To what extent is prion aggregation responsible for Alzheimer's disease?

To What extend is prion aggregation responsible for Alzheimers's disease?

Until recently, there was no 'hard evidence' implicating an infectious, self-propagating protein or prion (proteinaceous infectious particle) in Alzheimer's disease, or any convincing evidence that  a prion-like mechanism  is involved in this disease.

However, I quote from a recent review (Alzheimer’s and Parkinson’s diseases:  The prion concept in relation to assembled A$\beta$, tau, and alpha-synuclein) by a leading researcher in the Alzheimer's field:

  Transcellular propagation of protein pathogens, reminiscent of the spread of viruses, represents an unprecedented concept of disease. It is now known to extend beyond CJD [Creutzfeldt-Jakob disease], to include AD [Alzheimer's disease]  and PD [Parkinson's disease], which are the most common neurodegenerative diseases.

Pruisner,
 who
 received a Nobel prize
 for his work on prions ('a new biological principle of infection'), was one of the first to suggest that neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease, like Creutzfeldt-Jakob disease (CJD), may be due to a prion, or to a prion-like mechanism. He points out that over 80% of these diseases are sporadic, late-onset, and involve proteins present since birth (see
 A Unifying Role for Prions in Neurodegenerative Diseases
 ).

However, there  is one caveat.  The prion causing CJD, scrapie and kuri may be transmitted from one individual to another, and there is no evidence that Alzheimer's disease or Parkinson's disease may be so transmitted or  are in any way infectious.

What is Alzheimer's disease?

Alzheimer's disease is a neurodegenerative disease, and a disease of ageing, that causes severe dementia worsening over time. It affects 10% of those over 65 years of age, and 50% of those aged over 85  years. There is no known cause, and no known cure.  It is the leading cause of dementia, ahead of Parkinson's disease.  Most cases of AD are sporadic, but a small percentage have a genetic origin (familial AD).

The disease was first described (On certain peculiar diseases of old age)  by Alois Alzheimer in 1906. After histochemical analysis, Alzheimer described  two characteristic abnormalities in the postmortem brain of a 51-year old woman :  the (extracellular) neuritic plaques and the (intracellular) neurofibrillary tangles.

There is a very nice picture of both neuritic plaques and neurofibrillary tangles in Fig 1(A) of Goedert (2005).  For a great summary of the history of AD and references to the above summary, see  A Century of Alzheimer's Disease (2006) by Goedert & Spillantini.

What are the neuritic plaques?

Neuritic plaques are extracellular structures primarily composed of  a small peptide of (usually) either 40 or 42  amino acids known as  the amyloid-$\beta$ ($\beta$A), where the '$\beta$' refers to their tendency to form beta sheets.

This small peptide arises by proteolysis of a much larger protein of unknown function, the amyloid precursor protein (APP). The APP is a trans-membrane protein with  a single membrane-spanning segment, where the N-terminus (28 amino acids) is extracellular. Two proteases are responsible for generating $\beta$A :   $\beta$-secretase and $\gamma$-secretase

Peptide bond cleavage by   $\gamma$-secretase  occurs within the membrane-spanning region of APP and components of this proteolytic complex (the presenilins) are 'major players' in the Alzheimer's story.

It is thought that A$\beta$ is a 'normal' brain peptide, that is it does not arise from 'aberrant' proteolysis, but its function is unknown (Goedert & Spillantini, 2006).

Finally, mutations in the APP gene are known to cause familial AD, but account for only a minority of cases. (Goedert & Spillantini, 2006).

So, the structure of the neuritic plaques is known. They consist of a small peptide of unknown function derived from a much larger trans-membrane protein of unknown function.

And the neurofibrillary tangles?

Under the electron microscope, neurofibrillary tangles have a ribbon-like appearance called paired helical filaments.  It is now known that these structures are composed of a single protein, microtubule-associated protein Tau, or Tau protein  in an aggregated and hyper-phosphorylated state. There is  a very nice picture (electron micrograph) of a paired helical filament in  Fig 1(B) of Goedert (2005)

What is Tau Protein?

Tau is a 'normal' brain protein characterized by Kirschner and colleagues (see here and here)  as a microbutule-binding protein, long before its role in Alzheimer's disease was realized.

In humans, it consists of six isoforms generated by differential mRNA splicing of the transcript from a single gene, and 'imperfect repeats' within the amino-acid sequence are thought to be responsible for microtubule binding.

Mutations in the Tau gene are not known to cause Alzheimer's disease, but are responsible for very rare neurogenerative diseases (taupathies ) such as frontotemporal dementia  (FTD) (Goedert, 2005)

In the 'native' state Tau is phosphorylated, and is considered an intrinsically unstructured protein, (there is no crystal structure available), and it is now accepted that  'hyper-phosphorylated' Tau is the major structural component of the paired helical filament of Alzheimer's disease.

I simply seek clarification as to whether the onset of Alzheimer's disease could have a direct correlation with an aggregate of misfolded proteins

This is where things get interesting.  There is no doubt that aggregated proteins are involved in AD. The case of Tau and $\beta$A attest to that, and the paired helical filament could be considered a misfolded state.  Can either of these proteins act  as a prion and transmit the misfolded state?  That is, can Alzheimer's disease be considered a prion disease, where a 'rogue' form of a protein transmits its 'rogueness' to 'normal' proteins?

In the case  of Tau, it has been shown that extracellular Tau aggregates can "transmit a misfolded state from  the outside to the inside of a cell, similar to prions" by inducing fibrillization  of intracellular Tau .  In addition, aggregated intracellular  Tau can transfer to other cells. (Propagation of Tau Misfolding from the Outside to the Inside  of a Cell)

Testing of the hypothesis that prions or a prion-like mechanism is the cause of AD is a very active field and much more detail and discussion will be found in Goedert (2005).

What are the other 'players' in the Azheimer's story?

There are many 'players' in the modern understanding of AD.  Two further important ones are the presenilins and  apolipoprotein E  (APOE).

What are the presenilins?

Presenilins are part of the $\gamma$-secretase complex, a protease that cleaves trans-membrane proteins including APP. Mutations in the presenilin-1 gene are the  most common cause of familial AD; presenilin-2 mutations also known to cause AD. (See  Goedert & Spillantini, 2006).

And apolipoprotien E4?

A risk factor for sporadic AD is inheritance of the  ${\epsilon}_4$ allele of apolipoprotein E (APOE), a protein of fat metabolism,  but the molecular basis for this is a complete mystery.   (Goedert & Spillantini, 2006, Goedert, 2005). Inheriting a single copy of the APO-$\epsilon_4$ gene more than doubles the  likelihood of developing AD; inheriting two copies increases the risk by 12-fold (see Smith, Dana, 2018)

In what looks like a major advance, gene editing has been used to convert a  APO-$\epsilon_4$  phenotype to one resembling 'normal'  APO-$\epsilon_3$.  For a great recent article, see Scientists Fix Genetic Risk Factor for Alzheimer’s Disease in Human Brain Cells by  Dana Smith (2018).


"structural and regulatory elements of genes"

The expression of protein coding genes happens by the process of transcription. So promoters facilitate access of the RNA polymerase complex to DNA to begin transcribing a locus on the genome. The promoter of a gene often contains sequences that bind proteins called transcription factors, which play a role in various parts of the transcriptional process as well as components of RNA polymerase themselves (Such as a Pribnow box in prokaryotes, or a TATA box or an initiator element in animals).

So whether a gene is turned on and if so, how much it is turned on, is a property of how many transcription factor binding sites exist in the promoter, the nature of the transcription factors themselves in terms of their influence on transcription, and in eukaryotes and some archaea, epigenetic processes that control the access of transcriptional machinery to the locus being transcribed.

So when you think about the two elements in a gene, think of a light (the bit of a gene that codes for proteins) and a dimmer (which controls how much RNA is made by the protein-coding bit)


How does Tylenol relieve pain without making me drowsy?

Opiate pain killers or pain killers that act on opioid receptors have a different mechanism of action than NSAIDs. They tend to act as receptor agonists which exert their effect on the CNS (oxycodone as an example). Opioid receptors are associated with analgesia, CNS depression, sedation, etc. Tylenol on the other hand is thought to exert its effect by downmodulating cyclooxygenase, and therefore inhibiting the production of prostaglandins like H2, which is a precursor to lots of pro-inflammatory compounds.


Imagine you want to produce a widget. You have thousands of worker, but only one blueprint. Each worker needs the blueprint to build a widget (they're really forgetful and can't build from memory). So only one worker at a time can build your widgets.

What you would do is to create copies of your blueprint and distribute them to your workers. That way multiple workers can produce the widget at the same time.

DNA is the blueprint, and RNA is the copy. Your workers are the ribosomes that translate the RNA into proteins.

This is of course grossly simplified, and there are other reasons for the specific arrangement, but this is certainly one of the reasons why the intermediate RNA is used.


This is a bit tricky.

The blastocoel in e.g. amphibians separates ectoderm from endoderm and prevents cells of the blastocoel roof from inductive influence of vegetal cells. If you cut out the marginal zone and squish the roof onto vegetal cells, you will end up with mesoderm only:

Blastocoel is not homologous to blastocystic cavity. One could consider a tiny space between epiblast and hypoblast during gastrulation as a homologue of blastocoel, this however does not appear in mice. Blastocystic cavity forms at 32-cell stage thanks to Na+/K+ pumps as well as aquaporins. The inner cell mass is a mixture of cells expressing Gata6 and Nanog, which will form hypoblast and epiblast respectively.

But worry not, many people still call that cavity a blastocoel, in fact, I've seen it happen on Wikipedia. Anyway, I'd still recommend using separate terms for coeloblastula and blastocyst due to the non-homologous nature of blastocystic cavity and the blastocoel.

My sources:

https://kjcscientific.wordpress.com/project-excalibur/
Gilbert's Developmental Biology
Ćwiczenia z Biologii Rozwoju Zwierząt [Marek Maleszewski et al., University of Warsaw, Polish language publication]


Can signals travel "backwards" in the sensory pathway?

