see diagram from Wikipedia article, below).

He describes the results with yeast as follows:

  X-ray crystallography of yeast ATP synthase revealed a ring of c subunits attached to F1 even in the absence of other subunits of the F0 sector (9). This work not only suggested that a and b were not interdigitated with c but also revealed the surprising stoichiometry of c10. The C-terminal helix of the hairpin c subunit is at the outside of the ring and contains an essential aspartate or glutamate residue. This residue is believed to pick up an H+ and rotate away from an interaction with the α subunit. Thus, 10 protons should drive a 360° rotation of the c ring, which is structurally connected to γ, giving synthesis of 3 ATPs as γ rotates through 360° within F1; the H+/ATP ratio would be 10/3 = 3.3. The P/O ratio for NADH would be 10/(3.3 + 1) = 10/4.3 ≈ 2.3, thus moving below the range of values directly determined.

It was assumed that ATP synthases other than yeast would also have 10 c subunits, but, surprisingly, although bacterial ATP synthases also have 10 subunits, the bovine (and other vertebrate) one has only 8, suggesting a higher P/O ratio than yeast — greater, not poorer, efficiency.

Mitochondrial evolution in context

Whatever the actual P/O ratios in different aerobes, the more rapidly-dividing species do not show a clear increase in efficiency in this respect. I suggest that in this respect the evolutionary timescale shown below (adapted from The Cell: A Molecular Approach) should be considered.

What is clear is that the time for an improvement in efficiency of energy production to occur between the divergence of yeast and animals (A) is much less than that between the time at which mitochondria were acquired from bacteria by the first aerobic eukaryote (B–A). Note also the long period the system had to evolve in the aerobic bacterium that gave rise to mitochondria (C–B). My argument is that by the time of appearance of mitochondria, the system had time to evolve to the optimum that mechanistic considerations would allow. Otherwise one would have expected those bacteria to further evolve a system much superior to yeast or mammals in the C–B timescale.

Other aspects of the evolution of the mitochondrial energy generating system

It should be noted that there have been changes in the mitochondrial energy generating system over evolutionary time. For example, in the cytochrome oxidase system the same set of core subunits are found in prokaryotes and eukaryotes. However additional subunits have been acquired in primates. Rather than being concerned with the catalytic efficiency of the system, these additional subunits are thought to be concerned with regulation.

Better systems to study the effect of division time on evolution of eukaryotic ‘efficiency’?

Because mitochondria had probably reached optimal mechanistic efficiency in energy generation when they were acquired, they do not appear to be a good choice for studies of the type the poster envisages. Perhaps he might do better with something related to nuclei, which are not present in bacteria. However there are problems of interpretation. For example, if it were found  that some aspect of the DNA replication machinery in yeast allowed this process to proceed faster than that in mammals, could one conclude that this was due to the shorter generation time of yeast? No! One could equally argue (and it would seem to me more likely) that the lower generation time resulted from an evolutionary pressure for faster DNA replication, a pressure that does not exist in the more slowly dividing mammals.

FOOTNOTE *

ATP in mitochondria (and the inner membrane of aerobic bacteria) is synthesized from ADP using the free energy released by the oxidation of the reduced cofactors, NADH and FADH2 (produced from the oxidation of particular carbohydrates), by molecular oxygen. The mechanism of this, rather than involving simple coupled chemical reactions, involves the movement of hydrogen ions across a membrane in which there is a concentration gradient (strictly through a proton motive force, to which membrane charge also contributes) using an ATP synthase, a molecular machine, the structure of which clearly indicates the stoichiometry of input hydrogen ions to ATP synthesized. The hydrogen ion gradient results from three stages in the electron transport chain (complexes I, III and IV) where a hydrogen ion is translocated into the inner mitochondrial intermembrane space. This is described in standard text books of biochemistry such as Berg et al..


Are lactic acid and prolactin rise after exercise connected?

Prolactin (PRL) is a pleiotropic hormone. More than 300 different functions have been described for it (Bole-Feysot et al., 1998), although probably the most well known/studied1 is the maturation of the mammary gland during pregnancy and subsequent stimulation of milk production.

One of the fairly well known situations when PRL increases is after an acute stress (Neill, 1970; Seggie and Brown, 1975; Kant et al., 1983). Although the details of this are still a bit foggy, the reason seems to be connected to the anxiolytic properties of PRL (Torner et al., 2001, Donner et al., 2007).

Anaerobic excercise is considered as a stressor, and therefore the PRL response may be important to avoid hyperactivation of the stress pathway. This has been suggested before (Ohiwa et al., 2007) and the rise in PRL may be triggered by lactic acid, as administration of lactic acid alone can stimulate PRL secretion (Sculthe et al., 2013).
Note that this does not exclude that there may be other factors involved in this response.

1 at least in female mammals, but bear in mind that PRL is present in all vertebrates, males and females alike.


What histological stain can I use for beta-keratin?

Not sure if this is what you are looking for, but I did some searching around for histochemicals and reptilia.  I did come across a paper by L Alibardi, Dipartimento di Biologia evoluzionistica e sperimentale, University of Bologna, Bologna, Italy.  Now, that exact application doesn't seem to answer your question, it did open up a web page that contained numerous papers on reptilia and their beta-keratin structure and investigations into that (citations of the original paper, as well as papers by the same author).  I didn't see any that specifically spoke to the exact stain used, but then this is a little outside my area of expertise.  Perhaps this link will give you an avenue to pursue?

Wish I could help more.


Can single-cell organisms have through-holes? (Are donut-cells a thing?)

Yeah, holes seem to happen in leptomyxa:

L[eptomyxa] reticulata is an edaphic protozoan and a predator of bacteria and amoebae. [...] The plasmodium is very polymorphic; its size varies between 50 .mu.m and 1 cm. It generally spreads in the form of a very thin transparent protoplasmic layer. It may have the shape of a full blade, sometimes perforated with holes, or of a network; the pseudopodial zones with active locomotion present a typical fan-shaped contour.

There are some hi-res images from other sources showing the same

Image source: http://penard.de/Amoebozoa/Tubulinea/Leptomyxida/
It seems that what happens is that branches "merge back" after touching "at the tips" leaving holes in such organisms, but that's just speculation on my behalf. I haven't (yet) found a source discussing the dynamics of how these holes get formed.
And a couple more images from  a different source--a broader review of leptomyxidae.

[Above] Light microscopy of Leptomyxa arborea n. sp. and L. variabilis n. sp. (by S.
Geisen and C. Burberg) on the plastic bottom of a Petri dish (Phaco). A-F: Leptomyxa arborea,
various shapes and specimens of different size. G-M: Leptomyxa variabilis, various shapes of
trophozoites (G-K and M); cysts (L-M). Arrows indicate the most pronounced bunches of
adhesive filaments; arrowheads indicate pore like structures in cysts. Scale bar is 100 μm in A-E
50 μm in F-K and 25 μm in L-M.

[Above] Isolate of Leptomyxa sp. (by morphology of trophozoite indistinguishable from
L. reticulata) observed in the sample from Valamo Island, North-West Russia (by A.Smirnov).
A: usual appearance of a trophozoite. B-D: subsequent stages of contraction of the cell on the
object slide under the bright light beam. Figure D shows pseudopodia very similar to those or
Rhizamoeba; polypodial cell like this one can move relatively rapidly for some distance.
Molecualar data from this strain were not obtained. Scale bar is 50 μm.

By the way, the "branches" are more or less "legs"/"limbs" used in locomotion; but also this species is multinucleate:

Leptomyxa reticulata is the type species of the genus Leptomyxa. It is a
multinucleate, expanded organism with plasmodia-like organization of its ramose body,
possessing a simple life cycle [...] Moving amoebae usually form adhesive uroidal filaments along the posterior end of the body or an uroidal structure consisting of a pack(s) of such filaments (the latter often is seen when the locomotive cell adopts a shape of
an irregular ramose triangle, with the base directed anteriorly).

A more diagrammatic explanation:

Main morphological traits of leptomyxid amoebae. A-E: Leptomyxa cf. reticulata
(Valamo Island strain by AS). A: expanded, plasmodium-like ramose cell, slowly moving on the
substrate. This is the “textbook” appearance of Leptomyxa. B – more compact, faster moving and
actively feeding cell. C: Disturbed cell showing compact lobose pseudopodia. Leptomyxa accepts
shapes like this under certain influence (light, temperature, etc. in order to relocate rapidly). D:
solitary cyst with double wall. E: several cysts covered with the shared outer cyst wall (D-E are
drawn based on photos by Pussard and Pons 1976a)

(So yes, creepin' amoeba with holes and "limbs"!)
A more interesting question at this point is whether there are any (naturally occurring) single-nucleus examples of "cells with holes".


Why are there few quail any more in the Northeast of the US?

Work in the early 1990s (https://pubs.er.usgs.gov/publication/5210546) (https://www.nwf.org/en/Magazines/National-Wildlife/1993/The-Case-of-the-Disappearing-Quail) suggests development (curtailing habitat), climate crisis (and associated water loss), and decline in insect populations (reducing food supply) as possible causal factors.

Insects are an important energy source for birds, generally. They help pollinate plants, which help feed birds, and they are also a food source, themselves. Their loss (https://en.m.wikipedia.org/wiki/Decline_in_insect_populations) particularly hits bird populations hard. Unless we change our agricultural practices, it is predicted that most insects may be extinct within a century. This would decimate many forms of life (ourselves, included with quail and other birds) that depend on them.