Reverse signals (dendrite -> axon) do occur in neurons, and are called back propagating action potentials (bAPs). However, whatever role bAPs play in the nervous system at large is subtle/small enough that we don't really understand them at all.
In any case, as @luigi points out, pinched nerves don't have anything to do with bAPs. The reason why a pinch in one place (the neck) feels like it has an effect in another place (the arm) is because some neurons trace long (on the order of several feet) pathways through the body. Ultimately, the sensory input of everything below your head passes through neurons in your neck at some point. If there is a pinch in the neuron in your neck that relays sense information from your arm, that neuron in your neck can activate spuriously, even in the absence of any stimulus acting on your arm. In that case your brain will interpret the spurious activation of that neck neuron as being the result of some kind of strange arm stimulus, and so you feel pins and needles.
See here for more information on the sensory cortex in your brain and the "sense image" it maintains of your body.
Edit
To clarify what I mean by a "pathway",

The part marked "proprioceptors or mechanoreceptors" is what's buried in your skin. If you poke a mechanoreceptor, it evokes a signal in the neuron marked "first-order". In some cases, that first-order neuron will reach all the way to brainstem (as in the picture above), and in some cases that first-order neuron will interface with an intermediate neuron in the spine, but the effect is the same in any case. A first-order neuron stimulates a second-order neuron, which in turn stimulates a third-order neuron, etc., all the way until the original signal arising from the mechanoreceptor reaches the somatosensory cortex. A pinch in any of those first, second, etc. order neurons will potentially send spurious signals to the somatosensory cortex.
Second edit:
Rereading your question, I think a lot of the trouble that you're having has to do with your understanding of how the brain assembles sense information. In order to feel pain in your arm, it is not necessary for anything to be happening to the arm itself. Your arm could be perfectly healthy and normal, but as long as your brain is receiving a signal equivalent to the one produced by a damaged arm you will still feel the same sensation of pain.


What effect does ambient temperature have on the cardiovascular system?

In relation to the cardio vascular system a combination of adrenaline from exercise and the bodies natural response to the cold causes constriction of blood vessels in the skin and extremities. This helps to reduce heat loss.

The movement from running increases the amount of cold air that runs across your body and into your lungs, which would offset the effect of heat generated from running. According to the article about Thermoregulation in cold conditions on Wikipedia, the offset is great enough to make shivering while standing still a better way to keep warm.


What are some places where biofilms could develop?

They can certainly develop in the toilet. Just try not to disinfect for a week...

Another place is the surface of living organisms, e.g. dental plaque or the leaves of a plant, etc...


Are longer and shorter DNA similarly charged?

Each phosphate group has a single negative charge. Not just the terminals. The reason gel electrophoresis works so well with DNA is that charge is linearly proportional to size. The longer the fragment, the slower it moves. A double stranded DNA molecule with 100 nucleotides has a charge of -200. If it were twice as long, it would have twice as many, just as if it were 3.4 times longer, it would have 3.4 times as many negative charges. This way, charge is essentially ignored, so DNA migrates through the gel at a rate inversely proportional to its size.


Q: We know neurons can organize into very complex networks, but how?

The answer is your first guess: Neurons find other target neurons with specific chemical signals.

Q: What are the names of said mechanisms?

This process is called axon guidance, by which the growth cones of developing axons are directed to reach their targets. This process depends upon a slew of cellular and molecular cues. The first axons to grow in any particular brain region are called pioneer axons and are the most dependent upon these cues. Later axons are able to follow (and diverge from) previous axons by the interaction of cell adhesion molecules on their surfaces. Dendritic development is also important for your question, but dendrites tend not to travel as far.

Here are some of the molecules that we know to participate in axon guidance:

Cell adhesion molecules and substrate adhesion molecules, including IgSF CAMs and cadherins
Some chemokines, e.g. CXCL12
Netrins, ephrins, and semaphorins
Slits, via the Slit-Robo cell signaling pathway
Developmental morphogens, e.g. Wnts and Hedgehog

The list goes on, and this is an area of active research. Each of these cues is recognized by one or more specific receptors on the developing neuron, which upon recognition of the ligand molecule either attracts or repels the axon from (or both, depending on the context). Recognition can function either short-range (by direct contact with a ligand) or long-range (e.g. by detection of a concentration gradient), depending on the molecular cue.

For more information, you may want to read Sanes et al., Development of the Nervous System.


Yes, the spinocerebellar tract ends in the ipsilateral cerebellum.
The gracile tract is a bundle of axon fibers in the dorsal root. The neural cell bodies are in the dorsal root ganglions. The tectospinal tract is part of extrapyramidal tract that connects midbrain (mesencephalon) with the spinal cord.
Didin't get exactly what you meant but: the lateral corticospinal tract (part of pyramidal tracts) controls fine movement of ipsilateral limbs, while the anterior corticospinal tract (part of the pyramidal tracts) conducts voluntary motor impulses from the precentral gyrus.

Source: Wikipedia: Tectospinal tract, Spinocerebellar tract, Dorsal root ganglion, Pyramidal tracts, Anterior corticospinal tract, Lateral corticospinal tract.


Are there biochemical differences between the cell membranes of prokaryotes and eukaryotes?

There are differences. (Except mitochondrial eukaryotic membranes, which are indeed similar to bacterial membranes! (reviewed in van Meer et al., 2008)).

First, bare in mind that it is thought that even different eukaryotes, such as Fungi and Humans, have different cell membrane compositions and that this is reflected in the proteins (Sharpe et al, 2010). The outer membrane of Gram negative bacteria isn't even made of phospholipids, it's made of glycolipids (Kamio & Nikaido, 1976). Archean membranes have the most notable lipid compositions, including a bilayer-like monolayer, to adapt to the conditions they are found in (Oger et al 2013). My point being that saying "there are differences" is indeed an understatement.

This question has probably arisen because anti-microbial peptides seem to act with specificity, and that perhaps this specificity comes from direct peptide-lipid interaction. This is on the right lines. From wikipedia:

  The cell membranes of bacteria are rich in acidic phospholipids, such as phosphatidylglycerol and cardiolipin[23][27]. These phospholipid headgroups are heavily negatively charged. Therefore, the outmost leaflets of the bilayer which is exposed to the outside of the bacterial membranes are more attractive to the attack of the positively charged antimicrobial peptides.

Notably, no such charge exists in eukaryotes since the negative charge is found on the inner leaflet of the plasma-membrane rather than the outer leaflet.

There is such a massive variation, even within bacterial membrane composition (Bogdanov et al 2014), that I cannot even really begin to list it here. Furthermore, there are variations in the glycocalyx, surface proteins, and lipid composition dynamics due to lipid rafts.


A suggested ancestor of cyanobacteria consumed manganese. Why not magnesium?

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

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

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

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


How to get Population Genotype Frequency from 1000 genomes Perl API

If you want population specific allele frequencies you have three options: * For a single variant you can look at the population genetics page for a variant in our browser. This gives you piecharts and a table for a single site. * For a genomic region you can use our allele frequency calculator tool which gives a set of allele frequencies for selected populations * If you would like sub population allele frequences for a whole file, you are best to use the vcftools command line tool.

This is done using a combination of two vcftools commands called vcf-subset and fill-an-ac

An example command set using files from our phase 1 release would look like

grep CEU integrated_call_samples.20101123.ALL.panel | cut -f1 > CEU.samples.list

vcf-subset -c CEU.samples.list ALL.chr13.integrated_phase1_v3.20101123.snps_indels_svs.genotypes.vcf.gz | fill-an-ac |
    bgzip -c > CEU.chr13.phase1.vcf.gz

Once you have this file you can calculate your frequency by dividing AN (allele number) by AC (allele count)

Please note that some early VCF files from the main project used LD information and other variables to help estimate the allele frequency. This means in these files the AF does not always equal AC/AN. In the phase 1 and phase 3 releases, AC/AN should always match the allele frequency quoted.


What's the difference between male and female?

Sexes (male and female) are generally defined in terms of Anisogamy, which means that there are size differences between the gametes (i.e. the reproductive cells that fuse at fertilization). The sex with smaller gametes is defined as male and the sex with larger gametes is defined as female, and individuals that can produce both types of gametes are called hermaphrodites. This is the case in both animals and plants (plants have pollen vs. ovules and microsporangia vs. megasporangia), and the definition of sexes is therefore not dependent on chromosomal makeup as such or which sex that carries the young. Actual sex determiniation in a particular species is often based on chromosomal inheritance though, but other systems also exists (e.g. environmental cues or sequential hermaphroditism). Anisogamy also comes in several different types, where animals generally have Oogamy, where males have small mobile spermatozoa and females large stationary egg cells.

More generally, Anisogamy is a special case of mating types in sexually reproducing organisms, where fertilization (on syngamy) generally can only occur between gametes of different mating types. In for instance fungi, gametes of different mating types are of the same size (isogamous) and they are therefore only labelled as mating types (e.g +/-) and not different sexes. Functionally, if we are simplifying the issue, male gametes can be viewed only as carriers of genetic information, while female gametes also contain the nutrients necessary for the early development of a newly formed embryo.


The second law of thermodynamics and the cell (3 questions)?

First question: the answer is actually contained within the question.  The cell maintains order precisely by discharging heat.  The second law of thermodynamics states that the tendency of a closed system is to proceed from ordered to disordered.  Since thermal energy is (to our knowledge) the most disorderly form of energy that exists, in any given system where energy is involved, some energy will always be lost to heat.

For instance, if your cell performs the break down of ATP to drive some chemical need of the cell, some of the energy released in the breaking of the bonds in the ATP to form ADP will be lost as heat.  This means that the cell's heat is going up on average, and it must export heat to the environment.  If the heat was held inside the cell, the cell would rapidly become extremely disordered as proteins de-natured, non-enzymatic reactions sped up, and the cell basically self-destructed.

Second question:  I think you've slightly missed something.  Autotrophs (producer cells, such as plants) are the cells to actually "create order" in the biosystem.  They do this by capturing Carbon dioxide and water from the environment, and using light energy from the sun to bond them together and form complex biomolecules - usually carbohydrates.

These carbohydrates are then sent into the rest of the biosystem, where heterotrophs (consumers like me, you and the lion in the zoo) break them down to release their energy for tasks their cells need to do (cellular respiration, catabolism).  As time passes, all that energy is converted to heat and radiated from our bodies, and ultimately by the atmosphere off the Earth (barring excessive greenhouse gases.)

Third question: Not necessarily.  If the multi-cellular organism were a closed system, you are absolutely right.  The chemical energy would rapidly be all converted to thermal energy, and the order would disappear entirely.  However, bodies are not closed systems: they are continually radiating thermal energy and absorbing chemical energy, either from the sun through photosynthesis, or from autotrophs through ingestion and digestion.

A picture is worth 1,000 words:

(Image courtesy of stephsnature.com)


Does the species of snake that eats Amphidromous inversus have chiral dimorphism?

I don't know much about this particular species of snake but here are some info that may help.

What do we mean by right-handed snakes?

I doubt that in this context a snake could be ambidextrous. What they call handedness in these snakes (Pereatids) concerns the density and size of teeth on each side of the jaw (pictures from Hoso et al. (2010))

This asymmetry helps them to forage on snails.

Here is how they describe the snake feeding behaviour.

  The Japanese pareatid, P iwasakii, strikes an exposed soft
  part of a crawling snail from behind at a determined leftward angle
  to grasp the ventral shell surface with the upper jaw and the soft
  body by inserting the mandibles into the aperture. The snake then
  extracts the soft body by alternately protracting and retracting the
  asymmetric right and left mandibles.

On the figure below, the individual on the left is sinistral and the individual on the right is dextral. Note by the way that snails of different chirality have a hard time to mate together.

"Right-handed" snakes can easily forage on dextral snails (the most common and ancestral form), while they have a hard time to forage on dextral snails. Hoso et al. (2010) reports a survival probability of 0% for dextral snails and 87% for sinistral snails.

Left-handed snakes

Hoso et al. (2007) report that "left-handed" snakes have never been found in south-east Asia. This is surprising as noted by Hoso et al. (2010). Even in areas where sinistral snails are relatively common, all snakes were "right-handed".

They do not suggest any potential explanation for this lack of "left-handed" snakes but one could speculate that "handedness" in snakes might be under other selection pressures than those related to foraging. It is also possible that intermediate forms are deleterious and that mutation of large enough effect are rare. It is possible that the genetic variance for handedness is just not present. It is possible that even if in some areas there are more sinistral species of snails than dextral species, the abundance of dextral is still higher and therefore, there is no selection for switching to being right-handed.


There are two answers if the question refers to genomic DNA (neither enucleated ova nor mature RBCs have genomic DNA).  However, since the question doesn't specify genomic DNA, we can exclude enucleated ova, which would still have mitochondria and therefore mitochondrial genomic DNA.  Mature RBCS (at least in most mammals) do not have mitochondria, so the safest answer is probably b) Mature RBC.


How to conceptualize the action potential?

First of all, electric current is defined as movement of charges, $I=\frac{dQ}{dt}$. In electronics that you see around that is not very useful definition, because electrons move much slower than signals, that is changing electric field. Speed of electric field propagation reaches speed of light, whereas electrons move at 1%-30% or $c$.

In biology, especially regarding action potential, only movement of charges is important, not propagation of electric field, probably because conductance is much smaller than in copper wires. that is signal propagates not through interaction between charges, but via intermediate agent/amplifier -- ion channels.

Charge in body is more or less constant, because action potentials are cyclic: after depolarization membrane comes back to -70mV or something. There is no flow of charge out of the body.


The toxins of both Clostridium tetani and Corynebacterium diphtheriae are so toxic that you cannot use them for immunization, since the amount needed for proper antibody production would kill the individuals. For that purpose the toxins are "de-toxified" by reacting them with formaldehyde which takes away the toxicity but the resulting toxoids are still immunogenic.
This happens by the reaction of the formaledehyde with the free aminogroups of the sidechains of the amino acids to form azomethin groups. This changes the protein so much, that it cannot bind to glangliosides any more which renders it untoxic. The immune system can still recognize unmodified parts (for this 8-10 amino acids in one stretch are enough) and make antibodies.


Is it possible to discriminate tetrachromacy using sRGB color?

All the combinations of three sRGB primary colors are distinct for a trichromat. This immediately precludes any way to find out whether you are capable of more: if even a trichromat can distinguish all the colors, tetrachromat even more so.

But in principle, three colors are sufficient to check for tetrachromacy, but they can't be the sRGB primaries. The three colors you need must lie on one line on the chromaticity diagram, so that multiple mixtures of them could appear as the same color to a trichromat. Then a tetrachromat may be able to distinguish the two mixtures, which are metamers to a trichromat.


Does Spinning dancer has anything to do with your eyesight

For a bit of background, this test was devised by Nobuyuki Kayahara and it was originally thought that it shows the dominance of one part of the brain to the other. This was later on discarded as a misconception (reference). It is now widely believed that the clockwise - counter-clockwise rotation is a phenomenon called Bistable perception (Reference 1 and reference 2).

  Multistable perceptual phenomena are a form of perceptual phenomena in
  which there are unpredictable sequences of spontaneous subjective
  changes. While usually associated with visual perception, such
  phenomena can be found for auditory and olfactory percepts. Famous
  examples include the Necker cube, structure from motion, monocular
  rivalry and binocular rivalry, but many more visually ambiguous
  patterns are known. Since most of these images lead to an alternation
  between two mutually exclusive perceptual states, they are sometimes
  also referred to as bistable perception(reference 1 and
  reference 2).

No, the fact that you can only see her turn clockwise has not got anything to with your vision (for the record, I have never been able to see the girl go counter- clockwise myself).

  Sometimes, a person will stare at an image and it will never reverse.
  Dr. Toppino advises staring at one part of the image, such as the
  foot, and most of the time it will eventually flip. In people who
  can’t see the reversal, it may be that one underlying neural structure
  is more dominant, but once someone finally manages to see the flip, it
  will start to happen more often (reference).

This image would help you watch her rotate counter-clockwise.

Here she is spinning clockwise.


Cloning a gene of an organism with an nonsequenced genome

I assume that we are talking about eukaryotic genomes which are split into introns and exons. Depending on what you want to do with your cloned gene, you need different strategies. The method is based on the assumption that the gene sequence has only very little differences to the known sequences of other organisms.

If you want to express your gene from a vector, you need to find the right processed mRNA which is then processed into cDNA and then cloned. Here two strategies are possible: If you have a gene, which is strongly expressed, you can design a primer primer (based on the orthologous sequences) which is anchored in the poly-A tail and has a gene specific seuqence next to it. With this it should be possible to amplify your gene specifically and isolate it. If the gene is not strongly expressed (the resulting amount of cDNA would be very small, since there is no amplification involved), I would opt for making cDNA from total mRNA (use anchored polyA primers) and then amplify the sequence from the cDNA pool with two primers (again based on the orthologous sequences) to amplify the gene sequence. I would go for TA-cloning here, since you do not know, which restriction enzyme recognition sites are present on your gene.

When you need the complete sequence containing introns and exons, there are two possible strategies. First you can use primers to amplify the gene and subsequently clone it. Then it is possible (and this is probably what I would do) to use a set of primers which bind to the end of the gene (and also the reverse strand) to amplify the sequences at the end and then sequence these PCR products. This gives you the exact sequences at the 5' and 3' end of the gene and allows you to include possible regulatory sites, since you then can design exactly matching primers for this region. Again, I would go for TA cloning.

And finally you could start by sequencing the whole region based on homologous sequence primers first and then with primers designed on the newly analyzed sequences. This is the most exact way, but is also costly and takes some time (since you need to make new primers after each round of sequencing until you are done).


Does food really give our bodies the energies that we have determined by burning them in the lab?

The device you refer to is a bomb calorimeter. Inside one of these, a sample of material is completely combusted. Typically, the heat from the combustion warms a measured mass of water and the rise in temperature is used to calculate the Calories/Joules in the material.

Of course our cells don't ignite food and burn it to completion. Even if they did, some of the heat from the process would escape collection. Cells use the process of cellular respiration to harvest the energy. The basic version of cellular respiration describes the utilization of glucose to create ATP, by far the most used substance to power the energy needs of the cell. Here's just one source that takes you through the calculations of how efficient this process is: http://www.tiem.utk.edu/~gross/bioed/webmodules/ATPEfficiency.htm

So, at least for the very common sugar glucose, only about 40% of the total Joules, as measured in the calorimeter, end up as ATP. Most other food substances we use for energy share much of the same chemical pathway as glucose. I haven't seen calculations of their efficiency but suspect it would be roughly similar.

One of the most basic and important lays of physics is that no transfer of energy is 100% efficient. (Read more here: https://en.wikipedia.org/wiki/Energy_conversion_efficiency ). The remaining energy in the glucose that was not converted to energy in ATP is "lost" as heat. By lost, it is meant that it's not avaible to do any useful work other than heat us up. Of course, being homeothermic ("warm blooded") animals, that's useful too.


What is the 'job' of the byproduct water in the Electron Transport Chain?

Thanks for your question.
One reason is, if this chemical reaction does not happen so there will be a lot of electrons in mitochondria in a short time consequently the environment inside the mitochondria will be charged in negative and as we know the environment inside the all parts of cells should not change during the time
and on the other hand, these extra electrons may carry out some chemical reactions which result in producing some materials which are not good for cell, for ex H2O2, as we know it is a poisonous material for cell.
But maybe you ask why H2O and not another product? because H2O exists in cell, in a large amount, it is solvent for many materials, it is not poisonous for cell, and many other reasons.


From what stage can you speak of an inflammation?

From PubMed Health:

  When a wound swells up, turns red and hurts, it may be a sign of inflammation. Inflammation is – very generally speaking – the body’s immune system’s response to stimulus. This can be bacteria colonizing a wound or a splinter piercing your finger, for example. Inflammation happens when the immune system fights against something that may turn out to be harmful.