What is the most up-to-date CRISPR/Cas9 protocol?

It really depends on what you want to do with it. Sticking to genome engineering in Human cells, Nature Protocol 8(11):2281-308 · November 2013 is the de-facto standard. One improvement I suggest is to replace the "Surveyor Assay" with deconvolution analysis of sequencing traces using TIDE.


Text or source (preferably free) for learning developmental biology

Gilbert's Developmental Biology is an excellent text. It is in the 11th edition, though the 6th edition is available free on NCBI bookshelf.


Are genetic crosses between asexual organisms possible?

When it comes to viruses and bacteria, genetic cross is just as a vaguely defined concept as species. The latter is often defined on the percentage of the sequence similarity (for viruses) or the percentage of common genes (for bacteria).
If we speak about simply mixing genomes of different organisms, there are many possibilities, how this could happen. Just to give a couple of examples:

Some viruses integrate their genome into the host genome. In some cases these integrated genomes cease being functional viruses, and may evolve to be functional genes of the host. This is truly a genetic cross. See here, for example.
Bacteria and viruses routinely undergo horisontal gene transfer in which genes from one bacteria are integrated into the genome of the other one. A typical bacterial species has a few hundred core genes, and thousands of genes that are present only in some specimen or borrowed from other species, which significantly vary from one bacteria to another. Thus, every individual bacteria or bacterial community can be thought of as a genetic cross.


Plant respiration produces carbon dioxide, so why are plants regarded as decreasing its atmospheric concentration?

There are two factors here.  First is that you have to look at the plant's net production over time.  Say for instance (I'm just making up numbers here) that during the day the plant takes in 88 g of CO2 and uses photosynthesis to convert it to 64 g of O2 that's released into the air, and 24 g of C that is incorporated into the plant.  Then during the night it uses 12 g of the stored C for respiration (combining it with 44 g of O2 from the air), leaving a net daily production of 12 g C that goes into plant growth, and 44 g of O2 in the air.

Second problem is perhaps better classed as either linguistic confusion (to be polite) or ignorance.  CO2 is not "pollution": it is a normal part - more accurately, a fundamental part - of the carbon cycle https://earthobservatory.nasa.gov/features/CarbonCycle on which almost all life depends.  The problem is not plants (or animals) releasing CO2: it's humans digging up lots of fossil carbon and burning it, thus increasing atmospheric CO2 concentrations beyond the levels to which the ecosystem has adapted.

Now that you've changed the question, it's even more important to read the basic description of the carbon cycle at the link.  (Honestly, wasn't this covered in your high school biology class?)  Again, the bottom line is that plants produce a net surplus of O2, which animals consume along with the plants, so that the cycle remains balanced.


That is a Ten-lined June Beetle, (Polyphylla decemlineata) in the family Scarabeidae. You can tell its a scarab by its lamellate antennae. The stripes indicate the species.
https://en.wikipedia.org/wiki/Ten-lined_June_beetle


The easiest answer to this question is NO. We will not be able to print humans any time soon, if ever. Despite the potential of the technology, it will likely still make more sense to use stem cells to fight genetic diseases, create limited cellular masses such as hearts and other organs, and to do reconstructive surgeries such as skeletal repairs.

The reasons vary but will include:

The human being is not just a single series of cells, we are a complex melange of integrated systems connected together in a predetermined manner by our genetic code.
The standard 3D printing process might be most effective for producing a single type of cells or a simple organ whose structure is simple and whose configuration could be managed with computer aided design to produce the cells needed at the time of the organ's creation. Even an organ such as a liver will need connective tissues, for blood to be provided for the organ and those cells would need to be integrated as well.
Brain tissue would be the most difficult part of this process. Even having the tissue matrix derived from stem cells would not give us the understanding of how to create an actual brain from a printing process, which uses a layering method to deliver the material into a 3D structure.

It is certain that some things we may do in the future may be done by printing output that resembles cellular matter, i.e. bone repair and restructuring.

In the case of fixed materials such as bone, a 3D model could be taken and then replicated on a printer. The replicated material is then integrated into an area of the body and allowed to either grow in place or artificially stimulated to grow to replace the damaged area.
I use bones as an example since they have very limited purposes and once replicated artificially, would be relatively easy to put in place. This would certainly transform the dental industry, perhaps hip replacement surgeries.
If the technology could be applied internally to damaged tissues, perhaps spinal injuries could be repaired and with proper rehabilitation, a person who may have lost mobility due to an injury could have nervous tissue regrown and learn to walk again.

The potential for specific cellular development is outstanding but the method for growing complete humans has had millions of years evolution and not likely to be surpassed by Humanity in the next thirty to one hundred years unless we come to a far greater understanding of the human genome and the genetic/cellular relationships between systems in the human body as a collective whole.


Do transposons usually jump from one chromosome to another?

Yes of course; they are not like tandem duplications.

However, some transposons have site preferences; for example the Tn7 transposon.

EDIT:

I don't know what you mean by original location. Some transposons, especially LINEs, have expanded a lot in the human genome. For any individual you can check the germ cells for a reliable estimate on the original positions. There are mechanisms such as piRNA mediated silencing that suppress transposon activity in germ cells. The genome of the germ cells also tells you what exactly will be inherited by the offsprings.


Its because NADH is a powerful reducing agent. If you leave high concentrations of NADH in the cell, it would actually wreak havoc on the cell.

This is actually the reason why peroxisomes just remove FADH2s because they find no use for the extra energy and simply remove it.

So heres the simple answer. Energy is not always a good thing, because stability also matters. ATP is simply a good way to store and convert such energy.


Identified Species: Clathrus ruber

  Scientific classification

  Kingdom:  Fungi

  Division: Basidiomycota

  Class:    Agaricomycetes

  Order:    Phallales

  Family:   Phallaceae

  Genus:    Clathrus

  Species:  C. ruber

Source:
http://en.wikipedia.org/wiki/Clathrus_ruber


If my brain lost all of its activity for a moment, would my memory be gone too?

Memories are dynamic; that is not equivalent to "memories are evanescent". Cellular structure and composition controls memory, not just a continuous passage of signals. This point is already discussed in the comments.

Loss of energy (in the form of ATP) would cause memory deterioration and in some cases neuronal cell death too— strokes, which happen due to lack of blood supply to brain (and hence unavailability of nutrients and oxygen) can cause amnesia.

But one second will practically not affect anything.


What exactly happens during the crossover

Q1 In each pair, do chromosomes have to be of the same length?

Yes, approximatively.

  If yes, does it mean that this length is the same for all humans?

Yes, approximatively.

  Do chromosomes in different pairs have different lenghts?

Yes. E.g., in humans, chromosome 1 is 294 millions nucleotides long while the chromosome 22 is only 50 millions nucleotide long.

  Q2 In which exactly place do they get mixed?

These crossover can appear pretty much anywhere. The probability of a crossover to happen at a given locus (locus=location on a chromosome) is not a constant throughout the chromosome though. In any case, the crossover always (almost always) happen at the same locus for each pair of the chromosome. In other words, if ~3 millions nucleotides goes from the paternally inherited to the maternally inherited chromosome, then ~3 millions nucleotides goes from the maternally inherited to the paternally inherited chromosome.


To understand synthesis of e-NOS and n-NOS with respect to Ca and calmodulin

Does it mean that e-NOS and n-NOS are synthesized by mediation of Ca
  and calmodulin?

Calmodulin is activated by binding to calcium and NOS is activated by binding to Ca2+-calmodulin. The binding changes the structural conformation which renders the enzyme active. See this.

  Are e-NOS and n-NOS expressed on macrophages after induction [...]

Macrophages generally express iNOS upon induction by cytokines. The activity of iNOS is shown to be different in humans compared to mice; humans have low activity [ref]. However mouse macrophages have been shown to express eNOS constitutively and eNOS-knockout mice show reduced NFkB production and iNOS induction.


Animals can hurt themselves to save their life for example foxes and tigers falling in traps are known to chew their paws to escape from the trap. Thus one can argue that all living creatures want to live and to escape death as well as losing freedom.

looking at how animals live, an animal can always use its capabilities to escape danger or problems as well as to look for food for survival. In humans who commit suicide sometimes it is because  there is no "exit". for example some people commit suicide due to being unable to pay their loans it is the feeling of distress losing all hope and the fact that it is hard to escape from problems in a human society that lead to this thinking.

so a person doing so is trying to escape the problems instead of facing them. further, the fact that humans have the concept of "responsibility" and being held accountable by members of the society all these lead to this thinking as the only escape


Technically yes, but practically it depends on what the half-life of your isotope is relative to the half-life of your protein. For example, tritium has a half-life of a little over 12 years, but most protein labeling experiments take place over only a few days at most (it depends on your protein). So while technically the tritium is decaying during your experiment, the amount of decay will be below your detection limit, and therefore is negligible over the course of the experiment.

So basically it works best to choose an isotope that will not appreciably decay over the time course of your experiment so you don't have to worry about it. If this is not possible, then yes, you would need to correct for this.