So when inflammation occurs, chemicals from the body's white blood cells are released into the blood or affected tissues to protect your body from foreign substances. This release of chemicals increases the blood flow to the area of injury or infection, and may result in redness and warmth. Some of the chemicals cause a leak of fluid into the tissues, resulting in swelling.

Signs of an inflammation :

There are five signs that may indicate an acute inflammation:

Redness
Heat
Swelling
Pain
Loss of function

There is a loss of function, for example, when the inflamed limb can no longer be moved properly or when the sense of smell is worse during a cold.

This means that an inflammation does not start when a wound has been infected by bacteria, festers, or heals poorly, but already as the body is trying to fight against the harmful stimulus or a viral infection.

Not all five signs occur in every inflammation. Some inflammations occur silently and do not cause any symptoms.

So depending on the symptoms we can decide if there is an inflammation or no.


Are self pollinated plants genetically different?

Yes, it does.
In Meiosis there is genetic recombination (by recombinase) in the Meiosis-1. So even though it is self pollination, there is significant genetic variation.
Still for higher degree of variation cross pollination is exhibited.
It should be noted that cross pollination has greater evolutionary significance.
Few plants exhibit self-incompatibility to supress self pollination (in monoecious flowers/plants).


Why is it beneficial for trees to grow that tall?

Beside the reasons you've given I would add environmental disturbance (e.g. flooding) as a evolutionary factor that could explain selection for taller individuals. Many palms also inhabit and thrive in disturbed habitats (Frangi & Lugo, 1998; Salm, 2005), which indicates that this could potentially (i.e. speculative) be an important factor for this taxon. Palms also have the combination of tall height and a relatively low "wind profile" (relative to many other groups of trees), which indicates that they are adapted to exposed/disturbed habitats.

This, along with the reasons you've already given, seems to cover the most obvious evolutionary reasons for selection on tree height. However, these will naturally trade-off against negative effects on e.g. fecundity from investing and maintaining biomass.


Loss of antibiotic resistance due to long term storage

It is possible due to the fact that some antimicrobial resistance genes are induced by the presence of antibiotics themselves and are not promoted in the absence of a specific antibiotic, so the production of certain antimicrobial structures (enzymes, pumps, etc.) will be reduced once the bacterial medium is antibiotic free for enough time. This is sometimes refered to as "antibiotic pressure" referencing to some extent the genomic concept of selection pressure.

Take for example the phenomena reported in this paper's summary; they studied a patient hospitalized because of an infection by 2 K. pneumoniae strains. They knew beforehand that one of the strains was suceptible to carbapenems while the other one had a certain degree of resistance to this antibiotic. As the infection unfolded and a treatment with meropenem was administered, they took several samples and studied them via whole genome sequencing (WGS). They found out that the strain previously characterized as suceptible to carbapenems had acquired a plasmid (possibly by vertical transmission from the other strain) and hence now exhibited resistance to carbapenems, however when this strain was left in observation (and without being exposed to meropenem) it lost its previously acquired resistance.

In conclusion the sole presence of antibiotics induces resistance by different mechanisms in bacteria, but in some cases the lack of antibiotics in the medium can also revert resistance if this condition lasts for enough time. It is important to mention though that some resistance profiles will never be reverted no matter for how long the bacteria remains away from an antibiotic due to their nature. For example a gram-negative bacteria will always have instrinsic resistance to regular penicillin no matter what due to its cell structure itself (lack of a thick peptidoglican cell wall and presence of an outer cell membrane).


How do I prepare a solution? (Calculation)

This is relatively easy. First: Look up the molecular weight of sodium hydroxide: Wikipedia gives a molar weight of 39.997 grams/mole (lets round this to 40 g/mole thats easier to calculate and the error in this is marginal).

So when you dissolve 40 g of it in 1 l of water, you have a 1000 mM (or 1 M) solution. Since you only want to have a 400 mM solution, you need to multiply the final concentration with the molar weight to get the amount of NaOH for one litre:
40 g/mole * 0.4 mole/l = 16 g of NaOH per litre. Since you only need 100 ml, you only need 1/10th of the NaOH (1.6 g).

So to prepare 100 ml of a 400 mM NaOH solution you dissolve 1.6 g of NaOH in 80ml of water and fill up to 100ml in a appropriate messuring cylinder.


What is the optimum length of abstinence for maximum ejaculation volume in humans?

There don't appear to be many robust studies on this, but this study by De Longe et al in 2004 suggests that, whilst the volume of the ejaculate is increased after 5-days of abstinence (in most participants), for many this did not increase further after 8-days [1].

Here are the 11 participant included (along the x-axis), and for each participant there are four coloured boxes:  dark blue, day 1 (corresponds to 24 hours' abstinence); red, day 3 (corresponds to 3 days' abstinence); yellow, day 5 (corresponds to 5 days' abstinence); light blue, day 8 (corresponds to 8 days' abstinence).

This study has a very small sample size, and really shows how the variability between people is massive. There could be many other factors affecting individuals, from smoking and drinking behaviours, to exercise and stress.

What seems much clearer is that sperm concentration increases with abstinence [2]. This study included 27 men and did not specifically ask them to remain abstinent for periods of time, but asked them how long. The average abstinence is about 2-days.

I could not find any study which investigated abstinence for longer periods - but there are undoubtedly more that I did not see.

De Longe, at al. 2004. Influence of the abstinence period on human sperm quality. Fertility and Sterility (http://dx.doi.org/10.1016/j.fertnstert.2004.03.014)
Carlsen, et al, 2004. Effects of ejaculatory frequency and season on variations in semen quality. Fertility and Sterility (http://dx.doi.org/10.1016/j.fertnstert.2004.01.039)


If bortezomib, a cancer drug, inhibits cell proteasomes, wouldn't resulting protein aggregate in normal cells further increase the risk of cancer?

Proteasome inhibitors do affect normal cells to some extent, but the whole point of using them as cancer treatments is that (some) cancer cells are far more sensitive to proteasome inhibitors than are normal cells.  For example, multiple myeloma cells (the first clinical targets of Bortezomib) that overproduce immunoglobulins are dependent on proteasome degradation to eliminate them and are therefore sensitive to Bortezomib.  There are many other aspects of cancer cells that may make them more dependent on proteasome; see for instance

Proteasome inhibitors in cancer therapy: Treatment regimen and peripheral neuropathy as a side effect for some examples.

But of course there are effects on normal cells as well, such as the peripheral neuropathy mentioned in that review.


How does blue, yellow and orange coloured light affect photosynthesis?

Your thought process should revolve around optimal spectrum for photosynthesis, since whether that happens sufficiently will determine the health of your plant. Just poking around, I found this document.

What light will be usable for photosynthesis depends on which version of light absorbing protein is being used to capture energy from photons.

This diagram would indicate that pure yellow would be pretty ineffective for any pigment. Blue is fine, as is darker orange/red for chlorophyll A and B.

Keep in mind that a lightbulb, unless a very special one, will still have lots of other spectrum bleed.  It won't be a pure single color (even though it may look like a single color to your eye).

Another source from Khan Academy.


I think it's best to break this question up in to two parts:

What mutations account for red hair and fair skin in humans
How might these same mutations affect pain sensation

MC1R variants & red hair
The MC1R gene encodes a transmembrane receptor protein (belonging to a very common family of receptors), called melanocortin 1 receptor. It also has another name describing its best known role in the body: 'alpha melanocyte stimulating hormone receptor'.
This receptor binds ligands - both agonists and an antagonist - outside the cell, and passes signals to the pigment-producing pathways in melanocytes; activation favours eumelanin (brown) production over pheomelanin (red).
Common MC1R variants are all single point mutations which cause an amino acid substitution and reduce/impair the normal function of the receptor - i.e. loss-of-function mutations. E.g. Arg151Cys, Arg160Trp, Asp294His, the most common variants in european red-heads probably arose ~80,000ya in a eurasian population, and have a reduced ability to activate adenylate cyclase inside the cell.
How & why could the same mutations affect pain sensation?
Genetic linkage, or dual role of MC1R?
Firstly, it is possible that MC1R variants are linked to a mutation at a separate nearby gene; the two making a haplotype.

In this diagram, mutation A might be a red-hair MC1R mutant, and mutation B might be some other pain-sensitivity mutant. Through random effects on small populations, group Hg B might have 'seeded' the european population, say; meaning that the two mutations are inherited together in that population. If the two loci are very near, their linkage is less likely to be disturbed by recombination.
This is an obvious possibility whenever two seemingly unrelated traits co-occur.
However, there's good reason to believe that this case is due to a dual-role of MC1R...
Arguments against linkage; for dual role of MC1R: The existence of many different haplotypes in redheads argues against linkage, if this pain sensitivity effect is found across all/many redhead haplotypes, and not in wildtype MC1R europeans.

Indeed, this study shows that europeans with 2 MC1R mutant variants (homozygote or compound-heterozygote) have increased pain tolerance to electric shocks compared to people with 1 or more functional copies of MC1R. The second panel shows that a mu-opiod analgesic (morphine) has greater effect on those with no functional MC1R. The effect coincides with presence of functional MC1R, not a particular haplogroup.
MC1R is also expressed in a region of the midbrain responsible for pain modulation. This region produces endogenous opioids to control pain. As far as I can gather, researchers are trying to work out what exactly it does there.
The study by Mogil et al suggests MC1R in the brain somehow counteracts pain inhibition by the opioid receptors, and so MC1R mutant redheads have more effective ex/endogenous opioid pain inhibition, which reduces noxious pain.
This study found that redheads are slightly less susceptible to pain-sensitisation by capsaicin.
Whereas this study found a contradictory result, that redheads are more sensitive to thermal pain and that lidocaine is less effective for them. (This study didn't genotype the subjects, and red-hair may be caused by mutations in other genes.)
Overall, the number of subjects in these studies (both humans and mice) is fairly small; and the science of MCR pain modulation seems early-days.
But at least we can answer your question: the mutations apparently responsible for red hair and altered pain sensitivity are amino acid substitutions in MC1R causing loss-of-function variants.
The fact that MC1R probably has totally different roles in the brain and in the skin is an interesting general point of biology.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1288200/ < about the evolution of MC1R mutant variants.
http://www.ncbi.nlm.nih.gov/pubmed/10403794/ < about the mechanism of loss-of-function
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1736101/pdf/v042p00583.pdf < evidence of increased pain tolerance & greater morphine effectiveness
http://www.scandinavianjournalpain.com/article/S1877-8860%2810%2900111-4/abstract < evidence of resistance to hyperalgesia
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1692342/ < evidence of decreased pain tolerance & lesser lidocaine effectiveness


Why don't mosquitoes evolve towards muting themselves?