The Ishihara Color Test consists of plates containing one number. But that number may consist of two digits (Fig. 1). After scouring the internet I have also found variants of the test where the each of the two digit had a different coloring (Fig. 2), but these tests may not all be validated/standardized or used by health care professionals. The plates may also contain one or two wiggly lines that have to be traced (Fig.1). In all, my conclusion is that there are many variants of this specific test around, at least on the web. I am not aware whether there are certain standardized versions being used by health care professionals. In all, my answer to your question...

  Were there slides in the test that had two or more numbers, or was I hallucinating?

...is that there might have been two digits of different coloring in the plate, dependent on the specific make of your teacher's plates. You might, or might not have been hallucinating. To give a more affirmative answer, the specific test with the specific make would have been dug up by your teacher.

Fig. 1. Ishihara test with a plate containing one number of two digits (left) and one or more wiggly lines (right). source: Colour Blindness

Fig. 2. Ishihara variants, showing two digits with different shades in the middle panel. source: allinesnowmop, a personal web page, credibility questionable


Firstly, Spider ID? Also possible relation to ~100+ serious bite reactions in past 1-2yrs

It is a wolf spider. It grows from about 1cm to 5cm long. Wolf spiders are usually gray with brown to dark gray markings. It does not spin webs, instead it actively hunts it's prey. Wolf spiders are agile, robust and have excellent eyesight$^1$. That is why you have noticed that it is quite aware of your movements.
Hogna radiata:

Alopecosa Kochi:

The bite of this spider leaves prominent marks$^2$.

In severe cases, the surrounding area may develop redness, swelling, and even ulcers that spread beyond just the bite location. Allergic reactions may cause even more severe symptoms in some people$^2$.

Since the wolf spider is not poisonous its bite can be treated by cleaning the area with soap and water and then placing a bandage over it$^2$.
Note:
I am unable to identify the exact genus of the spider. I believe it could be Hogna or Alopecia. Someone more knowledgeable could inform me.
References:
1.Wikepedia
2.Healthline


Why do animal cells "mistake" rubidium ions for potassium ions?

There are multiple biological mechanisms that can be brought to bear for distinguishing between atoms. In addition to binding properties (e.g., ionic charge, electronegativity, bond strength), there is also the size of the atoms and even their vibrational properties.
For one of these mechanisms to actually be used, however, it needs to be evolutionarily selected for in some way. The binding properties are by far the simplest to select for, since they are fairly local and permissive in nature, while the others require much more carefully tuned mechanisms.
Thus, we should expect to see most biological selectivity to be developed in terms of binding properties, as seems to be the case. For same-group covalent-binding such as one encounters with oxygen vs. sulfur, there are major differences in the properties of the bonds, giving ample opportunity for biological selectivity.
For Group 1 alkali metals like sodium, potassium, and rubidium, however, ionic bonding is much more uniform. Thus, we should expect mechanisms that apply to one to apply to all unless strongly selected for distinguishing.  In the case of potassium versus sodium, which are both very important in biochemistry, a recently discovered mechanism in sodium-potassium pumps uses binding properties to grab both, then atomic size (via steric hindrance) to distinguish sodium versus potassium as described nicely in the answers to this question.
Presumably, there simply has not been sufficient evolutionary pressure to establish mechanisms for distinguishing rubidium from potassium in the same way.  While sodium and potassium have approximately equal abundance, rubidium is approximately two orders of magnitude less abundant than either. Cesium, in turn, is nearly two orders of magnitude less than rubidium, and rapidly decaying francium mostly doesn't exist.
Thus, unless there is a particularly problematic effect of occasional incorporation of rubidium or cesium, then, we should expect these elements to be essentially indistinguishable from potassium biologically, but not from sodium, since sodium/potassium distinguishing mechanisms will reject them all along with potassium into the "not the right size to be sodium" bin.


Why Goldman Equation cannot be used to calculate dynamic changes of membrane potential

What's the purpose of the Goldman equation?

I think that statement you posted from Kandel is a bit misleading, though not incorrect - I think he's just warning against a pitfall he's seen students make.

The Goldman Equation is an equation for steady-state voltage or in other words the reversal potential, not for Vm. It will only give you Vm in a (mostly) steady-state condition, like in the context of a resting membrane potential. However, that doesn't mean it isn't useful to calculate the Goldman equation voltage when Vm is changing or that it doesn't apply, but rather that it is not sufficient to use. It will still accurately tell you what the reversal potential is at any moment in time, but it can't tell you what Vm is at that moment.

How the Goldman equation can be helpful in understanding dynamic voltage changes:

Importantly, the rate of change of the voltage of the cell is going to be proportional to the difference between the reversal potential (from the Goldman equation) and the current voltage Vm, and after a long time the voltage will eventually asymptote to the Goldman voltage.

Therefore, if you know the current Vm, and you calculate the reversal potential with the Goldman equation, you can make some inference about what will happen to the voltage at the next moment in time: it will change in the direction of the reversal potential by a magnitude proportional to

Vm - Ereversal

Why the Goldman equation is not sufficient while Vm is changing:

I suspect what Kandel and others are warning about is that this isn't quite enough information to know what happens in the next moment of time:

It takes time to reach a steady voltage, and you need to know the membrane capacitance, which isn't represented in the Goldman equation, to know what the actual change in voltage is after $\delta$t, or how long it will take to reach a particular voltage.

Also, because of voltage-dependent conductances in a neuron, the permeabilities to different ions are also changing as a function of Vm, so the reversal potential is also changing constantly.

Furthermore, simulations of Vm sometimes need to consider the changing concentrations of individual ions, because the reversal potential will change as ion concentrations change. Therefore, it typically makes more sense to think about the driving force of individual ions given by the Nernst equation rather than the Goldman equation which gives you the net reversal potential across all ions.

Summary

In summary, authors that warn against using the Goldman equation when Vm is changing are reminding you that voltage changes take time and depend on membrane capacitance as well as changes in conductance from voltage-gated channels. However, the Goldman equation is still a correct way to calculate the instantaneous reversal potential at any moment in time (but not Vm), even if Vm is dynamic.

You could edit Kandel to say:

  The Goldman equation only outputs the present Vm when Vm is not changing; also, when Vm is changing, the output of the Goldman equation is also changing due to changing conductances and ion concentrations.

..but you can see this is a bit verbose.


Land recultivation? Land revegetation? Land reclamation? Land rehabilitation?

Reclamation can be used in this context, but I think in this situation the most appropriate word would be "remediation", from the Latin word remediare which means "heal" or "cure". It is most often used in the sense of fixing environmental problems such as pollution or contaminants.

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

A Google search suggests this is a widely used term in the mining industry for the situation you describe.
https://www.google.co.uk/search?q=remediation+mining

It does depend exactly which stages you're attempting to describe, though. From http://www.miningfacts.org/environment/what-happens-to-mine-sites-after-a-mine-is-closed/:

  The terms reclamation, remediation, rehabilitation, and restoration
  are all used to describe mine closure activities that attempt to alter
  the biological and physical state of a site. [11] The terms are
  sometimes used interchangeably, and are closely linked, but refer to
  distinct steps in the preparation of the site for another use: [11,
  12]

  Remediation: The cleanup of the contaminated area to safe levels by removing or isolating contaminants. At mine sites, remediation
  often consists of isolating contaminated material in pre-existing
  tailings storage facilities, capping tailings and waste rock piles
  with clean topsoil, and collecting and treating any contaminated mine
  water if necessary.

  Reclamation: The physical stabilization of the terrain (dams, waste rock piles), landscaping, restoring topsoil, and the return of
  the land to a useful purpose.

  Restoration: The process of rebuilding the ecosystem that existed at the mine site (where applicable) before it was disturbed. The
  science of mine reclamation has evolved from simple revegetation
  activities to a discipline which involves using native plants to mimic
  natural ecosystem development over an extended period of time. [13]

  Rehabilitation: The establishment of a stable and self-sustaining ecosystem, but not necessarily the one that existed before mining
  began. In many cases, complete restoration may be impossible, but
  successful remediation, reclamation, and rehabilitation can result in
  the timely establishment of a functional ecosystem.

See also this publication by USGS:
Finger, Church, and Guerard. Potential for Successful Ecological Remediation, Restoration, and Monitoring, Integrated Investigations of Environmental Effects of Historical Mining in the Animas River Watershed, San Juan County, Colorado, 2008; U.S. Geological Survey Professional Paper .


Dynamic of the number of cells over time as the embryo grows

A starting point could be this very recent amazing movies and the corresponding research article published yesterday.

This is not my field of expertise, but I think you will find relevant information in the references cited by this article.


Is oxidative phosphorylation less efficient in gram positive bacteria?

A similar question was already answered at How do Gram + bacteria use a proton gradient for F-type ATPase? . In those answers, there is a general belief that Gram negative bacteria do not have much control over their intermembrane space pH, because their outer membranes have many porins, such as OmpC, which allows free passage both ways for protons and other molecules smaller than 600 daltons. If that is true, there is not much of a difference between Gram positive and Gram negative ability to control pH just outside the inner membrane.

There is a long review at DOI: 10.1016/j.bbamem.2005.09.010 . The first two examples of pH sensitivity are E. coli (divides more slowly when pH goes from 7 to 8.7) and B. subtilis (divides more slowly when pH goes from 7 to 8.5). The first is Gram-negative, the second is Gram-positive. B. subtilis undergoes growth arrested at pH 9, suggesting it might be more sensitive, but again, the difference is just subtle.