Your question is really good, but in actuality, they do evolve towards muting themselves, actually, they have pretty much done "most of the work":

It is assumed that microscopic scales along veins and wind margin
play an important role as a silencer as downs on the flight feather of owl.

From this we can assume that the effectiveness of these scales are high, as they had plenty of time to evolve; thus the other factor they should alter to make them quieter is the frequency of their flapping $f$, which can be calculated from the following equation:

$$f=K m^{-1/6}$$

where $m$ is the mass of the animal and $K$ is the proportionality constant. The resulting number is around several hundred hertz (Remi.b observed a value around 440 Hz)

There are two options for them, either increasing the frequency up until our ear is incapable of hearing it which would be impossible as even the highest flapping frequency can hardly exceed 1000 Hz, which is nowhere near the required 20,000 Hz. By increasing their body mass they could decrease the frequency but the needed 15-20 Hz is pretty low compared to the actual several hundred, thus it would likely need a complete body structure change which is not something to happen in the near-future.

An another solution might be a different strategy in flying. Gliding attacks might pay off really well (that's why owls on the other hand can't be heard during flight), but even though there are some insects capable of such[1], it would need an immerse amount of time, not talking about the problems that might arise from the bumping into of our body.

I don't think that the mating signaling would be indispensable from an evolutionary perspective, but this statement of mine can't be proved.

These are the physical/biological difficulties of the problem, here is one from an evolutionary aspect: They are not likely to have experienced a strong selection against this feature, as most of the possible victims are incapable of doing much against a mosquito due to the absent of hands (and tails are seldom enough to stop them). The first possibly blood-sucking mosquito was found to be living 79 million years ago, while animals that might be able to "seal their fate" are much more recent, while not even having success most of the time.

https://www.jstage.jst.go.jp/article/jsmec1997/43/4/43_4_895/_pdf
http://www.geologica-acta.com/pdf/aghv3501a12.pdf
http://www.physics.emory.edu/faculty/weeks//lab/papers/jwang-arf05.pdf


Local storage of NCBI database in MongoDB

I've played with mongoDb.  It is a nearly schemaless data store - each record (analogous to a row) can have nearly any entry name set except for a unique ID that mongoDb uses.  In practice most of your records will have the same labels and names

Leaving SQL for noSQL is turning out not to be a great win.  MongoDB will excel in retrieving records quickly and processing records by their content.  It has some constraints too compared to SQL.  It requires that the main index be stored in RAM, which might or not be an issue.   For very large datasets mongoDB can be configured to shard the data automatically - splitting it up over a cluster of machines for high throughput fast processing applications.

If you need flexibility in your data record and you have a good machine (or a good cluster) to put it up on it could offer some advantages. We have a reasonable store of dbSNP on a recent MySQL machine and it performs okay.  Not thousands of transactions a second, but we can do reasonable throughput of record processing.


What's the use of RNA editing in kinetoplast?

You could have asked a similar question about splicing. The function of RNA editing seems to be similar: it's one of the ways to trigger production of alternative transcripts and proteins given the same DNA sequence.

The question is discussed, for example, in this review. The authors describe different known effects of alternative RNA editing:

Amino-acid substitutions
ORF extension
New unique ORFs
Alternative UTRs

Alternative editing is correlated with developmental stage, which is not surprising, given the fact that the parasites switch their energy metabolism in different hosts (1,2,3), with the mitochondria changing their structure accordingly.

The authors seem to be astonished as well and conclude: "RNA editing in kinetoplastid mitochondria is a beautiful example how evolution favors diversifying mechanisms even if they seem to be extremely wasteful from a
human perspective."


Why are urban birds still scared of humans?

Perhaps counter-intuitively, fear of humans is often a learned behaviour. There are accounts, such as one made by Charles Darwin following his visit to the Galapagos islands;

In Charles Island, which had then been colonized about six years, I saw a boy sitting by a well with a switch in his hand, with which he killed the doves and finches as they came to drink. He had already procured a little heap of them for his dinner, and he said that he had constantly been in the habit of waiting by this well for the same purpose. It would appear that the birds of this archipelago, not having as yet learnt that man is a more dangerous animal than the tortoise or the Amblyrhynchus, disregard him, in the same manner as in England shy birds, such as magpies, disregard the cows and horses grazing in our fields.
From "The Voyage of the Beagle" - http://www.ling.upenn.edu/courses/hum100/Beagle17.html

Birds born and bred in proximity to humans will have learned that we are actually to be avoided.
Ducks and swans, for instance, (and this is quite anecdotal) live in very close proximity to a lot of humans in cities, and feel confident walking picking up food. However if you try to get close to one they are very quick to get out of the way. The only exceptions to this are learned behaviours, such as when someone stands and feeds them.
In the wild animals may be cautious of humans if we are much bigger than them, but if they have no experience at all of human contact they  may just ignore them. This quite often happens with film crews in Antarctica, as in the below image from the BBC's Frozen Planet series.


Does mung bean nuclease cleave a phosphate group when it's chewing off 5' or 3' ssDNA ends?

According to Kroeker WD, Kowalski W, Laskowski M. 1976. Mung Bean Nuclease I. Terminally Directed Hydrolysis of Native DNA. Biochemistry 15(20):4463-4467

  It was concluded that the products of the terminally directed hydrolysis of native DNA possess 5’-phosphoryl groups because: (1) greater than 99% of acid-soluble activity applied to the column was recovered in products which coeluted with 5’-terminated standards and (2) the w-monophosphatase activity of mung bean nuclease would have dephosphorylated 3’-phosphoryl-terminated products. The endonucleolytic activity of mung bean nuclease on denatured DNA also results in the production of 5’-phosphoryl-terminated products.

Also, from Promega:

  Mung Bean Nuclease catalyzes the degradation of single-stranded DNA and RNA endonucleolytically to yield 5´-phosphoryl-terminated products


How are the images of both eyes combined to form one image?

The visual system contain several stages in which the information from both eyes is progressively mixed and analyzed, starting in the lateral geniculate nucleus.

Even if you feel seeing just one merged object with both eyes, your brain is using both images to calculate the 3D position of that object.

One fun fact: The image that you feel centric, it is actually bias towards one of your eyes, the called "dominant eye". You can check what is yours by a simple experiment


How to convert skin temperature to core temperature?

The measurement of core temperature (it is the right term*) is easy using an invasive method. It is also reliable since:

  Core temperature is easy to measure and temperatures are relatively
  homogeneous throughout the trunk and head[PMCID: PMC1752199];

However, the measurement of skin temperature is highly dependent on the location of measurement and also ambient temperature, as explained here[DOI: 10.1039/C6EE00456C]:

Also, Xu et. al. concluded in "Relationship between core temperature, skin temperature, and heat flux during exercise in heat" that:

  Algorithms for T_c measurement are location-specific and their
  accuracy is dependent, to a large degree, on sensor placement.

They also proposed two relationships for calculation of T_c based on T_s (Core temp. based on surface temp.) which is included in the paper (regarding copyright laws, I'm not allowed to put it here. you have the DOI and can look it up).

*Here is the list of few publications which are using "core temperature" to address the temperature inside the body:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1752199/

.../pubmed/23775374

.../pubmed/10655798

Gender Role:
In a study in University of North Texas Source it is concluded that men has different skin temperature, due to different methods of temperature regulation compared to women:

  We found gender differences at four different skin temperature locations. These changes might suggest that men retain more metabolic heat in various locations on the back when exercising in a hot, humid environment compared to women.

Also This Work shows that, although the temperature distribution pattern among genders are similar, women have lower skin temperature.

This Masters Thesis from University of South Florida indicates findings in regards to clothing and metabolic conditions role on core temperature, i.e. no statistical difference between T_c of genders. Look at Figure 3 in page 23 for heart rate vs. metabolic rates. In page 24 there is a table for measurements for T_c.


Short answer, yes. The fresh water concentration inside saltwater fish is higher than the surrounding sea water, and the salt concentration inside the fish is lower.  This means that fresh water continuously flows out of the fish through their gills via osmosis.  To combat this loss of fresh water, fish must constantly be drinking sea water to replenish the lost fresh water. This also requires that they pump out the excess salt in the sea water they drink using their kidneys and specialized chloride cells in their gills.

Some more information can be found here, or you can watch a short video on the subject here.


Actual determination of the DNA sequence in the shotgun approach?

The question appears to confuse the method of identifying and determining the order of bases in a fragment of DNA — Sanger* sequencing, Maxam–Gilbert or more modern ‘next generation’ methods — with the strategy for selecting fragments to analyse and reassemble into the larger contiguous sequence from which they were derived, of which shotgun sequencing is one.

Shotgun sequencing is a strategy in which the selection of fragments to sequence is random, the method of sequencing is a matter of choice (it was often the Sanger method when it was first developed), and the assembly is done by computer programs that identify matching stretches. (It fails — or is not completely successful — if by chance the fragments do not cover the whole DNA with suitable overlaps or there are certain types of repeated regions.)

Shotgun sequencing should be contrasted with what might be called ordered sequencing strategies in which one generally starts with a restriction map of the whole DNA and initially selects specific fragments to clone and sequence (by whatever method seems best). On the basis of the sequence of the fragment one can choose to sequence further from a position within the already sequenced fragment, and this procedure repeated. Here there is no apparent assembly step as this is inherent in the choice of fragments to sequence. (This is much slower than shotgun sequencing, and cannot be automated so that it is much more expensive. However, it is more precise.)