Transcription rate expressed in microarray per hour

The units here are relative units of intensity.  There may be about a picomole of probes on a microarray spot, but the units of intensity are not scaled to the precise concentration of DNA on the spot.

There are many variables which make exact measurements of intensity difficult to translate into the number of RNA bound to a spot.  The main one is nonspecific or non-target binding.  The oligomer on the array surface is typically between 25 and 50 bases long - it isn't the entire length of the RNA being tested by a given spot.  Another RNA may have some or most of the same sequence as a probe, or some labelled RNA will tend to get associated with some spots.  Usually factors such as the position of the spot on the array surface, the GC composition of the probe and variations in the batch of RNA preparation will also cause the intensity to vary.

Still, even with all this, with the same prep conditions and with an identical set of arrays, its valid to look at the intensity over time.  In this paper, the investigators took array measurements at different time points and at two different temperatures after 4-Thiouracil  is added to the cells, which allows one to follow RNA produced by transcription at a given time.

Since the units are arbitrary but still proportional to the mRNA found in the cells, a difference experiment like this is valid, even if the absolute concentration of any given RNA is still a bit of a mystery.


E. coli bioreactor or E. coli fermenter?

I don't think that there is a clear division between bioreactor and fermenter and the terms are often used interchangeably, but they do carry a difference in connotation (and marketing). The term "bioreactor" implies complexity, research driven, and/or maximal cell growth. Bioreactors are more state of the art and are used primarily for studying microorganisms or producing difficult to grow cells or for peak production of cells- while the term "fermenter" implies production of a substance besides or other than just the cells and might have the connotation of utility.  Fermenters also carry a historical connotation of brewing beer, wine, and other fermented food stuffs or materials. Also, it's important to bear in mind that bioreactors are used for fermenting, because bioreacting is not a real word.

If you just need a simple design for producing the bacteria or a bacterial product, then the term fermenter might be more appropriate. If you need computer control, or if you are using it to investigate/research growth and/or production parameters then you could call such vessels bioreactors without the risk of looking foolish. I think the best way to describe the difference is probably by example, but instead, I tried to itemize some of the distinguishing details, as follows:

Fermentors commonly have all or some the following elements: Agitator (of simple design), pH meter, temperature control (jacketed vessels are common), pipes for transferring nutrients, water, etc., and a sampling port (maybe). It may be made out of wood or clay, but if it is made from steel, plastic, glass, or other modern materials, that certainly wouldn't disqualify the term fermenter, but I would probably not call an oak barrel or a clay pot a bioreactor.

Bioreactors generally have the same things as fermenters, but bioreactors also usually have some or all of the following additional elements: oxygen probe, air or oxygen pump(s) and diffuser(s), other gas ports, additional ports/pipes for pH monitoring and control (often a programmable computer controlled pump is used for multiple solutions), electrolyte balance, radial or axial impellors- which operate at hundreds or thousand of RPMs, a vapor condensor (maybe), spectophotometer (for cell density measurements), nutrient processing data, and any variety of data measurement and/or recording is the often the point of interest, or when growth of tricky or finicky cells is necessary (especially like hybridomas, phytoplankton, or perhaps generally eukaryotic cell culturing). Also, there are different kinds of bioreactors like wave bioreactors (often in bioreactor bags on shaker tables instead of having an impellor).

In general, sterility is more important for bioreactors whereas many fermenters (or fermentation products, like yoghurt) can kind of take care of themselves, or a certain "cleanliness" will work. In both cases, steam sterilization is common. Again, the division is a bit blurry, and the terms might be used interchangeably by some people, like a jacket (light) versus a coat (heavy).

So, for your specific example, it would definitely be a fermentation system (not a bioreaction system), but regarding whether to call the vessels bioreactors or fermenters is more of an opinion, I'm afraid; but personally, I would probably say the fermentation system has two fermenters, since the idea is to produce a product and it sounds like they may be simple vessels. However, if the system has on-the-fly computational checks and balances, then I might be tempted to call the vessels bioreactors (if dazzle demands it).

Also, the smaller (200 L) vessel could be called an inoculation vessel without any connotations.


Why do we assume that the first humans were dark-skinned?

The first modern humans evolved about 200.000 years ago in Africa. When they lost their body hair (or at least most of it), they needed some other protection of their skin from the sun - otherwise they are prone to develop melanoma. Melanin is such a protection, and the rate of melanoma is much lower in dark skinned people.
There is also a nice correlation between latitude and skin color - the more to the north (and to some degree to the south as well) you get, the lighter the skin color of the population gets. The reason for this is likely the better ability to synthesize Vitamin D (for which you need sunlight on the skin):

The evolution of human skin coloration.
The evolution of human skin ans skin color.
Development of different human skin colors: a review highlighting
photobiological and photobiophysical aspects.
North-South gradients of melanomas and non-melanomas: A role of
vitamin D?

The lightening of the skin occurred after humans moved to Europe:

The Timing of Pigmentation Lightening in Europeans

And we even know, that this occured more than once, since the genetic reasons for lighter skins are different between europeans and light skinned asians.
A lot of this we know via sequence comparisions of genes involved in pigmentation, there you can trace mutations and see, where they show up first and how they migrate over time. One very good example is the melanocortin-1-receptor (MC1R), which is mutated pretty often in europeans (mutations in this gene are generally associated with lighter skin and hair color; people with red hair carry certain mutations in this gene) but its under selection pressure to not mutate in africa (there are almost no known mutations in MC1R for africans). Another example would be a mutation in the SLC24A5 gene, which is exclusively found in europeans, but not in asians and which accounts also for lighter skin. I stop here for the moment, if there are more specific question, go ahead.

The genetic architecture of normal variation in human pigmentation:
an evolutionary perspective and model
Genetic Variation at the MC1R Locus and the Time since Loss of Human
Body Hair
SLC24A5, a putative cation exchanger, affects pigmentation in
zebrafish and humans.


Is a haploid essentially half of a homologous pair?

Yes, you seem to have understood it correctly. On top of haploid and diploids, there are also cases of triploids, hexaploids, octoploids and others.

For example, some species of strawberries are decaploid (10 copies) (Hummer 2012). Then, there are the extremes. In Entamoeba populations, there can be variation in ploidy level among individuals ranging from diploid (2 copies) to tetracontaploid (40 copies) (Mukherjee et al. 2008)!


Can the immune system stop plasmodium from being active?

The experience of a former adviser of mine was that some people who are not taking anti-malarial medication can still resist infection with Plasmodium falciparum, one of the parasites responsible for malaria. The parasite's life cycle includes stages inside the Anopheles sp. mosquito, and they are transmitted to human host via the female mosquito's saliva when she bites to have a blood meal:

(from Wikimedia)

There is currently a great deal of research going on to understand the biology of the parasite and how it typically evades the immune system so well. Proteins expressed by the parasite can undergo antigenic variation, meaning that different forms are expressed at different stages of the life cycle, and just as the immune system may be forming a response to one version, it is down-regulated and another takes its place. This is one reason why making a vaccine has proved to be so difficult, as unlike the influenza virus, for example, a single strain of Plasmodium can alter its immunogenic appearance and escape antigen-specific immune responses.

While malaria is responsible for a high degree of morbidity - sickness - it is not necessarily fatal except in some cases, frequently when the victims are young, already ill, or are otherwise immune-compromised, or when the infection moves to the central nervous system and the brain. I can't speak from personal experience (fortunately!), but I have been told by numerous friends that malaria is something you want to avoid at all costs. The sickness can last for weeks in some cases, and apparently is quite debilitating at its worst. Brain fever can be deadly, and in many third-world countries and among the poor the lack of good medical care can lead to complications. There is the additional factor that the family has to care for the sick, and if the ill person is a wage-earner that can mean the difference between food on the table and going hungry.

So, your friends are not going to die (probably) if they don't take their tablets, but there is no reason not to take them unless you have strong side-effects, and in that case the doctor may be able to find you another one. Other common-sense measures include always sleeping with a bed net, putting screens in windows, covering exposed skin during active mosquito hours, wearing repellant if available, and eliminating places where standing water can collect, stagnate, and provide a breeding area for mosquitoes.


Creatine phosphate is used as a buffer in high energy using cells, such as muscles. In a cell you have a pool of ATP, which is needed for things like muscle contraction, and then you have your pool of creatine phosphate, which can not directly be used as energy for muscle contraction. The cell only stores so much energy as ATP. And during high energy activities it can be depleted quite fast. The problem is that it takes a lot of time to make ATP through oxidative phosphorylation. And while glycolysis is faster, you dont get nearly as much ATP. Creatine phosphate solves this problem by acting as a reserve of ATP, so when ATP is depleted, the creatine phosphate can transfer a phosphate to ADP, and thus restoring ATP without needing to wait for glycolysis or the electron transport chain to complete.


Trying to identify a bug that left a blood spot when killed

That looks like a species of syrphid fly (aka. hover fly, flower fly) — not sure about the red fluid, but it probably wasn't blood.  These flies are pollinators and the larvae eat pests such as aphids.

I don't know for sure what species that is, but it appears very similar to Toxomerus politus:

Other sources of information on this group of flies:

http://thingsupclose.com/syrphidae-hoverflies/
http://bugoftheweek.com/blog/2017/10/31/flies-that-mimic-wasps-masquerading-syrphid-fly-ihelophilusi-sp
http://bugoftheweek.com/blog/2016/10/19/a-flower-fly-grows-in-brooklyn-flowers-flies-syrphidae


You'll be interested in THIS Wikipedia article. It really depends on how you define "strongest" (Newtons, Wattage, Newtons per Kilogram, etc.). Here are a few relevant excerpts from the article:

In ordinary parlance, muscular "strength" usually refers to the ability to exert a force on an external object—for example, lifting a weight. By this definition, the masseter or jaw muscle is the strongest. The 1992 Guinness Book of Records records the achievement of a bite strength of 4,337 N (975 lbf) for 2 seconds. What distinguishes the masseter is not anything special about the muscle itself, but its advantage in working against a much shorter lever arm than other muscles.
If "strength" refers to the force exerted by the muscle itself, e.g., on the place where it inserts into a bone, then the strongest muscles are those with the largest cross-sectional area. This is because the tension exerted by an individual skeletal muscle fiber does not vary much. Each fiber can exert a force on the order of 0.3 micronewton. By this definition, the strongest muscle of the body is usually said to be the quadriceps femoris or the gluteus maximus.
The heart has a claim to being the muscle that performs the largest quantity of physical work in the course of a lifetime. Estimates of the power output of the human heart range from 1 to 5 watts.[14] This is much less than the maximum power output of other muscles; for example, the quadriceps can produce over 100 watts, but only for a few minutes. The heart does its work continuously over an entire lifetime without pause, and thus does "outwork" other muscles. An output of one watt continuously for eighty years yields a total work output of two and a half gigajoules.


What is the impact of stress on the human body?

Stress is the reaction, which our body reacts against the pressure or tension. There are many impact of stress on the human body, which includes

Emotional:  Moodiness, short temper, agitation, inability to relax, feeling lonely and always depressed.
Cognitive:  Memory problems, unable to concentrate, very poor judgment, negative thoughts, always anxious and worrying
Physical: Frequently suffering from pains and aches
Behavior: Addiction toward drugs, alcohol or cigarettes for relief, nervous, being alone, insomnia.
Other problems like headache, muscle pain, chest pain, fatigue, etc.


What kind of fish is this? Spotted or largemouth?

This looks like a spotted bass (Micropterus punctulatus).

Here's an image showing some quick differences between some common bass species:

Using the above photo and this source to guide our judgment we can see your specimen appears to:

Have a jaw that does not go posterior to the eye (as it otherwise would in a largemouth).
Have rows of pigment towards its ventral side (below the "lateral line").
Not have the typical darker horizontal line of scales characteristic of the largemouth bass .
Have smaller-sized cranial scales (those around the eye) characteristic of the spotted bass.

If you can provide additional pictures of the following, I can provide a more definitive ID:

Both dorsal fins -- if the 2 dorsal fins are connected, it would further suggest a spotted bass (as largemouth bass dorsal fins are not typically connected)
Tongue -- evidence of a tooth patch is more likely on the spotted bass.

According to the International Game Fish Association:

  Spotted bass can be found throughout the central and lower Mississippi basin to the Gulf of Mexico (from Texas to the Florida panhandle), including Georgia, Alabama, Tennessee, Kentucky and other nearby states where it occurs naturally or has been introduced.


Mitochondria produce a large quantity of reactive oxygen species (ROS) that damage the mitochondrial genetic material. These cell organelles do have a  DNA repair mechanism similar to that of the nucleus to some extent 3 which is not entirely understood however they have multiple copies and so the fusion and fission of mitochondria work together to maintain as many viable/healthy mitochondria as possible.

When two mitochondria fuse, their genetic material can recombine and thus exchange their damaged DNA. In this way, one of them repairs its DNA at the expense of the other accumulating more damaged DNA. Mitochondria that accumulate too much damaged DNA will 'die' - get eliminated, but they can be replaced by fission of healthy ones. Take a look at this wiki page, it has useful info.

Edit: This article may also be useful. (Mitochondrial fusion and division: regulation and role in cell viability
Giovanni BENARD and Mariusz KARBOWSKI, Semin Cell Dev Biol. 2009 May;20(3):365-74.)


I don't have an other explanation than pointing to evolution. It was obviously not a problem to evolve the way it did. One article I found (see "The Inverted Retina: Maladaptation or Pre-adaptation?") called it a sign of pre-adaptation, where forms exist before they get their final function.
Another pretty comprehensive review can be found here: "Evolution of Phototransduction, Vertebrate Photoreceptors and Retina."


There is a very different mechanism for generation (and detection) of ultraviolet, visible and infrared light vs radio waves.

For the first, it is possible to generate it using chemical reactions (that is, chemiluminescence, bioluminescence) with a typical energy of order of 2 eV (electronovolts). Also, it is easy to detect with similar means - coupling to a bond (e.g. using opsins).

For much longer electromagnetic waves, and much lower energies per photon, such mechanism does not work. There are two reasons:

typical energy levels for molecules (but it can be worked around),
thermal noise has energies (0.025 eV) which are higher than radio wave photon energies (<0.001 eV) (it rules out both controlled creation and detection using molecules).

In other words - radiation which is less energetic than thermal radiation (far infrared) is not suitable for communication using molecular mechanisms, as thermal noise jams transmission (making the sender firing at random and making the receiver being blind by noise way stronger than the signal).

However, one can both transmit, and detect it, using wires. In principle it is possible; however, without good conductors (like metals, not - salt solutions) it is not an easy task (not impossible though).


I came across this paper (Holt et al. 2002), does this answer your question? Look at Table 2 and 3. In this paper the lenght of 2L is  52393056 bp.


Do bacteria with capsular antigen always have a capsule?

In short: It can depend on your definition of encapsulation.

According to the Oxford Dictionary of Biochemistry, a capsular antigen is defined as

  any of the antigens, usually polysaccharide in nature, that are
  carried on the surface of bacterial capsules. The term K antigen is
  used for those that mask somatic (O) antigens.

In general, capsule polysaccharides have complex structures and are produced by a the action of several enzymes, with the genes necessary for production of the capsule typically making up a gene cluster in the genome (see for example Chen et al.: http://www.biomedcentral.com/1471-2180/10/274). On the face of it, it would seem somewhat unlikely that a bacterium would produce a known capsular polysaccharide antigen without retaining the ability to produce a capsule, as the selective advantage of the capsule then would be lost.

In actuality, the answer might depend on how you define "have capsular antigen" and "capsule". Historically, several methods have been used for demonstrating encapsulation. Methods based on staining microscopy or colony morphology observations tend to identify fewer strains as encapsulaed than does serotyping (reaction of serum with antigen). With this in mind, strains that can be shown to be encapsulated without serotyping are sometimes referred to as "highly encapsulated" to distinguish them from strains that test positive for encapsulation through serotyping only.

For discussions of capsule detection methods as applied to Staphylococcus aureus, see Sutra et al. (http://jcm.asm.org/content/28/3/447.full.pdf) and O'riordan and Lee (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC321462/).  O'riordan and Lee writes

  Isolates belonging to the remaning serotypes produce nonmucoid
  colonies on solid medium, and their colony morphology is
  indistinguishable from that of strains lacking a capsule. Some
  investigators have referred to nonmucoid, encapsulated S. aureus
  isolates as microencapsulated to distinguish them from the atypical
  mucoid strains.

Thus, if both "have capsular antigen" and "have a capsule" is defined by a positive serotyping result for a capsular antigen, then all strains with a capsular antigen as detected by serotyping have a capsule per definition. If on the other hand you define encapsulation based on ink staining microscopy or colony morphology, there are definitely strains that produce K-antigens and don't qualify as "encapsulated".

Note that while bacterial capsules consist mostly of polysaccharides, capsule proteins make up a second class of capsule antigens. One example is the Caf1 capsule antigen protein produced by Yersinia pestis: http://en.wikipedia.org/wiki/Caf1_capsule_antigen


There are 5 answers, all "yes" (though the first one is disputable).

First: there exists at least one animal which can produce its own chlorophyll:

A green sea slug appears to be part animal, part plant. It's the first critter discovered to produce the plant pigment chlorophyll.
The sea slugs live in salt marshes in New England and Canada. In addition to burglarizing the genes needed to make the green pigment chlorophyll, the slugs also steal tiny cell parts called chloroplasts, which they use to conduct photosynthesis. The chloroplasts use the chlorophyl to convert sunlight into energy, just as plants do, eliminating the need to eat food to gain energy.

The slug in the article appears to be Elysia chlorotica.

Elysia chlorotica is one of the "solar-powered sea slugs", utilizing solar energy via chloroplasts from its algal food. It lives in a subcellular endosymbiotic relationship with chloroplasts of the marine heterokont alga Vaucheria litorea.

UPDATE: As per @Teige's comment, this finding is somewhat disputable.

Second, animals need not produce their own Chlorophyll, and instead symbiotically host organisms that use Photosynthetis - e.g.  algae and cyanobacteria. This approach is called Photosynthetic symbioses.