Coda

Part of the confusion may arise from the fact that modern automated methods of sequencing genomes are designed to work on a mixture of many uncloned fragments of DNA, so inherently involve the shotgun sequencing strategy. They tend to employ technologies other than the classic Sanger method. If a ‘manual’ clone-based ordered sequencing strategy is required to ‘finish’ missing or ambiguous regions of a genome, this would most employ the Sanger method of determining the sequence. Hence, the contemporary writer might employ what is, in fact, a misleading contrast.

*Fred Sanger was an eminent Nobel laureate, so his surname is capitalized.


Can the eye distinguish between pure and composite colours and how do we measure this?

Yes, we do perceive a composite spectrum in a way which is analogous to how we perceive the corresponding single-peak spectrum. Human beings have trichromatic vision, meaning that there are 3 types of specialized cells in our eyes for seeing color. Each one has a different color of light which produces peak stimulus, although they all perceive a range of colors:

(the axes are wavelength and normalized response)

None of the color-sensing cells has a peak color of yellow. In order to perceive something as being yellow it either has to be pure yellow or stimulate the 3 types of color sensing cells in a very similar way as pure yellow would. However, if you took very careful readings of the output signals from the color sensing cells you might see some subtle differences in the exact waveforms of the responses.


Gene terminology - is one gene a concrete, single physical sequence?

'just two molecules of one gene'.

They are the same gene. Gene is more of an abstract concept. We say for example that humans have ~ 20,000 protein-coding  genes. It does not mean that we have only 20,000 molecules, one for each gene. We have many more molecules of course. What we mean is that we have 20,000 different entities, each coding for a specific type of protein. If you have two molecules of a sequence in a tube, it becomes questionable whether these sequences can be thought of as genes. I would say that those sequences lose their 'genicity' or their property of being genes because they are not coding for anything in a tube. They lack the cellular machinery that makes them code for something. I would just say you have 2 nucleotide sequences of the gene BCL2 but not that you have 2 copies of the gene BCL2. It's maybe just a personal difference I see though.


DNA replication: How many DNA polymerase molecules work in parallel?

In the (beautifully rendered) video you linked to, the green molecules are DNA polymerases. So you can already see that there are more than two DNA polymerases at work!

At each replication fork, there is generally one DNA polymerase working on the leading strand, but on the lagging strand, multiple DNA polymerases may be working at the same time (as depicted in the video). Note that different types of polymerase are thought to be primarily responsible for the leading (Pol ε) and lagging (Pol δ) strands in eukaryotes (but not prokaryotes, which use Pol III for both).

Next, note that at every origin of replication, there are two replication forks working simultaneously, one in each direction. So that's double the number of polymerase molecules.

On top of that, a single eukaryotic cell has multiple chromosomes. Each one must have at least one origin of replication of its own, which can operate in parallel. In reality, each eukaryotic chromosome has up to thousands of origins of replication (prokaryotic chromosomes generally only have one). Human cells have on the order of 100,000 origins of replication. So depending on how many origins are active simultaneously, there are likely many thousands of polymerase molecules acting at once to replicate the DNA of a single eukaryotic cell.

You could probably do a rough estimate of the number of polymerase molecules active simultaneously by taking the average duration of S phase in your cell of interest and dividing by the genome size and the speed of polymerase.


How many transcription factors are there?

This is the Curated database of mouse and human transcription factors. And this is the paper in which they describe how they curated the database. In summary, there are 3230 putative mouse TF, 1200 of which are described in scientific papers.


That is a red breasted nuthatch.(https://www.allaboutbirds.org/guide/Red-breasted_Nuthatch/id

Include a location next time,it helps with identification.


What is this beetle and what are the strange antennae for?

From the pattern on the elytra (hard upper wings), it looks like you might have a beautiful male Polyphylla fullo. Compare your photos with the P. fullo in this illustration, or photos on the Wikipedia page.

edit to fully respond to the comments:

I suspect you're right that the antennae plates in your picture are just tightly closed up, giving a different appearance. Here's a photo I took of a related species where you can see both appearances of the antennae.

And I think that Alan Boyd is correct about the antennae being used as chemoreceptors to locate females. The wikipedia page on the Ten-Lined June Bug also mentions both of these points.


This has been attempted, with some success, though on grapheme-color synesthesia, rather than sound-color synesthesia. Beyond conditioning, there have also been somewhat successful attempts to induce synesthesia through various psychoactive drugs. In both of these cases, however, the effects are temporary and generally weaker than genuine synesthetic perceptions.

There have been no studies (to my knowledge) about which associations can be induced and which cannot. I would say that sound-color might be a difficult association to generate, simply because no one would like to site and stare at a flashing screen while listening to various sounds, and it also predicates on the patients' ability to distinguish sounds, which can vary wildly from person to person. The grapheme-color experiment had the treatment group read materials with certain letters colored, which was much easier to implement.

This raises the question of whether synesthesia can be classified as a low-level interaction between typically non-interacting parts of the brain, or if it operates on a higher cognitive level (i.e. ideathesia).

See the article for details about the grapheme-color study:

"Pseudo-Synesthesia through Reading Books with Colored Letters"


How does an antisense RNA molecule restore protein function in CF patients?

The root of the problem for a majority of cystic fibrosis patients is that they have two defective genes for a particular protein and at least one of these genes is defective because it is missing a 3-base codon for the amino acid at position 508 of the protein.

Eluforsen, also known as QR-010, is a somewhat modified 33-base RNA molecule.  The bases in it are complementary to an area centered on the codon for amino acid 508 of the normal mRNA (messenger RNA) for the protein. Since the defective mRNA is missing 3 bases in the middle of this sequence, eluforsen binds to only 30 bases of the mRNA and has an unbound loop of three bases in the middle, as suggested by the wiggle in this diagram:

[image from SEC]

Such a double-stranded stretch of mRNA is abnormal, of course, but the effect of its presence at least some of the time is to cause the mRNA to undergo repair in the duplex area in a manner which makes a break in the main strand opposite the loop and inserts RNA bases that are complementary to the three "excess" bases present in the eluforsen loop.  Since these three bases are complementary to the normal mRNA bases at that point, the effect is to transform the defective mRNA into a normal mRNA.  When the repaired mRNA is translated by a ribosome, a normal protein is produced, and some of the symptoms of the CF condition are reduced because of the presence of normal protein.

The mechanism which causes the mRNA to be repaired in this manner is not yet well understood(1).  The condition improvement from a complementary mRNA fragment was noted back in 2004.(2)  One hypothesis is that RNAse H is involved in the repair.(1)  Some further information about QR‐010 effects can be found towards the end of reference (3).

(1) Matos & Matos, 2018

(2) Zamecnik et al., 2004

(3) Alton et al., 2016


Do any nonhuman species have effective ebola immunity?

While at least some other primates are suspectible to Ebola, pigs appear to be immune. From the WHO factsheet on Ebola (1):

  Although non-human primates have been a source of infection for
  humans, they are not thought to be the reservoir but rather an
  accidental host like human beings. Since 1994, Ebola outbreaks from
  the EBOV and TAFV species have been observed in chimpanzees and
  gorillas.

  RESTV has caused severe EVD outbreaks in macaque monkeys (Macaca
  fascicularis) farmed in Philippines and detected in monkeys imported
  into the USA in 1989, 1990 and 1996, and in monkeys imported to Italy
  from Philippines in 1992.

  Since 2008, RESTV viruses have been detected during several outbreaks
  of a deadly disease in pigs in People’s Republic of China and
  Philippines. Asymptomatic infection in pigs has been reported and
  experimental inoculations have shown that RESTV cannot cause disease
  in pigs.


Textbook/lab manual for mammalian cell culture

Culture of Animal Cells: A Manual of Basic Technique and Specialized Applications by Ian Freshney is the most popular book on the topic of animal cell culture.

You can also refer to ATCC animal cell culture guide which also has information about media formulations.


The escaping light causes unnecessary illumination, thus reducing the contrast.
This webpage has a couple of photos that demonstrate different microscope setups.


Does culling badgers restrict the spread of bovine tuberculosis?

This is apparently a debate since decades in the UK. As to the pathology:

  Eurasian badgers (Meles meles) are an important wildlife reservoir of
  tuberculosis (Mycobacterium bovis) infection in Ireland and the United
  Kingdom. As part of national programmes to control tuberculosis in
  livestock, considerable effort has been devoted to studying the
  disease in badgers and this has lead to a rapid increase in our
  knowledge of tuberculosis in this host.

L. A. Corner, D. Murphy, E. Gormley: Mycobacterium bovis infection in the Eurasian badger (Meles meles): the disease, pathogenesis, epidemiology and control.'' In: ''Journal of comparative pathology. 144, 1, January 2011, 1–24. doi:10.1016/j.jcpa.2010.10.003. PMID 21131004. (Review).

A summary of the pre-1997 debates is here:
http://archive.defra.gov.uk/foodfarm/farmanimal/diseases/atoz/tb/publications/krebs.htm

The up-to-date DEFRA informations are at:
http://www.defra.gov.uk/animal-diseases/a-z/bovine-tb/

For an alternative approach see:
http://www.ncbi.nlm.nih.gov/pubmed/19846226 (in short: educate them not to piss everywhere)

I have been asked to give also a summary. Tuberculosis is probably one of the nastiest bacterial infections in existence. It is a prototype of those diseases which are called latent: you can be infected for decades without symptoms, but when your immune system falters (or you have to take immune suppressants) it breaks out and kills you. One third of the human population has such a latent infection with Mycobacterium tuberculosis, and the HIV wave plus the high mycobacterial mutation rate with following extreme resistances make for interesting epidemiology. But this is also a result of our lifestyle, depending on huge cattle herds, as cattle can be cross-infected with human TB. In the west we have succeded to cut human infections by controlling cattle infection with human TB. Still, cattle can get bovine TB, and this may be economically disastrous. One of the pools of the infection is the badger population which can get bovine TB too and spread bacteria with their urine. It is unclear if protozoa may be an even more important pool. It is likewise unclear if culling of badgers would be successful for cattle TB control; the government bases its decision on a long-term study of regions where culling has happened. Alternative approaches include vaccination (which only affects uninfected animals), different cattle grazing regimes, habitat manipulations and badger latrine management. Physical exclusion of badgers from farm buildings is suggested as the simplest, and potentially most effective, method of reducing contact and opportunities for disease transmission between badgers and cattle. The government expert opinion clearly concluded that without such additional measures, culling won't be successful in reducing cattle TB.