Overall, 27 (49%) of the 55 eukaryotic groups identified by Baldauf (2003) have representatives which possess photosynthetic symbionts or their derivatives, the plastids. These include the three major groups of multicellular eukaryotes: the plants, which are derivatives of the most ancient symbiosis between eukaryotes and cyanobacteria; the fungi, many of which are lichenized with algae or cyanobacteria; and the animals. We, the authors, and probably many readers were taught that animals do not photosynthesize. This statement is true in the sense that the lineage giving rise to animals did not possess plastids, but false in the wider sense: many animals photosynthesize through symbiosis with algae or cyanobacteria.

Please note that while most organisms known for this are fungi, and some rare invertebrates (corals, clams, jellyfish, sponges, sea anemones), there is at least one example of vertebrate like this - spotted salamander (Ambystoma maculatum)

Non-chlorophyll synthesis

A 2010 study by researchers at Tel Aviv University discovered that the Oriental hornet (Vespa orientalis) converts sunlight into electric power using a pigment called xanthopterin. This is the first scientific evidence of a member of the animal kingdom engaging in photosynthesis, according to Wikipedia.

Another discovery from 2010 is possibly a second piece of evidence:

University of Arizona biologists researcher Nancy Moran and Tyler Jarvik discovered that pea aphids can make their own carotenoids, like a plant. “What happened is a fungal gene got into an aphid and was copied,” said Moran in a press release.

Their research article is http://www.sciencemag.org/content/328/5978/624, and they did not consider it conclusive:

The team warns that more research will be needed before we can be sure that aphids truly have photosynthesis-like abilities.

Third, depending on how you understand Photosynthesis, you can include other chemical reactions converting sunlight energy.
If the answer is "usual 6H2O + 6CO2 ----------> C6H12O6+ 6O2 reaction done via chlorophyll", then see answers #1,#2.
But if you simply literally translate the term (synthesizing new molecules using light), then you can ALSO include the process of generating Vitamin D from exposure to sunlight that
humans do thanks to cholesterol (link)

Non-biological answer.

As a side bonus, Ophiocordyceps sinensis is referred to as half-animal half-plant (not very scientifically IMHO). But it doesn't do photosynthesis.


While there is no such thing as perfect vision, growing evidence from Asia shows that looking often at distant objects (which one does naturally when being outside) can stop myopia progression. Vice versa, progression appears to increase when myopic children mainly live indoors.

D. J. Park, N. G. Congdon: Evidence for an "epidemic" of myopia. In: Annals of the Academy of Medicine, Singapore. 33, 1, Jan 2004, 21–26. PMID 15008557. (Review).

K. A. Rose, I. G. Morgan et al: Outdoor activity reduces the prevalence of myopia in children. In: Ophthalmology. 115, 8, Aug 2008, 1279–1285. DOI:10.1016/j.ophtha.2007.12.019. PMID 18294691.


Predictive Single Nucleotide Polymorphisms (SNPs) for Bipolar Disorder

Yes, there have been a variety of studies that do association analysis of variants with bipolar disorder. Here is a recent one that validated 11-30 variants depending on how you count.
However, in these kinds of analyses you should be somewhat cautious as the associations are extremely weak (as they generally are for complex traits in humans):

Eight of the 19 variants that were genome-wide significant (P < 5 × 10−8) in the discovery GWAS were not genome-wide significant in the combined analysis, consistent with small effect sizes and limited power but also with genetic heterogeneity.

The statistics of how you interpret such variants are rather dodgy/uncertain, so I would put very little stock in any particular variant. Maybe if you take the genome-wide significant variants only and added them all up you might start to get a little predictive power.
In terms of other more speculative observations (again from the abstract of that study):

The significant loci contain genes encoding ion channels, neurotransmitter transporters and synaptic components. Pathway analysis revealed nine significantly enriched gene sets, including regulation of insulin secretion and endocannabinoid signaling. Bipolar I disorder is strongly genetically correlated with schizophrenia, driven by psychosis, whereas bipolar II disorder is more strongly correlated with major depressive disorder.

I would suggest reading that paper and finding some further citations from it if you are interested in more detail.


In order for a vaccine to work, antigens in the vaccine must maintain their shape and charge. Freezing a vaccine, particularly vaccines that contain aluminum, can cause antigens or other important constituents of the vaccine to aggregate. This may be what prevents them from working correctly, though we don't know for sure, and it may be something else about the freeze-thaw process. The main thing that we know, though, is that (typically in animal models, as in the last reference) for certain vaccines, if you allow them to freeze, they don't produce a sufficient immune response.

You can look at this very large table of data about which vaccines are freeze stable and which are not.  There are a few patterns to this, as the OP seems to have noticed.

Aluminum adjuvant: Any vaccine that uses an aluminum adjuvant (a chemical used to enhance the immune response) will be damaged by freezing. Polysaccharide vaccines and other purified or recombinant antigens are more likely to require an adjuvant. This is one of the reasons antigen only vaccines are more likely to be freeze sensitive. Some antigen only vaccines can be frozen themselves, and reconstituted with the adjuvant prior to administration (for example, some Meningitis polysaccharide and polysaccharide protein conjugate vaccines).
Live attenuated vaccines: Almost all live attenuated vaccines are freeze stable (e.g., MMR, oral polio). The only ones that aren't, as far as I'm aware, are influenza vaccines: flumist and the live attenuated H1N1 influenza A vaccine. This may or may not just be a precaution, as I'm not aware of immunogenicity experiments that demonstrate freeze sensitivity.
Inactivated vaccines: Most killed or inactivated vaccines are sensitive to freezing. IPV is one of them. Rabies is an important counterexample. This is entirely speculation, but since many of these vaccines are formalin inactivated enveloped viruses or bacteria with cell membranes, freezing a perforated cell membrane may further damage it's antigenicity.

You can read about the basic principles of vaccination (e.g., how a vaccine works, what an adjuvant is, when you need it, etc) in Abbas Basic Immunology Chapter 8, and Murray Medical Microbiology Chapter 13.


What is meant by "a codon codes for an amino acid"?

It does not means "provides instructions for manufacturing an amino acid".  How could three little letters encode so much?

A codon is a three nucleotide sequence that matches the anti-codon of a t-RNA molecule capable of carrying one kind of amino acid.  The GGG codon, for instance, binds the t-RNA that binds to glyceine.  So the codon GGG in an mRNA ends up amounting to "put a glyceine here in the amino acid chain"


I can't understand what you mean by "Should the probability of having a daughter be multiplied?" But yes, the probability of having a normal daughter is 0.25, but she will be a carrier like her mother.

Let H represent normal allele for blood clotting (dominant); h represent allele for hemophilia, XY represent the male chromosomes and XX represent the female chromosomes.

Parental Phenotypes :

   Normal female(carrier) x Hemophiliac male

Parental Genotypes (2n) :

   X(H)X(h)         x     X(h)Y

Gametes (n) :

   X(H)     X(h)    x   X(h)     Y

Possible Outcomes :

X(H)X(h) - A normal female, carrier.

X(H)Y    - A normal male.

X(h)X(h) - A hemophiliac female.

X(h)Y    - A hemophiliac male.

So probability of having a normal daughter, that is X(H)X(h) is 0.25.


How long will a vegetable live for after being harvested?

The short answer is that as long as the vegetable/fruit is fresh looking - i.e. the cells have not disintegrated - they will be respiring, many cells will be functioning quite normally, and the plant is still technically alive. In cases where the part of the plant we treat as a vegetable is a part intended for reproduction (e.g. a seed, or a tuber like a potato) the plant will keep growing.

The point at which the plant dies is not clearly defined like it is in animals, but generally if you can still eat it, it's still alive.

Death in plants is quite different from that in animals - we refer to it as senescence. The key difference is that it happens to tissues and organs which can die and separate from the organism. Individual leaves can die without the plant's health being affected. Once this has happened to all the parts, the organism is considered dead, but if there is any respiring tissue left, it's still alive.


When was it understood that a male haemophilia sufferer can't pass it on to his sons?

Using Google Scholar, I've found the oldest publication on this item.
1911 - "The pathogenesis of hereditary haemophilia".
In this article you'll find a complete synthesis of all the works done about haemophilia till 1946.

OP adding a summary, in case of future link rot: The linked article is from 1946, based on research in the late 1930s and early 1940s into the statistics of haemophilia. It's attempting to estimate the mutation rates of X chromosomes in males and females, and to test if X-Y crossover allows the haemophilia mutation to skip generations. It assumes the knowledge that leads to the conclusion that a male sufferer can't pass it onto his sons.


How can you identify if a person is homozygous for a certain allele?

You could use a 3-primers strategy, where you have a common primer, one that only amplifies the mutant allele and one that only amplifies the wt. This may or may not be feasable depending on the type of mutation.
DNA from het people will amplify both product, while homozygous will only amplify one (wt or mutant).

Of course then, linking the mutation of a gene to the lack of a chemokine is not necessarily straightforward.

To be honest, however, I would use a different approach: take people who don't produce the chemokine, and people who do (simply by dosing the chemokine in the blood). Now sequence the gene in the two groups and look for mutations.


Given your questions taken together and your comment It would be interesting to know how much delay the brain can handle in understanding causality and associating events I think you are interested in intersensory asynchrony. A well-known example where two stimulus modalities are perceived as separate while they are in fact coming from the same event is a thunder heard after lightning. This is caused by the fact that sound travels at a speed much slower than light, and hence a thunder can lag lightning by seconds.

source: NASA
In many instances, however, one event generating perceptions across stimulus modalities are actually perceived as synchronous while they are in fact offset in time due to differences in physical characteristics of the stimuli. Taking the storm as an example - when it is far away, the thunder is perceived as separate because the thunder lags by seconds. But when the thunderstorm is close enough, the auditory crack and visual lightning are actually perceived as synchronous, while in fact they are still offset because of the sound travelling so much slower than light.
So the question becomes, as you rightfully ask, what are the margins in which stimuli across modalities can be asynchronous while perceived as one event? In other words, what is the window of integration?
A review by Vroomen and Keetels (2010) describes various psychophysical studies that have examined what the minimal asynchrony is between two stimuli of different modality that lead to a synchronized percept. The following values are for simple stimuli, such as tactile taps, auditory beeps and visual flashes.

Auditory and tactile stimuli: 80 ms
Auditory beeps and visual flashes: 25 - 50 ms
Visual and tactile stimili: 35 - 65 ms

Note that these lag differences are relatively large, given the speed of peripheral neural transduction (see the other answer of Nandor Poka below). Moreover, the window of integration between more complex stimuli can be much greater. For example, the window for speech and visual information can be as large as 203 ms.  Such large windows of integration point toward higher processes playing a role in the brain.
Note that only temporal lags below 20 msec are expected to go unnoticed because of hard-wired limitations on the resolution power of the individual senses,
Hence, Vroomen and Keetels (2010) argue there must be higher processes at work in the brain that actively synchronize percepts that are offset in time, but seem to belong to one and the same event. One such mechanism is referred to as temporal ventriloquism, which means that one perceptual modality is actively shifted in time to match it with another. This effect is most pronounced in visual stimuli, in that a visual percept is actively adjusted in time to match a sound or tactile stimulus. Likely visual percepts are shifted preferably by the brain, because the visual system is the slowest of all the senses.
Reference
- Vroomen & Keetels, Att Percept Psychophys 2010; 72(4): 871-84


I could find that topic related to Eminem's mother, Debbie Mathers-Briggs, who almost died delivering her first son(Eminem) at the end of a 73-hour labor or 73-hour birth. That "73 hour birth" means she was in labor(to undergo the efforts of childbirth) for "73 hours".


Is intelligence (or mental ability) genetically transferred (inherited characteristic) from the parent to the offspring or is it an acquired trait?

Standard IQ test are often considered the best proxy for intelligence. Studies show IQ heritability varying between 0.5 (ref) and 0.8 (ref).

TO make sense of these numbers, you will need to understand the concept of heritability. You can find info on this important concept in the post Why is a heritability coefficient not an index of how “genetic” something is?. Other posts also offer an intro to this concept (see this, this, this or this post). You can also simply have a look at wiki. You might want for example to be able to understand the equation $H_N^2=\frac{V_A}{V_P}$ without further explanations.

The H2DB database may interest you as well and of course the wiki page on heritability of IQ


Difference between Peptone, Peptide and Proteose

Quick Answer

Peptide refers to at least two amino acids joined by amide bonds.
Proteoses are products of acid proteolysis which precipitate with saturating ammonium sulfate.
Peptones are products of acid proteolysis which do not precipitate with saturating ammonium sulfate.
While peptide is a term of significant relevance today, proteose and peptone are anachronistic.

Long, Confusing and Out-Dated Details

The terms peptone and proteose were first used in the late 19th century, which makes finding substantive definitions, well, difficult. I refer you to the following paper (yes, 1891...). It is not the first to discuss proteoses, but I can't find any earlier ones and the explanation is quite clear (emphasis added).

Chittenden RH, Hartwell JA. 1891. The Relative Formation of Proteoses and Peptones in Gastric Digestion. J Physiol 12:12-22.

  In the digestion of proteid matter by pepsin-hydrochloric acid there are three well-defined products or classes of products, viz. acid-albumin or syntonin, albumoses or proteoses, and peptones. We look upon the first as the initial product of gastric digestion and identify it by its well known precipitation by neutralization. In the filtrate, the [proteoses] can be detected... best by saturation with ammonium sulphate, while the true peptones... are found in the filtrate from the latter precipitate... True peptones are bodies not precipitated by saturation with ammonium sulphate, and are the final products of pepsin digestion.

NB: proteid = protein

So, according to this paper (and apparently "all physiologists" at the time, see below), there are three main products resulting from pepsin-acid digestion of protein:

syntonin - the initial product, precipitates upon neutralization (likely due to acid denaturation)
proteose - the main product after continued digestion, characterized by precipitation with saturating ammonium sulfate

  Study of the individual proteoses formed in the gastric digestion of albumin, fibrin, globulin, myosin, casein and other proteids has seemingly already shown that these so-called preliminary bodies are the main products of the digestive action of pepsin

peptone - the final product of digestion, does not precipitate with saturating ammonium sulfate

  All physiologists are presumably agreed that peptone is the final product of gastric digestion

They further emphasize that peptone is a product of continued proteose digestion:

  Since the discovery of the [proteoses] and of their characteristics, frequent study of digestive mixtures has given convincing proof that in an ordinary gastric digestion of any common proteid only a comparatively small amount of peptone is formed; peptonization in the true sense of the word results only from the long-continued action of pepsin-acid, and even then complete peptonization rarely if ever occurs. The... proteoses are to be considered as the primary products of gastric digestion, while peptones are the end products of proteolytic action, the latter being formed by the gradual hydration of the primary products...

It would seem that peptone differs from proteose only in the length of its constituent peptides, with peptone containing shorter peptides due to continued proteose digestion. However, a more recent paper (with more recent meaning 1924) challenged this view and claimed that both proteose and peptone consist of small peptides which differ in amino acid composition rather than length. In their view, different composition rather than length explains their differential solubility in saturating ammonium sulfate.

Rudd GV. 1924. Proteoses, Peptones, and Polypeptides. Aust J Exp Biol Med Sci 1:187-190.

  ...each fraction must consist of a mixture of comparatively simple peptides, which differ among themselves in the amino-acid units of which they are constituted. The fact that some, at least, of these peptides are precipitated by ammonium sulphate shows that they belong to the group of proteoses, which therefore are partially, if not entirely, made up of simple peptides.

  It is possible that the terms, "proteose," "peptone," and "polypeptide,*' will all have to be considered to apply to substances of the nature of peptides... each built up of a small number of amino-acid units and differing from each other, not so much in the number of amino-acids in the molecule, but rather in the variety of these acids. The differences in solubility in various solutions shown by these compounds are thus to be attributed to differences in their chemical constitution, rather than in their molecular complexity. If this be so, these substances would be considered, not as successive stages in hydrolysis, but as products of one completed stage, differing in their solubility's.

They also quote another paper with supporting evidence:

  Fischer produced tripeptides and tetrapeptides of known composition and structure, which were precipitated when their aqueous solutions were saturated with ammonium sulphate. If these peptides were found in the solution obtained by the hydrolysis of a protein with pepsin they would be classed as proteoses.

I wasn't able to find any subsequent research. Nevertheless, such definitions from this period are based on macroscopic physical, rather than molecular, properties of the substance. This old terminology is not particularly informative in modern biology, and it would seem that they remain in use only as historic anachronisms. Today, both peptone and proteose are terms used almost exclusively when describing microbiological culture media (which dates from the period) or when making general reference to digestion products. In fact, they are often used in conjunction (ie proteose-peptone) which suggests they are now synonymous.


Is scalable growth the main reason why Darwinian systems select Fibonacci sequences?

I really wanted to put my thoughts into words as to why biological systems conform to Fibonacci's series.

What you say is entirely plausible and it does make sense. But what I wanted to address was why do these systems conform to it.

It is because of the interactions with the environment

Explaining this concept on multicellular organism first requires answering the same question in bacteria. Towards this end, I would like to point you towards this wiki page

It comes down to parameters such as medium concentration and hardness, parameters which we can influence. If we can extrapolate from this that cells, any cells will always follow a chemokine/nutrition gradient then we can start to understand why the system conforms to a fibonacci sequence.

Next, check out this video on a wound healing assay, what i would like to bring to your notice is that you'll find the cells replicate and move at the same rate.

If you follow a chemokine gradient, and move at approximately the same rate as your 2 billionth cousin, wouldn't you end up inevitably creating a symmetric structure?

Finally, I would, point you towards this article, where they explain a phenomenon called cell migration. This is particularly responsible for creating the symmetry which you see. And this is a similar article as the top one but it should be open access. Both support an idea which has been observed, I tried searching for the video but couldn't find it. The idea being that cells migrate collective, but there are some cells which are leaders and some followers. The leaders lead the collective migration (creating some sort of chemokine gradient) while the followers follow this gradient.

I attended a seminar last year by D Gilmour from EMBL. He showed us this particular video on collective cell migration and deposition of small clusters of cells which go on to establish the lateral line in zebrafish. You will find that a periodicity exists in this migration pattern. He relates it to a ligand activation. The related article to the video should be this one (I thought so after reading the abstract)


As a general rule, you might want to check wikipedia before posting here. On the other hand, I am glad you made me look the answer up.

Goose-bumps warm you up a little. "During the formation of goose bumps, the body is warmed from the muscle tension in piloerection."