How do animals contain and dispose of bacterial endotoxins (lipopolysaccharides)?

There are too many questions embeded here to cover in a single answer. I'll summarize and answer what I interpret to be the "central" question.

How do animals A) locate, B) isolate, and C) contain/eliminate bacterial endotoxins?

LPS in the blood stream is rapidly bound by LPS-binding protein (LBP) and localized to the liver for detoxification and excretion (1).
A) LBP recognizes and binds the Lipid-A region of the LPS molecule (2),
B) At this point LPS is released from bacterial cell membrane and sequestered into complexes with high-density lipoprotein (HDL). This is also the stage at which free LPS can activate CD14+ monocytes, triggering an acute inflammation response (3). However, additional HDL reduces monocyte activation, suggesting that these complexes inactivate LPS by "isolating" it from CD14 (4).
C) Finally, the LPS-HDL complex is taken up by the liver, either into Kupffer Cells (~25%) or liver sinusoidal endothelial cells (~75%), where enzymatic inactivation of LPS occurs either by dephosphorylation of the phosphates or deacetylation of the primary acyl components of lipid A (5)
Given the hydrophobic characteristics of LPS lipid-A and the fact that it's processed in the liver, I suspect that LPS and its metabolites are eliminated from the body via excretion into the bile ducts, but I haven't found a reference in the literature to confirm that suspicion.
References:

Wassenaar and Zimmermann, Eur J Microbiol Immunol. 2018 Sep 28; 8(3): 63–69.
Tobias et al., J Biol Chem. 1989 Jun 25;264(18):10867-71.
Vesy et al., Infect Immun. 2000 May; 68(5): 2410–2417.
Flegel et al, Infect Immun. 1989 Jul; 57(7): 2237–2245.
Yao et al. J Immunol. 2016 Sep 15; 197(6): 2390–2399.


By what mechanism does penicillin resistance usually develop in Streptococcus pneumoniae?

I think your guess is quite spot-on. According to this scientific article I found online, They did a whole genome sequencing on penicillin-resistant Streptococcus pneumoniae and their conclusion was

  ....is mediated by a mosaic of genes encoding altered
  penicillin-binding proteins (PBPs). Nonetheless, S. pneumoniae has
  also developed non-PBP mechanisms implicated in penicillin resistance.

In clinical medical laboratory point of view, S. pneumoniae's AST is done with oxacillin instead of Penicillin because OXA gives better cut-off between Susceptible, Intermediate and Resistance. You may see a big zone of inhibition when you used PEN disk but that doesn't mean the isolate is susceptible to PEN. This may suggests that "hydrolysis of the antibiotic by a beta-lactamase" is less likely to be the main mechanism?


Why is facial symmetry of the opposite sex attractive?

Facial symmetry is currently believed the be a sign of developmental stability and good health and thus good genes.  More precisely a sign of genetic diversity in a potential partner.


Is there any evidence for sperm parameters being connected to fitness of the offspring produced by that sperm?

The only way that natural selection can act on genes is when they're expressed, there's no mechanism for reading and assessing the "quality" of a gene in a sperm. Obviously the genes that effect the quality of the sperm will be selected for/against.


Molecules responsible for reading amino acid language

Clarifying the premise

As mentioned in my comment, the term “amino acid language” doesn’t really make sense as far as I’m concerned. Worse: nothing, to my knowledge, is ever reading an amino acid sequence in living systems.

Yet here we are. The term “amino acid language” itself is definitely used (though, once again, I’ve never heard of anything “reading” this language).

So, to answer the question, let’s define a meaning for the term “amino acid language”:

  The amino acid language is a language written by amino acids. In other words, a set of sequences consisting of amino acids.

The candidates

Now, your question is multiple choice so it’s sufficient to go through all possible choices and see if they fit:

  RNA polymerase enzyme

RNA polymerase reads either DNA (DNA-dependent RNA polymerase) or RNA (RNA-dependent RNA polymerase) and produces RNA. There are no amino acids involved. This is clearly not the right answer.

  mRNA

mRNA is an information-carrying molecule. But it does not “read” anything (at least not in its canonical function). Note that other RNAs are involved in recognising/reading things, but not mRNA. So, not the answer.

  tRNA

tRNAs (transfer RNAs) are RNAs that carry individual amino acids. Each individual tRNA recognises a codon on an mRNA via complementary base pairing and thus “translates” the codon into a specific amino acid by the rules of the genetic code. In the context of this question, it’s fair to say that tRNAs (in combination with other molecules) are writing the amino acid language.

  DNA

DNA, like mRNA, is an information-carrying molecule that does not read anything. Moving on.

The answer

tRNAs do not read amino acids in the conventional meaning of the phrase. But it’s the closest candidate here: not only does it indeed read a language, it translates symbols into amino acids. This is therefore almost certainly the expected answer, unless an acceptable answer is “none of the above”.


In the context of this book, dAT joining is a method used in molecular cloning to join two DNA molecules. Basically, terminal transferase is used to add polyA or polyT to the 3' ends of each DNA molecule. This creates cohesive ends which can anneal and then be ligated together, giving a covalently closed circular DNA molecule.

Image from: Jackson DA, Symons RH, Berg P. 1972. Biochemical Method for Inserting New Genetic Information into DNA of Simian Virus 40: Circular SV40 DNA Molecules Containing Lambda Phage Genes and the Galactose Operon of Escherichia coli. Proc Nat Acad Sci USA 69(10):2904-2909.

See also: Lobban PE, Kaiser AD. 1973. Enzymatic end-to-end joining of DNA molecules. J Mol Bio 78(3):453-460.

dAT joining can also refer to an assay of DNA ligase activity. Linear dAT oligomers are incubated with the ligase, which can circularize them and make them resistant to exonuclease digestion. This resistance to digestion correlates with DNA ligase activity.

Modrich P, Lehman IR. 1970. Enzymatic Joining of Polynucleotides. J Biol Chem 245(14):3626-3631.


Why are P and T waves curved and not straight (ECG)

P wave represents atrial depolarization (hence atrial contraction).

Atrial depolarization takes only a split second, therefore its corresponding wave will be smooth and rounded.

Variations from this shape could be consequences of various heart diseases: for example,a spiked P wave is called P pulmonale and suggests right atrial enlargement.

T wave represents ventricular repolarization: a normal T wave looks like an

  upright low amplitude broad hump following the QRS complex.

Abnormalities in T wave could be the signs for multiple heart diseases, varying from myocardial ischemia to hyperkalemia.

In particular, peaked T waves suggest an hyperkalemia diagnosis.

T wave abnormalities are well documented here

The QRS complex corresponds to ventricular depolarization, which is faster and more intense than atrial or ventricular repolarization: hence a normal QRS complex is peaked.

In conclusion, P wave and T wave are rounded because these correspond to low-intensity electrical events while the QRS complex is provoked by an intense electrical event.


You should check out Howald C, et al[1].  This is one of the many recent papers tied to the ENCODE data. They've used RT-PCR to amplify exon-exon junctions and then sequenced the results. Supplemental table 2 shows 3076 validated exon-exon junctions in putative processed transcripts which, in the main body of the paper may be sub-classified as:

  Non-coding, 3prime_overlapping_ncrna, Ambiguous_orf, Antisense,
  LincRNA, ncRNA_host, Retained_intron, Sense_intronic,
  Sense_overlapping, Processed transcript.

Howald C, Tanzer A, Chrast J, Kokocinski F, Derrien T, Walters N, Gonzalez JM, Frankish A, Aken BL, Hourlier T, Vogel JH, White S, Searle S, Harrow J, Hubbard TJ, Guigó R, Reymond A. 2012. Combining RT-PCR-seq and RNA-seq to catalog all genic elements encoded in the human genome. Genome Research, 22: 1698–1710, doi:10.1101/gr.134478.111.


The same reason some plants are poisonous: to stop animals from eating them.

The visible part of the fungus is called, rather misleadingly, the fruiting body. It exists to produce and spread spores and thus produce the next fungal generation. Getting eaten, rather obviously, inhibits its ability to do this. Being poisonous discourages animals from eating the fruiting body and thus permits it to complete its life cycle.


gene mutation occurs on two strands of DNA or just one strand?

A "mutation" is a permanent alteration of the genetic composition of an individual. To obey this definition, a base change in one strand must be accompanied by a corresponding change in the opposite strand. Only in this way a mutation can be transmitted to the offspring.
The situation where only one of the strands has undergone a base change constitutes a pre-mutational DNA damage, as the double strand will show a deformation at that site. The enzymes of DNA repair mechanisms recognize and correct many such "deformations", but sometimes they do not know which was the original base, and introduce a change that become fixed in the DNA sequence.


The J. Craig Venter Institute recently has indeed created a synthetic, self-replicating cell (see the press release). So it's definitely not impossible to create completely synthetic cells for use in synthetic biology, but that doesn't mean it makes much sense to do so. E. coli in particular have been used as bench tools for decades: lots of protocols exist for using them in the lab, their genome has been extensively sequenced and is well studied, and they're cheap. I'm not a bench biologist anymore, but I'm guessing these are the reasons they stripped living bacteria and replaced their DNA rather than trying to build a completely synthetic microbe from scratch.


Why do we get bored of certain food items after repeatedly eating them?