There are other reasons, which do not directly serve humans, but may be a remnant from evolution. In animals with fur, the erected hair makes thicker insulation and further protection from cold. "Goose bumps can also be a response to anger or fear: the erect hairs make the animal appear larger, in order to intimidate enemies."

More on wikipedia: http://en.wikipedia.org/wiki/Goose_bumps


Could someone help me identify this insect?

Looks like a Bibio, sometimes referred to as "March flies" and one species in particular known as "St Mark's Fly". Yours seems unlikely to be that one because it is found in England and it seems like nowhere else.

Most likely I think yours is a Bibio vestitus from the picture below (unfortunately I wasn't able to find multiple sources corroborating this, though, so take it with some caution), and although I had trouble finding definitive distribution data, it looks like the one in your picture has the copper-colored legs, and in addition the first image below claims to be from Massachusetts. There are many many species of Bibio though so I can't be certain of species.

Bibio vestitus
Reference


Agony, Hydrophobia and viruses in the light of evolutionary principles

The hydrophobia symptom is most likely a bi-product of the effects the virus has on the brain and not an evolutionarily derived strategy to create an appropriate environment to reproduce in. Just the same as other symptoms the infection causes, like fever for example, is a reaction the body has to the presence of the virus and not something the virus is doing on purpose to set up a better environment.

A bit old, but check out [1]: "Hydrophobia may represent an exaggerated respiratory tract irritant reflex with associated arousal potentiated by the selective destruction of brain stem inhibitory systmes."

So basically the virus is indirectly causing a fear of water. The destruction of brain cells and inflammation caused by the presence of the virus in the central nervous system cause a reflex in the respiratory tract which manifests as muscle spasms and renders the patient, who is already pretty out of it at this stage, unable and very unwilling to drink any fluids [2].

[1] http://europepmc.org/abstract/MED/982512 (Warrell DA, Transactions of the Royal Society of Tropical Medicine and Hygiene [1976, 70(3):188-195])

[2] http://publichealth.lacounty.gov/vet/rabiesmanual/clinical.htm


Microbiome Context for Amino Acid Essentials and Non-Essentials

If your body was filled with highly specialized bacteria living in nutrient-rich conditions, what you suggest could happen*.

But in practice, you're not filled with such bacteria, and most of the bacteria in your body are living in rather harsh conditions for rapid metabolism.

That said, gut bacteria do produce a range of other useful nutrients. Look for a review on gut microbiome metabolism, and you will find a number of examples.

*Some basic calculations:
Say we take an optimistic estimate for productivity of 1g AA/g biomass/day. (It's what they got in this paper (one of many) that characterized a strain of Corynebacterium glutamicum engineered to produce lysine for industrial purposes and growing in a bioreactor. There are better strains now, but still, let's call that an unbelievably optimistic estimate of what a bacterium in the body might produce in the right conditions). How much bacterial biomass is in the body? Not a trivial question to answer (How much weight/volume do microbes occupy within the human body?) but let's go with the middle of the road estimate of 1kg. So 1 kg of awesome lysine-producing bacteria might potentially produce 1 kg of lysine a day. Googling around for dietary requirements seems to get you somewhere in the 1-5 g/day range. So assuming vaguely similar productivities for other amino acids, we've got plenty of room to spare if we assume that our bacteria are highly specialized for this function and are exposed to friendly, oxygen-rich and nutrient-rich conditions.


Are heterozygotes always fitter than homozygotes? Can inbreeding be beneficial?

Certainly it is not necessarily the case that having two of the same allele is a bad thing - if there is a "bad" allele then there is a "good" allele. It can be that the heterozygote is equal, better than, or worse than either homozygote. When the heterozygote is fitter than both homozygotes it is called heterosis and, when this is the case, outbreeding/hybridisation is advantageous.

The process of inbreeding can actually improve fitness because it increases the rate at which deleterious mutations (bad mutations) are expressed, and therefore the efficacy of selection. If the population avoids fatal inbreeding depression it can have positive effects. This process of removing deleterious variants by inbreeding is called genetic purging.


How can a disease be transmissible animal-to-human but not human-to-human?

I have heard some debate about whether or not the Wuhan virus can be transmitted human-to-human, but this doesn't make sense to me. Why wouldn't it be able to?

A virus has to be able to physically get out of one person and then into another in order to infect them.  If it can't do that, it can't spread between people.  Just because you can get a virus by (for example) eating an infected animal doesn't mean you'll be able to spread it to other people, at least without them eating you.

  Are there diseases that can only be transmitted from animals, not humans?

Yes, and this is very common.  Rabies for instance can be transmitted from hundreds or maybe even thousands of animals to humans, but is virtually incapable of moving between people because it infects the nervous system which severely limits the ability of the virus to get into another host.


What is the chance a given gene will end up in a given gamete?

A cell contains two haplotypes (or two set of all chromosomes). One haplotype inherited from the mother, one from the father. A haploid cell, resulting from meiosis, will receive either the maternal (or grandmother if you prefer) or paternal (or grandfather if you prefer) haplotype. It cannot receive anything else. Hence the probably must be 0.5 (or 50%).

Note that you are using the term "gene" incorrectly. You should use the term "allele" instead. And while you are improving your genetic vocabulary you should also check the term "locus". Also, the term "desired gene" is never used. We talk about "beneficial allele" or "detrimental allele".


Change in synthesis rate of a molecule changes equilibrium concentration

Note: The term equilibrium is different from steady-state w.r.t chemical reactions. Steady state is the right term for the above example. Equilibrium is used in the sense of forward and reverse reactions in a single reversible reaction. The above example considers two irreversible reactions — production and degradation.

  ... ... the time required for the molecule to shift halfway from its old to its new equilibrium concentration is equal to its normal half-life

This is not true if the degradation reaction is zeroth order or if these reactions are nonlinear. But for a linear production degradation set of reactions ($X$ is a biomolecule formed at a constant rate $\alpha$ and degraded at a first order rate  $\beta$ ), the reaction rate can be represented by the following equation.

$$\frac{d[X]}{dt}\bigg|_1=\alpha _1 - \beta [X]$$

At steady state $\frac{d[X]}{dt}=0$, which means $[X_{ss_1}]=\Large\frac{\alpha _1}{\beta}$

Half life as defined, by setting $\alpha$=0 and solving the differential equation = ${\Large \frac{log(2)}{\beta}}$

When the formation rate is changed to a new value:

$$\frac{d[X]}{dt}\bigg|_2=\alpha _2 - \beta [X]$$

and $[X_{ss_2}]=\Large\frac{\alpha _2}{\beta}$

From the above equation following equation can be deduced (by integrating the differential equation):

$$-\frac{1}{\beta}.log(\alpha _2 - \beta [X]){\large|}_{X_{initial}} ^{X_{final}}= t_{\frac{1}{2}} $$

when you substitute $X_{initial}=X_{ss_1}=\frac{\alpha _1}{\beta}$ and $X_{final}=\Large\frac{\frac{\alpha _2}{\beta} - \frac{\alpha _1}{\beta}}{2}$ (halfway between new steady state and old steady state)

you would obtain: $$t_{\frac{1}{2}}= -\frac{1}{\beta}log\left(\frac{\alpha _2 -\beta\frac{\alpha _1}{\beta}}{\alpha _2 - \beta \frac{\frac{\alpha _2}{\beta} - \frac{\alpha _1}{\beta}}{2}}\right) = \frac{log(2)}{\beta} $$


Why does uniprot sometimes not label single-pass transmembrane proteins as "anchors"?

A membrane anchor is close to the end (N-terminus or C-terminus) of a protein. For "Single-pass type I membrane proteins" the transmembrane region is not necessarily close to N- or C-terminus, which is why single-pass type I membrane domain are not labeled as anchors.

Instead, relevant entries usually have a signal peptide annotated.

Note that we have replaced the example for single-pass type I membrane protein by http://www.uniprot.org/uniprot/P14778#subcellular_location which is more relevant (the modified version of the documentation will be available with release 2016_01).


What would happen if most the fat in your body was rapidly converted into energy in 2 minutes?

It depends, but you're going to die.

Specifically, it depends on how fat you are. Even Andreas Munzer is going to die. At only 3% body fat, burning all his fat (9kcal/g) would "only" increase his internal body temperature by 270 degrees C. Factoring in the energy required to boil off his body moisture and adding in body heat leaves Andreas at  ~200 C or so (pretty unevenly distributed) minus whatever heat he could give off through his skin in two minutes. He's definitely dead, but probably not on fire. The flash point of animal fat oil is about 300 C, so most of his body probably isn't going to be hot enough to burn on its own. There will probably be some smoking, though.

The average body fat percentage is more like 22%(for males), and the numbers there are unequivocal. That person is going to catch on fire, as their body temperature is going to go up about ~1800 C after boiling off all the water. That's enough to melt your titanium hip implants.

In short: you'll die pretty quickly, and then you might catch on fire before your two minutes are up, unless you're Andreas Munzer or another professional bodybuilder.


Do sieve tube cells have any extrachromosomal circular DNA at maturity?

This ref. says that the plastids and mitochondria are still intact.
Found by searching for "sieve cell development"
Neuberger, D.S., Evert, R.F. Structure and development of sieve cells in the primary phloem ofPinus resinosa . Protoplasma 87, 27–37 (1976). https://doi.org/10.1007/BF01623956
https://link.springer.com/article/10.1007/BF01623956