Humans inadvertently try to balance neophilia and neophobia - fancy names for preferring the new and fearing the new. With regards to food, most humans, and animals, take an overall stance of cautious curiosity. Curiosity as in discovering a new edible food that helps them survive and thrive, and caution as in any new food item may cause harm. Certain individuals will have less curiosity, being content with just eating a few foods, while others will seek new experiences when they can. That's part of the variety in humanity.

For example, people from the Eastern countries rarely ever get bored of certain foods, as they are a primary source of fuel, such as rice or noodles. Or like people from western countries, many of them eat bacon, eggs, and toast every morning for sixty years. They eat it repeatedly, almost everyday, yet they continue to do so without complaining of boredom.

The scientific explanation is just that the brain will get tired of the same thing. That's why do many fast foods are engineered so carefully tantalize (bliss factor) and yet not go over the point when the brain gets overloaded. This phenomenon doesn't really count as a factor of boredom, rather more like insensitive to repeated exposure. It's like when you are exposed to a strong smell (e.g. Perfume) for a longtime. The brain, neurotransmitters and olfactory receptors just ignores it and doesn't register it. It is suggested why we females keep putting more and more layers of perfume on, we just don't smell it anymore .

Hope that helps <3.


How is trangender female different from normal female biologically?

Remi gives a good introduction to the various terms and definitions you should know when learning about gender identity. However, he didn't really address your basic question:

  What is biological difference between transgender and a normal male/female[?]

Except for some likely genetic differences, which we aren't even close to beginning to understand, there is no biological difference between two persons born with $XX$ sex chromosomes, one of whom identifies as female (cis-gender) and one of whom identifies as male, or somewhere on the spectrum between female and male (trans-gender). There is no difference physically - both have the same organs, including sex organs, and both have the same secondary sex characteristics. One cannot tell the difference upon gross physical examination, X-ray, blood test, etc. Gender is a social construction, and while the majority of people in the West have a gender identity that matches their biological sex, some do not, for reasons that are not yet clear.


How does the "heat vision" of some snakes work?

Vipers, pythons and boas have holes on their faces called pit organs (Moon, 2011), which contain a membrane that can detect infrared radiation from warm bodies up to one meter away (Fig. 1). At night, the pit organs allow snakes to sense an image of their predator or prey (Source: Nature).

Fig. 1. Pit organs in python (top) and viper (bottom) as indicated by arrows. Source: Wikipedia

Nerve cells in the pit organ contain an ion channel called TRPA1, which detects infrared radiation as heat. The pit organ is part of the snake's somatosensory system, which detects touch, temperature and pain. It does not receive signals from the eyes. Hence, snakes sense infrared by detecting heat, not photons of light. Infrared radiation heats up the pit membrane tissue, and TRPA1 channels open when a threshold temperature is reached, allowing ions to flow into the nerve cells and triggering an electrical signal (Gracheva et al., 2010). Rattlesnake TRPA1 is activated by temperatures higher than about 28 °C — roughly the temperature a snake would 'feel' from a mouse or a squirrel about a meter away (Source: Nature).

Hence, this organ works best in cold environments where temperatures are low so that warmblooded prey stands out. Further, warmblooded animals won't be able to use this organ, as the pit would be ~37oC and not be able to detect anything below that temperature.

References
- Gracheva et al., Nature (2010); 464: 1006-11
- Moon, Anat Cell Biol (2011); 44(1): 8–13


What are "+" and "Ar" in consensus binding sequence of amino acids?

Ar means aromatic and + means positively charged residues. However, this is not a standard code (as of now).

From the same paper:

  Sequences closely matching these optimal binding motifs, R-X-[Ar/S]-[+]-pS-[LEAM]-P and R-[S/Ar]-[+]-pS-[LEAM]-P, denoted as mode 1 and mode 2 consensus sequences, were found to be present in many known 14-3-3 ligands ( Yaffe et al. 1997), where Ar denotes aromatic residues and + denotes basic residues.


There is an interesting relationship between the length of an animals femur, the thickness and the mass of the thickness. A point that should be taken into account is that bones can different densities and so might be able to support varying amounts. The muscle in you leg also does nothing for the support of you weight it is (basically) all in the bone. Really looking purely at the leg won't tell you much you need to strip back the tissue and get you measurements straight from that. Given the different gate strategies of various animals this can lead to differing levels of muscle surrounding the leg and could be confounding your answer.

Walter Lewin a professor of physics at MIT did a lecture series where in the first lecture he went off on one about the relative sizes and thickness of animal femurs and it is really interesting (http://www.youtube.com/watch?v=PmJV8CHIqFc - between 11 minutes and 22 minutes). The short answer was that the ratio between the thickness and the length stays similar relative to the length.


Iris curvature seems to be dependent on the state and health of the eyes.

See Prevention of blinking alters iris configuration in pigment dispersion syndrome and in normal eyes :

  Initial iris configuration was concave in all eyes with pigment dispersion syndrome, whereas in control eyes it was concave in four eyes, planar in four eyes, and convex in two eyes.

Other resources :

Accommodation-induced changes in iris curvature

Ultrasound biomicroscopic analysis of iris profile changes with accommodation in pigmentary glaucoma and relationship to age

Quantification of Iris Concavity


I'm pretty sure that's an Achelousaurus.

Two curved horns on top, plus hump on nose:
Front view:

Side view: (for nose)


Wild connection by Jennifer Verdolin is good, but it really depends on what you are looking for is there a specific area you are trying to learn about?

The Third chimpanzee might interest you, it compares human behavior to the other chimpanzee species, sex is only a small part but it it=s there.

I a can warn you against a book I used ot like,sperm wars by Baker, A lot of the research is his own and there have been a lot of issues with people being unable to replicate many of them, so a lot of it untrustworthy which is a shame becasue I really liked his writing style.


Starting of with the basics, reactions are the breaking of bonds in the reactants and the forming of bonds in the products.

To answer your questions about water, there is not always H2O present, although most of the times there is water. You are referring to the hydrolysis and dehydration synthesis reactions, in which water is added or removed, to break down and combine molecules, respectively.

Catabolic reactions are more defined as the net release of energy in the reaction. They break down bigger molecules to smaller molecules. There is a need for energy input to begin the reaction and break the bonds of the reactants, however, the release of energy when the bonds of the products form are far greater, resulting in a net release of energy.

Anabolic reactions are essentially the opposite, where smaller molecules are combined and built up to larger macromolecules, many times with the removal of H2O. This results in a net decrease in free energy, as energy is absorbed/stored in the larger molecule. Energy inputted to break bonds of the reactants are far greater than the small energy released as bonds form.

As you will learn soon, these reactions can be characterized by exergonic/exothermic, and endergonic/endothermic reactions. They can be considered synonymous in many cases.


If everybody DNA is different then how blood can match even with matching blood group?

A few components to my answer.

Red blood cells do not contain a nucleus, therefore, they do not harbour DNA.
The major determinant of blood compatibility is the blood antigen. There are only 4 types: O, A, B, AB. This is genetically encoded, and is expressed as a set of sugar coats on the blood cell membrane. However, the enzymes that encode for A or B should be identical from person to person.

I hope this gives you a preliminary answer to work off.


There is a mechanism in T and B cells called allelic exclusion. This means that most of the times only a single allele is used by building the light chain and the other is excluded. Incomplete allelic exclusion may contribute to auto-immune diseases, because cells using two different light chains can potentially recognize both pathogens and healthy human cells1,2,3,4,5,6,7,8.


What is the purpose of segments in citrus fruit?

The citrus fruits belongs to the type hesperidium, which is a highly specialised form of berry specific to citrus fruit.The hesperidium is derived entirely from the ovary, other features of hesperidium includes leathery exocarp, spongy mesocarp and juice filled endocarp.

A hesperidium has an aromatic, leathery exocarp (the "rind") and mesocarp and endocarp compartmentalized into sections (each representing a carpel), each of which contains one to several seeds. This type of berry is unique to the genus Citrus, which produces fruits such as oranges, grapefruit, lemons, limes and tangerines.
Reference

The edible flesh of a mature citrus fruit is divided into segments, each derived from an ovary locule.The number of segments varies widely but is typically between 10-15.Each segment is surrounded by tough endocarp membrane and filled with tightly packed juice sacks or vesticles.
Reference

There are several major ways that plants have evolved for constructing
fleshy fruits.  Oranges etc. belong to the family Rutaceae, which is
unique in filling its "locules" (the spaces in which seeds are produced)
with "juice sacs" that are attached to the outer walls.  Each of the
locules probably represents a structure, known as a "carpel" that was
at one time distinct, but now has fused together with its neighbors.
The outer skin of most citrus fruits shows no sign that the interior
is sectioned, but this is a result of the fusion occurring early in
the development of each individual fruit (rather than early in the
evolution of the Rutaceae).
Reference

Segmentation inside the citric fruits are due to its development from the ovary, as each of the segment is evolved from the ovary locule, the number of segments varies according to species(also there are variations in single species). The evolutionary advantage of segmentation inside the fruit is a debated topic.A digestible theory is that, each segment of the fruit contains 1-3(in the case of orange) seeds, due to the evolution by mammalian resources, keeping segments inside the fruits helps in the dispersal of seeds by different agents. When a ripe fruit falls down, its individual segments are broken apart and eaten by different animals/birds, this in turn helps in dispersal of seeds to geographically distinct(distant) locations. With each segments featuring seeds inside them, its a good adaptation to produce a single fruit which can be distributed by different agents.


By the picture and the official distribution it looks to be as you said a Lacerta viridis.

Some references and distribution here:

https://www.iucnredlist.org/species/61530/12507156
https://commons.wikimedia.org/wiki/Lacerta_viridis
http://reptile-database.reptarium.cz/species?genus=Lacerta&species=viridis

In Western Europe we have a brother specie Lacerta bilineata.

Example in Geneva:

The distribution maps shows that Lacerta viridis is mainly present in Easter Europe (including Hungary) and Lacerta bilineata is present in the Western Europe.

Both species are similar and the male get the throat blue generally during the breeding season.

This site have also a description of the specie.